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1
Braedt, G. "Different reading frames are responsible for IS1-dependent deletions and recombination." Genetics 118, no. 4 (1988): 561–70. http://dx.doi.org/10.1093/genetics/118.4.561.
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Abstract Two classes of plasmids in addition to the parent become apparent when plasmids that contain direct repeats of IS1. One class of plasmids has deleted sequences from the end of IS1 to nonrandom sites within the plasmid. The appearance of these plasmids in the population requires intact insA and insB reading frames, but not insC. The other class of plasmids has undergone an exchange within the direct repeats of IS1 on the plasmid. Their appearance requires InsC but neither InsA nor InsB. The two reactions may represent two distinguishable steps in IS1 transposition. The InsC-catalyzed exchange is independent of RecA and resembles hologous recombination since the frequency of recombinants arising from exchanges in different regions of IS1 appears to be roughly proportional to the size of the region. InsC can also catalyze an exchange between direct repeats of non-IS1 DNA.
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Shahavatov, Sabuhi. "Şiî Tefsir Geleneğinde Nesh Teorisi." Van İlahiyat Dergisi 8, no. 12 (2020): 88–99. https://doi.org/10.5281/zenodo.3894304.
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<em>Tarih boyunca Kur’an’ı anlama ve yorumlama faaliyetinin metodolojik bir zemine oturtulmasına yönelik çabaların semeresi olarak oluşup şekillenen klasik Ulûmu’l-Kur’an (Kur’an İlimleri) bahislerinden biri olan nesh (en-nâsih ve’l-mensûh) konusu Sünnî gelenekte olduğu kadar Şiî gelenekte de farklı yorumlara konu olmuştur. Şiî müfessirler çoğunlukla bu kavramın anlam ve izahı ile ilgili olarak Sünnî meslektaşlarıyla benzer tutumlar sergilemiş olsalar da belli kırılma noktalarında onların kendilerine özgü yaklaşımlara sahip olduğu da gözlemlenebilmektedir. Özellikle nesh ve bedâ kavramları arasındaki benzerlik ve karşıtlık noktaları ile neshin Kur’an dilindeki isimlerinden biri olan insâ kavramı bu farklı yaklaşımların temerküz ettiği hususlar arasında sayılabilir. Bu yazı söz konusu kavramın Şiî tefsir edebiyatı içerisinde nasıl anlaşılmış olduğunu izlemenin yanı sıra bu geleneğin Sünnî gelenekten ayrıştığı noktalara titizlikle işaret edebilmek için kimi değerlendirmeler yapmayı da amaçlamaktadır. Özellikle bedâ kavramı çerçevesinde Şiî tefsir ve daha genel anlamda Şiî düşünce hakkında ağırlıklı olarak dışarıdan teşekkül etmiş algı, bu düşüncenin ilahî bilgide değişiklik ya da eksiklik gibi illetleri mümkün gördüğü şeklindedir. Ne var ki doğrudan Şiî bilginlerin tefsir metinlerinde böyle bir yargıyı doğrulamak için yeterli veri bulunmamaktadır. İnsâ kavramı ise Şiî müfessirler tarafından, onların peygamberlerin ismeti konusundaki hassas tutumlarının neticesi olarak, farklı yorumlara ve mezhep içi tartışmalara konu olmuştur. Bu tartışmalarda Şiî bilginler imamlardan nakledilen rivayetlerin literal anlamlarına sadık kalmakla teorik tutarlılığı sürdürme arasında farklı konumları benimsemişlerdir. Bu bağlamda bu yazı, tefsir disiplini çerçevesinde benimsenen genel kabullerin metin yorumunda sebep olduğu gerilimlere ve açtığı diyalektik düşünme imkânlarına dair daha kapsamlı çalışmalar için bir tür giriş/başlangıç noktası oluşturmayı da hedeflemektedir. </em>
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Jakowec, M., P. Prentki, M. Chandler, and D. J. Galas. "Mutational analysis of the open reading frames in the transposable element IS1." Genetics 120, no. 1 (1988): 47–55. http://dx.doi.org/10.1093/genetics/120.1.47.
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Abstract IS1 is one of the smallest transposable elements found in bacteria (768 bp). It contains eight overlapping open-reading-frames (ORFs) greater than 50 codons, designated insA to insG and insB'. To determine which of the ORFs actually code for proteins involved in transposition, we have introduced amber codons into each ORF by site-directed mutagenesis which make neutral changes in the overlapping ORFs. Each mutant IS1 was then tested for its ability to mediate cointegrate formation in Su+ and Su- backgrounds. The mutant elements were also tested for trans-complementation in an IS1-free Salmonella background. Our results show that the products of the insA and insB genes are the only ones essential for cointegrate formation. We suggest that other ORFs may, however, encode accessory proteins.
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Dionne, Derek A., Søs Skovsø, Nicole M. Templeman, Susanne M. Clee, and James D. Johnson. "Caloric Restriction Paradoxically Increases Adiposity in Mice With Genetically Reduced Insulin." Endocrinology 157, no. 7 (2016): 2724–34. http://dx.doi.org/10.1210/en.2016-1102.
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Antiadiposity effects of caloric restriction (CR) are associated with reduced insulin/IGF-1 signaling, but it is unclear whether the effects of CR would be additive to genetically reducing circulating insulin. To address this question, we examined female Ins1+/−:Ins2−/− mice and Ins1+/+:Ins2−/− littermate controls on either an ad libitum or 60% CR diet. Although Igf1 levels declined as expected, CR was unable to reduce plasma insulin levels in either genotype below their ad libitum-fed littermate controls. In fact, 53-week-old Ins1+/−:Ins2−/− mice exhibited a paradoxical increase in circulating insulin in the CR group compared with the ad libitum-fed Ins1+/−:Ins2−/− mice. Regardless of insulin gene dosage, CR mice had lower fasting glucose and improved glucose tolerance. Although body mass and lean mass predictably fell after CR initiation, we observed a significant and unexpected increase in fat mass in the CR Ins1+/−:Ins2−/− mice. Specifically, inguinal fat was significantly increased by CR at 66 weeks and 106 weeks. By 106 weeks, brown adipose tissue mass was also significantly increased by CR in both Ins1+/−:Ins2−/− and Ins1+/+:Ins2−/− mice. Interestingly, we observed a clear whitening of brown adipose tissue in the CR groups. Mice in the CR group had altered daily energy expenditure and respiratory exchange ratio circadian rhythms in both genotypes. Multiplexed analysis of circulating hormones revealed that CR was associated with increased fasting and fed levels of the obesogenic hormone, glucose-dependent insulinotropic polypeptide. Collectively these data demonstrate CR has paradoxical effects on adipose tissue growth in the context of genetically reduced insulin.
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Papasani, Madhusudhan R., Barrie D. Robison, Ronald W. Hardy, and Rodney A. Hill. "Early developmental expression of two insulins in zebrafish (Danio rerio)." Physiological Genomics 27, no. 1 (2006): 79–85. http://dx.doi.org/10.1152/physiolgenomics.00012.2006.
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We have cloned a second insulin gene in zebrafish and studied temporal and spatial expression of two zebrafish insulin genes. Zebrafish insulin-a ( insa) and -b ( insb) mRNAs are derived from two different DNA contigs on chromosomes 5 and 14, respectively, representing two different insulin genes. Real-time PCR studies suggest that insa is a maternal and also a postzygotic transcript. insa was observed at 1 h postfertilization (hpf) and was rapidly degraded by 6 and 12 hpf but induced at 24 hpf (i.e., after pancreas formation). Expression levels at 24 hpf were ∼220-fold higher than at 6 hpf and were significantly different from earlier time points. At 72 hpf (at time of hatching), zebrafish insa mRNA levels tended to be higher than at 24 hpf and were ∼727-fold higher compared with 6 hpf. This further increase in insa expression may be one of the many rapid physiological changes associated with hatching. insb expression was observed from 1 hpf and was significantly decreased from 12 hpf onward. Its expression levels at 12 and 24 hpf were approximately twofold and sixfold lower, respectively, compared with expression at 6 hpf. insb expression levels at 48 hpf were significantly lower than at 24 hpf but not different from 72 hpf. Expression levels at 72 hpf were ∼61-fold lower than at 6 hpf. In situ hybridization studies showed insb expression in proliferating blastomeres at 3 and 4 hpf. At later time points, insb expression was restricted to the brain and pancreas (24 and 48 hpf). insa expression was observed in the pancreas at 24 and 48 hpf. Expression of insb in blastomeres and head suggests that insb could be acting as a pro-growth, survival, and neurotrophic factor during development. Pancreatic insa and insb may both be involved in regulation of glucose homeostasis as in mammals.
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Rudnicka, E., M. Kunicki, K. Suchta, P. Machura, M. Grymowicz, and R. Smolarczyk. "Inflammatory Markers in Women with Polycystic Ovary Syndrome." BioMed Research International 2020 (March 6, 2020): 1–10. http://dx.doi.org/10.1155/2020/4092470.
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Several studies have reported the association between polycystic ovary syndrome (PCOS) and low-grade chronic inflammation to be of uncertain cause: obesity, insulin resistance, or PCOS itself. The aim of the study was to investigate the WBC (white blood cell) count and CRP (C-reactive protein) concentration in women with PCOS and to determine the factors that affect their concentration. The study included 200 women aged 18-40 with PCOS and 105 healthy women as the control group, recruited in the Department of Gynaecological Endocrinology of Medical University in Warsaw from 2016 to 2018. Each patient underwent clinical, biochemical, and ultrasonographic assessments. WBC and CRP were significantly higher in the PCOS group (Z=−2,353, p=0,019 and Z=−2,453, p=0,014). WBC positively correlated with serum insulin at 0, 60, and 120 min during the oral glucose tolerance test (INS0: r=0,221, p=0,001; INS1: r=0,194, p=0,003; INS2: r=0,022, p=0,001), testosterone (r=0,130, p=0,046), androstenedione (r=0,212, p=0,001), and DHEAS (r=0,178, p=0,006) and negatively correlated with progesterone (r=−0,204, p=0,002), estradiol (r=−0,140, p=0,032), and SHBG (r=−0,308, p<0,001). CRP positively correlated with insulin concentration in 0, 60, and 120 min during the oral glucose tolerance test (INS0: r=0,343, p<0,001; INS1: r=0,276, p=0,001; INS2: r=0,320, p<001) and negatively correlated with progesterone (r=−0,194, p=0,030) and SHBG (-0,244, p=0,005). We also estimated positive correlation between BMI and serum CRP and WBC concentration. Multiple linear regression analysis showed that CRP values are positively associated with BMI (beta=0,374, p<0,001) and insulin level (INS1) (beta=0,282, p=0,004); and WBC results are negatively associated with SHGB (beta=−0,284, p<0,001) but positively associated with testosterone (beta=0,163, p=0,024) and BMI (beta=0,157, p=0,047). PCOS is associated with increased WBC and CRP concentrations. The main predicting factors of increased CRP are BMI and insulin resistance, but there is also a relationship between WBC count in PCOS and androgen concentration itself so that inflammation may be mediated not only through adiposity but also through increased androgen concentration.
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Almairac, Fabien, Hugues Duffau, and Guillaume Herbet. "Contralesional macrostructural plasticity of the insular cortex in patients with glioma." Neurology 91, no. 20 (2018): e1902-e1908. http://dx.doi.org/10.1212/wnl.0000000000006517.
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ObjectiveTo assess the homotopic structural plasticity in case of unilateral damage of the insula.MethodsTo detect changes in gray matter volumes of the contralesional insula from structural MRIs, we used voxel-based morphometry (VBM) in a sample of 84 patients with a diffuse low-grade glioma invading the left insula (insL group; n = 47) or the right insula (insR group; n = 37).ResultsThe region of interest–based VBM analysis highlighted a large cluster of voxels with gray matter volume increase in the contralesional insula in both patient groups (k = 2,214 voxels for insL and k = 879 voxels for insR, p < 0.05, family-wise error corrected) compared with 24 age-matched healthy controls. Gray matter volume was increased for the entire insula (t69 = 3.63, p = 0.0016 for insL; t59 = 3.54, p = 0.0024 for insR, Bonferroni corrected), whereas no significant changes were found in 2 control regions for both patient groups. Furthermore, an increase of 24.6% and 31.6% in the gray matter volume was observed in the insula-related VBM cluster for insL and insR patients, respectively, compared with healthy controls (t69 = 7.39, p = 2.59 × 10−10 and t59 = 7.51, p = 3.61 × 10−10).ConclusionsThe reported results demonstrate that slow-growing but massive lesion infiltration of the insula induces marked increase of gray matter volume in the contralateral one. Our findings give support for a homotopic reorganization that might be a physiologic basis for the high level of functional compensation observed in patients with glioma.
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Liu, Qing-Rong, Min Zhu, Faatin Salekin, et al. "An Insulin Upstream Open Reading Frame (INSU) Is Present in Skeletal Muscle Satellite Cells: Changes with Age." Cells 13, no. 22 (2024): 1903. http://dx.doi.org/10.3390/cells13221903.
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Insulin resistance, stem cell dysfunction, and muscle fiber dystrophy are all age-related events in skeletal muscle (SKM). However, age-related changes in insulin isoforms and insulin receptors in myogenic progenitor satellite cells have not been studied. Since SKM is an extra-pancreatic tissue that does not express mature insulin, we investigated the levels of insulin receptors (INSRs) and a novel human insulin upstream open reading frame (INSU) at the mRNA, protein, and anatomical levels in Baltimore Longitudinal Study of Aging (BLSA) biopsied SKM samples of 27–89-year-old (yrs) participants. Using RT-qPCR and the MS-based selected reaction monitoring (SRM) assay, we found that the levels of INSR and INSU mRNAs and the proteins were positively correlated with the age of human SKM biopsies. We applied RNAscope fluorescence in situ hybridization (FISH) and immunofluorescence (IF) to SKM cryosections and found that INSR and INSU were co-localized with PAX7-labeled satellite cells, with enhanced expression in SKM sections from an 89 yrs old compared to a 27 yrs old. We hypothesized that the SKM aging process might induce compensatory upregulation of INSR and re-expression of INSU, which might be beneficial in early embryogenesis and have deleterious effects on proliferative and myogenic satellite cells with advanced age.
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Camacho, Raul C., D. Brooks Lacy, Freyja D. James, E. Patrick Donahue та David H. Wasserman. "5-Aminoimidazole-4-carboxamide-1-β-d-ribofuranoside renders glucose output by the liver of the dog insensitive to a pharmacological increment in insulin". American Journal of Physiology-Endocrinology and Metabolism 289, № 6 (2005): E1039—E1043. http://dx.doi.org/10.1152/ajpendo.00247.2005.
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This study aimed to test whether stimulation of net hepatic glucose output (NHGO) by increased concentrations of the AMP analog, 5-aminoimidazole-4-carboxamide-1-β-d-ribosyl-5-monophosphate, can be suppressed by pharmacological insulin levels. Dogs had sampling (artery, portal vein, hepatic vein) and infusion (vena cava, portal vein) catheters and flow probes (hepatic artery, portal vein) implanted >16 days before study. Protocols consisted of equilibration (−130 to −30 min), basal (−30 to 0 min), and hyperinsulinemic-euglycemic (0–150 min) periods. At time ( t) = 0 min, somatostatin was infused, and basal glucagon was replaced via the portal vein. Insulin was infused in the portal vein at either 2 (INS2) or 5 (INS5) mU·kg−1·min−1. At t = 60 min, 1 mg·kg−1·min−1portal venous 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR) infusion was initiated. Arterial insulin rose ∼9- and ∼27-fold in INS2 and INS5, respectively. Glucagon, catecholamines, and cortisol did not change throughout the study. NHGO was completely suppressed before t = 60 min. Intraportal AICAR stimulated NHGO by 1.9 ± 0.5 and 2.0 ± 0.5 mg·kg−1·min−1in INS2 and INS5, respectively. AICAR stimulated tracer-determined endogenous glucose production similarly in both groups. Intraportal AICAR infusion significantly increased hepatic acetyl-CoA carboxylase (ACC, Ser79) phosphorylation in INS2. Hepatic ACC (Ser79) phosphorylation, however, was not increased in INS5. Thus intraportal AICAR infusion renders hepatic glucose output insensitive to pharmacological insulin. The effectiveness of AICAR in countering the suppressive effect of pharmacological insulin on NHGO occurs even though AICAR-stimulated ACC phosphorylation is completely blocked.
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Wang, Zhu, Fangwen Sun, Jian Liu, et al. "Electric field and uniaxial strain tunable electronic properties of the InSb/InSe heterostructure." Physical Chemistry Chemical Physics 22, no. 36 (2020): 20712–20. http://dx.doi.org/10.1039/d0cp02721a.
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Takahashi, Keisuke, and Lauren Takahashi. "Hydrophobic and antioxidant effects in In, Sn, and Sb based two dimensional materials." Dalton Transactions 45, no. 8 (2016): 3244–46. http://dx.doi.org/10.1039/c5dt04542h.
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Itoh, Masanobu, Mari Iwabuchi, Naoki Yorimoto, and Samuel H. Hori. "A transposable genetic element associated with positive regulation of G6PD gene expression in Drosophila melanogaster." Genetical Research 52, no. 3 (1988): 169–77. http://dx.doi.org/10.1017/s0016672300027622.
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SummaryThe DNA structures around the G6PD coding region in three high-G6PD activity mutants and their low-activity revertants of Drosophila melanogaster were analysed by Southern blot using a cloned G6PD gene as a probe. As a result, two kinds of insertion sequences were found; one was present just 5′ to exon I (Ins1), and the other within the intron (Ins2). The Ins1 sequence was 3·5 Kb in two mutants and 2·9 Kb in one mutant. In both cases, it consisted of a core sequence either 1·2 or 0·6 Kb long flanked by terminal repeats. On the other hand, low-activity revertants possessed either a defective Ins1 or no Ins1. The Ins2 sequence was found in all mutants and revertants, but not in Canton S. Although a recombinant phage carrying the DNA fragment spanning the entire Ins1 has not been obtained, sequencing data of the clone containing only the terminal repeats demonstrated that the repeats are defective P elements. Comparison of the genomic DNA structures of mutants and revertants suggested that the element responsible for the positive regulation of the G6PD gene in the mutants would probably be the core sequence, but not the flanking defective P elements. It was also conjectured that the 1·2 Kb core sequence might be composed of two identical elements, which might transpose independently.
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Kaminskii, V. M., Z. D. Kovalyuk, and V. I. Ivanov. "Structure and Physical Properties of In2Se3, InSe and InSe Layered Crystals." Фізика і хімія твердого тіла 16, no. 1 (2015): 44–48. http://dx.doi.org/10.15330/pcss.16.1.44-48.
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The influence of magnetic impurities on the properties of In2Se3 and InSе layered crystals was studied. The results indicate the formation of substitutional solid solutions in the In2Se3<1 wt. % Mn>, InSe<0.5 wt. % Mn> single crystals. Temperature dependences of electroconductivity across (σ^С) and along (σ||С) the С crystallographic axis of doped crystals were measured in the range of 80–400 K. The values of energy barrier height between the crystal layers ΔЕδ were evaluated for In2Se3<Mn> and InSe<Mn>. It was established that InSe<Fe> crystals exhibit ferromagnetic properties.
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Jindra, Christoph, Edmund K. Hainisch, Andrea Rümmele, Markus Wolschek, Thomas Muster, and Sabine Brandt. "Influenza virus vector iNS1 expressing bovine papillomavirus 1 (BPV1) antigens efficiently induces tumour regression in equine sarcoid patients." PLOS ONE 16, no. 11 (2021): e0260155. http://dx.doi.org/10.1371/journal.pone.0260155.
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Bovine papillomaviruses types 1 and 2 (BPV1, BPV2) commonly induce skin tumours termed sarcoids in horses and other equids. Sarcoids seriously compromise the health and welfare of affected individuals due to their propensity to resist treatment and reoccur in a more severe form. We have developed influenza (Flu) A and B virus vectors that harbour a truncated NS1 gene (iNS) assuring interferon induction and co-express shuffled BPV1 E6 and E7 antigens for sarcoid immunotherapy. In a safety trial involving 12 healthy horses, intradermal administration of iNSA/E6E7equ and iNSB/E6E7equ was well tolerated, with the only transient side effect being mild fever in four horses. Repeated screening of secretions and faeces by RT-PCR and plaque assay revealed no virus shedding, thus also confirming biological safety. In a patient trial involving 29 horses bearing BPV1-induced single or multiple sarcoids, at least one lesion per horse was intratumourally injected and then boosted with iNSA/E6E7equ and/or iNSB/E6E7equ. The treatment induced a systemic antitumour response as reflected by the synchronous regression of injected and non-injected lesions. Irrespective of vaccination schemes, complete tumour regression was achieved in 10/29 horses. In 10/29 horses, regression is still ongoing (May 2021). Intriguingly, scrapings collected from former tumour sites in two patients tested negative by BPV1 PCR. Nine severely affected individuals with a history of unsuccessful therapeutic attempts did not (6/29) or only transiently (3/29) respond to the treatment. INSA/E6E7equ and iNSB/E6E7equ proved safe and effective in significantly reducing the tumour burden even in severe cases.
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Crivello, Martín, María Marta Bonaventura, Astrid Chamson-Reig, et al. "Postnatal development of the endocrine pancreas in mice lacking functional GABAB receptors." American Journal of Physiology-Endocrinology and Metabolism 304, no. 10 (2013): E1064—E1076. http://dx.doi.org/10.1152/ajpendo.00569.2012.
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Adult mice lacking functional GABAB receptors (GABAB1KO) have glucose metabolism alterations. Since GABAB receptors (GABABRs) are expressed in progenitor cells, we evaluated islet development in GABAB1KO mice. Postnatal day 4 (PND4) and adult, male and female, GABAB1KO, and wild-type littermates (WT) were weighed and euthanized, and serum insulin and glucagon was measured. Pancreatic glucagon and insulin content were assessed, and pancreas insulin, glucagon, PCNA, and GAD65/67 were determined by immunohistochemistry. RNA from PND4 pancreata and adult isolated islets was obtained, and Ins1, Ins2, Gcg, Sst, Ppy, Nes, Pdx1, and Gad1 transcription levels were determined by quantitative PCR. The main results were as follows: 1) insulin content was increased in PND4 GABAB1KO females and in both sexes in adult GABAB1KOs; 2) GABAB1KO females had more clusters (<500 μm2) and less islets than WT females; 3) cluster proliferation was decreased at PND4 and increased in adult GABAB1KO mice; 4) increased β-area at the expense of the α-cell area was present in GABAB1KO islets; 5) Ins2, Sst, and Ppy transcription were decreased in PND4 GABAB1KO pancreata, adult GABAB1KO female islets showed increased Ins1, Ins2, and Sst expression, Pdx1 was increased in male and female GABAB1KO islets; and 6) GAD65/67 was increased in adult GABAB1KO pancreata. We demonstrate that several islet parameters are altered in GABAB1KO mice, further pinpointing the importance of GABABRs in islet physiology. Some changes persist from neonatal ages to adulthood (e.g., insulin content in GABAB1KO females), whereas other features are differentially regulated according to age (e.g., Ins2 was reduced in PND4, whereas it was upregulated in adult GABAB1KO females).
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Haas, Markus, and Bodo Rak. "Escherichia coli Insertion Sequence IS150: Transposition via Circular and Linear Intermediates." Journal of Bacteriology 184, no. 21 (2002): 5833–41. http://dx.doi.org/10.1128/jb.184.21.5833-5841.2002.
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ABSTRACT IS150, a member of the widespread IS3 family, contains two consecutive out-of-phase open reading frames, orfA and orfB, that partially overlap. These open reading frames encode three proteins, InsA, InsB, and the InsAB protein, which is jointly encoded by both open reading frames by means of programmed translational frameshifting. We demonstrate that the InsAB protein represents the IS150 element's transposase. In vivo, the wild-type IS150 element generates circular excision products and linear IS150 molecules. Circular and linear species have previously been detected with mutant derivatives of other members of the IS3 family. Our finding supports the assumption that these products represent true transposition intermediates of members of this family. Analysis of the molecular nature of these two species suggested that the circular forms are precursors of the linear molecules. Elimination of InsA synthesis within the otherwise intact element led to accumulation of large amounts of the linear species, indicating that the primary role of InsA may be to prevent abortive production of the linear species and to couple generation of these species to productive insertion events.
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Kovalyuk, Z. D. "Investigation of InS-InSe heterojunctions prepared using sulphurization of p-InSe." Semiconductor Physics Quantum Electronics and Optoelectronics 15, no. 1 (2012): 38–40. http://dx.doi.org/10.15407/spqeo15.01.038.
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Guo, Yan, and Shuangqian Liu. "Incompressible hydrodynamic approximation with viscous heating to the Boltzmann equation." Mathematical Models and Methods in Applied Sciences 27, no. 12 (2017): 2261–96. http://dx.doi.org/10.1142/s0218202517500440.
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The incompressible Navier–Stokes–Fourier (INSF) system with viscous heating was first derived from the Boltzmann equation in the form of the diffusive scaling by Bardos–Levermore–Ukai–Yang [Kinetic equations: Fluid dynamical limits and viscous heating, Bull. Inst. Math. Acad. Sin.[Formula: see text] 3 (2008) 1–49]. The purpose of this paper is to justify such an incompressible hydrodynamic approximation to the Boltzmann equation in [Formula: see text] setting in a periodic box. Based on an odd–even expansion of the solution with respect to the microscopic velocity, the diffusive coefficients are determined by the INSF system with viscous heating and the super-Burnett functions. More importantly, the remainder of the expansion is proven to decay exponentially in time via an [Formula: see text] approach on the condition that the initial data satisfies the mass, momentum and energy conversation laws.
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Kniep, Rüdiger, and Wilfried Welzel. "Phasenbeziehungen und intermediäre Verbindungen in Systemen GaX3 – Ga2S3 und InX3 – In2S3 (X = Cl, Br, I) / Phase Relations and Intermediate Compounds in Systems GaX3 – Ga2S3 and InX3 – In2S3 (X = Cl, Br, I)." Zeitschrift für Naturforschung B 40, no. 1 (1985): 26–31. http://dx.doi.org/10.1515/znb-1985-0108.
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The systems GaX3-Ga2S3 and InX3-In2S3 (X = Cl, Br, I) are quasi-binary and contain the intermediate phases GaSX and InSX with incongruent melting behaviour. Stability regions of GaSCl and GaSBr at elevated temperatures are shifted towards the respective binary halides and include compositions Ga9S8X11 which in an earlier work were reported as separate crystalline phases. InSCl and InSBr (CdCl2-type structure) also show a significant phase width towards the respective binary halides, but with the maximum melting temperature remaining at stoichiometric compositions. Cell parameters and symmetry of InSI are related to InSeI, but do not confirm the proposed isotypic relationship
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Szabat, Marta, Honey Modi, Reshma Ramracheya, et al. "High-content screening identifies a role for Na + channels in insulin production." Royal Society Open Science 2, no. 12 (2015): 150306. http://dx.doi.org/10.1098/rsos.150306.
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Insulin production is the central feature of functionally mature and differentiated pancreatic β -cells. Reduced insulin transcription and dedifferentiation have been implicated in type 2 diabetes, making drugs that could reverse these processes potentially useful. We have previously established ratiometric live-cell imaging tools to identify factors that increase insulin promoter activity and promote β -cell differentiation. Here, we present a single vector imaging tool with eGFP and mRFP, driven by the Pdx1 and Ins1 promoters, respectively, targeted to the nucleus to enhance identification of individual cells in a high-throughput manner. Using this new approach, we screened 1120 off-patent drugs for factors that regulate Ins1 and Pdx1 promoter activity in MIN6 β -cells. We identified a number of compounds that positively modulate Ins1 promoter activity, including several drugs known to modulate ion channels. Carbamazepine was selected for extended follow-up, as our previous screen also identified this use-dependent sodium channel inhibitor as a positive modulator of β -cell survival. Indeed, carbamazepine increased Ins1 and Ins2 mRNA in primary mouse islets at lower doses than were required to protect β -cells. We validated the role of sodium channels in insulin production by examining Nav1.7 ( Scn9a ) knockout mice and remarkably islets from these animals had dramatically elevated insulin content relative to wild-type controls. Collectively, our experiments provide a starting point for additional studies aimed to identify drugs and molecular pathways that control insulin production and β -cell differentiation status. In particular, our unbiased screen identified a novel role for a β -cell sodium channel gene in insulin production.
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Dzięgielewska-Gęsiak, Sylwia, Dorota Stołtny, Alicja Brożek, Małgorzata Muc-Wierzgoń, and Ewa Wysocka. "Are insulin-resistance and oxidative stress cause or consequence of aging." Experimental Biology and Medicine 245, no. 14 (2020): 1260–67. http://dx.doi.org/10.1177/1535370220929621.
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Insulin resistance (IR) may be associated with oxidative stress and leads to cardiovascular disorders. Current research focuses on interplay between insulin-resistance indices and oxidant-antioxidant markers in elderly individuals with or without insulin-resistance. The assessment involved anthropometric data (weight, height, BMI, percentage of body fat (FAT)) and biochemical tests (glucose, lipids, serum insulin and plasma oxidant-antioxidant markers: Thiobarbituric Acid-Reacting Substances (TBARS), Cu,Zn-superoxide dismutase (SOD-1) and total antioxidant status). Insulin resistance index (IR) assuming a cut-off point of 0.3 allows to divides groups into: insulin sensitive group (InsS) IR < 0,3 ( n = 35, median age 69.0 years) and insulin-resistant group (InsR) IR ≥ 0.3 ( n = 51, median age 71.0 years). Lipids and antioxidant defense system markers did not differentiate the investigated groups. In the InsR elderly group, the FAT was increased ( P < 0.000003) and TBARS ( P = 0.008) concentration decreased in comparison with InsS group. A positive correlation for SOD-1 and total antioxidant status ( P < 0.05; r = 0.434) and a negative correlation for TBARS and age ( P < 0.05 with r = −0.421) were calculated in InsR individuals. In elderly individuals, oxidative stress persists irrespective of insulin-resistance status. We suggest that increased oxidative stress may be consequence of old age. An insulin action identifies those at high risk for atherosclerosis, via congruent associations with oxidative stress and extra- and intra-cellular antioxidant defense systems. Thus, we maintain that insulin-resistance is not the cause of aging. Impact statement Insulin resistance is associated with oxidative stress leading to cardiovascular diseases. However, little research has been performed examining elderly individuals with or without insulin-resistance. We demonstrate that antioxidant defense systems alone is not able to abrogate insulin action in elderly individuals at high risk for atherosclerosis, whereas the combined oxidant-antioxidant markers (thiobarbituric acid-reacting substances (TBARS), Cu,Zn-superoxide dismutase (SOD-1), and total antioxidant status (TAS)) might be more efficient and perhaps produce better clinical outcome. In fact, a decrease in oxidative stress and strong interaction between antioxidant defense can be seen only among insulin-resistant elderly individuals. This is, in our opinion, valuable information for clinicians, since insulin-resistance is considered strong cardiovascular risk factor.
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Sulaiman, Nabil, Mahmood Yaseen Hachim, Anila Khalique, Abdul Khader Mohammed, Saba Al Heialy та Jalal Taneera. "EXOC6 (Exocyst Complex Component 6) Is Associated with the Risk of Type 2 Diabetes and Pancreatic β-Cell Dysfunction". Biology 11, № 3 (2022): 388. http://dx.doi.org/10.3390/biology11030388.
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EXOC6 and EXOC6B (EXOC6/6B) components of the exocyst complex are involved in the secretory granule docking. Recently, EXOC6/6B were anticipated as a molecular link between dysfunctional pancreatic islets and ciliated lung epithelium, making diabetic patients more prone to severe SARS-CoV-2 complications. However, the exact role of EXOC6/6B in pancreatic β-cell function and risk of T2D is not fully understood. Herein, microarray and RNA-sequencing (RNA-seq) expression data demonstrated the expression of EXOC6/6B in human pancreatic islets. Expression of EXOC6/6B was not affected by diabetes status. Exploration of the using the translational human pancreatic islet genotype tissue-expression resource portal (TIGER) revealed three genetic variants (rs947591, rs2488071 and rs2488073) in the EXOC6 gene that were associated (p < 2.5 × 10−20) with the risk of T2D. Exoc6/6b silencing in rat pancreatic β-cells (INS1-832/13) impaired insulin secretion, insulin content, exocytosis machinery and glucose uptake without cytotoxic effect. A significant decrease in the expression Ins1, Ins1, Pdx1, Glut2 and Vamp2 was observed in Exoc6/6b-silenced cells at the mRNA and protein levels. However, NeuroD1, Gck and InsR were not influenced compared to the negative control. In conclusion, our data propose that EXOC6/6B are crucial regulators for insulin secretion and exocytosis machinery in β-cells. This study identified several genetic variants in EXOC6 associated with the risk of T2D. Therefore, EXOC6/6B could provide a new potential target for therapy development or early biomarkers for T2D.
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TUĞLUK, Mehmet Emin. "A Lexıcographıc Approach to İnşâ (Inshâ) Works: The Example of Hâzâ İnşâ-i Merğûb." Akademik Dil ve Edebiyat Dergisi 6, no. 2 (2022): 56–76. http://dx.doi.org/10.34083/akaded.1151968.
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İnsanlar çeşitli şekillerde iletişim kurmuş ve iletişim kurmak istedikleri muhataplarına duygu ve düşüncelerini en güzel ve akıcı bir şekilde aktarmak istemişlerdir. Bundaki amaç sözlerinin etkisiyle muhatapları üzerinde olumlu bir etki bırakma isteğidir. Tarih boyunca uzakta bulunan kişilerle iletişim kurmanın en yaygın yollarından biri mektup göndermek olmuştur. Ancak mektup bir tür olup bu adla yazılan metinlerin hepsi aynı özelliği göstermemektedir. Osmanlı nesri sade nesir, orta nesir, sanatlı (edebî) nesir olmak üzere üçe ayrılıp Türk edebiyatında edebî nesir için genellikle inşâ terimi benimsenmiştir. Mektup, yaygın olarak her toplum ve kültürden insanların haberleşmesi için kullanılırken Türk edebiyatında edebî nesir için ve klasik edebiyata özgü bir terim olarak mektup karşılığında inşâ terimi kullanılmış ve inşâ bir ilim dalı olarak yaygınlaşmıştır. İnşâ metinlerinin yazımına kılavuzluk etmesi amacıyla pek çok eser kaleme alınmıştır. Yazılan bu eserler genellikle belirli kalıplar ile Arapça ve Farsça kelime ve tamlamalar içermektedir. Ancak eserden esere değişmekle birlikte bu eserlerin bazılarının genellikle sol ve sağ köşelerine bu kalıp, kelime ve tamlamaların Türkçe karşılıkları bir sözlük şeklinde verilmiştir. Bu çalışmada yazarı bilinmeyen ve inşâ ilminde kullanılan kelimeleri konu edinen Hâzâ İnşâ-i Merğûb adlı eser sözlükbilimsel açısından ele alınmış, eserin çevirisi çalışmanın sonuna eklenmiştir.
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LIU, Qian, Qing-xian HUANG, Fu-chen LOU, et al. "Effects of glucose and insulin on the H9c2 (2-1) cell proliferation may be mediated through regulating glucose transporter 4 expression." Chinese Medical Journal 126, no. 21 (2013): 4037–42. http://dx.doi.org/10.3760/cma.j.issn.0366-6999.20130685.
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Background The change of glucose transporter 4 (GLUT4) expression could influence glucose uptake in the myocardial cells and then effect myocardial metabolism, which maybe one of the factor for the diabetes cardiovascular disease. This study aimed to explore the influence of glucose and insulin at different concentrations on H9c2 (2-1) cell proliferation and its GLUT4 expression in vitro, and evaluate the correlation between myocardial cells proliferation and GLUT4 expression. This might be helpful for understanding the relationship between glucose metabolism and cardiovascular disease. Methods According to glucose concentrations in culture medium, cultured H9c2 rat myocardial cells were divided into five groups: control group (NC, glucose concentration 5.0 mmol/L), low glucose group (LG, glucose concentration 0.1 mmol/L), high glucose group 1 (HG1, glucose concentration 10 mmol/L), high glucose group 2 (HG2, glucose concentration 15 mmol/L), high glucose group 3 (HG3, glucose concentration 20 mmol/L). Then according to different insulin concentrations in culture medium, each group was further divided into two subgroups: normal insulin subgroup (INSc, insulin concentration 3.8 mU/L), high insulin subgroup (INSh, insulin concentration 7.6 mU/L). H9c2 (2-1) cells were cultured for 1, 2, 3 days, the proliferation of cells were assayed by cell counting Kit-8 assay, the expressions of GLUT4 mRNA and protein were detected with RT-PCR and Western Blotting technique, and the relation between myocardial cells proliferation and GLUT4 expression was evaluated. Results Compared with NC group, cell proliferation (OD value) was lower in LG, HG2, HG3 group but higher in HG1 group on the second and the third day (P <0.05). There was a negative correlation between OD value and the glucose level in HG1, HG2, HG3 groups (P <0.05). OD value in INSc subgroups was lower than that in INSh subgroups (P <0.05). GLUT4 mRNA was lower in LG, HG2, HG3 groups than that in NC group (P<0.05). Compared with NC group, GLUT4 mRNA level in HG1 group was higher on the first day but lower on the second and third day (P<0.05). In HG1, HG2 and HG3 groups, GLUT4 mRNA level had a negative correlation with the level of glucose (P <0.05). GLUT4 mRNA in INSc subgroups was lower than that in INSh subgroups (P <0.05). The expression of GLUT4 protein was similar to that of GLUT4 mRNA. There was a positive correlation between H9c2 cell proliferation and GLUT4 expression (P<0.02). Conclusions Glucose levels could regulate glucose uptake in myocardial cells through influencing GLUT4 expression, and thus affected the cell proliferation and cell function. Insulin levels could affect the myocardial cell function by regulating GLUT4 expression. Effects of glucose and insulin on the myocardial cells proliferation might be mediated through regulating GLUT4 expression. There may be a mechanism of hyperglycemia pre-accommodation (HGPA) in myocardial cells mediated through regulation of GLUT4 expression.
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Saeed, Rania, Abdul Khader Mohammed, Sarra E. Saleh, Khaled M. Aboshanab, Mohammad M. Aboulwafa та Jalal Taneera. "Expression Silencing of Mitogen-Activated Protein Kinase 8 Interacting Protein-1 Conferred Its Role in Pancreatic β-Cell Physiology and Insulin Secretion". Metabolites 13, № 2 (2023): 307. http://dx.doi.org/10.3390/metabo13020307.
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Mitogen-activated protein kinase 8 interacting protein-1 (MAPK8IP1) gene has been recognized as a susceptibility gene for diabetes. However, its action in the physiology of pancreatic β-cells is not fully understood. Herein, bioinformatics and genetic analyses on the publicly available database were performed to map the expression of the MAPK8IP1 gene in human pancreatic islets and to explore whether this gene contains any genetic variants associated with type 2 diabetes (T2D). Moreover, a series of functional experiments were executed in a rat insulinoma cell line (INS-1 832/13) to investigate the role of the Mapk8ip1 gene in β-cell function. Metabolic engineering using RNA-sequencing (RNA-seq) data confirmed higher expression levels of MAPK8IP1 in human islets compared to other metabolic tissues. Additionally, comparable expression of MAPK8IP1 expression was detected in sorted human endocrine cells. However, β-cells exhibited higher expression of MAPK8IP1 than ductal and PSC cells. Notably, MAPK8IP1 expression was reduced in diabetic islets, and the expression was positively correlated with insulin and the β-cell transcription factor PDX1 and MAFA. Using the TIGER portal, we found that one genetic variant, “rs7115753,” in the proximity of MAPK8IP1, passes the genome-wide significance for the association with T2D. Expression silencing of Mapk8ip1 by small interfering RNA (siRNA) in INS-1 cells reduced insulin secretion, glucose uptake rate, and reactive oxygen species (ROS) production. In contrast, insulin content, cell viability, and apoptosis without cytokines were unaffected. However, silencing of Mapk8ip1 reduced cytokines-induced apoptosis and downregulated the expression of several pancreatic β-cell functional markers including, Ins1, Ins2, Pdx1, MafA, Glut2, Gck, Insr, Vamp2, Syt5, and Cacna1a at mRNA and/or protein levels. Finally, we reported that siRNA silencing of Pdx1 resulted in the downregulation of MAPK8IP1 expression in INS-1 cells. In conclusion, our findings confirmed that MAPK8IP1 is an important component of pancreatic β-cell physiology and insulin secretion.
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MATSUTANI, SACHIKO. "THE INTERNAL SEQUENCE OF IS1STIMULATES RNA SYNTHESIS FROM THE IS1OWN AND EXOGENOUS PROMOTERS." Journal of Biological Systems 13, no. 03 (2005): 313–29. http://dx.doi.org/10.1142/s0218339005001513.
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The bacterial IS1 contains the genes insA and B′-insB encoding transposition related-proteins. The expression of these genes is driven by a promoter within the left end of IS1. Using IS1-lacZ constructs in which lacZs were fused in-frame at various sites of IS1 genes, it was found that the presence of the internal region of insA results in about a 100-fold increase in lacZ expression. The lacZ expression of the fusion constructs in which the IS1 own promoter was displaced by an exogenous promoter, was also stimulated by the presence of the IS1 internal region. Similarly, when lacZ was transcriptionally fused to the internal region of IS1, the lacZ expression from an exogenous promoter was stimulated. This result shows that the IS1 internal region acts as a cis-element to stimulate RNA synthesis from the upstream promoter. This was confirmed by Northern blot analyses. Furthermore, the gene which encodes the factor working with the IS1 internal sequence to stimulate transcription, was cloned. The gene was artA in the transfer region of the Escherichia coli F factor. Interestingly, the cis-element for transcription stimulation is found downstream, whereas many such elements are located upstream, of the promoter.
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Baikova, Iuliia P., Leonid A. Ilchuk, Polina D. Safonova, et al. "Two Novel Mouse Models of Duchenne Muscular Dystrophy with Similar Dmd Exon 51 Frameshift Mutations and Varied Phenotype Severity." International Journal of Molecular Sciences 26, no. 1 (2024): 158. https://doi.org/10.3390/ijms26010158.
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Duchenne muscular dystrophy (DMD) is a severe X-linked genetic disorder caused by an array of mutations in the dystrophin gene, with the most commonly mutated regions being exons 48–55. One of the several existing approaches to treat DMD is gene therapy, based on alternative splicing and mutant exon skipping. Testing of such therapy requires animal models that carry mutations homologous to those found in human patients. Here, we report the generation of two genetically modified mouse lines, named “insT” and “insG”, with distinct mutations at the same position in exon 51 that lead to a frameshift, presumably causing protein truncation. Hemizygous males of both lines exhibit classical signs of muscular dystrophy in all muscle tissues except for the cardiac tissue. However, pathological changes are more pronounced in one of the lines. Membrane localization of the protein is reduced to the point of absence in one of the lines. Moreover, an increase in full-length isoform mRNA was detected in diaphragms of insG line mice. Although further work is needed to qualify these mutations as sole origins of dissimilarity, both genetically modified mouse lines are suitable models of DMD and can be used to test gene therapy based on alternative splicing.
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Mr. Dharmesh Dhabliya. "Intelligent Banal type INS based Wassily chair (INSW)." International Journal of New Practices in Management and Engineering 1, no. 01 (2012): 01–08. http://dx.doi.org/10.17762/ijnpme.v1i01.2.
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The navigation of physically impaired requires a continuous positioning with certain accuracy in their environments. This paper proposes an automated wheel chair developed for the indoor navigation using Inertial Navigation System (INS) for the physically blight persons. The Wassily chairs are the mobile chairs that facilitate the movement of the user in pre-functioned places. This is an intelligent vehicle which has all the feasibility for the usage of the physically impaired. This mobile chair replaces the traditional gear system with the keypad system to reach the destined places and to locate the things in the destined places. This makes the vehicle smart and user-friendly augmenting the viability to carry out their day to day activities. It has an additional feature, the automatic airbag system which provides hip bone protections.
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Sharma, Rahul, Sujay K. Maity, Partha Chakrabarti, et al. "PIMT Controls Insulin Synthesis and Secretion through PDX1." International Journal of Molecular Sciences 24, no. 9 (2023): 8084. http://dx.doi.org/10.3390/ijms24098084.
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Pancreatic beta cell function is an important component of glucose homeostasis. Here, we investigated the function of PIMT (PRIP-interacting protein with methyl transferase domain), a transcriptional co-activator binding protein, in the pancreatic beta cells. We observed that the protein levels of PIMT, along with key beta cell markers such as PDX1 (pancreatic and duodenal homeobox 1) and MafA (MAF bZIP transcription factor A), were reduced in the beta cells exposed to hyperglycemic and hyperlipidemic conditions. Consistently, PIMT levels were reduced in the pancreatic islets isolated from high fat diet (HFD)-fed mice. The RNA sequencing analysis of PIMT knockdown beta cells identified that the expression of key genes involved in insulin secretory pathway, Ins1 (insulin 1), Ins2 (insulin 2), Kcnj11 (potassium inwardly-rectifying channel, subfamily J, member 11), Kcnn1 (potassium calcium-activated channel subfamily N member 1), Rab3a (member RAS oncogene family), Gnas (GNAS complex locus), Syt13 (synaptotagmin 13), Pax6 (paired box 6), Klf11 (Kruppel-Like Factor 11), and Nr4a1 (nuclear receptor subfamily 4, group A, member 1) was attenuated due to PIMT depletion. PIMT ablation in the pancreatic beta cells and in the rat pancreatic islets led to decreased protein levels of PDX1 and MafA, resulting in the reduction in glucose-stimulated insulin secretion (GSIS). The results from the immunoprecipitation and ChIP experiments revealed the interaction of PIMT with PDX1 and MafA, and its recruitment to the insulin promoter, respectively. Importantly, PIMT ablation in beta cells resulted in the nuclear translocation of insulin. Surprisingly, forced expression of PIMT in beta cells abrogated GSIS, while Ins1 and Ins2 transcript levels were subtly enhanced. On the other hand, the expression of genes, PRIP/Asc2/Ncoa6 (nuclear receptor coactivator 6), Pax6, Kcnj11, Syt13, Stxbp1 (syntaxin binding protein 1), and Snap25 (synaptosome associated protein 25) associated with insulin secretion, was significantly reduced, providing an explanation for the decreased GSIS upon PIMT overexpression. Our findings highlight the importance of PIMT in the regulation of insulin synthesis and secretion in beta cells.
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Karaca, Melis. "Transgenic expression of human INS gene in Ins1/Ins2 double knockout mice leads to insulin underproduction and diabetes in some male mice." Frontiers in Bioscience 12, no. 1 (2007): 1586. http://dx.doi.org/10.2741/2171.
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Murakami-Kawaguchi, Shoko, Shin Takasawa, Tohru Onogawa, et al. "Expression of Ins1 and Ins2 genes in mouse fetal liver." Cell and Tissue Research 355, no. 2 (2013): 303–14. http://dx.doi.org/10.1007/s00441-013-1741-4.
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Gallon Pitta, Manoela, Kelly Zhang, Gustavo Henrique De Mello Rosa, Lucas Hipolito Do Espírito Santo, Elaine Caldeira De Oliveira Guirro, and João Eduardo De Araujo. "Effects of Cholinergic Receptor Activation and Magnetic Fields on Motor Behavior in Ischemic Gerbils." Interdisciplinary Rehabilitation / Rehabilitacion Interdisciplinaria 4 (February 11, 2024): 70. http://dx.doi.org/10.56294/ri202470.
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Introduction: Ischemic stroke stands as a leading global cause of death and disability, prompting the need for animal model experiments in stroke research and the protection of motor function. Recently, magnetic fields have gained significant interest in various biological contexts, showing promise in preserving neurons and reversing behavioral and morphological changes in stroke models. This study explores the potential synergy between static magnetic field and nAChR agonist administration in safeguarding motor behavior in ischemic gerbils. Objective: To determine whether the combined use of a static magnetic field and an agonist for nicotinic acetylcholine receptors (nAChR) can preserve motor behavior in ischemic gerbils.Methods: In this experimental study, 72 Mongolian gerbils were randomly allocated into nine groups (n=8): S, SISM, SINSM, ISM, INP, ISP, INSM, INNP, INSP, distributed according to surgical procedure and treatment. The animals were trained and evaluated on the Rotarod (RR) to assess motor performance.Results: The main finding was the preservation of motor behavior in the Sham Ischemia and Nicotine and Sham Magnetic Stimulation (SINSM) and Ischemia and Nicotine and South Pole Magnetic Field (INSP) groups, as evidenced by the results of the RR test.Conclusions: The findings are consistent with previous literature and provide insight into the mechanism of potentiation, as results showed that adding a nAChR agonist to the magnetic field preserved motor performance in the RR test of ischemic animals.
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Akinci, Ersin, Anannya Banga, Lucas V. Greder, James R. Dutton та Jonathan M. W. Slack. "Reprogramming of pancreatic exocrine cells towards a beta (β) cell character using Pdx1, Ngn3 and MafA". Biochemical Journal 442, № 3 (2012): 539–50. http://dx.doi.org/10.1042/bj20111678.
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Pdx1 (pancreatic and duodenal homeobox 1), Ngn3 (neurogenin 3) and MafA (v-maf musculoaponeurotic fibrosarcoma oncogene family, protein A) have been reported to bring about the transdifferentiation of pancreatic exocrine cells to beta (β) cells in vivo. We have investigated the mechanism of this process using a standard in vitro model of pancreatic exocrine cells, the rat AR42j-B13 cell line. We constructed a new adenoviral vector encoding all three genes, called Ad-PNM (adenoviral Pdx1, Ngn3, MafA construct). When introduced into AR42j-B13 cells, Ad-PNM caused a rapid change to a flattened morphology and a cessation of cell division. The expression of exocrine markers is suppressed. Both insulin genes are up-regulated as well as a number of transcription factors normally characteristic of beta cells. At the chromatin level, histone tail modifications of the Pdx1, Ins1 (insulin 1) and Ins2 (insulin 2) gene promoters are shifted in a direction associated with gene activity, and the level of DNA CpG methylation is reduced at the Ins1 promoter. The transformed cells secrete insulin and are capable of relieving diabetes in streptozotocin-treated NOD-SCID (non-obese diabetic severe combined immunodeficiency) mice. However the transformation is not complete. The cells lack expression of several genes important for beta cell function and they do not show glucose-sensitive insulin secretion. We conclude that, for this exocrine cell model, although the transformation is dramatic, the reprogramming is not complete and lacks critical aspects of the beta cell phenotype.
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Leroux, L., P. Desbois, L. Lamotte, et al. "Compensatory responses in mice carrying a null mutation for Ins1 or Ins2." Diabetes 50, Supplement 1 (2001): S150—S153. http://dx.doi.org/10.2337/diabetes.50.2007.s150.
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SEKINO, N. "IS1-encoded proteins, InsA and the InsA-B?-InsB transframe protein (transposase): Functions deduced from their DNA-binding ability." Advances in Biophysics 31 (1995): 209–22. http://dx.doi.org/10.1016/0065-227x(95)99393-4.
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Wafa, T. "Contribution of BRCA1 and BRCA2 mutations to breast cancer in Tunisia." Journal of Clinical Oncology 27, no. 15_suppl (2009): e22191-e22191. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e22191.
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e22191 Background: Hereditary breast cancer accounts for 3–8% of all breast cancers. It was recently estimated that a combination of BRCA1 and BRCA2 genes mutations is responsible for 30% of hereditary breast cancer cases. Methods: To investigate the prevalence of BRCA1 and BRCA2 gene mutations in breast cancer patients with affected relatives in Tunisia, 36 patients who had at least one first degree relative affected with breast and/or ovarian cancer were analysed. Thirty three patients are suggestive of BRCA1 mutation and 3 are suggestive of BRCA2 mutation. Results: Four mutations in BRCA1 gene were described among which, one novel splice site mutation (330 dupA) and 3 frameshift mutations including the 4160 delAG, the 2789 delG and the 5385 insC. Our study is the first to describe the 5385 insC mutation which was described only among Jewish Ashkenazi population. Two frameshift mutations (1537 del4 and 5909 insA) were screened in BRCA2 gene. Nineteen percent (7/36) of the familial cases were altered on BRCA1 or BRCA2 genes with deleterious mutations at heterozygous state and 55% (20/36) by mutation with uncertain value (UV) or by single nucleotide polymorphisms (SNPs). Conclusions: Almost all the cases mutated by deleterious mutations on BRCA1 gene reported a family history of breast and/or ovarian cancer in the index case or in their relatives. On the contrary, patients with an UV mutation or SNPs have no history of ovarian cancer in their corresponding families. Our data are the first to contribute to information on mutation spectrum of BRCA genes and offer a recommended screening mode for clinical genetic testing policy in Tunisia. No significant financial relationships to disclose.
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Pusch, Emily, Małgorzata Krążek, Tatiana Wojciechowicz, et al. "GIP_HUMAN [22–51] Peptide Encoded by the Glucose-Dependent Insulinotropic Polypeptide (GIP) Gene Suppresses Insulin Expression and Secretion in INS-1E Cells and Rat Pancreatic Islets." Genes 14, no. 10 (2023): 1910. http://dx.doi.org/10.3390/genes14101910.
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GIP_HUMAN [22–51] is a recently discovered peptide that shares the same precursor molecule with glucose-dependent insulinotropic polypeptide (GIP). In vivo, chronic infusion of GIP_HUMAN [22–51] in ApoE−/− mice enhanced the development of aortic atherosclerotic lesions and upregulated inflammatory and proatherogenic proteins. In the present study, we evaluate the effects of GIP_HUMAN [22–51] on insulin mRNA expression and secretion in insulin-producing INS-1E cells and isolated rat pancreatic islets. Furthermore, we characterize the influence of GIP_HUMAN [22–51] on cell proliferation and death and on Nf-kB nuclear translocation. Rat insulin-producing INS-1E cells and pancreatic islets, isolated from male Wistar rats, were used in this study. Gene expression was evaluated using real-time PCR. Cell proliferation was studied using a BrdU incorporation assay. Cell death was quantified by evaluating histone-complexed DNA fragments. Insulin secretion was determined using an ELISA test. Nf-kB nuclear translocation was detected using immunofluorescence. GIP_HUMAN [22–51] suppressed insulin (Ins1 and Ins2) in INS-1E cells and pancreatic islets. Moreover, GIP_HUMAN [22–51] promoted the translocation of NF-κB from cytoplasm to the nucleus. In the presence of a pharmacological inhibitor of NF-κB, GIP_HUMAN [22–51] was unable to suppress Ins2 mRNA expression. Moreover, GIP_HUMAN [22–51] downregulated insulin secretion at low (2.8 mmol/l) but not high (16.7 mmol/l) glucose concentration. By contrast, GIP_HUMAN [22–51] failed to affect cell proliferation and apoptosis. We conclude that GIP_HUMAN [22–51] suppresses insulin expression and secretion in pancreatic β cells without affecting β cell proliferation or apoptosis. Notably, the effects of GIP_HUMAN [22–51] on insulin secretion are glucose-dependent.
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Khalique, Anila, Abdul Khader Mohammed, Nujood Mohammed Al-khadran та ін. "Reduced Retinoic Acid Receptor Beta (Rarβ) Affects Pancreatic β-Cell Physiology". Biology 11, № 7 (2022): 1072. http://dx.doi.org/10.3390/biology11071072.
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Various studies have suggested a link between vitamin A (VA), all-trans-retinol, and type 2 diabetes (T2D). However, the functional role/expression of vitamin A receptors (Rarα, β, and γ) in pancreatic β-cells is not clear yet. Accordingly, we performed a series of bioinformatics, molecular and functional experiments in human islet and INS-1 cells to evaluate the role of Rarβ on insulin secretion and pancreatic β-cell function. Microarray and RNA-sequencing (RAN-seq) expression analysis showed that RARα, β, and γ are expressed in human pancreatic islets. RNA-seq expression of RARβ in diabetic/hyperglycemic human islets (HbA1c ≥ 6.3%) revealed a significant reduction (p = 0.004) compared to nondiabetic/normoglycemic cells (HbA1c < 6%). The expression of RARβ with INS and PDX1 showed inverse association, while positive correlations were observed with INSR and HbA1c levels. Exploration of the T2D knowledge portal (T2DKP) revealed that several genetic variants in RARβ are associated with BMI. The most associated variant is rs6804842 (p = 1.2 × 10−25). Silencing of Rarβ in INS-1 cells impaired insulin secretion without affecting cell viability or apoptosis. Interestingly, reactive oxygen species (ROS) production levels were elevated and glucose uptake was reduced in Rarβ-silenced cells. mRNA expression of Ins1, Pdx1, NeuroD1, Mafa, Snap25, Vamp2, and Gck were significantly (p < 0.05) downregulated in Rarβ-silenced cells. For protein levels, Pro/Insulin, PDX1, GLUT2, GCK, pAKT/AKT, and INSR expression were downregulated considerably (p < 0.05). The expression of NEUROD and VAMP2 were not affected. In conclusion, our results indicate that Rarβ is an important molecule for β-cell function. Hence, our data further support the potential role of VA receptors in the development of T2D.
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Karatug Kacar, A., S. Gezginci-Oktayoglu, and S. Bolkent. "4-Methylcatechol stimulates apoptosis and reduces insulin secretion by decreasing betacellulin and inhibin beta-A in INS-1 beta-cells." Human & Experimental Toxicology 37, no. 11 (2018): 1123–30. http://dx.doi.org/10.1177/0960327118758365.
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Insulinoma INS-1 cell line is a pancreatic beta cell tumor which is characterized with high insulin content and secretion in response to increasing glucose levels. 4-Methylcatechol (4-MC) is a metabolite of quercetin, which is known as a potential drug for inhibition of tumorigenesis. The aim of this study was to determine the applying doses of 4-methylcatechol (4-MC) for triggening cell death and decreasing the cell function of rat insulinoma INS-1 beta cells. The rate of apoptosis and the amount of insulin in the cell and the secretions were determined by the ELISA method. Betacellulin (BTC) and inhibin beta-A amounts in both the cell and the glucose induced secretion were investigated by Western blotting. Furthermore, BTC, Inhibin beta-A, Ins1, Ins2, and GLUT2 gene expression levels were determined by the by the real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) method. We noted a significant decrease in cell viability, while an increase in apoptotic cell death by 4-MC treatment. It caused a decrease in the secretion of BTC, expressions of both BTC and inhibin beta-A. We showed a decrease in the expressions of Ins1 and GLUT2, while there is no alteration in the level of insulin protein. Insulin secretion levels increased in INS-1 cells given 4-MC by basal glucose concentration while they did not response to high concentration of glucose, which indicates that 4-MC disrupts the functionality of INS-1 cells. These results revealed that 4-MC induces apoptosis and decreases insulin secretion by reducing BTC and inhibin beta-A in insulinoma INS-1 cells. Thus, 4-MC may be offered as a potential molecule for treatment of insulinoma.
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Liu, Hua-Yu, Meng Fang, and Yu-Qing Zhang. "In Vivo Hypoglycaemic Effect and Inhibitory Mechanism of the Branch Bark Extract of the Mulberry on STZ-Induced Diabetic Mice." Scientific World Journal 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/614265.
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Branch bark extract (BBE) derived from the mulberry cultivar Husang 32 (Morus multicaulisL.) with aqueous alcohol solution has been investigated as an inhibitor ofα-glycosidasein vitro. Mulberry BBE was orally administered to STZ-induced diabetic mice for three weeks, and it improved the weight gain and ameliorated the swelling of liver and kidney in diabetic mice. Obviously, mulberry BBE not only can reduce the abnormally elevated levels of serum insulin and ameliorate insulin resistance induced by STZ, but also it regulates dyslipidemia in diabetic mice. To understand this therapeutic effect and the regulatory mechanisms of BBE in diabetic mice, a qRT-PCR experiment was performed, indicating that the mulberry BBE can regulate the mRNA expression of glycometabolism genes in diabetic mice, including glucose-6-phosphatase (G6Pase), glucokinase (GCK), and phosphoenolpyruvate carboxykinase (PEPCK), thereby regulating sugar metabolism and reducing the blood glucose level in diabetic mice. The mulberry BBE can increase the mRNA expression of the genes Ins1, Ins2 and pancreatic duodenal homeobox-1 (PDX-1) and may decrease the insulin resistance in diabetic mice. Those results provide an important basis for making the best use of mulberry branch resources and producing biomedical drugs with added value.
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Shamshidin, A. S., I. S. Beishova, E. V. Belaya, A. M. Kovalchuk, and T. V. Ulyanova. "GENETIC ARCHITECTURE OF SIGNS OF MEAT PRODUCTIVITY IN CATTLE OF KAZAKH WHITE-HEADED AND AULIEKOLSKY BREEDS." Bulletin of the Korkyt Ata Kyzylorda University 66, no. 3-2 (2023): 131–40. http://dx.doi.org/10.52081/bkaku.2023.v66.i3.106.
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Мақалада:қазақтың ақбас ірі қара мал тұқымының бұқашықтары және «Москалевское» ЖШС, «АФ Диевское» ЖШС, 497 бас әулиекөл ірі қара мал тұқымының бұқашықтары туралы айтылған. Ірі қара малының ет өнімділігінің генетикалық негізін анықтау мал шаруашылығы үшін маңызды. Бұл мақаланың мақсаты – қазақтың ақбас және әулиекөл тұқым малының ет өнімділігі негізінде жатқан генетикалық құрылымға жан-жақты шолу жасау, гендер арасындағы күрделі өзара әрекеттесуді түсіндіру. Алдыңғы зерттеулерді талдай және қорытындылай келе, кемшіліктер анықталып, болашақ зерттеулерге бағыттар ұсынылды. Мақалада қазақтың ақбас және әулиекөл тұқымдарының ет өнімділігін қалыптастыру кезінде әртүрлі гендердің қатысуы туралы ақпарат берілген. Қазақтың ақбас ірі қара мал бұзауларының тірі салмағының гендік құрылымы – ADGRL2, ADAM22 және VTI1A, ал әулиекөл тұқымы INSR, OSBPL10, MAPK10, INSC, PLSCR2, HSP90AA1, SLC4A4, SCAF8, EPN2, ALDH5A1, PIGR, NIPAL1, WDR20, ADGB, WDR20 және CARD10 гендерінен тұрады. Олар арқылы жүретін биологиялық процестердің ішінде жасушалық процестер басым (тиісінше қазақтың ақбас және әулиекөл ірі қара мал тұқымдарында 25,0 және 28,5%); биологиялық реттеу процестері (12,50% және 21,43%), жасушаларды оқшаулау процестері (12,50% және 17,86%), даму процестері мен сигналинг біршама төмен деңгейде (12,5% және 10,71%) болды. Бұл мақала ауыл шаруашылығы малының генетикасымен айналысатын ғылыми қауымдастық үшін қазақтың ақбас және әулиекөл тұқымдарының ет өнімділігін қалыптастыруды оңтайландыру үшін мақсатты стратегияларын әзірлеуге көмектесетін құнды дереккөз болып табылады.
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Zhang, Xiaoling, Yawei Liu, Liwen Zhang, and Qingduan Meng. "Deformation Analysis of 128×128 Infrared Detector with Reticulated InSb Pixel Array." Open Electrical & Electronic Engineering Journal 9, no. 1 (2015): 273–77. http://dx.doi.org/10.2174/1874129001509010273.
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The reticulated InSb pixel array was successfully employed in the design of large format InSb infrared focal plane arrays (IRFPAs) detector, to remove the thermal strain accumulated in InSb IRFPAs with the thermal shock test. In order to explore the deformation rules in the InSb IRFPAs with reticulated InSb pixel array, in light of the proposed equivalent modeling, a three-dimensional modeling of InSb IRFPAs is created, and the Z-component of strain is selected to compare the displacements in the various layers of InSb IRFPAs. Analyzing results that show the top surface deformation of InSb IRFPAs originates from the thermal mismatch between the silicon readout integrated circuit (ROIC) and the indium bump array directly above. After passing through the intermediate layer and the silicon substrate, the deformation amplitude along Z-direction is reduced firstly from 0.113 μm to 0.0395 μm, finally to 0.0042 μm. Here the intermediate layer is made up of the indium bump array and the reticulated InSb pixel array. These deformation data suggest that the InSb IRFPAs with reticulated InSb pixel array is superior to that designed with the underfill filled structure in the fabricating large format InSb IRFPAs.
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Pankov, Yury Alexandrovich. "Diabetes mellitus and other pathology in patients with INS and INSR mutations." Diabetes mellitus 15, no. 4 (2012): 11–16. http://dx.doi.org/10.14341/2072-0351-5532.
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Over 20 missense mutations and Y108X nonsense mutation in INS are dominant and induce synthesis of chimeric proteins that may interfere with folding and processing of all insulin molecules. In heterozygous state they cause insulin deficiency and PND. Over 10 recessive mutations and the p.Q62X nonsense mutation of INS do not induce synthesis of anomalous protein, being associated with PND only in homozygous state. Most of significant mutations that induce insulin resistance, lipodystrophy, and other pathology were found in INSR gene. Lipodistrophy suggests an important role of insulin in stimulating fat accumulation and controlling lipid consumption in energy metabolosm.
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Chen, Yang, Lili Huang, Xinzhou Qi, and Chen Chen. "Insulin Receptor Trafficking: Consequences for Insulin Sensitivity and Diabetes." International Journal of Molecular Sciences 20, no. 20 (2019): 5007. http://dx.doi.org/10.3390/ijms20205007.
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Insulin receptor (INSR) has been extensively studied in the area of cell proliferation and energy metabolism. Impaired INSR activities lead to insulin resistance, the key factor in the pathology of metabolic disorders including type 2 diabetes mellitus (T2DM). The mainstream opinion is that insulin resistance begins at a post-receptor level. The role of INSR activities and trafficking in insulin resistance pathogenesis has been largely ignored. Ligand-activated INSR is internalized and trafficked to early endosome (EE), where INSR is dephosphorylated and sorted. INSR can be subsequently conducted to lysosome for degradation or recycled back to the plasma membrane. The metabolic fate of INSR in cellular events implies the profound influence of INSR on insulin signaling pathways. Disruption of INSR-coupled activities has been identified in a wide range of insulin resistance-related diseases such as T2DM. Accumulating evidence suggests that alterations in INSR trafficking may lead to severe insulin resistance. However, there is very little understanding of how altered INSR activities undermine complex signaling pathways to the development of insulin resistance and T2DM. Here, we focus this review on summarizing previous findings on the molecular pathways of INSR trafficking in normal and diseased states. Through this review, we provide insights into the mechanistic role of INSR intracellular processes and activities in the development of insulin resistance and diabetes.
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Ishida, K., T. Nomura, H. Tokunaga, H. Ohtani, and T. Nishizawa. "Miscibility gaps in the GaPInP, GaPGaSb, InPInSn and InAsInSb systems." Journal of the Less Common Metals 155, no. 2 (1989): 193–206. http://dx.doi.org/10.1016/0022-5088(89)90228-2.
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Zhang, Jiang-Feng, Xiao-Han Tian, Xiao-Ling Zhang, and Qing-Duan Meng. "Splashed gold bump dependence of cleavage of InSb chip under cyclic liquid nitrogen shocking tests." Acta Physica Sinica 71, no. 2 (2022): 028502. http://dx.doi.org/10.7498/aps.71.20211535.
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Local cleavage of indium antimonide (InSb) chip always occurs in the manufacture of the InSb infrared focal plane detectors (IRFPAs), and this specific fracture phenomenon restricts the improvement of the yield of the InSb IRFPAs. After analysis, we think that the cleavage of InSb chip in the edge region of the InSb IRFPAs is related to the splashed gold bump existing in this region, and this failure phenomenon dominates in the low-cyclic liquid nitrogen shocking tests. In order to clarify the influence of the splashed gold bump on the cleavage of the InSb chip, we establish a structural model of the InSb IRFPAs containing the splashed gold bump, and analyze the influence of the splashed gold bump on the thermal stress distribution in the InSb chip. Besides, we preset the initial cracks with different lengths at the stress concentration sites to describe the dislocations in InSb wafers. Using the energy release rate as criterion, we obtain the relationship between the cleavage of the InSb chip and the dislocation line length in the presence of splashed gold bump. The main conclusions are drawn as follows. 1) The influence of the splashed gold bump on the cleavage of the InSb chip is localized, and two stress concentration sites are formed in the outermost part of the contact region between the splashed gold bump and the InSb chip. 2) The energy release rate surrounding the preset crack increases promptly with the preset crack length increasing. 3) Cleavage of the InSb chip caused by the splashed gold bump belongs to the type I fracture failure mode. In the cyclic liquid nitrogen shocking tests, the dislocation line gradually punches through the InSb chip under the driving of the concentrating stress, and forms the macro cleavage of the InSb chip.
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Kazimov, M. V., G. B. Ibragimov, G. I. Isakov, and B. G. Ibragimov. "Physical-chemical properties of InSb+Mg3Sb2 eutectic systems: synthesis, characterization, and applications." Journal of Optoelectronic and Biomedical Materials 14, no. 4 (2022): 187–90. http://dx.doi.org/10.15251/jobm.2022.144.187.
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InSb+Mg3Sb2 systems are synthesized by the vertical Bridgman–Stockbarger method. InSb and Mg3Sb2, a form of lamellar eutectic. XRD analysis and microstructural study of InSb+Mg3Sb2 composites show that Mg3Sb2 lamellar are uniformly distributed in the InSb matrices. The initial and final melting temperatures for InSb+Mg3Sb2 eutectic alloys are 770K and 772K, respectively.
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Takahashi, Masayuki, Kei Daizumoto, Tomoya Fukawa, et al. "The significance of insulin receptor expression to predict the resistance to VEGFR-TKIs and induce PD-L1 expression in advanced clear cell renal cell carcinoma." Journal of Clinical Oncology 37, no. 7_suppl (2019): 592. http://dx.doi.org/10.1200/jco.2019.37.7_suppl.592.
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592 Background: Previously we have identified the prognostic gene set of ccRCC patients, where insulin receptor (INSR) expression was decreased in the patients with poor outcome (Proc Natl Acad Sci U S A., 2001). We examined the clinical significance of decreased INSR expression and sought to elucidate the underlying mechanisms. Methods: The INSR expression was immunohistochemically examined in the nephrectomy specimens of RCC patients (n = 33) who then received axitinib. We established patient derived Xenograft model (PDX) of ccRCC and examined the INSR expression in the axitinib resistant PDX tumors by Western blotting. As the INSR is expressed in the vascular endothelial cells, we co-cultured the RCC cell lines with the human renal glomerular endothelial cells (HGEC) treated with si-RNA of INSR (si-INSR) and the microarray experiment was conducted. Results: In RCC patients with axitinib, those with low INSR expression had poor outcome (median PFS 19.5 vs 2.3 months, p < 0.001; median OS 34.2 vs 5.6 months, p = 0.001). The INSR expression was the significantly independent predictor of PFS (p = 0.006). In the axitinib-resistant PDX tumors, the expression of INSR was decreased. In the co-culture experiments, the microarray experiments revealed that the decreased INSR expression in the HGECs may be involved with the important signaling pathway including interferon response in Caki-1 cells. Interferon- β was highly expressed in HGECs with si-INSR. The decreased INSR expression and the increased interferon-β expression in HGEC were confirmed when axitinib was administered. The Caki-1 cells that was co-cultured with HGECs treated with si-INSR demonstrated high expression of PD-L1. The PD-L1 expression was increased in a concentration-dependent manner of recombinant interferon-β and increased phosphorylation of STAT1 and STAT3 were observed. Conclusions: In conclusion, the decreased INSR expression could be a biomarker to predict the resistance to VEGFR-TKIs. The decreased INSR expression was correlated with the increased interferon-β expression in HGECs, which leads to the induction of PD-L1 through increased phosphorylation of STAT1 and STAT3.
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Meng, Qing Duan, Xiao Ling Zhang, Xiao Lei Zhang, and Wei Guo Sun. "Finite Element Analysis on Structural Stress of 64×64 InSb Infrared Focal Plane Array." Applied Mechanics and Materials 34-35 (October 2010): 212–16. http://dx.doi.org/10.4028/www.scientific.net/amm.34-35.212.
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Two-step method is used to research stress and its distribution in 64×64 InSb infrared focal plane array (IRFPA) employing finite element method. First, a small 8×8 InSb IRFPA is systemically studied by varying indium bump diameters, standoff heights and InSb chip thicknesses in suitable range, with indium diameter 30μm, thickness 9μm and InSb thickness 12μm, von Mises stress in InSb chip is the smallest and its distribution is uniform at contacting areas. Then, the sizes of InSb IRFPA is doubled once again from 8×8 to 64×64 to learn the effect from chip sizes, thus, the stress and its distribution of 64×64 InSb IRFPA is obtained in a short time. Simulation results show that von Mises stress maximum in InSb chip almost increases linearly with array scale, yet von Mises stress maximum in Si ROIC decreases slightly with increased array sizes, and the largest von Mises stress is located in InSb chips. Besides, stress distribution on the bottom surface of InSb chip is radiating, and decreases from core to four corners, and stress value at contacting area is smaller than those on its surrounding areas, contrary to stress distribution on top surface of InSb chip.
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Wilson, Miranda S. C., Simon J. Bulley, Francesca Pisani, Robin F. Irvine, and Adolfo Saiardi. "A novel method for the purification of inositol phosphates from biological samples reveals that no phytate is present in human plasma or urine." Open Biology 5, no. 3 (2015): 150014. http://dx.doi.org/10.1098/rsob.150014.
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Inositol phosphates are a large and diverse family of signalling molecules. While genetic studies have discovered important functions for them, the biochemistry behind these roles is often not fully characterized. A key obstacle in inositol phosphate research in mammalian cells has been the lack of straightforward techniques for their purification and analysis. Here we describe the ability of titanium dioxide (TiO 2 ) beads to bind inositol phosphates. This discovery allowed the development of a new purification protocol that, coupled with gel analysis, permitted easy identification and quantification of InsP 6 (phytate), its pyrophosphate derivatives InsP 7 and InsP 8 , and the nucleotides ATP and GTP from cell or tissue extracts. Using this approach, InsP 6 , InsP 7 and InsP 8 were visualized in Dictyostelium extracts and a variety of mammalian cell lines and tissues, and the effects of metabolic perturbation on these were explored. TiO 2 bead purification also enabled us to quantify InsP 6 in human plasma and urine, which led to two distinct but related observations. Firstly, there is an active InsP 6 phosphatase in human plasma, and secondly, InsP 6 is undetectable in either fluid. These observations seriously question reports that InsP 6 is present in human biofluids and the advisability of using InsP 6 as a dietary supplement.