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1
Calles-Enríquez, Marina, Benjamin Hjort Eriksen, Pia Skov Andersen, Fergal P. Rattray, Annette H. Johansen, María Fernández, Victor Ladero, and Miguel A. Alvarez. "Sequencing and Transcriptional Analysis of the Streptococcus thermophilus Histamine Biosynthesis Gene Cluster: Factors That Affect Differential hdcA Expression." Applied and Environmental Microbiology 76, no. 18 (July 23, 2010): 6231–38. http://dx.doi.org/10.1128/aem.00827-10.
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ABSTRACT Histamine, a toxic compound that is formed by the decarboxylation of histidine through the action of microbial decarboxylases, can accumulate in fermented food products. From a total of 69 Streptococcus thermophilus strains screened, two strains, CHCC1524 and CHCC6483, showed the capacity to produce histamine. The hdc clusters of S. thermophilus CHCC1524 and CHCC6483 were sequenced, and the factors that affect histamine biosynthesis and histidine-decarboxylating gene (hdcA) expression were studied. The hdc cluster began with the hdcA gene, was followed by a transporter (hdcP), and ended with the hdcB gene, which is of unknown function. The three genes were orientated in the same direction. The genetic organization of the hdc cluster showed a unique organization among the lactic acid bacterial group and resembled those of Staphylococcus and Clostridium species, thus indicating possible acquisition through a horizontal transfer mechanism. Transcriptional analysis of the hdc cluster revealed the existence of a polycistronic mRNA covering the three genes. The histidine-decarboxylating gene (hdcA) of S. thermophilus demonstrated maximum expression during the stationary growth phase, with high expression levels correlated with high histamine levels. Limited expression was evident during the lag and exponential growth phases. Low-temperature (4°C) incubation of milk inoculated with a histamine-producing strain showed lower levels of histamine than did inoculated milk kept at 42°C. This reduction was attributed to a reduction in the activity of the HdcA enzyme itself rather than a reduction in gene expression or the presence of a lower cell number.
2
Han, Bing, Wen Bo Zhao, Xian Ye Qin, Yan Hong Li, and Wei Wei. "Catalytic Methoxycarbonylation of 1,6-Hexamethylenediamine with Methyl Carbamate to Dimethylhexane-1,6-Dicarbamate." Advanced Materials Research 634-638 (January 2013): 490–93. http://dx.doi.org/10.4028/www.scientific.net/amr.634-638.490.
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A series of metal oxides were employed as catalysts for the synthesis of dimethylhexane -1,6-dicarbamate(HDC) from 1,6-hexamethylenediamine(HDA) and methyl carbonate(MC). Lead dioxide showed excellent catalytic activity, 100% HDA conversion and 93% HDC yield could be achieved at 463K for 6h. The effects of reaction temperature, reaction time and catalyst amount on the yield of HDC were investigated in details.
3
Martin, S. A. M., and Crahame Bulfield. "Genetic analysis of a new haplotype of the histidine decarboxylase gene complex in C57BL/6 mice." Genetical Research 47, no. 2 (April 1986): 131–34. http://dx.doi.org/10.1017/s0016672300022965.
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SUMMARYThe histidine decarboxylase (HDC) gene complex, [Hdc], comprises the structural gene for mouse kidney HDC and closely linked regulatory elements which determine enzyme concentration and its response to hormones. One of these regulatory elements, Hdc-e, determines the response (induction or repression) of kidney HDC to oestrogen. HDC is oestrogen-inducible in C57BL/10 and oestrogen-repressible in DBA/2 and C57BL/6; alleles of Hdc-e segregate in crosses between C57BL/10 and DBA/2 and between the C57BL substrains. Two different haplotypes of[Hdc] have been defined previously, B.10 (Hdc-sb, Hdc-cb, Hdc-eb) in C57BL/10 and D (Hdc-sa, Hdc-cd, Hdc-ed) in DBA/2. C57BL/6 represents a third haplotype (B.6) (Hdc-sb, Hdc-cb, Hdc-ed) which differs from both B.10 and D. Hdc-e may therefore be a component of the complex independent of Hdc-s and Hdc-c.
4
Ohning, Gordon V., Min Song, Helen C. Wong, S. Vincent Wu, and John H. Walsh. "Immunolocalization of gastrin-dependent histidine decarboxylase activity in rat gastric mucosa during feeding." American Journal of Physiology-Gastrointestinal and Liver Physiology 275, no. 4 (October 1, 1998): G660—G667. http://dx.doi.org/10.1152/ajpgi.1998.275.4.g660.
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The localization of histidine decarboxylase (HDC) activity in the enterochromaffin-like (ECL) cells of the oxyntic mucosa was studied during fasting and refeeding using monoclonal (CURE no. 44178) and polyclonal (CURE no. 94211) antibodies directed against the COOH terminus of HDC (HDC-CT). Changes in HDC immunostaining were correlated with mucosal HDC enzyme activity. Immunoneutralization of circulating gastrin and atropine treatment during refeeding were used to determine the relative importance of gastrin and cholinergic mechanisms in the regulation of HDC activity and immunostaining. Fasting caused a rapid reduction in the number of ECL cells immunostaining for HDC that was correlated with an almost complete loss of mucosal HDC enzyme activity. Refeeding restored both HDC immunostaining and enzyme activity within 2–4 h, and this response was inhibited by gastrin immunoneutralization but not by atropine treatment. Immunostaining was uniformly decreased and restored in the lower half of the oxyntic mucosa, which corresponds to the predominant area of ECL cells in the gastric gland. Histamine immunostaining and mucosal histamine content were not significantly changed during fasting and refeeding or by gastrin antibody and/or atropine treatment during refeeding. These findings indicate that HDC activity correlates with HDC-CT immunostaining and that both HDC activity and HDC-CT immunostaining are regulated by gastrin during refeeding.
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Colucci, Rocchina, John V. Fleming, Ramnik Xavier, and Timothy C. Wang. "l-Histidine decarboxylase decreases its own transcription through downregulation of ERK activity." American Journal of Physiology-Gastrointestinal and Liver Physiology 281, no. 4 (October 1, 2001): G1081—G1091. http://dx.doi.org/10.1152/ajpgi.2001.281.4.g1081.
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A poorly defined negative feedback loop decreases transcription of thel-histidine decarboxylase (HDC) gene. To help understand this regulation, we have studied the effect of HDC protein expression on HDC gene transcription in transfected AGS-B cells. Expression of the rat HDC protein inhibited HDC promoter activity in a dose-dependent fashion. The region of the HDC promoter mediating this inhibitory effect corresponded to a previously defined gastrin and extracellular signal-related kinase (ERK)-1 response element. Overexpression of the HDC protein reduced nuclear factor binding in this region. Experiments employing specific histamine receptor agonists indicated that the inhibitory effect was not dependent on histamine production, and studies with the HDC inhibitor α-fluoromethylhistidine revealed that inhibition was unrelated to enzyme activity. Instead, an enzymatically inactive region at the amino terminal of the HDC enzyme (residues 1–271) was shown to mediate inhibition. Fluorescent chimeras containing this domain were not targeted to the nucleus, arguing against specific inhibition of the HDC transcription machinery. Instead, we found that overexpression of HDC protein decreased ERK protein levels and ERK activity and that the inhibitory effect of HDC protein could be overcome by overexpression of ERK1. These data suggest a novel feedback-inhibitory role for amino terminal sequences of the HDC protein.
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Graf, Allyson, Fanyin Meng, Laura Hargrove, Lindsey Kennedy, Yuyan Han, Taylor Francis, Kyle Hodges, et al. "Knockout of histidine decarboxylase decreases bile duct ligation-induced biliary hyperplasia via downregulation of the histidine decarboxylase/VEGF axis through PKA-ERK1/2 signaling." American Journal of Physiology-Gastrointestinal and Liver Physiology 307, no. 8 (October 15, 2014): G813—G823. http://dx.doi.org/10.1152/ajpgi.00188.2014.
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Histidine is converted to histamine by histidine decarboxylase (HDC). We have shown that cholangiocytes 1) express HDC, 2) secrete histamine, and 3) proliferate after histamine treatment via ERK1/2 signaling. In bile duct-ligated (BDL) rodents, there is enhanced biliary hyperplasia, HDC expression, and histamine secretion. This studied aimed to demonstrate that knockdown of HDC inhibits biliary proliferation via downregulation of PKA/ERK1/2 signaling. HDC−/− mice and matching wild-type (WT) were subjected to sham or BDL. After 1 wk, serum, liver blocks, and cholangiocytes were collected. Immunohistochemistry was performed for 1) hematoxylin and eosin, 2) intrahepatic bile duct mass (IBDM) by cytokeratin-19, and 3) HDC biliary expression. We measured serum and cholangiocyte histamine levels by enzyme immunoassay. In total liver or cholangiocytes, we studied: 1) HDC and VEGF/HIF-1α expression and 2) PCNA and PKA/ERK1/2 protein expression. In vitro, cholangiocytes were stably transfected with shRNA-HDC plasmids (or control). After transfection we evaluated pPKA, pERK1/2, and cholangiocyte proliferation by immunoblots and MTT assay. In BDL HDC−/− mice, there was decreased IBDM, PCNA, VEGF, and HDC expression compared with BDL WT mice. Histamine levels were decreased in BDL HDC−/−. BDL HDC−/− livers were void of necrosis and inflammation compared with BDL WT. PKA/ERK1/2 protein expression (increased in WT BDL) was lower in BDL HDC−/− cholangiocytes. In vitro, knockdown of HDC decreased proliferation and protein expression of PKA/ERK1/2 compared with control. In conclusion, loss of HDC decreases BDL-induced biliary mass and VEGF/HIF-1α expression via PKA/ERK1/2 signaling. Our data suggest that HDC is a key regulator of biliary proliferation.
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Middleton, Richard J., Kathleen Williamson, and Grahame Bulfield. "A new allele of the testosterone-responsive gene, Hdc-a, in the histidine decarboxylase gene complex of the mouse." Genetical Research 50, no. 3 (December 1987): 213–17. http://dx.doi.org/10.1017/s0016672300023727.
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SummaryIn C57BL/10 and the majority of other strains of mice, females have about 20-fold higher kidney histidine decarboxylase levels than males; in DBA/2 mice, however, HDC in females is only 3- to 4-fold higher than males. The low ratio HDC phenotype of DBA/2 animals is due to decreased sensitivity of the HDC gene complex to repression by testosterone in males. From conventional crosses and by the use of the BXD recombinant inbred lines we conclude that the C57BL/ 10: DBA/2 difference, in testosterone sensitivity of HDC, is due to an allelic difference in the regulatory gene Hdc-a of the HDC gene complex, [Hdc], on chromosome 2; DBA/2 contains a third allele of this gene, Hdc-ad.
8
Sandvik, A. K., R. Dimaline, R. Marvik, E. Brenna, and H. L. Waldum. "Gastrin regulates histidine decarboxylase activity and mRNA abundance in rat oxyntic mucosa." American Journal of Physiology-Gastrointestinal and Liver Physiology 267, no. 2 (August 1, 1994): G254—G258. http://dx.doi.org/10.1152/ajpgi.1994.267.2.g254.
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Gastrin release histamine from the oxyntic mucosa, stimulates the enzymatic activity of histidine decarboxylase (HDC), increases HDC mRNA abundance, and has a trophic effect on the enterochromaffin-like (ECL) cell. In the present study, we examined the effect of exogenous gastrin on HDC activity and mRNA and the time scale of increase and decline of HDC activity and mRNA. Rats received intravenous infusion of gastrin-(1-17) in different doses or periods of time. Oxyntic mucosal HDC activity and mRNA abundance increased significantly with serum gastrin concentrations in the physiological range. The onset of response was rapid and maximal for both parameters after 2 h. Poststimulatory decrease was maximal 2 h after cessation of gastrin infusion. Those observations suggest that HDC enzymatic activity and mRNA abundance are important in meal-to-meal regulation of gastric secretion. Furthermore, HDC enzymatic activity and mRNA abundance varied in parallel, indicating that HDC mRNA abundance is important in the overall regulation of gastric mucosal HDC activity.
9
Middleton, Richard J., S. A. M. Martin, and Grahame Bulfield. "A new regulatory gene in the histidine decarboxylase gene complex determines the responsiveness of the mouse kidney enzyme to testosterone." Genetical Research 49, no. 1 (February 1987): 61–67. http://dx.doi.org/10.1017/s0016672300026744.
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SummaryThe level of histidine decarboxylase in mouse kidney normally differs between the sexes with females higher than males. In a strain derived from feral Danish mice (DAN), however, both males and females have the same, high, HDC activity due to the males being insensitive to repression by testosterone. Genetic analysis indicates that this insensitivity is caused by a variant allele of a new gene in the histidine decarboxylase gene complex, Hdc-a; the Hdc-ab allele in C57BL/10 confers high sensitivity to testosterone whereas the Hdc-aw allele in the DAN strain confers low sensitivity. In addition, the DAN strain has a novel haplotype for the other three known elements of [Hdc]: the allele Hdc-sd of the structural gene, the Hdc-cd allele of the gene determining enzyme concentration, and the oestrogen-inducible allele Hdc-eb.
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Labaki, Chris, Sarah Abou Alaiwi, Andrew Lachlan Schmidt, Talal El Zarif, Ziad Bakouny, Pier Vitale Nuzzo, Wenxin Xu, David A. Braun, Bradley Alexander McGregor, and Toni K. Choueiri. "Effect of high-dose corticosteroid use on efficacy of immune checkpoint inhibitors in patients with renal cell carcinoma (RCC)." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): 4583. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.4583.
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4583 Background: The use of High-Dose Corticosteroids (HDC) has been linked to poor outcomes in patients with lung cancer treated with immune checkpoint inhibitors (ICIs) (Ricciuti B, JCO, 2019). There is no data on the effect of HDC on renal cell carcinoma patients (RCC) treated with immunotherapy. We hypothesized that HDC use would be associated with worse outcomes in RCC patients receiving ICIs. Methods: This study evaluated a retrospective cohort of patients with RCC at Dana-Farber Cancer Institute in Boston, MA. Clinical information including demographics, IMDC risk score, RCC histology, steroid administration, ICI regimen, line of therapy, time to treatment failure (TTF) and overall survival (OS) were collected. Patients were divided into those receiving HDC (prednisone ≥10 mg or equivalent for ≥ 1 week, HDC group) or not receiving HDC (No-HDC group). HDC administration was evaluated in relation to TTF and OS in a univariate analysis (Log-rank test) and a multivariate analysis (Cox regression). Results: 190 patients with RCC receiving ICIs were included, with a median age of 59 years. HDC were administered to 56 patients and 134 patients received no (N= 116) or only low-dose (N=18) steroids. In the HDC group, 40 patients received steroids for immune-related adverse events, 8 for other cancer-related indications, and 8 for non-oncological indications. There was no difference in TTF between the HDC and No-HDC groups (12-mo TTF rate: 34.8 vs. 32.3%, respectively; log-rank p=0.65). Similarly, there was no difference in OS between the HDC and No-HDC groups (36-mo OS rate: 56.7 vs. 62.4%, respectively; log-rank p=0.97). After adjusting for IMDC risk group, RCC histology, ICI regimen type, and line of therapy, TTF and OS did not differ in the HDC group as compared to No-HDC group (HR=1.14 [95%CI: 0.80-1.62], p=0.44 and HR=1.17 [95%CI: 0.65-2.11], p=0.59, respectively). Conclusions: In this retrospective study of patients with RCC treated with ICIs, administration of high-dose corticosteroids was not associated with worse outcomes.[Table: see text]
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Ayada, Kentaro, Makoto Watanabe, and Yasuo Endo. "Elevation of histidine decarboxylase activity in skeletal muscles and stomach in mice by stress and exercise." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 6 (December 1, 2000): R2042—R2047. http://dx.doi.org/10.1152/ajpregu.2000.279.6.r2042.
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The effects of different types of stress (water bathing, cold, restraint, and prolonged walking) on histidine decarboxylase (HDC) activity in masseter, quadriceps femoris, and pectoralis superficial muscles, and in the stomach were examined in mice. All of these stresses elevated gastric HDC activity. Although water bathing, in which muscle activity was slight, was sufficiently stressful to produce gastric hemorrhage and to increase gastric HDC activity, it produced no detectable elevation of HDC activity in any of the muscles examined. The other stresses all elevated HDC activity in all three muscles. We devised two methods of restraint, one accompanied by mastication and the other not. The former elevated HDC activity in the masseter muscle, but the latter did not. These results suggest that 1) HDC activity in the stomach is an index of responses to stress, 2) the elevation of HDC activity in skeletal muscles during stress is induced partly or wholly by muscle activity and/or muscle tension, and 3) stress itself does not always induce an elevation of HDC activity in skeletal muscles.
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MORII, HIDEAKI, KENTARO KASAMA, and RAUL HERRERA-ESPINOZA. "Cloning and Sequencing of the Histidine Decarboxylase Gene from Photobacterium phosphoreum and its Functional Expression in Escherichia coli." Journal of Food Protection 69, no. 8 (August 1, 2006): 1768–76. http://dx.doi.org/10.4315/0362-028x-69.8.1768.
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The major causative agent of scombroid poisoning is histamine formed by bacterial decarboxylation of histidine. We reported previously that histamine was exclusively formed by the psychrotrophic halophilic bacteria Photobacterium phosphoreum in scombroid fish during storage at or below 10°C. Moreover, histamine-forming ability was affected by two histidine decarboxylases (HDCs): constitutive and inducible enzymes. In this study, the gene encoding P. phosphoreum HDC was cloned into Escherichia coli and sequenced. A sequence analysis of the DNA corresponding to the hdc gene revealed an open reading frame of 1,140 bp coding for a pyridoxal-5′-phosphate-dependent HDC of 380 amino acid residues with a predicted molecular mass of 42.6 kDa. The HDC amino acid sequences formed a phylogenetic clade with strong bootstrap support and revealed high sequence similarities among the P. phosphoreum isolate and species of the family Enterobacteriaceae and a separate phylogenetic branch with the lowest sequence similarity between the isolate and the taxonomically closer Listonella anguillarum. The T7 promoter was used to overexpress the hdc gene in E. coli cells. The recombinant clone, E. coli BL21(DE3), displayed significant levels of HDC activity. The recombinant hdc gene was suggested to code the inducible HDC; therefore, the optimum reaction conditions of the recombinant HDC were similar to those of the inducible HDC in the P. phosphoreum isolate. In addition, a putative catabolite-repressor protein binding site, amino acid permease gene, and histidine-tRNA synthetase gene were found in flanking regions of the hdc gene.
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Hocker, M., Z. Zhang, D. A. Fenstermacher, S. Tagerud, M. Chulak, D. Joseph, and T. C. Wang. "Rat histidine decarboxylase promoter is regulated by gastrin through a protein kinase C pathway." American Journal of Physiology-Gastrointestinal and Liver Physiology 270, no. 4 (April 1, 1996): G619—G633. http://dx.doi.org/10.1152/ajpgi.1996.270.4.g619.
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The enzyme L-histidine decarboxylase (HDC; EC 4.1.1.22), which converts L-histidine to histamine, plays a key role in the regulation of acid secretion. In the rat and human stomach, the peptide hormone gastrin appears to be one of the main regulators of HDC expression. In rats, marked elevation of gastric HDC mRNA abundance was observed within 12 h after induction of hypergastrinemia by a single injection of the proton-pump blocker omeprazole. In situ hybridization revealed that HDC expression occurred in the basal third of gastric glands where enterochromaffin-like cells are localized. To study the regulation of HDC gene transcription, 1,291 nucleotides of the 5'-flanking region of the rat HDC gene and the noncoding portion of exon 1 were cloned and sequenced. Gastrin and cholecystokinin (CCK) octapeptide equipotently stimulated the transcriptional activity of the rat HDC promoter three- to fourfold, and deletion analysis revealed the presence of a gastrin response element within 201 nucleotides upstream of the translational start site. Time-course studies revealed maximal activation of the HDC promoter after 12-36 h. Direct stimulation of protein kinase C (PKC) with the phorbol ester phorbol 12-myristate 13-acetate (PMA) substantially elevated rat HDC promoter activity, whereas induction of Ca2+ -dependent signaling pathways with thapsigargin was without effect. Downregulation or blockade of PKC abolished the effects of gastrin and PMA on the HDC promoter. These data indicate that stimulation of the CCK-B/gastrin receptor activates the rat HDC promoter in a time- and dose-dependent fashion and that this effect is primarily mediated via a PKC-dependent signaling pathway. Use of HDC as a model gene will allow further investigation of the intracellular pathways that are involved in gastrin-dependent gene regulation.
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Li, Lingling, Junping Shi, and Jialiang Kou. "Experimental Study on Mechanical Properties of High-Ductility Concrete against Combined Sulfate Attack and Dry–Wet Cycles." Materials 14, no. 14 (July 19, 2021): 4035. http://dx.doi.org/10.3390/ma14144035.
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Concrete will deteriorate and damage under sulfate attack.In order to study the degradation characteristics of HDC under sulfate attack, the mechanical properties of high-ductility concrete (HDC) were investigated using the uniaxial compressive strength test of HDC specimens soaked in different concentrations of sulfate solution and subjected to different times of dry–wet cycles. The variations in the compressive strength, loss rate of compressive strength, and the max compressive strength under the action of sulfate attack and dry–wet cycles were analyzed. The analytical expressions of damage variables were given. SEM was used to observe the microstructure of the sample, and the microdamage mechanism of the HDC was explored. The deterioration of the HDC was found to be the result of the combined action of sulfate attack and dry–wet cycles and was caused by physical attack and chemical attack. PVA prevented the rapid development of deterioration. On the basis of the change of compressive strength, the damage variable was established to quantitatively describe the degree of damage to HDC. The experimental results showed that with the increase in the number of dry–wet cycles, the compressive strength of HDC generally increased first and then decreased. As the concentration of the sulfate solution increased, the loss rate of the compressive strength of HDC generally increased and the max compressive strength gradually decreased. With the increase inthe number of dry–wet cycles, HDC first showed self-compacting characteristics and then gradually became destroyed. Compared with ordinary concrete (OC), HDC is superior to OC in sulfate resistance and dry–wet cycles. This study provided a test basis for the engineering application of HDC in sulfate attack and dry–wet cycles environment.
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Zahnow, Cynthia A., Pertti Panula, Atsushi Yamatodani, and David E. Millhorn. "Glucocorticoid hormones downregulate histidine decarboxylase mRNA and enzyme activity in rat lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 275, no. 2 (August 1, 1998): L407—L413. http://dx.doi.org/10.1152/ajplung.1998.275.2.l407.
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Histidine decarboxylase (HDC) is the primary enzyme regulating histamine biosynthesis. Histamine contributes to the pathogenesis of chronic inflammatory disorders such as asthma. Because glucocorticoids are effective in the treatment of asthma, we examined the effects of 6 h of exogenously administered dexamethasone (0.5–3,000 μg/kg ip), corticosterone (0.2–200 mg/kg ip), or endogenously elevated corticosterone (via exposure of rats to 10% oxygen) on HDC expression in the rat lung. HDC transcripts were decreased ∼73% with dexamethasone treatment, 57% with corticosterone treatment, and 50% with exposure to 10% oxygen. Likewise, HDC enzyme activity was decreased 80% by treatment with dexamethasone and corticosterone and 60% by exposure to 10% oxygen. Adrenalectomy prevented the decreases in HDC mRNA and enzyme activity observed in rats exposed to 10% oxygen, suggesting that the adrenal gland is necessary for the mediation of hypoxic effects on HDC gene expression. These results demonstrate that corticosteroids initiate a process that leads to the decrease of HDC mRNA levels and enzyme activity in rat lung.
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Ghosh, Ajoy Kumar, Noriyasu Hirasawa, Hiroshi Ohtsu, Takehiko Watanabe, and Kazuo Ohuchi. "Defective Angiogenesis in the Inflammatory Granulation Tissue in Histidine Decarboxylase–deficient Mice but not in Mast Cell–deficient Mice." Journal of Experimental Medicine 195, no. 8 (April 8, 2002): 973–82. http://dx.doi.org/10.1084/jem.20011782.
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We have analyzed the role of histamine in the angiogenesis of the granulation tissue in histidine decarboxylase–deficient (HDC−/−) mice, mast cell–deficient mice (WBB6F1-W/WV), and their corresponding wild-type mice (HDC+/+ and WBB6F1+/+). In HDC+/+ mice, subcutaneous implantation of a cotton thread in the dorsum induced granulation tissue formation with angiogenesis, while the topical injection of antivascular endothelial growth factor (VEGF) IgG strongly suppressed them. In HDC−/− mice which showed lower VEGF levels in the granulation tissue, there was notably less angiogenesis and granulation tissue formation than in HDC+/+ mice. The topical injection of histamine or the H2 agonist dimaprit rescued the defective angiogenesis and granulation tissue formation in HDC−/− mice. There was no significant difference in the granulation tissue formation and angiogenesis between WBB6F1-W/WV and WBB6F1+/+ mice. In addition, macrophages in the granulation tissue were found to express HDC. Our findings indicate that histamine derived from nonmast cells plays a significant role in the angiogenesis of the inflammatory granulation tissue.
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Weaver, T. A., and R. A. White. "headcase, an imaginal specific gene required for adult morphogenesis in Drosophila melanogaster." Development 121, no. 12 (December 1, 1995): 4149–60. http://dx.doi.org/10.1242/dev.121.12.4149.
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The majority of adult organs of a holometabolic insect like Drosophila melanogaster are derived from specific imaginal cells. These cells differ from their larval equivalents in many important cellular characteristics, ranging from the nature of the cell cycle to the timing and pattern of cellular differentiation. Here we describe the cellular, molecular and genetic characterization of a gene, headcase (hdc), which is required for imaginal cell development. hdc is the first gene to be described which is specifically expressed in all imaginal cells; this has allowed us to identify many imaginal primordia in the embryo and larval development. The Hdc protein is an extremely basic (pI 9.6) cytoplasmic protein with no obvious sequence similarities or conserved motifs. Interestingly, the spatial-temporal pattern of hdc expression prefigures imaginal cell re-entry into the mitotic cell cycle and persists until the final cell divisions. hdc null alleles have been isolated and found to cause pupal lethality, with dead pharate adults exhibiting defects in the differentiation of many adult tissues, most notably in head development. Ectopic expression of hdc, provided by a hdc-minigene, rescues the pupal lethality. Imaginal disc morphology in null mutants appears normal, therefore loss of hdc expression does not affect imaginal cell growth, but instead interferes with the ability of the imaginal primordia to differentiate properly during pupal development, suggesting that hdc may be involved in hormonal responsiveness during metamorphosis.
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Price, Katharine Andress Rowe, Ashish V. Chintakuntlawar, Robert Leonard Foote, Yolanda I. Garces, Daniel Ma, Michelle A. Neben-Wittich, Eric J. Moore, et al. "Long-term survival of adjuvant high-dose (HDC) vs weekly cisplatin (WC) for human papilloma-virus (HPV) and non-HPV head and neck squamous cell carcinoma (HNSCC)." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): 6071. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.6071.
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6071 Background: Phase III data suggests a benefit of HDC in the adjuvant setting, but the effect of HDC and WC on long term survival and for HPV+ HNSCC is unknown. Methods: Data from a published retrospective study (Geiger Oral Onc 2013) of HDC vs WC in resected HNSCC was updated. Overall survival (OS) and recurrence-free survival (RFS) was assessed by Kaplan-Meier method for all pts and by HPV status. Multivariate analyses were performed to assess impact of HPV status, smoking, age, HDC vs WC, and cumulative cisplatin dose ( < 200mg/m2 vs ≥200 mg/m2). Results: 51 patients (pts) received HDC and 53 WC. Median follow-up was 8.7 yrs (0.8-13.7). For the whole cohort, HDC had significantly improved OS over WC (p = 0.0095; 5- and 10-yr OS 84% and 80% vs 72% and 60%). No OS benefit for HDC was seen in pts with HPV+HNSCC (5- and 10-yr OS 90% and 87% for HDC and 81% and 81% for WC; p = 0.51). For HPV-negative HNSCC, OS had borderline significance with HDC vs WC (5- and 10-yr OS 73% and 68% vs 65% and 44%; p = 0.06). For the whole cohort, there was no difference in 5- and 10-yr RFS (78% and 74% for HDC vs 72% and 62% for WC; p = 0.32). When analyzed by HPV status, there was no difference in RFS with HDC or WC for either HPV+ (p = 0.43) or HPV-negative HNSCC (p = 0.97). On multivariate analyses of OS for all pts, only HPV status was significant (p = 0.0011; HR 0.27, CI 0.12-0.62). For HPV+ HNSCC, there was no significant predictor of OS. For non-HPV HNSCC, the benefit of HDC approached significance with a decreased risk of death (HR 0.38; p = 0.07). For all pts, those who received ≥200mg/m2 had significantly improved OS (5-yr 90% vs 72% and 10-yr 86% vs 61%; p = 0.004). By HPV status, cumulative dose had no significant effect on OS. Conclusions: OS is better with HDC and with cumulative dose > 200 mg/m2 in unselected patients. The benefit of cisplatin is likely higher for non-HPV HNSCC. A difference in OS with no difference in RFS suggests non cancer-related causes of death in the WC cohort. Ability to receive HDC could be a surrogate marker of comorbidity. [Table: see text]
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Peters, Geoffrey David, Robin Milne, Anne Bernard, Kate Elizabeth Roberts, Matthew C. Foote, Benedict Panizza, Sandro Virgilio Porceddu, and Jermaine Coward. "The influence of cisplatin de-escalation on survival outcomes in oropharyngeal head and neck squamous cell carcinoma (OPC)." Journal of Clinical Oncology 35, no. 15_suppl (May 20, 2017): e17551-e17551. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e17551.
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e17551 Background: Chemoradiotherapy (CRT) with 3 cycles (#) of high-dose cisplatin (HDC) (100mg/m2 weeks 1,4 & 7) and 70Gy over 7 weeks is associated with improved overall survival (OS) compared with radiotherapy (RT) alone in locally advanced OPC. Human Papilloma Virus (HPV) related tumours have superior outcomes and de-escalating treatment is a contemporary issue. Our study objectives were to determine if 2# HDC were non-inferior to 3#, how this was influenced by prognostic factors including stage, smoking history and p16 status, and to explore toxicity attributed to HDC. Methods: A single centre, retrospective analysis was undertaken for OPC patients who received CRT with HDC between Oct 2009 -Dec 2012. Those with distant metastatic disease or receiving induction chemotherapy were excluded. Data extracted included HPV and smoking status, tumour stage by 7thEd AJCC TNM and ICON-S classification, # HDC completed, toxicity and OS. Log-rank test was used for OS analysis. Results: 63, 96 and 4 patients received 3, 2 and 1 # HDC respectively. Median RT dose was 70Gy (range 66-70). 110 (67.5%) were p16 +, 28 (17.2%) were p16 negative and 25 (15.3%) unknown. 52 had omission of #3 HDC predominantly due to neutropenia (33%), nephrotoxicity (23%) and ototoxicity (12%). 19 had delays in #2 HDC resulting in omission of #3 due to completion of RT. There was no difference in OS between 3 #(mean OS (yrs)+/- SEM: 6.05+/- 0.22) or 2# HDC (5.70+/- 0.21) in all comers (p = 0.255). For RTOG0129 low risk p16+ patients, there was no significant difference (p = 0.896) between 3# (6.33+/- 0.24; n = 24) and 2# (6.18+/- 0.25; n = 44) HDC. Similar results were evident for ICON-S stage I for 3# (6.36+/-0.19; n = 25) vs 2# (6.30+/- 0.19; n = 42) HDC (p = 0.932). For RTOG 0129 intermediate risk p16 + OPC there was a significant difference (p = 0.017) in OS favouring 3# (6.29+/-0.22; n = 20) versus 2# (4.81+/-0.67; n = 10) HDC. For p16 negative patients there was no difference (p = 0.265) in OS between 3# (4.06+/-0.94; n = 9) and 2# (5.17+/-0.48; n = 22) HDC. Conclusions: This data suggests that cisplatin de-escalation does not confer inferior OS in low risk HPV related OPC. Significant toxicities with HDC influenced the ability to complete prescribed treatment.
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Meisenberg, B. R., W. E. Miller, R. McMillan, M. Callaghan, C. Sloan, T. Brehm, M. P. Kosty, et al. "Outpatient high-dose chemotherapy with autologous stem-cell rescue for hematologic and nonhematologic malignancies." Journal of Clinical Oncology 15, no. 1 (January 1997): 11–17. http://dx.doi.org/10.1200/jco.1997.15.1.11.
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PURPOSE A prospective study to determine the feasibility of high-dose chemotherapy (HDC) and autologous stem-cell rescue (ASCR) in the outpatient setting. METHODS One hundred thirteen consecutive patients underwent 165 cycles of HDC/ASCR for a variety of malignancies. HDC regimens were disease-specific. Initially, patients were hospitalized for HDC, discharged on completion, and maintained as outpatients unless toxicities required rehospitalization (subtotal outpatient transplantation [STOT]). Once this was established as safe, a total outpatient transplant (TOT) program was developed in which patients received all of the HDC, as well as supportive care, as outpatients. Patients who declined the outpatient programs received the same HDC and supportive care as inpatients. RESULTS In 140 of 165 (85%) HDC cycles, patients agreed to participate in one of the outpatient transplant programs. Five patients in the STOT program could not be discharged from the hospital because of toxicities that developed during HDC; thus, 135 patients were monitored the outpatient setting, 95 (70%) of whom were never readmitted. The mean +/- SEM total hospital length of stay (LOS), including all readmissions and excess days after chemotherapy, was 18.33 +/- 5.06 days for patients who refused the outpatient program, 8.22 +/- 5.76 days for patients in the STOT program, and 2.81 +/- 7.66 days for those in the TOT program (P < .001). One treatment-related death occurred in each treatment setting: day 120 inpatient, day 17 STOT, and day 110 TOT. CONCLUSION Outpatient management of HDC/ASCR is safe and acceptable for the vast majority of patients. The STOT program resulted in significant reduction in hospital LOS, while the TOT program appears equally safe and further reduces LOS. Hospitalization for HDC/ASCR is unnecessary in most patients.
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Nieto, Yago, Shi-Ming Tu, Matthew T. Campbell, Roland Bassett, Nizar M. Tannir, John Francis Ward, Wayne Lewis Hofstetter, et al. "Infusional gemcitabine + docetaxel/melphalan/carboplatin (GemDMC) ± bevacizumab (BEV) as an effective high-dose chemotherapy (HDC) regimen for refractory of poor-risk relapsed germ-cell tumors (GCT)." Journal of Clinical Oncology 35, no. 15_suppl (May 20, 2017): 4519. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.4519.
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4519 Background: Tandem HDC with carbo/etoposide (CE) is curative for a portion of relapsed GCT pts. However, outcomes of refractory or high-risk relapsed pts remain poor. We tested a new HDC regimen of GemDMC, based on DNA damage repair inhibition. We combined BEV with HDC given their potential synergy and the high vascularity of GCT metastases. Methods: Eligibility: Intermediate (int)/high-risk (Beyer Model), creatinine ≤1.8 mg/dL and adequate organ function. HDC included BEV (5 mg/kg) preceding GemDMC (HDC #1) and ifosfamide/CE (ICE) (HDC #2). Following accrual of 42 pts, we amended the trial omitting BEV. The trial was powered to distinguish a target 50% 2-yr RFS from an expected 25% in this population. Results: We enrolled 69 male pts in cohorts 1 (BEV, N=42) and 2 (no BEV, N=27) (Table). Pts were heavily pretreated and most had refractory tumors. Main AE: mucositis and renal (4 HDC-related deaths in cohort 1, 1 in cohort 2). Tumor markers normalized in 90% pts with active tumors at HDC. After HDC, 19 pts were in CR and 28 in PRm- (of these, 22 had residual lesions resected with no viable tumor found in 20/22, 2 xRT, 4 monitored). Median f/u = 39 (2-105) mo. The 2-yr RFS rates in cohorts 1 and 2 = 52% and 78%, respectively. Their respective 2-yr OS rates = 55% and 81%. Conclusions: Sequential HDC with GemDMC–ICE shows encouraging outcomes in heavily pretreated and refractory GCT, exceeding the anticipated results. Addition of BEV increases toxicity but not tumor control. Clinical trial information: NCT00936936. [Table: see text]
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Komori, Hirofumi, Yoko Nitta, Hiroshi Ueno, and Yoshiki Higuchi. "Structural basis for the histamine synthesis by human histidine decarboxylase." Acta Crystallographica Section A Foundations and Advances 70, a1 (August 5, 2014): C458. http://dx.doi.org/10.1107/s2053273314095412.
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Histamine is a bioactive amine responsible for a variety of physiological reactions, including allergy, gastric acid secretion, and neurotransmission. In mammals, histamine production from histidine is catalyzed by histidine decarboxylase (HDC). Mammalian HDC is a pyridoxal 5'-phosphate (PLP)-dependent decarboxylase and belongs to the same family as mammalian glutamate decarboxylase (GAD) and mammalian aromatic L-amino acid decarboxylase (AroDC). The decarboxylases of this family function as homodimers and catalyze the formation of physiologically important amines like GABA and dopamine via decarboxylation of glutamate and DOPA, respectively. Despite high sequence homology, both AroDC and HDC react with different substrates. For example, AroDC catalyzes the decarboxylation of several aromatic L-amino acids, but has little activity on histidine. Although such differences are known, the substrate specificity of HDC has not been extensively studied because of the low levels of HDC in the body and the instability of recombinant HDC, even in a well-purified form. However, knowledge about the substrate specificity and decarboxylation mechanism of HDC is valuable from the viewpoint of drug development, as it could help lead to designing of novel drugs to prevent histamine biosynthesis. We have determined the crystal structure of human HDC in complex with inhibitors, histidine methyl ester (HME) and alpha-fluoromethyl histidine (FMH). These structures showed the detailed features of the PLP-inhibitor adduct (external aldimine) in the active site of HDC. These data provided insight into the molecular basis for substrate recognition among the PLP-dependent L-amino acid decarboxylases.
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Weidlich, Tomáš, Barbora Kamenická, Klára Melánová, Veronika Čičmancová, Alena Komersová, and Jiří Čermák. "Hydrodechlorination of Different Chloroaromatic Compounds at Room Temperature and Ambient Pressure—Differences in Reactivity of Cu- and Ni-Based Al Alloys in an Alkaline Aqueous Solution." Catalysts 10, no. 9 (September 1, 2020): 994. http://dx.doi.org/10.3390/catal10090994.
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It is well known that the hydrodechlorination (HDC) of chlorinated aromatic contaminants in aqueous effluents enables a significant increase in biodegradability. HDC consumes a low quantity of reactants producing corresponding non-chlorinated and much more biodegradable organic compounds. Two commonly used precious metals free Al alloys (Raney Al-Ni and Devarda’s Al-Cu-Zn) were compared in reductive action in an alkaline aqueous solution. Raney Al-Ni alloy was examined as a universal and extremely effective HDC agent in a diluted aqueous NaOH solution. The robustness of Raney Al-Ni activity is illustrated in the case of HDC of polychlorinated aromatic compounds mixture in actual waste water. In contrast, Devarda’s Al-Cu-Zn alloy was approved as much less active for HDC of the tested chlorinated aromatic compounds, but with a surprisingly high selectivity on cleavage of C-Cl bonds in the meta and sometimes the ortho position in chlorinated aniline and sometimes chlorinated phenol structures. The reaction of both tested alloys with chlorinated aromatic compounds in the aqueous NaOH solution is accompanied by dissolution of aluminum. Dissolved Al in the alkaline HDC reaction mixture is very useful for subsequent treatment of HDC products by coagulation and flocculation of Al(OH)3 caused by simple neutralization of the alkaline aqueous phase after the HDC reaction.
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Berry, Donald A., Gloria Broadwater, John P. Klein, Karen Antman, Joseph Aisner, Jacob Bitran, Mary Costanza, et al. "High-Dose Versus Standard Chemotherapy in Metastatic Breast Cancer: Comparison of Cancer and Leukemia Group B Trials With Data From the Autologous Blood and Marrow Transplant Registry." Journal of Clinical Oncology 20, no. 3 (February 1, 2002): 743–50. http://dx.doi.org/10.1200/jco.2002.20.3.743.
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PURPOSE: To assess survival of patients with metastatic breast cancer treated with high-dose chemotherapy (HDC) versus standard-dose chemotherapy (SDC). PATIENTS AND METHODS: SDC in four Cancer and Leukemia Group B (CALGB) trials was compared with hematopoietic stem-cell support in patients from the Autologous Blood and Marrow Transplant Registry. Cox proportional hazard regression incorporated potentially confounding effects. A total of 1,509 women were enrolled onto CALGB trials, and 1,188 women received HDC. No significant survival differences existed by CALGB trial or HDC regimen. Consideration was restricted to candidates for both SDC and HDC. The resulting sample included 635 SDC and 441 HDC patients. The outcome of interest was overall survival. RESULTS: The HDC group displayed better performance status. The SDC group had slightly better survival in first year after treatment. The HDC group had lower hazard of death from years 1 to 4 and had somewhat higher probability of 5-year survival (adjusted probabilities [95% confidence intervals], 23% [17% to 29%] v 15% [11% to 19%], P = .03). CONCLUSION: After controlling for known prognostic factors in this nonrandomized analysis of two large independent data sets, women receiving HDC versus SDC for metastatic breast cancer have a similar short-term probability of survival, and might have a modestly higher long-term probability of survival.
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Hegyesi, Hargita, Cs Szalai, A. Falus, and G. Csaba. "The Histidine Decarboxylase (HDC) Gene of Tetrahymena Pyriformis is Similar to the Mammalian One. A Study of HDC Expression." Bioscience Reports 19, no. 2 (April 1, 1999): 73–79. http://dx.doi.org/10.1023/a:1020102308791.
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RNA was isolated from Tetrahymena pyriformis GL and using human histidine decarboxylase (HDC) gene primers, the RT-PCR product was sequenced. A fraction containing 207 base pairs was compared to the published sequences of prokaryotic and mammalian (rat, mouse and human) HDC cDNA (exons). The HDC-cDNA fraction of Tetrahymena was similar to the mammalian cDNA-s and it was completely different from the prokaryotic HDC-gene. The results indicate the presence of a mammalian-like HDC-gene already in a unicellular eukaryote organism and demonstrates also that the divergence of the prokaryotic–eukaryotic common gene took place already at this low evolutionary level.
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Ding, X. Q., D. Chen, E. Rosengren, L. Persson, and R. Hakanson. "Comparison between activation of ornithine decarboxylase and histidine decarboxylase in rat stomach." American Journal of Physiology-Gastrointestinal and Liver Physiology 270, no. 3 (March 1, 1996): G476—G486. http://dx.doi.org/10.1152/ajpgi.1996.270.3.g476.
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We compared the responses of rat stomach ornithine decarboxylase (ODC) and histidine decarboxylase (HDC) to food intake, oral treatment with antisecretagogues, NaHCO3, and hypertonic NaCl, antrectomy, intravenous infusion of gastrin-17, the selective cholecystokinin (CCK)-B/gastrin receptor antagonist L-365,260, and the somatostatin analogue RC-160. The serum gastrin concentration and oxyntic mucosal ODC and HDC activities were higher in freely fed rats than in fasted rats. Food intake in fasted rats raised the serum gastrin concentration and the ODC and HDC activities. Ranitidine, omeprazole, and NaHCO3 raised the serum gastrin concentration and activated ODC and HDC. Hypertonic NaCl raised the ODC activity 200-fold, whereas circulating gastrin and HDC activity were increased only moderately. Infusion of gastrin-17 activated HDC but not ODC. L-365,260 prevented the activation of HDC but not of ODC in response to food intake and treatment with omeprazole, NaHCO3, or hypertonic NaCl. Antrectomy prevented the food- and omeprazole-evoked rise in oxyntic mucosal HDC activity but not the rise in ODC activity. RC-160 suppressed HDC activity after food intake and treatment with omeprazole, NaHCO3, or NaCl. In contrast, RC-160 suppressed omeprazole- and NaHCO3-evoked ODC activation but not that evoked by food intake or NaCl. The results support the view that HDC in the oxyntic mucosa is activated by gastrin and suppressed by somatostatin. The induction of ODC is not mediated by gastrin; ODC activation appears to be related to acid inhibition per se or to mucosal maintenance and repair; somatostatin, or rather the lack of it, might contribute to the induction of ODC after acid blockade. The mechanism behind the activation of rat stomach ODC seems to differ depending on the type of stimulus.
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Bozcuk, H. S., M. Ozdogan, H. S. Coskun, H. Mutlu, A. Kargi, M. Uysal, and B. Savas. "High-dose chemotherapy and stem cell support in the management of metastatic germ cell cancer: A quantitative review." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): e16094-e16094. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e16094.
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e16094 Background: To analyze the independent associates of outcome in metastatic germ cell cancer (MGCC) patients treated with high dose chemotherapy (HDC) and stem cell rescue. Methods: Thirty-two published patient cohorts with MGCC (encompassing 2176 patients; 510 patients treated upfront and 1666 at relapse) were identified from PUBMED and Cochrane Registry of Clinical Trials. Weighed Regression Analyses of these trials were conducted to define prognosticators. Results: Correlate of overall survival (OAS) and survival with no evidence of disease (NED) in upfront HDC trials was number of chemotherapeutics in HDC (OAS with 2 agents: 60% vs. 3 or more agents: 72%, p = 0.047, survival with NED with 2 agents: 47% vs. 3 or more agents: 64%, p = 0.009). In trials of HDC at relapse, independent associates of OAS with multivariate analysis were line of chemotherapy index, an indicator of line of chemotherapy utilization (p = 0.004), and median age (≤30: 42%, >30: 49%, p = 0.023), whereas independent correlates of better survival with NED were again number of chemotherapeutics in HDC (2 agents: 54% vs. 3 or more agents: 33%, p = 0.001), and seminoma fraction (seminoma fraction ≤9%: 28% vs. seminoma fraction >9%: 49%, p < 0.001 ). Toxic mortality of HDC regimens employed in these trials ranged between 0% and 17%. Conclusions: HDC can cure patients with MGCC both as initial or salvage therapies. However, this study shows that type and setting of HDC, as well as patient age, and seminoma fraction all appear to be linked with benefit from HDC in MGCC. Future trials should continue to address the usage of tandem HDC cycles with multiagent protocols in high risk patients with MGCC. No significant financial relationships to disclose.
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Cagnoni, P. J., Y. Nieto, E. J. Shpall, S. I. Bearman, A. E. Barón, M. Ross, S. Matthes, S. E. Dunbar, and R. B. Jones. "High-dose chemotherapy with autologous hematopoietic progenitor-cell support as part of combined modality therapy in patients with inflammatory breast cancer." Journal of Clinical Oncology 16, no. 5 (May 1998): 1661–68. http://dx.doi.org/10.1200/jco.1998.16.5.1661.
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PURPOSE To evaluate the feasibility of high-dose chemotherapy (HDC) with autologous hematopoietic progenitor-cell support (AHPCS) as part of combined modality therapy (CMT) in patients with inflammatory breast cancer (IBC). PATIENTS AND METHODS From April 1993 to March 1997, 30 patients with IBC were treated at our program. Twenty-three patients received neoadjuvant chemotherapy (NAC) before HDC; 18 patients also received adjuvant chemotherapy following surgery, but before HDC. All patients received HDC with high-dose cyclophosphamide, cisplatin, and carmustine (BCNU) with AHPCS. Every patient underwent surgery either before (27 patients) or after (three patients) HDC. Patients received radiotherapy after HDC in addition to tamoxifen if their tumors were estrogen receptor-positive. RESULTS Thirteen patients experienced grade 3 or 4 nonhematologic noninfectious toxicities. In 12 patients (40%), this represented drug-induced lung injury, which in all cases responded to a 10-week course of corticosteroids. The only treatment-related death was secondary to hemolytic-uremic syndrome (HUS). Another patient suffered grade 4 CNS toxicity, which was completely reversible. All patients engrafted promptly. Eight patients relapsed, five of whom had a poor pathologic response to NAC. Relapses were local (five patients), local plus systemic (one), or systemic only (two). Median follow-up time from diagnosis and HDC is 23.5 (range, 7 to 49) and 19 (range, 4 to 44) months, respectively. Twenty-one patients (70%; 95% confidence interval [CI], 51% to 86%) remain alive and free of disease 4 to 44 months after HDC. Median disease-free survival (DFS) and overall survival have not yet been reached. CONCLUSION HDC as part of CMT is feasible in patients with IBC. The toxicity of this treatment program is significant, but tolerable. Despite the short follow-up duration, the promising DFS observed in this group of patients warrants randomized studies that include a HDC-containing arm in patients with IBC.
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Zhu, Qing Feng, Zhi Hao Zhao, Xiang Jie Wang, and Jian Zhong Cui. "Effect of Electromagnetic Field on Horizontal Direct Chill Casting of 7075 Aluminum Alloy." Materials Science Forum 654-656 (June 2010): 982–85. http://dx.doi.org/10.4028/www.scientific.net/msf.654-656.982.
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The influence of different electromagnetic fields on the horizontal direct chill (HDC) casting of aluminum alloy is studied. 7075 aluminum alloy with 100-mm in diameter is produced by HDC casting process; single electromagnetic field located before or around the mold and an out-phase electromagnetic field (OPEMF) are applied in the HDC casting process. The effect of different electromagnetic fields on the HDC casting solidification behavior and as-cast structure is investigated. The electromagnetic field can effectively make uniform thermal distribution in the molten pool and refine the as-cast structure. The OPEMF is more efficient than the single electromagnetic field in improving the as-cast structure of HDC cast ingots.
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Kanki, Masashi, Tomoko Yoda, Teizo Tsukamoto, and Eiichiroh Baba. "Histidine Decarboxylases and Their Role in Accumulation of Histamine in Tuna and Dried Saury." Applied and Environmental Microbiology 73, no. 5 (January 12, 2007): 1467–73. http://dx.doi.org/10.1128/aem.01907-06.
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ABSTRACT Histamine-producing bacteria (HPB) such as Photobacterium phosphoreum and Raoultella planticola possess histidine decarboxylase (HDC), which converts histidine into histamine. Histamine fish poisoning (HFP) is attributable to the ingestion of fish containing high levels of histamine produced by HPB. Because freezing greatly decreases the histamine-producing ability of HPB, especially of P. phosphoreum, it has been speculated that HFP is caused by HDC itself from HPB cells autolyzing during frozen storage, even when HPB survive frozen storage. Here we constructed recombinant HDCs of P. phosphoreum, Photobacterium damselae, R. planticola, and Morganella morganii and investigated the ability of HDCs to produce sufficient histamine to cause HFP. To elucidate the character of these HDCs, we examined the specific activity of each recombinant HDC at various temperatures, pH levels, and NaCl concentrations. Further, we also investigated the stability of each HDC under different conditions (in reaction buffer, tuna, and dried saury) at various temperatures. P. damselae HDC readily produced sufficient histamine to cause HFP in fish samples. We consider that if HDC is implicated as an independent cause of HFP in frozen-thawed fish, the most likely causative agent is HDC of P. damselae.
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Vitolo, Umberto, Giuseppe Rossi, Maria Giuseppina Cabras, Anna Marina Liberati, Annalisa Chiappella, Alessandro Levis, Enzo Pavone, et al. "Effect of Adding Rituximab (R) to Induction Treatment and High Dose Chemotherapy (HDC) Prior to Autologous Stem Cell Transplantation (ASCT) as First Line Therapy in Stage III-IV Diffuse Large B-Cell Lymphoma (B-DLCL) at Poor Prognosis." Blood 106, no. 11 (November 16, 2005): 676. http://dx.doi.org/10.1182/blood.v106.11.676.676.
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Abstract Introduction: We investigated efficacy and safety of adding Rituximab (R) to induction and intensified HDC as part of first line treatment in pts with aa-IPI at Intermediate-High (IH) or High (H) risk with B-DLCL at diagnosis. We compared two groups of similar pts enrolled in two consecutive non-randomized phase II clinical trials with up-front HDC and ASCT with or without R with identical inclusion criteria conducted by GIMURELL. Patients and methods: 118 previously untreated pts <61 years with B-DLCL, stage III-IV at aaIPI IH or H risk were treated: 41 pts were enrolled into HDC trial (control group; August 1991-August 1995) and 77 pts into R-HDC trial (study group; January 2001-December 2004). Treatment in R-HDC study group consisted in an induction treatment lasting two months with four courses of R-MegaCEOP chemotherapy (R 375 mg/m2 day1, CTX 1200 mg/m2 + EPI 110 mg/m2 + VCR 1.4 mg/m2 day3 and PDN 40 mg/m2 days 3–7) every 14 days with G-CSF support; then two courses of intensified chemoimmunotherapy R-MAD (Mitoxantrone 8 mg/m2 + ARAC 2000 mg/m2/12h + Dexamethasone 4 mg/m2/12h for 3 days and R 375 mg/m2 day4 and before PBSC harvest) followed by ASCT with BEAM as conditioning regimen. Treatment in HDC control group consisted in an induction treatment lasting two months with MACOPB chemotherapy x 8 weekly infusions followed by the same intensified and HDC regimens (MADx 2 courses + BEAM and ASCT). All pts were given antibacterial and antifungal prophylaxis throughout the whole treatment. IF RT was given to areas of previous bulky disease in both trials. Results: Pts characteristics in both trials were comparable with no statistically significant differences: median age was 45 years (19–60); 51% were at H risk; 36% had bone marrow (BM) involvement, 80% had LDH level >normal and 42% extranodal sites>1. Complete Response at the end of the treatment was: 60 pts (78%) in R-HDC group and 28 (68%) in HDC group (p=.25). Failures (17% vs 24%) and toxic deaths (5% vs 7%) were comparable between the two groups (R-HDC vs HDC). Short-term toxicity appeared similar. Median follow-up was 27 months in study group and 69 months in control group. Two-year failure-free survival (FFS) and 2-yr overall survival (OS) rates in R-HDC group compared to HDC group were: FFS 70% vs 49% (p=.036); OS 78% vs 56% (p=.009). A better outcome for pts treated with R-HDC was confirmed in both IPI groups (IH and H risk). A Cox’s model was performed to adjust the effect of treatment for competing risk factors (age, IPI, BM involvement, number of extranodal sites). In this multivariate analysis the risk of failure and death was confirmed as significantly reduced in R-HDC group: adjusted hazard ratio (R-HDC vs HDC) was 0.54 (95% CI=0.30–0.98, p=.02) for FFS and 0.42 (95% CI=0.21–0.84, p=.03) for OS. Germinal center and non germinal center subtype analysis is ongoing in both treatment groups. Conclusions: these results suggest that the addition of Rituximab to induction and intensified chemotherapy before BEAM and ASCT is effective and safe in B-DLCL at poor prognosis improving the outcome of these pts.
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Modak, Shakeel, Sharon Gardner, Ira J. Dunkel, Casilda Balmaceda, Marc K. Rosenblum, Douglas C. Miller, Steven Halpern, and Jonathan L. Finlay. "Thiotepa-Based High-Dose Chemotherapy With Autologous Stem-Cell Rescue in Patients With Recurrent or Progressive CNS Germ Cell Tumors." Journal of Clinical Oncology 22, no. 10 (May 15, 2004): 1934–43. http://dx.doi.org/10.1200/jco.2004.11.053.
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Purpose To evaluate the efficacy and toxicity of high-dose chemotherapy (HDC) followed by autologous stem-cell rescue (ASCR) in patients with relapsed or progressive CNS germ cell tumors (GCTs). Patients and Methods Twenty-one patients with CNS GCTs who experienced relapse or progression despite having received initial chemotherapy and/or radiotherapy were treated with thiotepa-based HDC regimens followed by ASCR. Results Estimated overall survival (OS) and event-free survival (EFS) rates for the entire group 4 years after HDC were 57% ± 12% and 52% ± 14%, respectively. Seven of nine (78%) patients with germinoma survived disease-free after HDC with a median survival of 48 months. One patient died as a result of progressive disease (PD) 39 months after HDC, and another died as a result of pulmonary fibrosis unrelated to HDC 78 months after ASCR without assessable disease. However, only four of 12 patients (33%) with nongerminomatous germ cell tumors (NGGCTs) survived without evidence of disease, with a median survival of 35 months. Eight patients with NGGCTs died as a result of PD, with a median survival of 4 months after HDC (range, 2 to 17 months). Patients with germinoma fared better than those with NGGCTs (P = .016 and .014 for OS and EFS, respectively). Patients with complete response to HDC also had significantly better outcome (P < .001 for OS and EFS) compared with patients with only a partial response or stable disease. There were no toxic deaths because of HDC. Conclusion Dose escalation of chemotherapy followed by ASCR is effective therapy for patients with recurrent CNS germinomas and might be effective in patients with recurrent NGGCTs with a low tumor burden.
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McCusker, Michael Gerard, Ranee Mehra, Jason K. Molitoris, Rodney Taylor, Kevin J. Cullen, and Olga G. Goloubeva. "Cisplatin every three weeks versus weekly cisplatin or carboplatin with definitive radiotherapy for squamous cell carcinoma of the head and neck is associated with improved overall survival in a representative national population." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): 6536. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.6536.
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6536 Background: For patients with primary untreated locally advanced head and neck squamous cell carcinoma (PULA-HNSCC), high dose once every 3 weeks cisplatin (HDC; 100 mg/m2) added to curative radiotherapy (RT) prolongs survival, but is associated with severe toxicities. Concurrent chemoradiation (CRT) with low dose weekly cisplatin (LDC; 30-40 mg/m2), carboplatin (C), or RT alone is often substituted for HDC. We estimated and compared overall survival (OS) and acquired toxicities among Medicare beneficiaries treated with CRT using HDC, LDC, C, or RT. Methods: Patients diagnosed from 2004-2011 with PULA-HNSCC (stages III-IVB AJCC 6th and 7th editions) of the oropharynx (OPC), hypopharynx (HP), or larynx (L) who received definitive RT or CRT were identified using the linked SEER-Medicare database. An analytic cohort of patients receiving CRT with HDC, LDC, or C was constructed using well-established eligibility criteria. OS was estimated and compared between patients grouped by treatment received utilizing a multivariable stratified propensity scores weighted Cox regression model, including demographic and disease characteristics. Toxicities were compared using exact common odds-ratio and Fisher’s tests. Results: We identified 1,335 patients that received RT: OPC (n = 731), HP (n = 174), or L (n = 430). Out of those, patients were treated with HDC (n = 264), LDC (n = 259), C (n = 353), or RT alone (n = 459). Median OS (years) was 5.61 (95% CI = 4.58-7.69) for HDC, 3.7 (95% CI = 3.1-4.79) for LDC, 3.1 (95% CI = 2.48-3.86) for C, and 1.36 (95% CI = 1.19-1.58) for RT, respectively. OS was significantly greater for HDC than for LDC (HR = 1.35, 95% CI = 1.06-1.72, p= 0.02), C (HR = 1.41, 95% CI = 1.12-1.76, p= 0.003), or RT (HR = 2.1, 95% CI = 1.68-2.61, p= < 0.001). Treatment with HDC compared to LDC was not associated with increased prevalence of dysphagia or neutropenia. HDC was associated with hearing loss when assessed at 9-12 months post-diagnosis ( p =0.03). Conclusions: In SEER-Medicare beneficiaries with PULA-HNSCC of the OPC, HP, or L, OS was significantly better for HDC than LDC when accounting for baseline clinical and demographic characteristics and propensity score weights. Toxicities were similar between regimens, except for an increased incidence of the late acute toxicity of hearing loss in HDC. A regimen of HDC improves OS, but needs to be carefully assessed against increased toxicity risk, with hearing loss in particular.
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Kazumori, Hideaki, Shunji Ishihara, Mohammad A. K. Rumi, Cesar F. Ortega-Cava, Yasunori Kadowaki, and Yoshikazu Kinoshita. "Transforming growth factor-α directly augments histidine decarboxylase and vesicular monoamine transporter 2 production in rat enterochromaffin-like cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 286, no. 3 (March 2004): G508—G514. http://dx.doi.org/10.1152/ajpgi.00269.2003.
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For the production and vesicle storage of histamine, Enterochromaffin-like (ECL) cells express histidine decarboxylase (HDC) and vesicular monoamine transporter 2 (VMAT2). Although HDC and VMAT2 show dynamic changes during gastric ulcer healing, the control system of their expression has not been fully investigated. In the present study, we investigated the effect of transforming growth factor-α (TGF-α) and proinflammatory cytokines on HDC and VMAT2 expression in rat ECL cells. Time course changes in the expression of TGF-α during the healing of acetic acid-induced ulcers were studied. EGF receptor (EGFR) expression was also examined in ECL cells, whereas the direct effects of TGF-α and proinflammatory cytokines on HDC and VMAT2 expression in ECL cells were investigated using in vivo and in vitro models. During the process of ulcer healing, expression of TGF-α mRNA was markedly augmented. Furthermore, EGFR was identified in isolated ECL cells. TGF-α stimulated HDC and VMAT2 mRNA expression and protein production and also increased histamine release from ECL cells. Selective EGFR tyrosine kinase inhibitor tyrphostin AG1478 almost completely inhibited HDC and VMAT2 gene expression induced by TGF-α in vivo and in vitro. During gastric mucosal injury, TGF-α was found to stimulate ECL cell functions by increasing HDC and VMAT2 expression.
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Juang, Yu-Chi, Xavier Fradera, Yongxin Han, and Anthony William Partridge. "Repurposing a Histamine Detection Platform for High-Throughput Screening of Histidine Decarboxylase." SLAS DISCOVERY: Advancing the Science of Drug Discovery 23, no. 9 (June 8, 2018): 974–81. http://dx.doi.org/10.1177/2472555218778053.
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Histidine decarboxylase (HDC) is the primary enzyme that catalyzes the conversion of histidine to histamine. HDC contributes to many physiological responses as histamine plays important roles in allergic reaction, neurological response, gastric acid secretion, and cell proliferation and differentiation. Small-molecule modulation of HDC represents a potential therapeutic strategy for a range of histamine-associated diseases, including inflammatory disease, neurological disorders, gastric ulcers, and select cancers. High-throughput screening (HTS) methods for measuring HDC activity are currently limited. Here, we report the development of a time-resolved fluorescence resonance energy transfer (TR-FRET) assay for monitoring HDC activity. The assay is based on competition between HDC-generated histamine and fluorophore-labeled histamine for binding to a Europium cryptate (EuK)-labeled anti-histamine antibody. We demonstrated that the assay is highly sensitive and simple to develop. Assay validation experiments were performed using low-volume 384-well plates and resulted in good statistical parameters. A pilot HTS screen gave a Z′ score > 0.5 and a hit rate of 1.1%, and led to the identification of a validated hit series. Overall, the presented assay should facilitate the discovery of therapeutic HDC inhibitors by acting as a novel tool suitable for large-scale HTS and subsequent interrogation of compound structure–activity relationships.
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Berry, Donald A., Naoto T. Ueno, Marcella M. Johnson, Xiudong Lei, Jean Caputo, Sjoerd Rodenhuis, William P. Peters, et al. "High-Dose Chemotherapy With Autologous Stem-Cell Support As Adjuvant Therapy in Breast Cancer: Overview of 15 Randomized Trials." Journal of Clinical Oncology 29, no. 24 (August 20, 2011): 3214–23. http://dx.doi.org/10.1200/jco.2010.32.5910.
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Purpose Adjuvant high-dose chemotherapy (HDC) with autologous hematopoietic stem-cell transplantation (AHST) for high-risk primary breast cancer has not been shown to prolong survival. Individual trials have had limited power to show overall benefit or benefits within subsets. Methods We assembled individual patient data from 15 randomized trials that compared HDC versus control therapy without stem-cell support. Prospectively defined primary end points were relapse-free survival (RFS) and overall survival (OS). We compared the effect of HDC versus control by using log-rank tests and proportional hazards regression, and we adjusted for clinically relevant covariates. Subset analyses were by age, number of positive lymph nodes, tumor size, histology, hormone receptor (HmR) status, and human epidermal growth factor receptor 2 (HER2) status. Results Of 6,210 total patients (n = 3,118, HDC; n = 3,092 control), the median age was 46 years; 69% were premenopausal, 29% were postmenopausal, and 2% were unknown menopausal status; 49.5% were HmR positive; 33.5% were HmR negative, and 17% were unknown HmR status. The median follow-up was 6 years. After analysis was adjusted for covariates, HDC was found to prolong relapse-free survival (RFS; hazard ratio [HR], 0.87; 95% CI, 0.81 to 0.93; P < .001) but not overall survival (OS; HR, 0.94; 95% CI, 0.87 to 1.02; P = .13). For OS, no covariates had statistically significant interactions with treatment effect, and no subsets evinced a significant effect of HDC. Younger patients had a significantly better RFS on HDC than did older patients. Conclusion Adjuvant HDC with AHST prolonged RFS in high-risk primary breast cancer compared with control, but this did not translate into a significant OS benefit. Whether HDC benefits patients in the context of targeted therapies is unknown.
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Deng, Mingke, Jian Han, Haibo Liu, Meng Qin, and Xingwen Liang. "Analysis of Compressive Toughness and Deformability of High Ductile Fiber Reinforced Concrete." Advances in Materials Science and Engineering 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/384902.
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The compressive toughness evaluation index of HDC (high ductile fiber reinforced concrete) is studied through three groups of uniaxial compressive tests of HDC specimens with different fiber mixing amounts, and an equivalent analysis of their deformability is carried out, coming to the following conclusion:(1)the peak strain of HDC under uniaxial compression can be up to 3.41~3.67 times as large as that of the mortar matrix;(2)the equivalent compressive toughness index reflects the unit volume deformation energy of specimens under uniaxial compression and it can be used as the compressive toughness evaluation index of HDC;(3)the fiber bridging effect of HDC increases the equivalent compressive toughness index and the compressive deformability up to 3 times of the mortar matrix;(4)the relationship between the equivalent compressive toughness indexWcu0.85and the fiber mixing amountφis established according to the test results; and(5)the fiber bridging effect of the matrix in HDC can be equaling as a large number of constraint stirrups installed in the specimens, which significantly enhances the compressive toughness and the compressive deformability of specimens.
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Song, Min, Hong Yang, John H. Walsh, Gordon Ohning, Helen Wong, and Yvette Taché. "Intracisternal TRH analog increases gastrin release and corpus histidine decarboxylase activity in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 4 (April 1, 1999): G901—G908. http://dx.doi.org/10.1152/ajpgi.1999.276.4.g901.
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Thyrotropin-releasing hormone (TRH) acts in brain stem nuclei to induce vagally mediated stimulation of gastric secretion. The effects of intracisternal injection of the TRH analog RX-77368 on plasma gastrin levels and corpus histidine decarboxylase (HDC) activity were studied in 48-h fasted conscious rats. RX-77368 (25–100 ng) increased plasma gastrin levels by threefold at 30 min, which remained significantly higher than control at 2 and 4 h postinjection. Corpus HDC activity began to increase at 2 h and reached a peak at 4 h postinjection with a 21-fold maximum response observed at 50 ng. Morphological changes in the appearance of corpus HDC-immunoreactive cells correlated well with HDC activity. Pretreatment with gastrin monoclonal antibody completely prevented RX-77368 stimulatory effects on HDC activity. Atropine significantly attenuated gastrin increase at 30 min by 26%. These results indicated that in conscious fasted rats, TRH analog acts in the brain to increase corpus HDC activity in the enterochromaffin-like cells, which involves gastrin release stimulated by central TRH analog.
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August, E. Michael, Lori Patnaude, Jerry Hopkins, Joey Studts, Elda Gautschi, Anthony Shrutkowski, Anthony Kronkaitis, Martha Brown, Alisa Kabcenell, and Daniel Rajotte. "Development of a High-Throughput Assay to Measure Histidine Decarboxylase Activity." Journal of Biomolecular Screening 11, no. 7 (September 14, 2006): 816–21. http://dx.doi.org/10.1177/1087057106290803.
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Histamine is a well-known mediator of allergic, inflammatory, and neurological responses. More recent studies suggest a role for histamine and its receptors in a wide range of biological processes, including T-cell maturation and bone remodeling. Histamine serum levels are regulated mainly by the activity of the histamine-synthesizing enzyme histidine decarboxylase (HDC). Despite the importance of this enzyme in many physiological processes, very few potent HDC inhibitors have been identified. HDC assays suitable for high-throughput screening have not been reported. The authors describe the development of a fluorescence polarization assay to measure HDC enzymatic activity. They used a fluorescein-histamine probe that binds with high affinity to an antihistamine antibody for detection. Importantly, they show that probe binding is fully competed by histamine, but no competition by the HDC substrate histidine was observed. The automated assay was performed in a total volume of 60 μL, had an assay window of 80 to 100 mP, and had a Z′ factor of 0.6 to 0.7. This assay provides new tools to study HDC activity and pharmacological modulation of histamine levels.
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Deng, Mingke, and Yangxi Zhang. "Seismic Performance of High-Ductile Fiber-Reinforced Concrete Short Columns." Advances in Civil Engineering 2018 (2018): 1–11. http://dx.doi.org/10.1155/2018/3542496.
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This study mainly aims to investigate the effectiveness of high-ductile fiber-reinforced concrete (HDC) as a means to enhance the seismic performance of short columns. Six HDC short columns and one reinforced concrete (RC) short column were designed and tested under lateral cyclic loading. The influence of the material type (concrete or HDC), axial load, stirrup ratio, and shear span ratio on crack patterns, hysteresis behavior, shear strength, deformation capacity, energy dissipation, and stiffness degradation was presented and discussed, respectively. The test results show that the RC short column failed in brittle shear with poor energy dissipation, while using HDC to replace concrete can effectively improve the seismic behavior of the short columns. Compared with the RC short column, the shear strength of HDC specimens was improved by 12.6–30.2%, and the drift ratio and the energy dissipation increases were 56.9–88.5% and 237.7–336.7%, respectively, at the ultimate displacement. Additionally, the prediction model of the shear strength for RC columns based on GB50010-2010 (Chinese code) can be safely adopted to evaluate the shear strength of HDC short columns.
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Bredenfeld, Henning, Elena Gilman, Beate Pfistner, Volker Diehl, and Andreas Engert. "A Comparison of Outcome and Second Malignancies in Adolescents and Adult Patients with Hodgkin’s Lymphoma (HL). Results from the German Hodgkin Study Group." Blood 106, no. 11 (November 16, 2005): 2670. http://dx.doi.org/10.1182/blood.v106.11.2670.2670.
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Abstract Introduction: Whether adolescent (alc) patients with HL represent a distinct patient group, requiring a therapy strategy separated from adults, is currently focussed in international debates. Most study groups are treating adult (ad) patients (pts) (age > 18 years) apart from younger patients (age < 18 years), considering a difference in treatment related toxicity and therapy outcome in both patient groups. Between 1988 and 1998, the GHSG trial generations 2 (G2) and 3 (G3) included younger patients from the age of 15 (G2), and 16 (G3), in identically therapy regimen with adults up to 65, and 75 years. The trials for early stages HD were comparing radiation therapy (RX) arms only (HD4, recruited 1988–1993), and, RX vs 2 cycles polychemotherapy plus RX (HD7, 1993–1998). Intermediate stages HD received 2 cycles of different chemotherapy regimen plus identically RX (HD5, 1988–1993), and, 2 identically cycles of chemotherapy plus different RX (HD8, 1993–1998). Advanced stages HL were treated with either 4 cycles conventional polychemotherapy plus EF, or, 4 cycles of a hybrid regimen plus EF RX (HD6, 1988–1993); the following trial (HD9, 1993–1998) compared 3 arms of different polychemotherapy followed by RX on bulky disease. Methods: In G2 and G3, a total of 573 adolescents (15–21 yrs) in early, intermediate, and advanced stages HL were compared with 4917 pts (15–75 yrs) for complete remission rate (CR), 5 yrs survival rate (SV), 5 yrs freedom from treatment failure (FFTF), and, secondary neoplasias (2nd NPL). (table 1) Conclusion: Based on this large analysis of HL patients treated in prospectively randomized trials, the prognosis of patients aged 15–21 years is rather similar to the prognosis of adult patients. A more detailed evaluation including age-adapted prognosis will be presented. Results: Adolescents /Adults CR % 5 yrs FFTF % 5 yrs SV % Alc Ad Alc Ad Alc Ad Early stages HD4 97.7 97.3 81.6 80.5 97.6 95.1 HD7 93.3 94.3 82.0 83.3 100 94.1 Intermediate stages HD5 93.5 93.4 83.3 81.7 94.3 90.5 HD8 93.8 92.6 84.5 82.7 97.3 91.3 Advanced stages HD6 77.8 77.0 61.0 58.8 85.3 78.6 HD9 93.5 90.3 85.8 79.2 92.4 88.0
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Takahara, Kazuhiko, Takuya Arita, Sumika Tokieda, Nobuyuki Shibata, Yoshio Okawa, Hiroaki Tateno, Jun Hirabayashi, and Kayo Inaba. "Difference in Fine Specificity to Polysaccharides of Candida albicans Mannoprotein between Mouse SIGNR1 and Human DC-SIGN." Infection and Immunity 80, no. 5 (February 13, 2012): 1699–706. http://dx.doi.org/10.1128/iai.06308-11.
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ABSTRACTC-type lectin SIGNR1 directly recognizesCandida albicansand zymosan and has been considered to share properties of polysaccharide recognition with human DC-SIGN (hDC-SIGN). However, the precise specificity of SIGNR1 and the difference from that of hDC-SIGN remain to be elucidated. We prepared soluble forms of SIGNR1 and hDC-SIGN and conducted experiments to examine their respective specificities. Soluble SIGNR1 (sSIGNR1) bound several types of liveC. albicansclinical isolate strains in an EDTA-sensitive manner. Inhibition analyses of sSIGNR1 binding by glycans from various yeast strains demonstrated that SIGNR1 preferentially recognizes N-glycan α-mannose side chains inCandidamannoproteins, as reported in hDC-SIGN. Unlike shDC-SIGN, however, sSIGNR1 recognized not onlySaccharomyces cerevisiae, but alsoC. albicansJ-1012 glycan, even after α-mannosidase treatment that leaves only β1,2-mannose-capped α-mannose side chains. In addition, glycomicroarray analyses showed that sSIGNR1 binds mannans fromC. albicansandS. cerevisiaebut does not recognize Lewisa/b/x/yantigen polysaccharides as in shDC-SIGN. Consistent with these results, RAW264.7 cells expressing hDC-SIGN in which the carbohydrate recognition domain (CRD) was replaced with that of SIGNR1 (RAW-chimera) produced comparable amounts of interleukin 10 (IL-10) in response to glycans fromC. albicansandS. cerevisiae, but those expressing hDC-SIGN produced less IL-10 in response toS. cerevisiaethanC. albicans. Furthermore, RAW–hDC-SIGN cells remarkably reduced IL-10 production after α-mannosidase treatment compared with RAW-chimera cells. These results indicate that SIGNR1 recognizesC. albicans/yeast through a specificity partly distinct from that of its homologue hDC-SIGN.
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Meng, Xiaoni, Manshu Song, Marija Vilaj, Jerko Štambuk, Mamatyusupu Dolikun, Jie Zhang, Di Liu, et al. "Glycosylation of IgG Associates with Hypertension and Type 2 Diabetes Mellitus Comorbidity in the Chinese Muslim Ethnic Minorities and the Han Chinese." Journal of Personalized Medicine 11, no. 7 (June 29, 2021): 614. http://dx.doi.org/10.3390/jpm11070614.
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Objectives: Hypertension and type 2 diabetes mellitus comorbidity (HDC) is common, which confers a higher risk of cardiovascular disease than the presence of either condition alone. Describing the underlying glycomic changes of immunoglobulin G (IgG) that predispose individuals to HDC may help develop novel protective immune-targeted and anti-inflammatory therapies. Therefore, we investigated glycosylation changes of IgG associated with HDC. Methods: The IgG N-glycan profiles of 883 plasma samples from the three northwestern Chinese Muslim ethnic minorities and the Han Chinese were analyzed by ultra-performance liquid chromatography instrument. Results: We found that 12 and six IgG N-glycan traits showed significant associations with HDC in the Chinese Muslim ethnic minorities and the Han Chinese, respectively, after adjustment for potential confounders and false discovery rate. Adding the IgG N-glycan traits to the baseline models, the area under the receiver operating characteristic curves (AUCs) of the combined models differentiating HDC from hypertension (HTN), type 2 diabetes mellitus (T2DM), and healthy individuals were 0.717, 0.747, and 0.786 in the pooled samples of Chinese Muslim ethnic minorities, and 0.828, 0.689, and 0.901 in the Han Chinese, respectively, showing improved discriminating performance than both the baseline models and the glycan-based models. Conclusion: Altered IgG N-glycan profiles were shown to associate with HDC, suggesting the involvement of inflammatory processes of IgG glycosylation. The alterations of IgG N-glycome, illustrated here for the first time in HDC, demonstrate a biomarker potential, which may shed light on future studies investigating their potential for monitoring or preventing the progression from HTN or T2DM towards HDC.
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Zhu, Qing Feng, Zhi Hao Zhao, Xiang Jie Wang, and Jian Zhong Cui. "Floating Grains in the HDC Casting 7075 Aluminum Alloy Ingot." Applied Mechanics and Materials 117-119 (October 2011): 1531–34. http://dx.doi.org/10.4028/www.scientific.net/amm.117-119.1531.
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7075 aluminum alloy ingot with the diameters of 100 mm was produced by Horizontal Direct-Chill (HDC). The temperature in the melt was measured and the ingots were examined in detail with the aim to reveal the floating grains in the HDC ingot. Experimental results show that very large floating grains with coarse dendrite arm spacing (DAS) mainly concentrate in the half-moon area near bottom surface of the HDC casting ingot, under the function of gravity. The floating grains in the HDC casting process is much bigger than that founded in Vertical Direct-Chill (VDC) casting process.
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Ledermann, J. A. "Lessons learned from a decade of clinical trials of high-dose chemotherapy in ovarian cancer." International Journal of Gynecologic Cancer 18, Suppl 1 (2008): 53–58. http://dx.doi.org/10.1111/j.1525-1438.2007.01107.x.
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Ovarian cancer is one of the most chemosensitive solid tumors and therefore a good example to explore high-dose chemotherapy (HDC). Interest in pursuing this treatment arose in the late 1980s following the success of HDC in treating hematological cancers and improvements in supportive care with peripheral blood stem cells. Experience from phase II trials and analysis of Bone Marrow Transplant Registry data led to the launch of several randomized phase III trials in the late 1990s. Initial enthusiasm for this treatment was in part due to the preliminary positive data emerging from HDC in breast cancer. Five randomized trials of HDC in ovarian cancer have been conducted and all experienced difficulty in recruitment. Their different designs and results are reviewed, as well as some of the lessons that have been learned about HDC in solid tumors in the last decade
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Fan, Yan-Ying, Wei-Wei Hu, Hai-Bin Dai, Jian-Xiang Zhang, Lu-Yi Zhang, Ping He, Yao Shen, Hiroshi Ohtsu, Er-Qing Wei, and Zhong Chen. "Activation of the Central Histaminergic System is Involved in Hypoxia-Induced Stroke Tolerance in Adult Mice." Journal of Cerebral Blood Flow & Metabolism 31, no. 1 (June 30, 2010): 305–14. http://dx.doi.org/10.1038/jcbfm.2010.94.
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We hypothesized that activation of the central histaminergic system is required for neuroprotection induced by hypoxic preconditioning. Wild-type (WT) and histidine decarboxylase knockout (HDC-KO) mice were preconditioned by 3 hours of hypoxia (8% O2) and, 48 hours later, subjected to 30 minutes of middle cerebral artery (MCA) occlusion, followed by 24 hours of reperfusion. Hypoxic preconditioning improved neurologic function and decreased infarct volume in WT or HDC-KO mice treated with histamine, but not in HDC-KO or WT mice treated with α-fluoromethylhistidine (α-FMH, an inhibitor of HDC). Laser-Doppler flowmetry analysis showed that hypoxic preconditioning ameliorated cerebral blood flow (CBF) in the periphery of the MCA territory during ischemia in WT mice but not in HDC-KO mice. Histamine decreased in the cortex of WT mice after 2, 3, and 4 hours of hypoxia, and HDC activity increased after 3 hours of hypoxia. Vascular endothelial growth factor (VEGF) mRNA and protein expressions showed a greater increase after hypoxia than those in HDC-KO or α-FMH-treated WT mice. In addition, the VEGF receptor-2 antagonist SU1498 prevented the protective effect of hypoxic preconditioning in infarct volume and reversed increased peripheral CBF in WT mice. Therefore, endogenous histamine is an essential mediator of hypoxic preconditioning. It may function by enhancing hypoxia-induced VEGF expression.
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Nieto, Yago, Nizar M. Tannir, Shi-Ming Tu, Roy B. Jones, Amado J. Zurita, Ana Aparicio, Roland Bassett, et al. "Phase II trial of bevacizumab (BEV)/high-dose chemotherapy (HDC) for refractory germ-cell tumors (GCT)." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): 4533. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.4533.
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4533 Background: HDC is a curative therapy for relapsed GCT. However, multiple prior relapses, cisplatin refractoriness (relapse/progression (PD) within 4 weeks) or absolute refractoriness (no prior response), or very high tumor markers at relapse predict poor early event-free survival (EFS). The validated Beyer model (JCO 1996;14:2638) identifies groups with poor risk (5% EFS at 1-year post-HDC), intermediate risk (25% EFS) or good risk (≥50% EFS). Given high VEGF expression in metastatic GCT and synergy between BEV and chemotherapy, we studied concurrent BEV/HDC in refractory GCT. Methods: Eligibility includes ≥ 1st relapse/PD, poor/interm risk and no contraindications to HDC or BEV. Treatment consisted of 2 cycles of HDC with stem-cell support following BEV (5 mg/kg) 1 week before each cycle. HDC-1 consists of a novel regimen of infusional gemcitabine with docetaxel/melphalan/carboplatin (BBMT 2005;11:297). HDC-2 includes ifosfamide/carboplatin/etoposide. Target accrual is 25 pts, to distinguish a 1-yr expected EFS of 15% (median time to progression [TTP], 9 months) from 50% 1-year EFS (median TTP, 2 years). Results: 21 pts have been treated, median age 22 (range, 19-45) poor risk (N=15) or interm risk (N=6), cisplatin refractoriness (N=9) or absolute refr (N=12), median 3 prior relapses (1-4), median 3 prior regimens (2-6), PD at HDC: 11 pts. Tumor sites: lungs (N=15), liver (8), bones (5), brain (5), retroperit (15), mediast (12). Histol at Dx: embryonal ca (4), chorio (3), mixed with teratoma (14). Prior surgery for metastases: 8 pts (6 abdomen, 1 liver, 1 brain). Prior radiation: 6 pts. Toxicity of HDC-1: grade 3 mucositis in all pts, rash (8 G2, 2 G3) and transaminase elevation; 2 pts with marginal baseline renal function died from early sepsis; 1 pt died from late fungal pneumonia. After HDC-1, markers normalized in 14/17 evaluable pts. 15 pts received HDC-2 at a median 49 (38-66) days after 1st stem cell infusion, which was well tolerated. 8 pts had residual lesions resected with findings of either teratoma (N=2) or no viable tumor (N=6). With median follow-up of 23 (3-43) months, 14 pts are alive in CR (67% EFS). Conclusions: BEV with HDCx2 shows encouraging preliminary results in heavily pretreated refractory GCT.
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Nitz, U. "Stammzellgestützte Hochdosischemotherapie (HDC) des Ovarialkarzinoms." Der Gynäkologe 30, no. 2 (February 27, 1997): 126–32. http://dx.doi.org/10.1007/pl00003025.
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Zhang, Zhiwei, Suling Ding, Xiangdong Yang, and Junbo Ge. "Analysis of Immune Associated Co-Expression Networks Reveals Immune-Related Long Non-Coding RNAs during MI in the Presence and Absence of HDC." International Journal of Molecular Sciences 22, no. 14 (July 9, 2021): 7401. http://dx.doi.org/10.3390/ijms22147401.
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Myocardial infarction (MI) is one of the most common cardiovascular diseases. Although previous studies have shown that histidine decarboxylase (HDC), a histamine-synthesizing enzyme, is involved in the stress response and heart remodeling after MI, the mechanism underlying it remains unclear. In this study, using Hdc-deficient mice (Hdc−/− mice), we established an acute myocardial infarction mouse model to explore the potential roles of Hdc/histamine in cardiac immune responses. Comprehensive analysis was performed on the transcriptomes of infarcted hearts. Differentially expressed gene (DEG) analysis identified 2126 DEGs in Hdc-deficient groups and 1013 in histamine-treated groups. Immune related pathways were enriched in Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Then we used the ssGSEA algorithm to evaluate 22 kinds of infiltrated immunocytes, which indicated that myeloid cells and T memory/follicular helper cells were tightly regulated by Hdc/histamine post MI. The relationships of lncRNAs and the Gene Ontology (GO) functions of protein-coding RNAs and immunocytes were dissected in networks to unveil immune-associated lncRNAs and their roles in immune modulation after MI. Finally, we screened out and verified four lncRNAs, which were closely implicated in tuning the immune responses after MI, including ENSMUST00000191157, ENSMUST00000180693 (PTPRE-AS1), and ENSMUST-00000182785. Our study highlighted the HDC-regulated myeloid cells as a driving force contributing to the government of transmission from innate immunocytes to adaptive immunocytes in the progression of the injury response after MI. We identified the potential role of the Hdc/histamine-lncRNAs network in regulating cardiac immune responses, which may provide novel promising therapeutic targets for further promoting the treatment of ischemic heart disease.
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Ali, Zain. "An Evidential Argument for Islamic Theism." European Journal for Philosophy of Religion 10, no. 4 (December 13, 2018): 55–78. http://dx.doi.org/10.24204/ejpr.v10i4.2515.
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In this paper, I argue that Islamic theism is best explained by the hypothesis of Divine Commission (HDC), whereby Muhammad is viewed as being divinely commissioned to serve the overall salvific purposes of God. To this end, I present three observation reports relating to Islamic theism and evaluate HDC against an alternative hypothesis, the hypothesis of Non-Commission (NC) whereby Muhammad is not viewed as being divinely commissioned. I argue that the probability of the observation reports is greater on the assumption that HDC is true than on the assumption that NC is true. Accordingly, this gives us reason to prefer HDC as a better explanation of Islamic theism.