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1

Pan, Xue, Haiying Li, Dingfang Chen, et al. "Comparison of Essential Oils of Houttuynia cordata Thunb. from Different Processing Methods and Harvest Seasons Based on GC-MS and Chemometric Analysis." International Journal of Analytical Chemistry 2021 (July 16, 2021): 1–13. http://dx.doi.org/10.1155/2021/8324169.

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Houttuyniae Herba (HH) refers to the dried aerial part of Houttuynia cordata Thunb. (DHC) or the fresh whole grass of Houttuynia cordata Thunb. (FHC), where DHC are harvested in summer and FHC around the year. However, harvest seasons and processing methods (i.e., medicinal parts and drying process) might affect the quality of HH. To compare the essential oils (EOs) of DHC and FHC and their two harvest seasons, GC-MS analysis combined with chemometric analysis was applied. The results showed that the oil yield of FHC (0.076 ± 0.030%) was higher than that of DHC (0.038 ± 0.029%), and oil yield was higher in summer than in autumn (0.044 ± 0.029% for DHC1, 0.036 ± 0.028% for DHC2, 0.084 ± 0.026% for FHC1, and 0.067 ± 0.033% for FHC2, respectively). Moreover, hierarchical cluster analysis (HCA) and principal component analysis (PCA) successfully distinguished the chemical constituents of DHC and FHC oils. Additionally, according to orthogonal partial least squares discriminant analysis (OPLS-DA), eleven components were selected as chemical markers for discriminating DHC and FHC, and two and four chemical markers for discriminating two harvest seasons of DHC and FHC, respectively. Among these markers, the average contents of α-pinene, limonene, β-phellandrene, α-terpineol, 4-tridecanone, and ethyl decanoate were higher in FHC oils. In contrast, the average contents of nonanal, 1-nonanol, β-cyclocitral, n-hexadecanoic acid, and octadecanol were higher in DHC oils. Additionally, the contents of 4-tridecanone and ethyl decanoate were both higher in DHC1 oils than in DHC2 oils. Moreover, the contents of β-myrcene and β-phellandrene were higher in FHC1 oils, while the contents of 2,6-octadien-1-ol, 3,7-dimethyl-, acetate, and (z)-phytol were higher in FHC2 oils. For these reasons, this study provides a scientific basis for quality control and clinical medication.
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2

Hemmann, Jethro L., Tristan Wagner, Seigo Shima, and Julia A. Vorholt. "Methylofuran is a prosthetic group of the formyltransferase/hydrolase complex and shuttles one-carbon units between two active sites." Proceedings of the National Academy of Sciences 116, no. 51 (2019): 25583–90. http://dx.doi.org/10.1073/pnas.1911595116.

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Methylotrophy, the ability of microorganisms to grow on reduced one-carbon substrates such as methane or methanol, is a feature of various bacterial species. The prevailing oxidation pathway depends on tetrahydromethanopterin (H4MPT) and methylofuran (MYFR), an analog of methanofuran from methanogenic archaea. Formyltransferase/hydrolase complex (Fhc) generates formate from formyl-H4MPT in two consecutive reactions where MYFR acts as a carrier of one-carbon units. Recently, we chemically characterized MYFR from the model methylotrophMethylorubrum extorquensand identified an unusually long polyglutamate side chain of up to 24 glutamates. Here, we report on the crystal structure of Fhc to investigate the function of the polyglutamate side chain in MYFR and the relatedness of the enzyme complex with the orthologous enzymes in archaea. We identified MYFR as a prosthetic group that is tightly, but noncovalently, bound to Fhc. Surprisingly, the structure of Fhc together with MYFR revealed that the polyglutamate side chain of MYFR is branched and contains glutamates with amide bonds at both their α- and γ-carboxyl groups. This negatively charged and branched polyglutamate side chain interacts with a cluster of conserved positively charged residues of Fhc, allowing for strong interactions. The MYFR binding site is located equidistantly from the active site of the formyltransferase (FhcD) and metallo-hydrolase (FhcA). The polyglutamate serves therefore an additional function as a swinging linker to shuttle the one-carbon carrying amine between the two active sites, thereby likely increasing overall catalysis while decreasing the need for high intracellular MYFR concentrations.
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3

Vardhan, Harsh, Apurb Rashmi Bhengraj, Rajneesh Jha, Pragya Srivastava, Hem Chandra Jha, and Aruna Mittal. "Higher expression of ferritin protectsChlamydia trachomatisinfected HeLa 229 cells from reactive oxygen species mediated cell death." Biochemistry and Cell Biology 88, no. 5 (2010): 835–42. http://dx.doi.org/10.1139/o10-027.

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Apoptosis plays an important role in modulating the pathogenesis of a variety of infectious diseases. Chlamydial infection protects cells against different forms of apoptosis: extrinsic, intrinsic, and granzyme B mediated. Redox reactions are central to the life and death decision of cells and pathogens and an intimate relationship exists between oxidative stress and iron metabolism. The link between redox status and ferritin was largely unexplored in chlamydia-infected cells. In the present study, we showed that Chlamydia trachomatis (CT) infection induced FHC protein in HeLa cells. FHC induction by CT-infected cells stably expressing FHC blunted ROS production compared with mock infected cells, and the infected cells were relatively resistant to apoptosis induced by H2O2. We also demonstrated that endogenous FHC overexpression correlates well with the stabilization of the mitochondrial membrane potential in CT-infected cells. Increased expression of FHC is independent of iron supplementation (FAC) and depletion (DFO) in CT-infected cells. These data suggest that FHC up-regulation is an acute response of HeLa cells against CT infection and that FHC exerts anti-apoptotic activity against oxidative stress.
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4

Schiffman, Joshua David, Ken R. Smith, Zachary Burningham, Wendy Kohlmann, and Karen Curtin. "Family history of cancer and clinical outcome in pediatric oncology." Journal of Clinical Oncology 30, no. 15_suppl (2012): 9525. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.9525.

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9525 Background: We previously reported in a small study (n=363) that children diagnosed with cancer who have a family history of cancer (FHC) may have worse prognosis than those without FHC, specifically children diagnosed with Hodgkin Disease (HD) and acute lymphoblastic leukemia (ALL) (Eichstadt et al., ASCO 2009). The Utah Population Database (UPDB), a unique resource, includes a Surveillance Epidemiology and End Results (SEER) registry (the Utah Cancer Registry) record-linked to extensive genealogies for 6.5 million people in which most Utah families are represented. A majority of pedigrees include ≥3 generations and several span 7+ generations. The UPDB provides an accurate, objective assessment of FHC. We expanded our original study by examining cancer mortality of 4,482 pediatric cases (age ≤18) diagnosed from 1966-2009 with adequate follow-up (median 9.5 years) and family information. Methods: We compared survival from cancer-caused mortality for pediatric cases diagnosed from 1966-2009 with FHC of any cancer diagnosed <80 yo in 1st-degree, 2nd-degree, or 3rd-degree relatives to pediatric cases without FHC. Nonparametric estimates of survivor function were determined by the life-table method and a log-rank test of homogeneity was used to test for differences between pediatric probands with FHC compared to no FHC. Results: Overall survival was significantly lower in children with positive FHC (n=1,128) than in children with no FHC (n=3,354) independent of stage (p<0.0001; 10yr survival, 69% with FHC vs.78% with no FHC). We observed lower survival in children with any leukemia and FHC (n=279) compared to children with leukemia and no FHC (n=871; p<0.0001). In particular, cases with ALL and FHC had lower survival (p<0.0001; 10yr survival, 61% vs. 75%). Pediatric lymphoma cases had lower survival when positive for FHC (n=150) vs. no FHC (n=428; p<0.0001), specifically for an HD diagnosis (p=0.0004; 10yr survival, 83% vs. 94%). Conclusions: Pediatric cancer cases with FHC of any cancer (children or adults) have decreased survival compared to cases with no FHC, specifically in children diagnosed with ALL or HD, thus validating our earlier findings. Familial factors likely contribute to increased pediatric cancer mortality.
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5

Cortellini, Alessio, Sebastiano Buti, Daniele Santini, et al. "Family history of cancer as surrogate predictor for immunotherapy with anti-PD-1/PD-L1 immune checkpoint inhibitors: The FAMI-L1 study." Journal of Clinical Oncology 37, no. 15_suppl (2019): 2559. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.2559.

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2559 Background: In the preliminary analysis of the FAMI-L1 study, we found a significant association between family history of cancer (FHC) and better clinical outcomes with anti-PD1/PD-L1 inhibitors. Methods: We retrospectively evaluated advanced cancer patients treated with single agents PD1/PD-L1 inhibitors. Patients were categorized as follow: FHC-high (in case of at least one cancer diagnoses in both straight and collateral family line), FHC-low (in case of a cancer diagnoses in only one family line) and FHC-negative. FHC was collected till the second degree of relatedness. Results: Between September 2013 and May 2018, 772 consecutive patients were evaluated. Median age was 68 years; male/female ratio was 521/251. Primary tumors were: NSCLC (58.3%), melanoma (22.1%), renal cell carcinoma (16.6%) and others (3%). 114 patients (14.9%) had ECOG-PS ≥ 2. 341 patients (44.3) were FHC-positive: 268 of them (34.75) were FHC-low while 74 (9.6%) were FHC-high. FHC-high patients had a significantly higher incidence of irAEs compared to FHC-negative (55.4% vs 35.6%; p = 0.0012) and to FHC-low (41.4%; p = 0.0323). No significant differences were found in terms of ORR among subgroups (data not shown). At median follow-up of 15.8 months, median PFS was 9.1 months (95%CI: 8.1-10.4; 452 events) and median OS was 19.7 months (95%CI: 15.7-24.4; 436 censored). No significant differences were found regarding PFS (data not shown). Median OS of FHC-high patients was 31.6 months (95%CI: 26.2-31.6; 50 censored patients), which was significantly longer than 18.2 months (95%CI: 14.7-21.3; 229 censored patients) of FHC-negative patients (HR = 0.60 [95%CI: 0.39–0.92), p = 0.0213). No significant differences in terms of OS were found between FHC-high/low patients (data not shown). After adjusting for primary tumor, sex, treatment-line, number of metastatic sites and ECOG-PS, FHC-high was confirmed an independent predictor of longer OS compared to FHC-negative (HR: 0.57 [95%CI: 0.37-0.88], p = 0.0098). Conclusions: FHC-high seems to be an independent predictor for longer OS in cancer patients treated with anti-PD-1/PD-L1. DNA damage and response (DDR) genes alterations may underlie that results.
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6

Eichstadt, S. L., G. V. Dahl, P. G. Fisher, J. M. Ford, and J. D. Schiffman. "Correlation of a family history of cancer with risk of relapse and death in pediatric cancer patients." Journal of Clinical Oncology 27, no. 15_suppl (2009): 10029. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.10029.

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10029 Background: The association between family history of cancer (FHC) and outcome remains uncertain. Relapse and survival of children with FHC has not been well studied. Such information would be valuable for prognosis, refining treatment protocols, and long-term follow-up in pediatric patients with FHC. Methods: An historical cohort study of all pediatric patients diagnosed with cancer at Lucile Packard Children's Hospital at Stanford from 1999 - 2002 was performed (n = 363, mean age: 8.4 yrs [0–28 yrs]). FHC among 1st, 2nd and 3rd degree relatives was obtained from the first 10 consecutive encounters in the electronic medical record. Relapse, secondary malignancy, and survival data were also acquired. The relative risks for these endpoints were calculated between patients with FHC among 1st and/or 2nd degree relatives and those with negative FHC. Patients without documented FHC were excluded (n = 100). Results: 108 (41%) newly diagnosed pediatric patients had reported FHC (1st Degree: n = 14 [5%], 2nd Degree: n = 58 [22%], 3rd Degree: n = 36 [14%]). Patients with reported FHC among 1st and/or 2nd degree relatives were at increased relative risk [RR] for relapse (1.96, 95% confidence interval [CI] 1.27–3.02) compared to patients with negative FHC (n = 191). In particular, patients with Hodgkin Disease (HD) and FHC (n = 12) were more likely to relapse (RR 1.79, 95% CI 1.19–2.72) and at increased risk of death (RR 1.72, 95% CI 1.18–2.53), compared to HD with negative FHC (n = 8). Similarly, patients diagnosed with ALL and FHC (n = 22) had increased risk of death (RR 2.25, 95% CI 1.06–4.8) compared to ALL patients with negative FHC (n = 56). For patients diagnosed with any pediatric cancer and positive FHC in 1st degree relative, RR of death was significantly elevated (3.74, 95% CI 1.20–11.70). Conclusions: Pediatric cancer patients with positive FHC among 1st and/or 2nd degree relatives appear to have higher relative risk of relapse compared to those with negative FHC. Additionally, an increased risk of death was associated with HD and ALL patients with positive FHC. Patients with 1st degree relative with malignancy had an increased risk for death compared to those without cancer among 1st degree relatives. These findings may reflect underlying genetic predispositions in children which contribute to outcome. No significant financial relationships to disclose.
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7

Rajan, Sudarsan, Sarah S. Williams, Ganapathy Jagatheesan, et al. "Microarray analysis of gene expression during early stages of mild and severe cardiac hypertrophy." Physiological Genomics 27, no. 3 (2006): 309–17. http://dx.doi.org/10.1152/physiolgenomics.00072.2006.

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Familial hypertrophic cardiomyopathy (FHC) is a disease characterized by ventricular hypertrophy, fibrosis, and aberrant systolic and/or diastolic function. We previously developed two transgenic mouse models that carry FHC-associated mutations in α-tropomyosin (TM): FHC α-TM175 mice show patchy areas of mild ventricular disorganization and limited hypertrophy, whereas FHC α-TM180 mice exhibit severe hypertrophy and fibrosis and die within 6 mo. To obtain a better understanding of the molecular mechanisms associated with the early onset of cardiac hypertrophy, we conducted a detailed comparative analysis of gene expression in 2.5-mo-old control, FHC α-TM175, and α-TM180 ventricular tissue. Results show that 754 genes (from a total of 22,600) were differentially expressed between the nontransgenic (NTG) and the FHC hearts. There are 178 differentially regulated genes between NTG and the FHC α-TM175 hearts, 388 genes are differentially expressed between NTG and FHC α-TM180 hearts, and 266 genes are differentially expressed between FHC α-TM175 and FHC α-TM180 hearts. Genes that exhibit the largest increase in expression belong to the “secreted/extracellular matrix” category, and those with the most significant decrease in expression are associated with “metabolic enzymes.” Confirmation of the microarray analysis was conducted by quantitative real-time PCR on gene transcripts commonly associated with cardiac hypertrophy.
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8

Aversa, Ilenia, Roberta Chirillo, Emanuela Chiarella та ін. "Chemoresistance in H-Ferritin Silenced Cells: The Role of NF-κB". International Journal of Molecular Sciences 19, № 10 (2018): 2969. http://dx.doi.org/10.3390/ijms19102969.

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Nuclear Factor-κB (NF-κB) is frequently activated in tumor cells contributing to aggressive tumor growth and resistance to chemotherapy. Here we demonstrate that Ferritin Heavy Chain (FHC) protein expression inversely correlates with NF-κB activation in cancer cell lines. In fact, FHC silencing in K562 and SKOV3 cancer cell lines induced p65 nuclear accumulation, whereas FHC overexpression correlated with p65 nuclear depletion in the same cell lines. In FHC-silenced cells, the p65 nuclear accumulation was reverted by treatment with the reactive oxygen species (ROS) scavenger, indicating that NF-κB activation was an indirect effect of FHC on redox metabolism. Finally, FHC knock-down in K562 and SKOV3 cancer cell lines resulted in an improved cell viability following doxorubicin or cisplatin treatment, being counteracted by the transient expression of inhibitory of NF-κB, IκBα. Our results provide an additional layer of information on the complex interplay of FHC with cellular metabolism, and highlight a novel scenario of NF-κB-mediated chemoresistance triggered by the downregulation of FHC with potential therapeutic implications.
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9

Santaella Gonçalves, Rodrigo. "FHC (1993-1994):." Conhecer: debate entre o público e o privado 8, no. 21 (2018): 117–50. http://dx.doi.org/10.32335/2238-0426.2018.8.21.1070.

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Este estudo busca elucidar aspectos da relação entre teoria e prática em Fernando Henrique Cardoso (FHC), desde o início de sua produção teórica até sua primeira candidatura presidencial, em 1994. Esta análise contrasta com as interpretações que encontram nas formulações sobre dependência a origem determinada da trajetória política de FHC – seja com um viés de continuidade, como se a teoria prévia houvesse determinado a prática, seja de ruptura, como se a prática fosse fruto de um corte com a teoria original. Buscamos demonstrar como a definição de uma nova hegemonia no país no final dos anos 1980 criou as condições para a consolidação desse pragmatismo em FHC, que passou a justificar “teoricamente” suas ações a partir do retorno a uma dicotomia moderno ´ arcaico que ele próprio ajudara a superar com a teoria da dependência. Nesse sentido, enfocamos os dois anos imediatamente anteriores à sua chegada à Presidência da República, para ilustrar os últimos anos de consolidação de uma nova visão do Brasil para FHC, como forma de subsidiar a compreensão do que foram seus governos, tanto no que diz respeito às políticas públicas quanto à própria concepção de Estado que norteava suas ações.
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10

Yu, Yun-Zhou, Na Li, Rui-Lin Wang, et al. "Evaluation of a Recombinant Hc of Clostridium botulinum Neurotoxin Serotype F as an Effective Subunit Vaccine." Clinical and Vaccine Immunology 15, no. 12 (2008): 1819–23. http://dx.doi.org/10.1128/cvi.00239-08.

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ABSTRACT A new gene encoding the Hc domain of Clostridium botulinum neurotoxin serotype F (FHc) was designed and completely synthesized with oligonucleotides. A soluble recombinant Hc of C. botulinum neurotoxin serotype F was highly expressed in Escherichia coli with this synthetic FHc gene. Subsequently, the purified FHc was used to vaccinate mice and evaluate their survival against challenge with active botulinum neurotoxin serotype F (BoNT/F). After the administration of FHc protein mixed with Freund adjuvant via the subcutaneous route, a strong protective immune response was elicited in the vaccinated mice. Mice that were given two or three vaccinations with a dosage of 1 or 10 μg of FHc were completely protected against an intraperitoneal administration of 20,000 50% lethal doses (LD50) of BoNT/F. The BoNT/F neutralization assay showed that the sera from these vaccinated mice contained high titers of protective antibodies. Furthermore, mice were vaccinated once, twice, or three times at four different dosages of FHc using Alhydrogel (Sigma) adjuvant via the intramuscular route and subsequently challenged with 20,000 LD50 of neurotoxin serotype F. A dose response was observed in both the antibody titer and the protective efficacy with increasing dosage of FHc and number of vaccinations. Mice that received one injection of 5 μg or two injections of ≥0.04 μg of FHc were completely protected. These findings suggest that the recombinant FHc expressed in E. coli is efficacious in protecting mice against challenge with BoNT/F and that the recombinant FHc subunit vaccine may be useful in humans.
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11

Pritzkow, Hans, Klaus Rall, Stefan Reimann-Andersen, and Wolfgang Sundermeyer. "Inverse Amine-Stabilized Sulfenes F2CSO2 and FHCSO2." Angewandte Chemie International Edition in English 29, no. 1 (1990): 60–61. http://dx.doi.org/10.1002/anie.199000601.

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12

Guo, Jianqiao, Yajun Yin, and Gang Peng. "Fractional-order viscoelastic model of musculoskeletal tissues: correlation with fractals." Proceedings of the Royal Society A: Mathematical, Physical and Engineering Sciences 477, no. 2249 (2021): 20200990. http://dx.doi.org/10.1098/rspa.2020.0990.

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Self-similar fractals are widely obtained from biomaterials within the human musculoskeletal system, and their viscoelastic behaviours can be described by fractional-order derivatives. However, existing viscoelastic models neglect the internal correlation between the fractal structure of biomaterials and their fractional-order temporal responses. We further expanded the fractal hyper-cell (FHC) viscoelasticity theory to investigate this spatio-temporal correlation. The FHC element was first compared with other material elements and spring–dashpot viscoelastic models, thereby highlighting its discrete and fractal nature. To demonstrate the utility of an FHC, tree-like, ladder-like and triangle-like FHCs were abstracted from human cartilage, tendons and muscle cross-sections, respectively. The duality and symmetry of the FHC element were further discussed, where operating the duality transformation generated new types of FHC elements, and the symmetry breaking of an FHC altered its fractional-order viscoelastic responses. Thus, the correlations between the staggering patterns of FHCs and their rheological power-law orders were established, and the viscoelastic behaviour of the multi-level FHC elements fitted well in stress relaxation experiments at both the macro- and nano-levels of the tendon hierarchy. The FHC element provides a theoretical basis for understanding the connections between structural degeneration of bio-tissues during ageing or disease and their functional changes.
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Ostovarfar, Jeyran, Mohammad Hossein Kaveh, Leila Ghahramani, Masoud Karimi, Abdolrahim Asadollahi, and Razie Zare. "The Validity and Reliability of the Persian Version of the Family Health Climate Scale (FHC-Scale) in Female Students and Their Mothers in Iran 2019." BioMed Research International 2021 (February 5, 2021): 1–9. http://dx.doi.org/10.1155/2021/8845716.

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Objectives. This study examined the validity and reliability of the Family Health Climate Scale (FHC-Scale) among Iranian families. Second, can it be attributed to other family members by measuring the health climate in one person? Method. In total, 261 female students and 196 mothers completed the FHC-Scale. The study instrument was a Persian version of the FHC-Scale prepared through a translation and back-translation process. Results. The results showed that the Persian version of the FHC-Scale is acceptable. Cronbach’s alpha coefficient for FHC-PA in female students and their mothers, respectively, was 0.88 and 0.86 for the whole scale. Cronbach’s alpha coefficient for FHC-NU in female students and their mothers, respectively, was 0.83 and 0.92 for the whole scale. The CVI values for all the items were equal to or above 0.8, and the CVR value for the total scale was 0.90. Conclusion. The Persian version of the FHC-Scale is therefore an effective tool for evaluating the different dimensions of family health climate in the Iranian population.
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Żylicz, Jan J., and Edith Heard. "Molecular Mechanisms of Facultative Heterochromatin Formation: An X-Chromosome Perspective." Annual Review of Biochemistry 89, no. 1 (2020): 255–82. http://dx.doi.org/10.1146/annurev-biochem-062917-012655.

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Facultative heterochromatin (fHC) concerns the developmentally regulated heterochromatinization of different regions of the genome and, in the case of the mammalian X chromosome and imprinted loci, of only one allele of a homologous pair. The formation of fHC participates in the timely repression of genes, by resisting strong trans activators. In this review, we discuss the molecular mechanisms underlying the establishment and maintenance of fHC in mammals using a mouse model. We focus on X-chromosome inactivation (XCI) as a paradigm for fHC but also relate it to genomic imprinting and homeobox ( Hox) gene cluster repression. A vital role for noncoding transcription and/or transcripts emerges as the general principle of triggering XCI and canonical imprinting. However, other types of fHC are established through an unknown mechanism, independent of noncoding transcription ( Hox clusters and noncanonical imprinting). We also extensively discuss polycomb-group repressive complexes (PRCs), which frequently play a vital role in fHC maintenance.
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N Ntafam, Carnot, Chigozie Nwobi Ivor, David Otohinoyi, Okikiade Adedeji, and Joseph Dimas. "Sonographic Assessment of the Fetal Heart Circumference as a Predictor of the Gestational Age." Journal of applied health sciences 7, no. 2 (2021): 127–36. http://dx.doi.org/10.24141/1/7/2/3.

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Introduction: Ultrasound is a non-invasive imaging modality, safe for both the mother and the fetus, which uses a high frequency sound to generate images of body tissues and organs. It has been widely used for fetal evaluation and dating. Purpose: To determine normative values of fetal heart circumference (FHC) as a predictor of the gestational age (GA) in black population and compare it to those of the Caucasian population. Material and Methods: A prospective cross-sectional study was carried at the University of Maiduguri Teaching Hospital (UMTH), Nigeria. 324 women with a singleton pregnancy between 12-40 weeks, who conceived naturally, were scanned using a 2D ultrasound machine with a 3.5 MHz curvilinear probe. Two fetal heart diametersat right angle to each other were taken at the level of the four-heart chamber view, during diastole. Results: There is a strong positive linear correlation between the FHC and the GA (r2= 0.964, p<0.001). The equation of GA prediction is Y=0.246X + 5.06 (where y=GA, X=FHC). FHC weekly growth rate is 3.81mm. FHC is more accurate between 12-20 weeks GA and its accuracy decreases as the pregnancy progresses. There is a strong correlation between FHC and biparietal diameter (BPD) (r2=0.959), HC(r2=0.946) and FL (r2= 0.962). Conclusion: The study has derived a nomogram of FHC as a predictor of the GA in Nigerian population and has shown that the FHC is a good predictor of GA especially in the early second trimester. Also, there was a statistically significant difference between the FHC in our study population (blacks) and those of the Caucasian population.
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16

Korneva, V. A., T. Yu Bogoslovskaya, T. Yu Kuznetsova, M. Yu Mandelshtam, and V. B. Vasilev. "Phenotype receptor gene mutations in low-density lipoprotein in patients with familial hypercholesterolemia in Karelia." CardioSomatics 6, no. 1 (2015): 46–49. http://dx.doi.org/10.26442/cs45144.

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Familial hypercholesterolemia (FHC) - hereditary dyslipidemia, which is based on mutations in the gene for low-density lipoprotein receptor.However, there is variability in the clinical manifestations of the disease difficult to assess individual risk.Materials and methods. Under our supervision for 10 years were 109 patients with FHC, 17 mutation in the receptor density lipoprotein. FHC diagnosis established by the criteria of the British leadership Simon Broom. To search for mutations in low-density lipoprotein receptor was performed automated fluorescent SSCP-analysis of exons of the gene analysis of restriction fragment length polymorphism and the direct sequencing of DNA on a gel sequencer ALFExpress-2 (Amersham Biosciences) using the program ALFwin Sequence Analyzer.The Results. We analyzed five clinical cases of patients with genetically confirmed diagnosis of FHC. Shows a wide phenotypic variability FHC: the possibility of early debut of coronary heart disease, coronary tropism for the pool some patients and cerebral - others, the possibility of a long asymptomatic disease.Conclusion. The absence of clinical manifestations of atherosclerosis and wide phenotypic variability at FHC require targeted screening for FHC, at least among patients with coronary heart disease in order to timely and adequate preventive measures, especially in cases where the mutation is set low density lipoprotein receptor.
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LATIFI, SHAHRAM. "SUBCUBE EMBEDDABILITY OF FOLDED HYPERCUBES." Parallel Processing Letters 01, no. 01 (1991): 43–50. http://dx.doi.org/10.1142/s0129626491000203.

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The Folded Hypercube (FHC) has been proven to be an attractive hypercube-based network. This paper closely compares the FHC to its standard hypercube counterpart from the subcube allocation viewpoint. It is shown that the FHC(n) outperforms the n-dimensional hypercube (n-cube for short) in offering subcubes of size k by a factor of [Formula: see text]. In an environment where subcubes of the original network must be allocated to incoming tasks, the FHC achieves an excellent processor utilization by assigning subcubes in an efficient and compact manner. Using the concept of virtual hypercubes, an efficient way is suggested to recognize the available subcubes in the FHC by adapting the already developed subcube recognition algorithms. An alternative approach to the subcube recognition problem is also given.
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Pandya, Bhavyata, Vagisha Ravi, and James Connor. "TMIC-43. ROLE OF EXTRACELLULAR FERRITIN HEAVY CHAIN PROTEIN IN GLIOBLASTOMA MULTIFORME." Neuro-Oncology 21, Supplement_6 (2019): vi257. http://dx.doi.org/10.1093/neuonc/noz175.1077.

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Abstract Increased expression of Ferritin heavy chain (FHC) protein has been associated with poor prognosis in Glioblastoma Multiforme (GBM) which is one of the most aggressive and common types of brain cancer. GBM patients have also been found to have increased extracellular ferritin levels, in their serum and cerebrospinal fluid (CSF), which are lowered once the source/tumor has been resected. Extracellular FHC can function as an iron delivery protein, and increasing amount of iron has been known to contribute to tumor initiation and proliferation. To study the effect of extracellular FHC in GBM cells we used patient derived GBM, CD133+ cancer stem cells (GSCs) from the pro-neural (T3691) and mesenchymal (T387) subtypes. Using recombinant FHC, conjugated with quantum dots (QD), we observed significant increase in cellular viability and intracellular uptake of FHC by the GSCs in a dose dependent manner. Our lab has previously shown that extracellular FHC interacts with T-Cell Immunoglobulin Mucin Receptor 1 (Tim-1) in the human oligodendrocytes. In order to determine if GSCs express the Tim-1 receptor we first confirmed its expression on GSCs using immunoblotting and immunocytochemistry. To test if FHC interacts with Tim-1, we performed knockdown of Tim-1 using siRNAs. However, the siRNA was not able to downregulate the Tim-1 receptors. Next, we exposed the GSCs to Sema4A, which has been shown in our previous studies to interact with Tim-1 receptor on human oligodendrocytes and is toxic to oligodendrocytes. The GSCs however were not affected by the saturable concentration of Sema4A. Thus, through this study we have shown the expression of potential FHC receptors on GSCs and a robust effect of H-ferritin on GSCs proliferation. Further experiments are warranted in this direction to understand this extracellular FHC uptake pathway and its role in GBM cell proliferation.
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Sallum Jr, Brasilio. "Sobre o dossiê FHC." Tempo Social 11, no. 2 (1999): 1–2. http://dx.doi.org/10.1590/s0103-20701999000200001.

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Vercellotti, Gregory M., Chunsheng Chen, Carol M. Bruzzone, et al. "H-Ferritin Ferroxidase Activity Induces Cytoprotective Pathways and Inhibits Microvascular Stasis in Transgenic Sickle Mice." Blood 120, no. 21 (2012): 378. http://dx.doi.org/10.1182/blood.v120.21.378.378.

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Abstract Abstract 378 Hemolysis, oxidative stress, inflammation, vaso-occlusion and organ infarction are hallmarks of sickle cell disease (SCD). We hypothesize that intravascular heme, liberated from hemoglobin S derived from hemolyzed sickle red blood cells, is fundamental to inflammation and vaso-occlusion in SCD. Heme can be degraded by heme-oxygenase-1 (HO-1), releasing Fe2+, carbon monoxide (CO), and biliverdin/bilirubin. We have previously shown that increases in HO-1 activity inhibit vascular inflammation and vaso-occlusion in transgenic mouse models of SCD. HO-1 products, CO and biliverdin/bilirubin, also are protective in SCD, but Fe2+ released from the heme ring requires further processing. The released Fe2+ from heme is oxidized by ferritin heavy chain (FHC) ferroxidase activity and safely stored as catalytically-inactive Fe3+ inside ferritin clusters. FHC overexpression has been shown to be cytoprotective in response to inflammation and oxidative stress in vivo and in vitro. In this study, we hypothesize that overexpression of FHC with its ferroxidase activity will inhibit inflammation and microvascular stasis in transgenic sickle mice in response to stroma-free hemoglobin. We utilized a Sleeping Beauty transposase plasmid to deliver a human wt-ferritin heavy chain (wt-FHC) transposable element by hydrodynamic tail vein injections to NY1DD SCD mice. Control mice were infused with the same volume of lactated Ringer's solution LRS) or a triple missense (ms-) human FHC plasmid encoding no ferroxidase enzyme activity. Eight weeks after injection, the mice were implanted with dorsal skin-fold chambers to access microvascular blood flow. LRS-treated mice had 40% microvascular stasis (% non-flowing venules) when infused with stroma-free hemoglobin, while wt-FHC overexpressing mice had only 5% stasis (p<0.05), suggesting vascular protection by wt-FHC. Ferroxidase activity was critical in this protection as mice overexpressing ms-FHC were not protected from microvascular stasis (33%). The wt-FHC SCD mice had marked increases in FHC mRNA and protein, light chain ferritin, 5-aminolevulinic acid synthase (5-ALA-synthase), cellular heme content, ferroportin, nuclear factor erythroid 2-related factor 2 (Nrf2), nuclear FHC and microsomal HO-1 activity and protein, and a decrease in activated phosho- and total nuclear factor-kappa B (NF-κB) p65 in the nuclei of the livers. We conclude that wt-FHC ferroxidase activity enhances 5-ALA-synthase activity and cytoprotective Nrf2-regulated proteins including HO-1 resulting in decreased NF-κB-activation, inflammation and microvascular stasis in transgenic SCD mice. Therapies directed at increasing ferritin heavy chain production and decreasing reactive iron availability may be beneficial in limiting sickle cell crises and end organ damage. Disclosures: Vercellotti: Sangart Inc: Consultancy, Research Funding. Chen:Sangart Inc: Research Funding. Hebbel:Sangart Inc: Consultancy, Research Funding. Belcher:Sangart Inc: Research Funding.
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Zafiraki, Vitalii K., Alim M. Namitokov, and Elena D. Kosmacheva. "FAMILIAL HYPERCHOLESTEROLEMIA: DIAGNOSTIC ISSUES AND THERAPEUTIC POSSIBILITIES." Kuban Scientific Medical Bulletin 26, no. 1 (2019): 175–86. http://dx.doi.org/10.25207/1608-6228-2019-26-1-175-186.

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Familial hypercholesterolemia (FHC) is a common monogenic disease that occurs with a frequency of ~1:250 and is characterised by a high content of low-density lipoprotein (LDL) in the blood. This disease leads to the early development of atherosclerotic cardiovascular diseases (ACVD). Although the screening and diagnostics issues concerned with FHC are well developed and the modern lipid-lowering therapy can significantly improve the prognosis, the detectability of this disease remains extremely low. In recent years, the concept of FHC has undergone significant changes under the influence of large epidemiological studies, including verification of the FHC diagnosis using genetic tests. The article is aimed at discussing the clinical manifestations of FHC, as well as modern medical and extracorporal approaches to its treatment.Conclusion.Until the advent of modern lipid-lowering drugs, FHC had remained to be a disease with a poor prognosis due to early ACVD and the associated premature death. Today, the diseases is amenable to successful treatment, which, though not eliminating the genetic defect, allows almost the same life duration as in the general population to be achieved. However, all the possibilities of modern approaches to the treatment of this serious disease can be realized provided that a state-level screening program for such patients has been implemented.Conflict of interest: the authors declare no conflict of interest.
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Johnson, Ali C., Ted Gooley, Alvaro Guillem, et al. "Parenterial iron sucrose-induced renal preconditioning: differential ferritin heavy and light chain expression in plasma, urine, and internal organs." American Journal of Physiology-Renal Physiology 317, no. 6 (2019): F1563—F1571. http://dx.doi.org/10.1152/ajprenal.00307.2019.

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Experimental data suggest that iron sucrose (FeS) injection, used either alone or in combination with other prooxidants, can induce “renal preconditioning,” in part by upregulating cytoprotective ferritin levels. However, the rapidity, degree, composition (heavy vs. light chain), and renal ferritin changes after FeS administration in humans remain to be defined. To address these issues, healthy human volunteers ( n = 9) and patients with stage 3–4 chronic kidney disease( n = 9) were injected once with FeS (120, 240, or 360 mg). Plasma ferritin was measured from 0 to 8 days postinjection as an overall index of ferritin generation. Urinary ferritin served as a “biomarker” of renal ferritin production. FeS induced rapid (≤2 h), dose-dependent, plasma ferritin increases in all study participants, peaking at approximately three to five times baseline within 24–48 h. Significant urinary ferritin increases (~3 times), without dose-dependent increases in albuminuria, neutrophil gelatinase-associated lipocalin, or N-acetyl-β-d-glucosaminidase excretion, were observed. Western blot analysis with ferritin heavy chain (Fhc)- and light chain (Flc)-specific antibodies demonstrated that FeS raised plasma Flc but not Fhc levels. Conversely, FeS increased both Fhc and Flc in urine. To assess sites of FeS-induced ferritin generation, organs from FeS-treated mice were probed for Fhc, Flc, and their mRNAs. FeS predominantly raised hepatic Flc. Conversely, marked Fhc and Flc elevations developed in the kidney and spleen. No cardiopulmonary ferritin increases occurred. Ferritin mRNAs remained unchanged throughout, implying posttranscriptional ferritin production. We conclude that FeS induces rapid, dramatic, and differential Fhc and Flc upregulation in organs. Renal Fhc and Flc increases, in the absence of nephrotoxicity, suggest potential FeS utility as a clinical renal “preconditioning” agent.
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Chen, Liye, Hui Shi, Jack Yuan, and Paul Bowness. "Position 97 of HLA-B, a residue implicated in pathogenesis of ankylosing spondylitis, plays a key role in cell surface free heavy chain expression." Annals of the Rheumatic Diseases 76, no. 3 (2016): 593–601. http://dx.doi.org/10.1136/annrheumdis-2016-209512.

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ObjectiveAssociation of position 97 (P97) residue polymorphisms in human leucocyte antigen (HLA)-B, including HLA-B*27, with ankylosing spondylitis (AS) has recently been reported. We studied the effect of P97 variations on cell surface expression of the AS-associated HLA-B*27 and HLA-B*51, and the AS-protective HLA-B*7.MethodsFlow cytometry was used to measure surface expression of HLA-B*27 in C1R/HeLa cells expressing HLA-B*27 (N97) and six mutants at P97 (N97T, N97S, N97V, N97R, N97W and N97D). Transporter associated with antigen processing-deficient T2, tapasin-deficient 220, β2m-deficient HCT15 and endoplasmic reticulum aminopeptidase 1 or β2m-clustered regularly interspaced short palindromic repeats/Cas9-knockout HeLa cells were used to provide evidence for specific protein interactions. Surface expression of HLA-B*7/HLA-B*51 P97 mutants was also studied.ResultsMutation of HLA-B*27 P97 to the AS risk residue threonine increased cell surface free heavy chain (FHC) expression. Protective residues (serine or valine) and non-AS-associated residues (arginine or tryptophan) did not alter FHC expression. The N97D mutation reduced expression of conventional and FHC forms of HLA-B*27. Differences in FHC expression levels between HLA-B*27, HLA-B*27-N97T and HLA-B*27-N97D were dependent on the presence of functional β2m. HLA-B*7, which has an AS-protective serine at P97, expressed lower levels of FHC than HLA-B*27 or HLA-B*51. Introduction of asparagine at P97 of both HLA-B*7 and HLA-B*51 increased FHC expression.ConclusionsThe nature of P97 residue affects surface expression of HLA-B*27, B*7 and B*51, with AS-associated residues giving rise to higher FHC expression levels. The association of P97 amino acid polymorphisms with AS could be, at least in part, explained by its effect on HLA-B*27 FHC cell surface expression.
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24

Zhang, Baoqin, Tiantian Li, Chao Wang, Jing Han, Baiqing Wang, and Guangbin Sun. "LncRNA MALAT1: A potential therapeutic target in DSSinduced ulcerative colitis progression in vitro." Tropical Journal of Pharmaceutical Research 19, no. 9 (2020): 1871–77. http://dx.doi.org/10.4314/tjpr.v19i9.11.

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Purpose: Ulcerative colitis is a severe disease affecting human health worldwide. Studies have shown that lncRNA MALAT1 has a significant correlation with breast, pancreatic, colon and liver cancers, but its effects on colitis is yet to be discovered. In this study, the potential role of lncRNA MALAT1 and the underlying molecular mechanism in DSS-induced colitis were investigated in vitro.Methods: Colorectal mucosal cell line FHC was induced with dextran sulphate sodium (DSS) to form an in vitro colitis model. Transfection procedure was employed to up- or down-regulate the expressions of lncRNA MALAT1 or miR-30c-5p in FHC cells. Cell viabilities were detected by CCK-8 assay. RT-qPCR was applied for evaluating gene expressions in normal FHC and DSS-induced FHC cell lines, while protein expression levels of target genes were examined by Western blot analysis. Starbase was used to predict the molecular interaction between MALAT1 and miR-30c-5p, while luciferase reporter assay was utilized to verify the binding sites between the two genes.Results: Expression of MALAT1 in the DSS-induced FHC cells was high with low cell viabilities, compared to the normal FHC cells. In the DSS-induced colitis-like FHC cells, overexpression of MALAT1 inhibited cell viabilities, while its downregulation promoted it. MiR-30c-5p directly targets MALAT1 and inhibited its expression in DSS-treated FHC cells. Upregulation of miR-30c-5p increased cell viabilities. Bcl-xL expression was inhibited by the up-regulation of MALAT1, while that of Bax was enhanced and the mimics of miR-30c-5p reversed these observations, suggesting that the enhancement of apoptosis promoted by oe-MALAT1 could be inhibited by miR-30c-5p. The interaction between MALAT1 and miR-30c-5p regulated NF-κB/TGF-β/Wnt-β-catenin signaling pathway.Conclusion: Overexpression of MALAT1 led to inhibition of cell viability, while apoptosis and inflammation were promoted by targeting miR-30c-5p via NF-κB/TGF-β/Wnt-β-catenin signaling pathway. These findings suggest MALAT1 as a therapeutic target for treating colitis.
 Keywords: Colitis, MALAT1, miR-30c-5p, NF-κB/TGF-β/Wnt-β-catenin
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Mangal, Utkarsh, Jae Joon Hwang, Heon Jo, et al. "Effects of Changes in the Frankfort Horizontal Plane Definition on the Three-Dimensional Cephalometric Evaluation of Symmetry." Applied Sciences 10, no. 22 (2020): 7956. http://dx.doi.org/10.3390/app10227956.

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The plane formed by the intersection of bilateral porions (PoR and PoL) and left orbitale (OrL) is conventionally defined as the Frankfort horizontal (FH) plane. We aim to test the influence of the FH plane definition on a 3D cephalometric assessment. We selected 38 adult patients (20 males, 18 females; average age: 22.87 ± 5.17 years) without any gross asymmetry from retrospective records and traced and analyzed their cone-beam computed tomographic images. The findings were categorized into the following four groups: FH1: conventional; FH2: PoR, PoL, right orbitale (OrR); FH3: OrR, OrL, PoL; FH4: OrR, OrL, PoR. The average menton (Me) deviation from the MSP was statistically significant for the FH1 group (0.56 ± 0.27 mm; p < 0.001), compared to the FH3 (1.37 ± 1.23 mm) and FH4 (1.33 ± 1.16 mm) groups. The spatial orientation level (SOL) of the FH plane showed a marked difference (p < 0.05) between the FH2 (0.602° ± 0.503°) and FH4 (0.944° ± 0.778°) groups. The SOL of the MSP was comparatively small (p < 0.001) for FH2 (0.015° ± 0.023°) in comparison to both FH 3 (0.644° ± 0.546°) and FH 4 (0.627° ± 0.516°). Therefore, the FH plane definition can significantly influence the interpretation of cephalometric findings. Future studies should focus on standardization to improve the reliability and reproducibility of 3D cephalometry.
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26

Touraine, Alain. "O campo político de FHC." Tempo Social 11, no. 2 (1999): 3–22. http://dx.doi.org/10.1590/s0103-20701999000200002.

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Lafer, Celso. "FHC: o intelectual como político." Novos Estudos - CEBRAP, no. 83 (March 2009): 39–63. http://dx.doi.org/10.1590/s0101-33002009000100004.

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Este artigo parte do exame dos múltiplos papéis que nas sociedades contemporâneas os intelectuais desempenham na vida política. Aponta a tendência à imperícia no trato da realidade política por parte dos intelectuais no exercício do poder. Neste contexto, discute-se como e por que FHC é um raro caso de um intelectual bem-sucedido na vida política de um país complexo, de escala continental, com as características do Brasil contemporâneo. Aquilata-se, finalmente, a maneira pela qual FHC conjugou teoria e experiência nos seus juízos políticos perante as especificidades das conjunturas com as quais lidou na presidência e como combinou, na sua liderança, a dimensão da mudança e da pacificação, tendo sempre presente o "quadro mental" e o sentido de direção da sua visão intelectual.
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28

Guo, Yuxiu, Juan Ding, and Wenjuan Yan. "MiR-579-3p Protects Intestinal Mucosal Epithelial Cells from Hypoxia-Reoxygenation Injury by Targeting Cyclin-Dependent Kinase Inhibitor 1B." Journal of Biomaterials and Tissue Engineering 11, no. 6 (2021): 1084–90. http://dx.doi.org/10.1166/jbt.2021.2653.

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Intestinal ischemia/reperfusion (I/R) injury is a common tissue and organ injury during surgery. This study explores miR-579-3p’s effect on the hypoxia-reoxygenation injury of intestinal mucosal epithelial cells via cyclin-dependent kinase inhibitor 1B (CDKN1B). Fetal human cells (FHC) cells, which are human normal colorectal mucosal epithelial cells, were cultured in vitro to establish a hypoxia-reoxygenation (H/R) cell model. Nano-based qRT-PCR and Western blot detected miR-579-3p and CDKN1B expressions in HCCLM3 cells treated with H/R. CCK-8 method and flow cytometry measured miR-579-3p and CDKN1B expressions on cell activity and death after H/R treatment. Dual-Luciferase reporter experiment and Western blot analyzed the relationship between miR-579-3p and CDKN1B. After the FHC cells were treated with H/R, miR-579-3p expression was decreased, whereas CDKN1B expression was increased (P < 0.05). FHC cells’ activity was decreased, and its apoptosis rate was upregulated; also, TNF-α and IL-6 protein levels were significantly enhanced (P < 0.05). Nevertheless, the activity of FHC cells treated with H/R after miR-579-3p overexpression was significantly increased, while the apoptosis rate was upregulation, and TNF-α level, IL-6 levels were reduced (P < 0.05). The effect of inhibiting CDKN1B expression was the same as that of overexpression miR-579-3p. After CDKN1B overexpression, the H/R-treated FHC cells’ viability was reduced, while the apoptosis rate was elevated, and TNF-α and IL-6 levels were elevated (P < 0.05). Compared to miR-579-3p overexpression, FHC cell activity in treated with H/R after the overexpression of miR-579-3p+CDKN1B was reduced. At the same time, the apoptosis rate and the level of TNF-α and IL-6 protein were elevated (P < 0.05). In summary, MiR-579-3p’s targeting of CDKN1B protects FHC cells from H/R injury by alleviating H/R-induced apoptosis and inflammation.
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Fertrin, Kleber Yotsumoto, Carolina Lanaro, Carla Fernanda Franco-Penteado, et al. "High Transferrin Saturation Is Associated with Lower Monocytic Ferritin Heavy Chain Expression in Sickle Cell Anemia Patients." Blood 124, no. 21 (2014): 4058. http://dx.doi.org/10.1182/blood.v124.21.4058.4058.

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Abstract The pathophysiology of sickle cell anemia (SCA) involves hemolysis, vaso-occlusion and a chronic inflammatory state. Iron overload secondary to blood transfusions is a frequent complication in these patients, but cannot be adequately estimated by serum ferritin levels, because ferritin is also an acute phase reactant. Although excess iron elevates both ferritin levels and transferrin saturation (TSAT) in SCA patients, there is notorious discrepancy between these parameters. Ferritin is composed of heavy (FHC) and light chains (FLC), and ferroxidase activity by FHC is an important cytoprotective mechanism against redox-iron, a product of heme breakdown and largely present in overt iron overload. Previous studies have shown that overexpression of FHC in sickle cell mice prevented free hemoglobin-induced vaso-occlusion. Since ferritin is also highly expressed in circulating monocytes, and these cells have been shown to interact with other cellular types in the sickle cell vaso-occlusive process, we aimed to characterize ferritin chains in monocytes and investigate the relationship with biomarkers of iron metabolism, inflammation and hemolysis. Peripheral blood monocytes from sixteen adult sickle cell anemia patients in steady state were isolated using a double Ficoll-Percoll density gradient to separate monocytes from neutrophils and lymphocytes. FHC, FLC, TLR4 (toll-like receptor 4), and SLC40A1(ferroportin) gene expressions were determined by RT-qPCR. Blood samples were also collected to determine serum ferritin, iron, and TSAT, and plasma levels of lactate dehydrogenase, soluble transferrin receptor, erythropoietin, and C reactive protein. We found that the expression of TLR4, a receptor known to be activated by heme, correlated with FLC, but not FHC expression. Higher TLR4 expression was also associated with higher serum iron, but not with ferritin, TSAT, or LDH. Interestingly, we did not find a correlation between C reactive protein levels and ferritin in this group of patients. As expected, the expressions of both ferritin chains were correlated with each other (P=0.027, r=0.55), but we found the strongest correlation between FHC and TSAT (P=0.0008, r=-0.652). Patients with a TSAT over 40% had significantly lower expression of monocytic FTH (P=0.003). This suggests that either excessive iron can lead to FHC downregulation in monocytes, or that a decrease in monocytic ferritin ferroxidase activity in some SCA patients may impair safe iron storage in ferritin and contribute to the development of higher TSAT, independently from ferritin levels. Our data support that human monocyte regulation of ferritin chains in SCA patients mirrors what has been described in hepatic cells in a sickle cell mouse model. Patients with increased TSAT may be relatively deprived of the cytoprotective ferroxidase activity of FHC, and a relationship between FHC deficiency and complications in SCA remains to be investigated. Further studies should also address whether FHC in monocytes influences cell adhesion, thus supporting an important role for iron trafficking in cells involved in sickle cell vaso-occlusion, and corroborating other studies associating organ damage in SCA with iron metabolism dysregulation. Disclosures No relevant conflicts of interest to declare.
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30

Alpert, Norman R., Saidi A. Mohiddin, Dorothy Tripodi, et al. "Molecular and phenotypic effects of heterozygous, homozygous, and compound heterozygote myosin heavy-chain mutations." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 3 (2005): H1097—H1102. http://dx.doi.org/10.1152/ajpheart.00650.2004.

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Autosomal dominant familial hypertrophic cardiomyopathy (FHC) has variable penetrance and phenotype. Heterozygous mutations in MYH7 encoding β-myosin heavy chain are the most common causes of FHC, and we proposed that “enhanced” mutant actin-myosin function is the causative molecular abnormality. We have studied individuals from families in which members have two, one, or no mutant MYH7 alleles to examine for dose effects. In one family, a member homozygous for Lys207Gln had cardiomyopathy complicated by left ventricular dilatation, systolic impairment, atrial fibrillation, and defibrillator interventions. Only one of five heterozygous relatives had FHC. Leu908Val and Asp906Gly mutations were detected in a second family in which penetrance for Leu908Val heterozygotes was 46% (21/46) and 25% (3/12) for Asp906Gly. Despite the low penetrance, hypertrophy was severe in several heterozygotes. Two individuals with both mutations developed severe FHC. The velocities of actin translocation ( Vactin) by mutant and wild-type (WT) myosins were compared in the in vitro motility assay. Compared with WT/WT, Vactin was 34% faster for WT/D906G and 21% for WT/L908V. Surprisingly Vactin for Leu908Val/Asp906Gly and Lys207Gln/Lys207Gln mutants were similar to WT. The apparent enhancement of mechanical performance with mutant/WT myosin was not observed for mutant/mutant myosin. This suggests that Vactin may be a poor predictor of disease penetrance or severity and that power production may be more appropriate, or that the limited availability of double mutant patients prohibits any definitive conclusions. Finally, severe FHC in heterozygous individuals can occur despite very low penetrance, suggesting these mutations alone are insufficient to cause FHC and that uncharacterized modifying mechanisms exert powerful influences.
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31

Pereira, William Eufrásio Nunes, Ana Cristina dos Santos Morais, Francisco Danilo da Silva Ferreira, and Severino Felix de Souza. "Localização das aglomerações do setor industrial nas regiões Nordeste e Sudeste:uma análise comparativa nos governos FHC e Lula." Economia & Região 9, no. 1 (2020): 5. http://dx.doi.org/10.5433/2317-627x.2021v9n1p5.

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O presente artigo tem por objetivo verificar as alterações no padrão locacional do setor industrial no Sudeste e Nordeste do País, durante os governos Fernando Henrique Cardoso (FHC) e Luiz Inácio Lula da Silva (Lula), com a utilização do coeficiente locacional de Hoover. Para a operacionalização do índice, foi utilizado o emprego formal no setor industrial nos anos de 1995, 2002, 2003 e 2010, correspondentes respectivamente aos anos iniciais e finais dos governos FHC e Lula. Os resultados alcançados revelam que houve perdas na indústria no Governo FHC, assim como, a hegemonia na concentração do emprego industrial no Sudeste foi reduzida relativamente nos anos seguintes do seu Governo. No governo Lula, a região Nordeste perdeu empregos.
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32

Pritzkow, Hans, Klaus Rall, Stefan Reimann-Andersen, and Wolfgang Sundermeyer. "Über die invers durch Amine stabilisierten Sulfene F2CSO2 und FHCSO2." Angewandte Chemie 102, no. 1 (1990): 80–81. http://dx.doi.org/10.1002/ange.19901020120.

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33

Marques, Erica Mendonça, and Rodrigo Vilela Rodrigues. "Crescimento econômico com restrição externa: uma análise da Lei de Thirwall para os períodos FHC e Lula." Brazilian Keynesian Review 5, no. 2 (2019): 239–68. http://dx.doi.org/10.33834/bkr.v5i2.180.

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Este artigo buscou avaliar os períodos dos governos FHC e Lula, bem como o período completo de 1995 a 2010, com objetivo de investigar em que medida o Brasil teve seu potencial de crescimento econômico limitado por restrições no balanço de pagamentos e quais diferenças observáveis entre os períodos. Para a análise empírica, adotou-se o procedimento econométrico de cointegração, empregado para estimativas de elasticidades-preço e renda da demanda por importação dos períodos, tendo como resultado um relaxamento na restrição externa no período Lula comparativamente ao governo FHC. Os resultados indicam que embora as restrições externas tenham reduzido durante o governo Lula em relação ao governo FHC, há evidências de que continuaram desempenhando papel relevante sobre a taxa de crescimento de longo prazo do Brasil.
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34

Baránková, Hana, and Ladislav Bardos. "Hollow cathode and hybrid atmospheric plasma sources." Pure and Applied Chemistry 80, no. 9 (2008): 1931–37. http://dx.doi.org/10.1351/pac200880091931.

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Generation and features of the radio frequency (RF) hollow cathode discharge (HCD) are compared for the atmospheric and moderate pressures. The atmospheric-pressure plasma systems, fused hollow cathode (FHC) and hybrid hollow electrode-activated discharge (H-HEAD), are described. Examples of applications where both FHC and H-HEAD have already been employed are given, and potentials for new processes are discussed.
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Andrade, Antonia Costa, Carlos Lucena, and Ilma Andrade Barleta. "A precarização do trabalho, o REUNI e o novo desenvolvimentismo." Revista HISTEDBR On-line 18, no. 1 (2018): 234–57. http://dx.doi.org/10.20396/rho.v18i1.8645868.

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Este artigo ao centralizar-se nos governos FHC e Lula e a ressignificação do neodesenvolvimentismo, tomou o REUNI como referência, em termos educacionais, com o objetivo de realizar um estudo comparativo entre os referidos governos, respaldado nas mudanças no neodesenvolvimento e seus impactos na sociedade e na educação. A pesquisa foi dividida em duas partes: a primeira analisa o governo FHC e os primórdios da implantação do Plano Real. A segunda, por sua vez, debate o governo Lula, demonstrando seus pressupostos, continuidades e rupturas com o governo FHC e uma ênfase final no projeto de expansão do ensino superior público denominado REUNI. Foram pesquisadas fontes primárias manifestas em jornais da época, documentos governamentais e análise do discurso dos principais atores políticos do projeto em questão. O que demonstramos é que o governo Lula não rompeu com a lógica monetarista inerente ao governo FHC, no qual houve expansão do ensino superior privado, manifestando projetos precarizantes do trabalho dos professores. No governo Lula, o processo de interiorização da Universidade pública manifestou a contradição do acesso a alunos no ensino superior, porém em condições também precárias para o desenvolvimento da Ciência e Tecnologia.
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Cunha, Luiz Antônio. "O ensino superior no octênio FHC." Educação & Sociedade 24, no. 82 (2003): 37–61. http://dx.doi.org/10.1590/s0101-73302003000100003.

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Este artigo se propõe a analisar o ensino superior brasileiro durante o período 1995/2002, para o que são focalizadas, principalmente, as políticas do governo federal. Depois de apresentar as mudanças determinadas pela Lei de Diretrizes e Bases da Educação Nacional (1996), o artigo relaciona e analisa as medidas do Governo Fernando Henrique Cardoso que constituíram uma verdadeira normatização fragmentada do ensino superior, a saber: o acesso aos cursos de graduação, o poder docente na gestão universitária, o Conselho Nacional de Educação, a avaliação e o formato institucional. O artigo finaliza com um balanço dos oito anos do Governo Fernando Henrique Cardoso no campo do ensino superior, o qual revela uma intensificação da privatização no período, assim como um deslocamento da fronteira entre o setor público e o setor privado.
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Chen, Li-Hui. "Evaluating total operational value and associated risks of financial holding companies in Taiwan." Yugoslav Journal of Operations Research 20, no. 2 (2010): 275–92. http://dx.doi.org/10.2298/yjor1002275c.

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This study comprises several different parts. The first part applies a normal benchmark valuation model established by Penman to assess the potential whole operational values of FHCs. The second part applies the concept of measuring financial risk as earnings variance to establish a financial risk measurement model. This model can be used to examine the degrees of financial risk before and after FHC?s establishment, and to distinguish different combinations of FHC based on risk diversion efficiency. The final part of this research constructs a new value-risk relation model that can be applied to cross-analysis for measuring total operation value of FHCs with different degrees of financial risk. Through completion of the above steps this study will demonstrate what combination of FHC offers the co-benefits of risk diversion and high whole operational value.
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Przylepa, Mariclei. "POLÍTICAS CURRICULARES NO BRASIL NOS GOVERNOS FHC E LULA: CONTINUIDADE?" LAPLAGE EM REVISTA 1, no. 2 (2015): 119. http://dx.doi.org/10.24115/s2446-622020151225p.119-131.

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O presente artigo objetiva problematizar as políticas curriculares elaboradas e efetivadas nos governos FHC e Lula, a partir do contexto de reforma de Estado materializada na década de 1990. Nessa direção o estudo inicia abordando a política curricular no contexto da reforma de Estado, evidencia a proposta educacional do governo FHC, discute sua política curricular, via parâmetros curriculares nacionais, e finaliza analisando a política curricular implementada no primeiro ano do governo Lula.
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39

Passini, João José, and Mirian Beatriz Schneider. "Políticas Públicas para o Desenvolvimento Rural no Brasil: FHC e Lula." Revista de Desenvolvimento e Políticas Públicas 4, no. 1 (2020): 3–20. http://dx.doi.org/10.31061/redepp.v4n1.3-20.

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Esse artigo tem por objetivo apresentar e discutir as principais políticas públicas voltadas ao desenvolvimento rural brasileiro nos governos dos presidentes Fernando Henrique Cardoso (FHC) e Luiz Inácio Lula da Silva. Ao fazer isso, pretende-se oferecer um panorama das estratégias escolhidas pelos governos estudados e avaliar a continuidade ou ruptura nas políticas implantadas. De forma geral, o governo FHC adotou os preceitos neoliberais, propondo um desenvolvimento endógeno com o propósito de diminuir a presença e atuação do Estado. Em contrapartida, o governo Lula apostou no desenvolvimento endógeno como forma da sociedade apropriar-se da riqueza gerada, tendo o Estado como entidade promotora desse desenvolvimento. Como ponto em comum, a criação do Pronaf, na gestão de FHC, consolida-se em uma referência na promoção do desenvolvimento rural sustentável na gestão de Lula, e tornar-se uma importante ferramenta de políticas públicas destinadas à produção e distribuição de alimentos.
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40

Coelho, Fabiano. "Reforma Agrária no Governo FHC: perfil, tensões, número de famílias assentadas e áreas obtidas." Diálogos 20, no. 2 (2016): 179. http://dx.doi.org/10.4025/dialogos.v20i2.34575.

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O governo do presidente Fernando Henrique Cardoso (FHC/1995-2002) teve papel relevante na consolidação de políticas voltadas ao campo e ao processo de reforma agrária no Brasil. O objetivo do artigo é refletir sobre o perfil e as tensões envoltas na política de reforma agrária do governo FHC, e os desdobramentos dessa política face ao número de famílias assentadas e áreas obtidas para fins de reforma agrária no Brasil. Utiliza-se como fonte textos de pesquisadores que estudaram os caminhos e descaminhos da reforma agrária brasileira e dados do “Banco de Dados da Luta Pela Terra” (DATALUTA/NERA/Unesp/Presidente Prudente). Compreende-se que, no Governo FHC, apesar do número de famílias assentadas e áreas obtidas terem avançado de forma considerável em relação a governos anteriores, a reforma agrária foi tratada de forma marginal, e o governo, por vezes, negou as lutas e o protagonismo dos movimentos sociais do campo.
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41

Wang, Fang, Nicolas M. Brunet, Justin R. Grubich та ін. "Facilitated Cross-Bridge Interactions with Thin Filaments by Familial Hypertrophic Cardiomyopathy Mutations inα-Tropomyosin". Journal of Biomedicine and Biotechnology 2011 (2011): 1–12. http://dx.doi.org/10.1155/2011/435271.

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Familial hypertrophic cardiomyopathy (FHC) is a disease of cardiac sarcomeres. To identify molecular mechanisms underlying FHC pathology, functional and structural differences in three FHC-related mutations in recombinantα-Tm (V95A, D175N, and E180G) were characterized using both conventional and modified in vitro motility assays and circular dichroism spectroscopy. Mutant Tm's exhibited reducedα-helical structure and increased unordered structure. When thin filaments were fully occupied by regulatory proteins, little or no motion was detected at pCa 9, and maximum speed (pCa 5) was similar for all tropomyosins. Ca2+-responsiveness of filament sliding speed was increased either by increasedpCa50(V95A), reduced cooperativityn(D175N), or both (E180G). When temperature was increased, thin filaments with E180G exhibited dysregulation at temperatures ~10°C lower, and much closer to body temperature, than WT. When HMM density was reduced, thin filaments with D175N required fewer motors to initiate sliding or achieve maximum sliding speed.
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42

Campbell, Stuart G., and Andrew D. McCulloch. "Multi-scale computational models of familial hypertrophic cardiomyopathy: genotype to phenotype." Journal of The Royal Society Interface 8, no. 64 (2011): 1550–61. http://dx.doi.org/10.1098/rsif.2011.0184.

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Familial hypertrophic cardiomyopathy (FHC) is an inherited disorder affecting roughly one in 500 people. Its hallmark is abnormal thickening of the ventricular wall, leading to serious complications that include heart failure and sudden cardiac death. Treatment is complicated by variation in the severity, symptoms and risks for sudden death within the patient population. Nearly all of the genetic lesions associated with FHC occur in genes encoding sarcomeric proteins, indicating that defects in cardiac muscle contraction underlie the condition. Detailed biophysical data are increasingly available for computational analyses that could be used to predict heart phenotypes based on genotype. These models must integrate the dynamic processes occurring in cardiac cells with properties of myocardial tissue, heart geometry and haemodynamic load in order to predict strain and stress in the ventricular walls and overall pump function. Recent advances have increased the biophysical detail in these models at the myofilament level, which will allow properties of FHC-linked mutant proteins to be accurately represented in simulations of whole heart function. The short-term impact of these models will be detailed descriptions of contractile dysfunction and altered myocardial strain patterns at the earliest stages of the disease—predictions that could be validated in genetically modified animals. Long term, these multi-scale models have the potential to improve clinical management of FHC through genotype-based risk stratification and personalized therapy.
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43

Ribeiro e Silva Medeiros, Thaynara Helena, Sally Cristina Moutinho Monteiro, José De Ribamar Medeiros Lima Júnior, Adriana Karina Beckman Ferreira Alves, Thaynara Nascimento da Silva Sampaio, and Brenda Emmylly Marinho Teles. "Fenótipo de cintura hipertrigliceridêmica e lesão renal em pacientes hipertensos." Saúde Coletiva (Barueri) 11, no. 66 (2021): 6611–32. http://dx.doi.org/10.36489/saudecoletiva.2021v11i66p6611-6632.

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Objetivo: Verificar a associação entre o fenótipo de cintura hipertrigliceridêmica (FCH) e a estimativa da taxa de filtração glomerular (eTFG) em pacientes hipertensos. Método: Tratou-se de um estudo transversal e retrospectivo, composto por 146 prontuários de hipertensos consultados entre os anos de 2013 a 2017 no Centro de Prevenção de Doenças Renais HUUFMA. Considerou-se dados sociodemográficos, condições clínicas e exames laboratoriais, estes foram analisados pelo programa estatístico SPSS 21.0®. Resultados: O FCH esteve presente em 84,2% (n=123) da amostra e 65% (n=, desta, eram mulheres. A eRFG apresentou média de 69,3 ± 23,9 mL / min em 1,73 m² no grupo com FCH e média de 91,4 ± 42,6 mL / min em 1,73 m² no grupo sem FCH, com associação significativa (p <0,05). Conclusões: A presença do FHC associou-se à diminuição da eTFG, ao aumento dos exames laboratoriais, medidas antropométricas e índices antropométricos.
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44

Wu, De Li, Quan Min Wang, Yong Feng, and Lu Ming Ma. "Effect of Inorganic Anions on Reduction of Nitrobenzene in Water by Structural Ferrous Iron." Advanced Materials Research 518-523 (May 2012): 1737–43. http://dx.doi.org/10.4028/www.scientific.net/amr.518-523.1737.

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Nitrobenzene is an important contaminant existed in water and wastewater widely. Because of its toxicity to organisms, it is hardly biodegradable. A new structural Fe(II): Ferrous Hydroxy Complex (FHC) was prepared with ferrous sulfate to investigate the reduction of nitrobenzene by structural ferrous iron. This study focused on the effects of inorganic anions on the reactivity of FHC towards nitrobenzene. It was found that soluble Fe(II) could hardly reduce any nitrobenzene within 2h while FHC could reduce nitrobenzene to aniline rapidly within 0.5h. Various anions such as CO32-, PO43-, SiO32-, S2- might have significant impact on the reactivity of structural Fe(II) in nitrobenzene reduction. These anions would slow down the rate of the reaction. Among these anions, SiO32- and PO43- had a greater effect on the reduction of nitrobenzene than CO32- and S2-. Structural ferrous iron (SFI) was prepared by two ways: (i) Aqueous Fe2+ was directly added to wastewater, then adjusted the pH value of water to 8-9; (ii) FHC prepared in advance was added to wastewater, SFI(II). Results indicated that the effect of anions on reactivity of SFI(I) was greater than that of SFI(II). When the initial concentration of nitrobenzene was 60mg/L and ferrous iron dosage was 240mg/L, NO3- with the concentration of 4mM had little effect on the reduction of nitrobenzene by both forms of Fe(II); NO2- had greater effect on reactivity of SFI(I) than that of SFI(II).
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45

Škvor, J., and P. Čapek. "Hypertrophic Cardiomyopathy." Methods of Information in Medicine 45, no. 02 (2006): 169–72. http://dx.doi.org/10.1055/s-0038-1634062.

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Summary Objectives: Our research is a pilot study that specializes in the molecular genetic investigation of the TNNT2 gene in Czech patients with HCM/FHC disease. This study was initiated with exons 9 and 11 of TNNT2 because of their crucial role in the binding ability of cardiac troponin T to α-tropomyosin, and continued with analyses in other regions of the gene. Methods: Hundred and eighty-one Czech probands with HCM/FHC were enrolled in this study. The study group consisted of 24 families with FHC and probands without FHC history but with HCM diagnosis. The clinical diagnosis was based on echocardiography. DNA was isolated from peripheral blood lymphocytes and subsequently analyzed by the polymerase chain reaction (PCR), followed by DNA sequencing analyses, which were cross-sequenced. Results: The ΔGlu160 mutation was observed in a sequence of the TNNT2 gene in a patient with the severe form of hypertrophic cardiomyopathy. No sequence alteration was found in exons 9 and 11 of the TNNT2 gene found in the rest of the DNA samples. Conclusion: The ΔGlu160 mutation was observed in patients with severe forms of hypertrophic cardiomyopathy. This region is responsible for binding troponin T to α-tropomyosin. This mutation may lead to functional and structural effects on the troponin T protein. Mutations in this region are reported relatively rarely and therefore it was unique to observe the ΔGlu160 mutation in our study.
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Fonseca-Silva, Maria da Conceição, Vinícius Fonseca-Nunes, and Edvania Gomes da Silva. "Política externa e deslizamento de sentido nos discursos dos governos FHC e Lula ( External politics and slippage of sense in the discourse of FHC’s government and Lula’s government )." Estudos da Língua(gem) 9, no. 2 (2011): 27. http://dx.doi.org/10.22481/el.v9i2.1153.

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Neste trabalho, apresentamos resultado de pesquisa sobre deslizamento de sentido de política externa nos discursos dos governos FHC e Lula. Defendemos a hipótese de que o governo Lula, diferente do governo FHC, assumiu o papel de hegemonia, não só regionalmente, mas também em foros maiores onde o país assumiu uma postura de liderança frente aos países em desenvolvimento. No entanto, há continuidades entre a política externa do governo de Fernando Henrique Cardoso e do governo de Luiz Inácio Lula da Silva.PALAVRAS-CHAVE: Política externa. Governo FHC. Governo Lula.
 ABSTRACT In the work, we present result of research about slippage of sense Brazilian external politics in the discourse the FHC’s government and the Lula’s government. We defend the hypothesis that Lula’s government, differently the FHC’s government, assumed the role of hegemony, not only regionally, but also in larger forums where the country assumed the leadership of the developing countries. However, there is much continuity between the external politics of Fernando Henrique Cardoso and that of Luiz Ina?cio Lula da Silva’s government.KEYWORDS: External politics. FHC’s government. Lula’s government.
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47

Sallum Jr., Brasilio. "O segundo governo FHC: um balanço crítico." Tempo Social 15, no. 2 (2003): 5–7. http://dx.doi.org/10.1590/s0103-20702003000200001.

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Adorno, Sérgio. "Lei e ordem no segundo governo FHC." Tempo Social 15, no. 2 (2003): 103–40. http://dx.doi.org/10.1590/s0103-20702003000200005.

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Liu, Jin, and Tuan D. Pham. "FHC: The fuzzy hyper-prototype clustering algorithm." International Journal of Knowledge-based and Intelligent Engineering Systems 16, no. 1 (2012): 35–47. http://dx.doi.org/10.3233/kes-2012-0231.

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50

Bashyam, M. D., G. R. Savithri, M. S. Kumar, C. Narasimhan, and P. Nallari. "Molecular genetics of familial hypertrophic cardiomyopathy (FHC)." Journal of Human Genetics 48, no. 2 (2003): 0055–64. http://dx.doi.org/10.1007/s100380300007.

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