Journal articles: 'RETN'

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Schwartz, Daniel R., Erika R. Briggs, Mohammed Qatanani, Heloisa Sawaya, Igal A. Sebag, Michael H. Picard, Marielle Scherrer-Crosbie, and Mitchell A. Lazar. "Human Resistin in Chemotherapy-Induced Heart Failure in Humanized Male Mice and in Women Treated for Breast Cancer." Endocrinology 154, no. 11 (November 1, 2013): 4206–14. http://dx.doi.org/10.1210/en.2013-1399.

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Resistin is a circulating mediator of insulin resistance mainly expressed in human monocytes and responsive to inflammatory stimuli. Recent clinical studies have connected elevated resistin levels with the development and severity of heart failure. To further our understanding of the role of human resistin in heart failure, we studied a humanized mouse model lacking murine resistin but transgenic for the human Retn gene (Hum-Retn mice), which exhibits basal and inflammation-stimulated resistin levels similar to humans. Specifically, we explored whether resistin underlies acute anthracycline-induced cardiotoxicity. Remarkably, doxorubicin (25mg/kg ip) led to a 4-fold induction of serum resistin levels in Hum-Retn mice. Moreover, doxorubicin-induced cardiotoxicity was greater in the Hum-Retn mice than in littermate controls not expressing human resistin (Retn−/−). Hum-Retn mice showed increased cardiac mRNA levels of inflammatory and cell adhesion genes compared with Retn−/− mice. Macrophages, but not cardiomyocytes, from Hum-Retn mice treated with doxorubicin in vitro showed dramatic induction of hRetn (human resistin) mRNA and protein expression. We also examined resistin levels in anthracycline-treated breast cancer patients with and without cardiotoxicity. Intriguingly, serum resistin levels in women undergoing anthracycline-containing chemotherapy increased significantly at 3 months and remained elevated at 6 months in those with subsequent cardiotoxicity. Further, elevation in resistin correlated with decline in ejection fraction in these women. These results suggest that elevated resistin is a biomarker of anthracycline-induced cardiotoxicity and may contribute in the development of heart failure via its direct effects on macrophages. These results further implicate resistin as a link between inflammation, metabolism, and heart disease.

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Ibrahim, Sherine M., and Afaf A. Bastawy. "The Relevance of Single-nucleotide Polymorphism +62 G>A to the Expression of Resistin Gene Affecting Serum Resistin Levels in Metabolic Syndrome in the Egyptian Population." Current Pharmaceutical Biotechnology 21, no. 7 (June 16, 2020): 626–34. http://dx.doi.org/10.2174/1389201021666191210122851.

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Background: Metabolic Syndrome (MS) is a clinical condition consisting of risk factors associated with type two diabetes and developing cardiovascular disease. It has been suggested that resistin is a linkage between obesity, inflammation and type two diabetes. This study aims to investigate whether Resistin Gene (RETN) polymorphism (+62G>A) is linked to MS and resistin levels among the Egyptian population. Methods: This study was performed with 310 Egyptian volunteers: 160 MS subjects and 150 controls. Anthropometric parameters and biochemical variables were determined. The RETN +62G>A polymorphism was genotyped by PCR-RFLP technique. Results: The resistin levels of the MS group were significantly higher than those of the control group. Resistin levels were positively correlated with anthropometric parameters and liver biomarkers in the MS group. According to RETN +62G>A polymorphism, carriers with the A allele (GA/AA) had significantly increased resistin levels than subjects with the GG genotype, consequently, the RETN +62G >A polymorphism was found to be related to MS, biochemical parameters and anthropometric variables. Conclusions: These findings propose that the RETN +62G>A polymorphism has a great impact on the circulating resistin concentrations, and that resistin levels are strongly related to MS. Therefore, this RETN polymorphism is related to the risk of the prevalence of MS in the Egyptians.

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Suriyaprom, Kanjana, Rungsunn Tungtrongchitr, and Pisit Namjuntra. "Associations of Resistin Levels with Resistin Gene Polymorphism and Metabolic Syndrome in Thais / Asocijacija Nivoa Rezistina Sa Polimorfizmom Gena Za Rezistin I Metaboličkim Sindromom Kod Tajlanđana." Journal of Medical Biochemistry 34, no. 2 (April 1, 2015): 170–78. http://dx.doi.org/10.2478/jomb-2014-0034.

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Summary Background: Metabolic syndrome (MS) is a clinical constellation comprising risk factors associated with developing cardiovascular disease and type 2 diabetes. Resistin has been suggested as a linkage between obesity, inflammation and type 2 diabetes. This study aimed to investigate resistin concentrations and hematological-biochemical parameters in MS subjects and controls, and to determine whether two resistin gene (RETN) polymorphisms (-420C>G & +299G>A) are linked to resistin levels and MS among Thais. Methods: This case-control study was performed with 322 Thai volunteers: 160 MS subjects and 162 controls. Anthropometric parameters and hematological-biochemical variables were determined. The RETN -420C>G (rs1862513) and +299G>A (rs3745367) polymorphisms were genotyped by PCR-RFLP technique. Results: The resistin levels of the MS group were significantly higher than those of the control group. Resistin levels were positively correlated with anthropometric parameters and WBC count in the MS group. According to RETN -420C>G polymorphism, MS subjects with the G allele (CG/GG) (3.9 mg/L) had significantly higher resistin con- centrations than in subjects with the CC genotype (2.4 mg/L); with regard to RETN +299G>A polymorphism, carriers with the A allele (GA/AA) (3.8 mg/L) had significantly higher resistin levels than subjects with the GG genotype (2.7 mg/L), after adjusting for potential covariates. How - ever, the RETN -420C>G and +299G>A poly morphisms were not found to be associated with MS, hematologicalbiochemical parameters and anthropometric variables. Conclusions: These findings suggest resistin levels are linked with MS and the RETN -420C>G and +299G>A polymorphisms have impacted the circulating resistin concentrations. However, these two RETN polymorphisms pro - bably do not influence susceptibility to MS among Thais.

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Mahmoudi, Touraj, Khatoon Karimi, Maral Arkani, Hamid Farahani, Mohsen Vahedi, Reza Dabiri, Hossein Nobakht, et al. "Resistin -420C>G Promoter Variant and Colorectal Cancer Risk." International Journal of Biological Markers 29, no. 3 (July 2014): 233–38. http://dx.doi.org/10.5301/jbm.5000079.

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Purposes Obesity is associated with an increased risk of colorectal cancer (CRC), and ghrelin (GHRL) and resistin (RETN) are thought to be related to obesity. Our aim was to investigate whether GHRL and RETN gene variants are associated with CRC risk. Materials and Methods All 414 subjects, including 197 cases with CRC and 217 controls, were genotyped for the GHRL (rs26802) and RETN (rs1862513) or -420C>G gene variants using the PCR-RFLP method. Results Our findings indicated that the RETN -420C>G “CC” genotype, compared with the “GG” and “GC” genotypes, was a marker of decreased CRC susceptibility; the difference remained significant after adjustment for age, BMI, gender, smoking status, NSAID use, and family history of CRC (p=0.020; OR=0.52, 95% CI=0.30-0.90). Furthermore, after adjustment for confounding factors, the -420C>G “CC” genotype, compared with the “GG” genotype, was associated with a decreased risk for CRC (p=0.044; OR=0.53, 95% CI=0.29-0.98). In addition, no significant difference was observed for the GHRL (rs26802) gene variant. Conclusions To our knowledge, this is the first study suggesting that the RETN -420C>G “CC” genotype is a marker of decreased CRC susceptibility. This observation is relevant from a scientific perspective and deserves further investigations.

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Pravenec, Michal, Petr Mlejnek, Václav Zídek, Vladimír Landa, Miroslava Šimáková, Jan Šilhavý, Hynek Strnad, et al. "Autocrine effects of transgenic resistin reduce palmitate and glucose oxidation in brown adipose tissue." Physiological Genomics 48, no. 6 (June 2016): 420–27. http://dx.doi.org/10.1152/physiolgenomics.00122.2015.

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Resistin has been originally identified as an adipokine that links obesity to insulin resistance in mice. In our previous studies in spontaneously hypertensive rats (SHR) expressing a nonsecreted form of mouse resistin ( Retn) transgene specifically in adipose tissue (SHR- Retn), we have observed an increased lipolysis and serum free fatty acids, ectopic fat accumulation in muscles, and insulin resistance. Recently, brown adipose tissue (BAT) has been suggested to play an important role in the pathogenesis of metabolic disturbances. In the current study, we have analyzed autocrine effects of transgenic resistin on BAT glucose and lipid metabolism and mitochondrial function in the SHR- Retn vs. nontransgenic SHR controls. We observed that interscapular BAT isolated from SHR- Retn transgenic rats compared with SHR controls showed a lower relative weight (0.71 ± 0.05 vs. 0.91 ± 0.08 g/100 g body wt, P < 0.05), significantly reduced both basal and insulin stimulated incorporation of palmitate into BAT lipids (658 ± 50 vs. 856 ± 45 and 864 ± 47 vs. 1,086 ± 35 nmol/g/2 h, P ≤ 0.01, respectively), and significantly decreased palmitate oxidation (37.6 ± 4.5 vs. 57 ± 4.1 nmol/g/2 h, P = 0.007) and glucose oxidation (277 ± 34 vs. 458 ± 38 nmol/g/2 h, P = 0.001). In addition, in vivo microPET imaging revealed significantly reduced 18F-FDG uptake in BAT induced by exposure to cold in SHR- Retn vs. control SHR (232 ± 19 vs. 334 ± 22 kBq/ml, P < 0.05). Gene expression profiles in BAT identified differentially expressed genes involved in skeletal muscle and connective tissue development, inflammation and MAPK and insulin signaling. These results provide evidence that autocrine effects of resistin attenuate differentiation and activity of BAT and thus may play a role in the pathogenesis of insulin resistance in the rat.

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Al-Hilali, Hammadi A., and Mohammed Jaafar AL-Anssari. "Resistin (RETN) Gene rs1862513 Polymorphisms and Acne vulgaris Patients." International Journal of Current Microbiology and Applied Sciences 5, no. 12 (December 10, 2016): 415–22. http://dx.doi.org/10.20546/ijcmas.2016.512.045.

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Wang, Chao-Qun, Chih-Hsin Tang, Huey-En Tzeng, Lulu Jin, Jin Zhao, Le Kang, Yan Wang, et al. "Impacts of RETN genetic polymorphism on breast cancer development." Journal of Cancer 11, no. 10 (2020): 2769–77. http://dx.doi.org/10.7150/jca.38088.

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de Luis, Daniel Antonio, Olatz Izaola, David Primo, Beatriz de la Fuente, Ines Mulero, and Rocío Aller. "The rs1862513 Variant in Resistin Gene-Modified Insulin Resistance and Insulin Levels after Weight Loss Secondary to Hypocaloric Diet." Annals of Nutrition and Metabolism 69, no. 3-4 (2016): 256–62. http://dx.doi.org/10.1159/000453676.

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Background/Aims: Polymorphisms of a single nucleotide in RETN have been associated with indexes of insulin resistance. Our aim was to analyze the effects of the rs1862513 RETN gene polymorphism on insulin resistance, insulin levels, and resistin levels changes after 3 months of a low-fat hypocaloric diet. Design: A Caucasian population of 133 obese patients was analyzed before and after 3 months on a low-fat hypocaloric diet. Results: Fifty-six patients (42.1%) had the genotype GG (wild group) and 77 (57.9%) patients had the other genotypes; GC (59 patients, 44.4%) or CC (18 patients, 13.5%; mutant group). In wild and mutant genotype groups, weight, body mass index, fat mass, waist circumference, and systolic blood pressure decreased. In the wild genotype group, the decrease in total cholesterol was -13.1 ± 25.3 mg/dL (vs. -4.4 ± 13.7 mg/dL in mutant group: p = 0.004 for group deltas), low density lipoprotein (LDL)-cholesterol was -13.0 ± 21.5 mg/dL (-4.3 ± 10.5 mg/dL: p = 0.007), glucose -7.2 ± 3.5 mg/dL (-0.8 ± 0.2 mg/dL: p = 0.01), insulin -5.6 ± 2.5 mUI/L (-2.9 ± 1.2 mUI/L: p = 0.03) and homeostasis model assessment-insulin resistance (HOMA-IR) -2.5 ± 1.1 (-0.6 ± 1.4: p = 0.02). Leptin levels decreased in both genotypes (-10.1 ± 9.5 ng/dL in wild type group vs. -13.1 ± 0.2 ng/dL in mutant type group: p > 0.05). Conclusion: The present study suggests that the G/G genotype of RETN rs1862513 could be a predictor of the reduction of HOMA-IR, insulin, fasting glucose and LDL cholesterol secondary to a hypocaloric diet in obese subjects.

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Kawamura, Ryoichi, Yasuharu Tabara, Akiko Tsukada, Michiya Igase, Jun Ohashi, Ryo Yamada, Yasunori Takata, et al. "Genome-wide association study of plasma resistin levels identified rs1423096 and rs10401670 as possible functional variants in the Japanese population." Physiological Genomics 48, no. 11 (November 1, 2016): 874–81. http://dx.doi.org/10.1152/physiolgenomics.00040.2016.

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Resistin is a cytokine inducing insulin resistance in mice. We previously identified single nucleotide polymorphisms (SNPs) at −420 (rs1862513) and −358 (rs3219175) located in the human resistin gene ( RETN) promoter as strong determinants for circulating resistin in the Japanese population. The objective was to identify additional functional variants for circulating resistin. We conducted a genome-wide association study in 448 Japanese subjects. A peak association signal was found on chromosome 19 where RETN is located. The top-hit SNP was SNP −358 G>A, followed by rs1423096 C>T, SNP −420 C>G, and rs10401670 C>T ( P = 5.39×10−47, 1.81×10−22, 2.09×10−16, and 9.25×10−15, respectively). Meta-analysis including another two independent general Japanese populations showed that circulating resistin was most strongly associated with SNP-358, followed by SNP-420, rs1423096, and rs10401670. Rs1423096 and rs10401670 were located in the 3′-region of RETN and were in strong linkage disequilibrium. Although these SNPs were also in linkage disequilibrium with the promoter SNPs, conditional and haplotype association analyses identified rs1423096 and rs10401670 as independent determinants for circulating resistin. Functionally, nuclear proteins specifically recognized T but not C at rs10401670 as evidenced by an electrophoretic mobility shift assay. The promoter activity of a luciferase reporter with T at either rs1423096 or rs10401670 was lower than that with C in THP-1 human monocytes. Therefore, rs1423096 and rs10401670, in addition to SNP-420 and SNP-358, were identified as possible functional variants affecting circulating resistin by the genome-wide search in the Japanese population.

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Elkhattabi, Lamiae, Imane Morjane, Hicham Charoute, Soumaya Amghar, Hind Bouafi, Zouhair Elkarhat, Rachid Saile, Hassan Rouba, and Abdelhamid Barakat. "In Silico Analysis of Coding/Noncoding SNPs of Human RETN Gene and Characterization of Their Impact on Resistin Stability and Structure." Journal of Diabetes Research 2019 (May 20, 2019): 1–9. http://dx.doi.org/10.1155/2019/4951627.

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Resistin (RETN) is a gene coding for proinflammatory adipokine called resistin secreted by macrophages in humans. Single nucleotide polymorphisms (SNPs) in RETN are linked to obesity and insulin resistance in various populations. Using dbSNP, 78 nonsynonymous SNPs (nsSNPs) were retrieved and tested on a PredictSNP 1.0 megaserver. Among these, 15 nsSNPs were predicted as highly deleterious and thus subjected to further analyses, such as conservation, posttranscriptional modifications, and stability. The 3D structure of human resistin was generated by homology modeling using Swiss model. Root-mean-square deviation (RMSD), hydrogen bonds (h-bonds), and interactions were estimated. Furthermore, UTRscan served to identify UTR functional SNPs. Among the 15 most deleterious nsSNPs, 13 were predicted to be highly conserved including variants in posttranslational modification sites. Stability analysis predicted 9 nsSNPs (I32S, C51Y, G58E, G58R, C78S, G79C, W98C, C103G, and C104Y) which can decrease protein stability with at least three out of the four algorithms used in this study. These nsSNPs were chosen for structural analysis. Both variants C51Y and C104Y showed the highest RMS deviations (1.137 Å and 1.308 Å, respectively) which were confirmed by the important decrease in total h-bonds. The analysis of hydrophobic and hydrophilic interactions showed important differences between the native protein and the 9 mutants, particularly I32S, G79C, and C104Y. Six SNPs in the 3′UTR (rs920569876, rs74176247, rs1447199134, rs943234785, rs76346269, and rs78048640) were predicted to be implicated in polyadenylation signal. This study revealed 9 highly deleterious SNPs located in the human RETN gene coding region and 6 SNPs within the 3′UTR that may alter the protein structure. Interestingly, these SNPs are worth to be analyzed in functional studies to further elucidate their effect on metabolic phenotype occurrence.

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Miyamoto, Yuji, Sebastian Stintzing, Wu Zhang, Shu Cao, Yan Ning, Satoshi Okazaki, Martin D. Berger, et al. "Polymorphisms in adipokine-related genes to predict treatment outcomes in patients (pts) with metastatic colorectal cancer (mCRC) treated with bevacizumab-based chemotherapy." Journal of Clinical Oncology 35, no. 4_suppl (February 1, 2017): 600. http://dx.doi.org/10.1200/jco.2017.35.4_suppl.600.

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600 Background: The molecular effects of obesity are mediated by alterations in the levels of adipokines, which are produced mainly by adipose tissue. Adipokines have multiple effects, including insulin sensitivity, cell proliferation, inflammation, and angiogenesis. We previously reported that single-nucleotide polymorphisms (SNPs) in obesity-related genes were associated with the recurrence probability of CRC treated with 5-FU based adjuvant chemotherapy. This study aimed to evaluate whether SNPs in adipokine-related genes may predict clinical outcomes in bevacizumab treated mCRC pts. Methods: Genomic DNA was obtained from mCRC pts receiving bevacizumab plus FOLFIRI as first-line treatment and analyzed by using PCR-based direct sequencing. Eleven functional SNPs in 7 genes ( LEP, LEPR, ADIPOQ, ADIPOR1, RETN, TNFa and NAMPT) were tested in 291 pts in FIRE3 trial bevacizumab cohort (NCT00433927). Main characteristics were the following: male/female = 193/98; median age = 65; High BMI pts (BMI ≥ 25 Kg/m2)/low BMI pts (BMI < 25 Kg/m2) = 162/129; median PFS = 10.1 months; median OS = 24.2 months, median follow-up time = 40.8 months. Results: LEPR rs1137100 G/G variants (n = 24) showed worse PFS than any A variants (n = 246) in univariate (10.4 months (M) vs. 9.2 M, HR = 1.75, 95%CI = 1.12-2.74, P = 0.011) and multivariate analyses (HR = 1.75, 95%CI = 1.11-2.74, P = 0.016). NAMPT rs61330082 T/T (n = 24) showed worse PFS than any C variants (n = 243) in multivariate analysis (HR = 1.65, 95% = 1.02-2.67, P = 0.042). RETN rs1862513 C/C (n = 23) showed worse OS than any G variants (n = 246) in univariate analysis (14.1 m vs. 25.1 M, HR = 1.65, 95%CI = 1.04-2.60, P = 0.029). In subgroup analyses of high BMI pts, the prognostic effect of LEPR rs1137100 G/G and RETN rs1862513 C/C was confirmed and no association was observed among low BMI pts. Conclusions: Our study showed for the first time that genetic variations in adipokine-related genes are associated with prognosis of mCRC pts treated with bevacizumab based chemotherapy.

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Uchiyama, Tomoko, Asako Itaya-Hironaka, Akiyo Yamauchi, Mai Makino, Sumiyo Sakuramoto-Tsuchida, Ryogo Shobatake, Hiroyo Ota, Maiko Takeda, Chiho Ohbayashi, and Shin Takasawa. "Intermittent Hypoxia Up-Regulates CCL2, RETN, and TNFα mRNAs in Adipocytes via Down-regulation of miR-452." International Journal of Molecular Sciences 20, no. 8 (April 22, 2019): 1960. http://dx.doi.org/10.3390/ijms20081960.

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Sleep apnea syndrome (SAS), characterized by recurrent episodes of oxygen desaturation and reoxygenation (intermittent hypoxia [IH]), is a risk factor for insulin resistance. Recently, IH is considered to independently cause adipose tissue inflammation/dysfunction, leading to worsening insulin resistance; however, the detailed mechanism remains unknown. We exposed mouse 3T3-L1 and human SW872 adipocytes to experimental IH or normoxia for 24 h, and analyzed mRNA expression of several adipokines. We found that the mRNA levels of RETN, TNFα, and CCL2 in SW872 and 3T3-L1 adipocytes were significantly increased by IH, whereas the promoter activities of these genes were not increased. A target mRNA search of microRNA (miR)s revealed that all human mRNAs have a potential target sequence for miR-452. The miR-452 level of IH-treated cells was significantly decreased compared to normoxia-treated cells. MiR-452 mimic and non-specific control RNA (miR-452 mimic NC) were introduced into SW872 cells, and the IH-induced up-regulation of the genes was abolished by introduction of the miR-452 mimic but not by the miR-452 mimic NC. These results indicate that IH stress down-regulates the miR-452 in adipocytes, resulting in increased levels of RETN, TNFα, and CCL2 mRNAs, leading to insulin resistance in SAS patients.

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Wu, Xiaoyan, Elise R. den Boer, Manon Vos-Loohuis, Frank G. van Steenbeek, Glen R. Monroe, Isaäc J. Nijman, Peter A. J. Leegwater, and Hille Fieten. "Investigation of Genetic Modifiers of Copper Toxicosis in Labrador Retrievers." Life 10, no. 11 (October 31, 2020): 266. http://dx.doi.org/10.3390/life10110266.

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Copper toxicosis is a complex genetic disorder in Labrador retrievers characterized by hepatic copper accumulation eventually leading to liver cirrhosis. The variation of hepatic copper levels in Labrador retrievers has been partly explained by mutations in ATP7A c.980C>T and ATP7B c.4358G>A. To further elucidate the genetic background of this disease, we used targeted Next Generation Sequencing (NGS) in a cohort of 95 Labrador retrievers to analyze 72 potential modifier genes for variations associated with hepatic copper levels. Variants associated with copper levels were subsequently evaluated in a replication cohort of 144 Labrador retrievers. A total of 44 variants in 25 different genes were identified, of which four showed significant association with copper levels. Of the four variants found associated with hepatic copper levels in the NGS cohort, one was validated in the replication cohort. The non-reference allele of the variant NC_006602.3.g.52434480C>T in RETN resulting in amino-acid change p.Leu7Phe was associated with decreased hepatic copper levels. In humans, resistin is associated with severity of non-alcoholic fatty liver disease, fibrosis, cirrhosis and mitochondrial dysfunction in hepatocytes. Further studies are needed to investigate the biological function of RETN p.Leu7Phe in the development of copper toxicosis in Labrador retrievers.

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Alharithy, Rowyda N. "Polymorphisms in RETN gene and susceptibility to colon cancer in Saudi patients." Annals of Saudi Medicine 34, no. 4 (July 2014): 334–39. http://dx.doi.org/10.5144/0256-4947.2014.334.

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Pechlivanis, Sonali, Justo Lorenzo Bermejo, Barbara Pardini, Alessio Naccarati, Ludmila Vodickova, Jan Novotny, Kari Hemminki, Pavel Vodicka, and Asta Försti. "Genetic variation in adipokine genes and risk of colorectal cancer." European Journal of Endocrinology 160, no. 6 (June 2009): 933–40. http://dx.doi.org/10.1530/eje-09-0039.

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ObjectiveObesity has been related to an increased risk of colorectal cancer (CRC). Adipokines produced by the adipose tissue are directly linked to obesity and may thus contribute to the pathogenesis of CRC. We hypothesized that potentially functional polymorphisms in the adipokine genes leptin (LEP), leptin receptor (LEPR), resistin (RETN), and adiponectin (ADIPOQ) may be associated with CRC.Design and methodsWe studied the association of four putatively functional single nucleotide polymorphisms (SNPs) with CRC risk using a hospital-based study design with 702 cases and 752 controls from the Czech Republic. We used likelihood ratio tests to select the best model to represent the relationship between genotypes and risk of CRC. Age-adjusted odds ratios (ORs) under the best model were calculated for each SNP. Previous genotyping data on insulin (INS)-related genes were used to explore interactions between genes in obesity- and diabetes-related pathways by using two independent methods, logistic regression, and multifactor-dimensionality reduction.ResultsA trend to associate between the RETN SNP rs1862513 (C-420G) and CRC risk was observed (per allele OR 1.18, 95% confidence interval (0.99–1.40). Statistically, significant interactions were observed between the INS SNP rs3842754 (+1127INSPstI) genotypes and both the LEPR SNP rs1137101 (Q223R) and the ADIPOQ SNP rs266729 (C-11374G) genotypes.ConclusionsOur results suggest that variants in the adipokine genes may affect CRC risk in combination with variants in diabetes-related genes.

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Mahmoudi, Touraj, Keivan Majidzadeh-A, Khatoon Karimi, Hamid Farahani, Reza Dabiri, Hossein Nobakht, Asadollah Asadi, Negar Karimi, Maral Arkani, and Mohammad Reza Zali. "Gly972Arg Variant of Insulin Receptor Substrate 1 Gene and Colorectal Cancer Risk in Overweight/Obese Subjects." International Journal of Biological Markers 31, no. 1 (January 2016): 68–72. http://dx.doi.org/10.5301/jbm.5000159.

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Background Given the major role of obesity and insulin resistance (IR) in colorectal cancer (CRC), we investigated whether genetic variants in ghrelin ( GHRL), resistin ( RETN) and insulin receptor substrate 1 ( IRS1) were associated with CRC risk. Methods This study was conducted as a case-control study, and 750 subjects, including 438 controls and 312 patients with CRC, were enrolled and genotyped using the PCR-RFLP method. Results No significant differences were observed for GHRL (rs696217), RETN (rs3745367) and IRS1 (rs1801278, Gly972Arg or G972R) gene variants between the cases and controls. However, the IRS1 G972R R allele compared with the G allele and the G972R RR+GR genotype compared with the GG genotype appeared to be markers of decreased CRC susceptibility in the overweight/obese subjects (p = 0.024; odds ratio [OR] = 0.42, 95% confidence interval [95% CI], 0.20-0.91; and p = 0.048; OR = 0.42, 95% CI, 0.17-0.99, respectively). Furthermore, the R allele and RR+GR genotype were also associated with decreased risks for obesity in the patients with CRC (p = 0.007; OR = 0.35, 95% CI, 0.15-0.77; and p = 0.015; OR = 0.35, 95% CI, 0.15-0.72, respectively). Conclusions In accordance with previous studies, our findings suggest that the IRS1 G972R R allele and RR+GR genotype have protective effects for CRC in overweight/obese patients and for obesity in patients with CRC. Nevertheless, further studies are required to confirm these findings.

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Chang, Ming-Ling, Su-Wei Chang, Shiang-Chi Chen, Rong-Nan Chien, Chia-Lin Hsu, Ming-Yu Chang, and Cathy S. J. Fann. "Genetic Association of Hepatitis C-Related Mixed Cryoglobulinemia: A 10-Year Prospective Study of Asians Treated with Antivirals." Viruses 13, no. 3 (March 11, 2021): 464. http://dx.doi.org/10.3390/v13030464.

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Genetic profiles of hepatitis C virus (HCV)-associated mixed cryoglobulinemia (MC) in Asians remain elusive. A 10-year prospective cohort study was conducted with 1043 consecutive HCV Ab-positive Taiwanese surveyed with 13 single nucleotide polymorphisms (SNPs). Of 1043, 589 (56.5%) had baseline MC, 934 (89.5%) had positive HCV RNA, 796 completed anti-HCV therapy, and 715 had sustained virological responses (SVRs). SNP associations were surveyed withgenotypic, allelic, trend, permutation and multivariate analyses. At baseline, higher male sex and MC rates were noted in HCV RNA-positive than RNA-negative patients; higher female sex and positive HCV RNA rates but lower HCV RNA levels were noted in patients with than those without MC. Baseline associations were: HLA II-rs9461776 A allele, IFNL3-rs12979860 T allele, SERPINE1-rs6976053 C allele and MC with HCV RNA positivity; IFNL3-rs12979860 C allele, ARNTL-rs6486122 T allele and HCV RNA positivity with baseline MC. In SVR patients, RETN-rs1423096 C allele and SERPINE1-rs6976053 T allele were associated with 24-week and 10-year post-therapy MC, respectively. Conclusions: HCV RNA, IFNL3-rs12979860 and ARNTL-rs6486122 were associated with baseline MC; RETN-rs1423096 and SERPINE1-rs6976053 were associated with short- and long-term post-therapy MC in SVR patients, respectively. Links with HCV RNA and immune-associated SNPs suggest MC an immune reaction to expel HCV.

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Hastuti, Pramudji, Tasmini Tasmini, Rizki Fajar Utami, Meirlin Rambu Kaita Riwa, Steven Steven, and Ahmad Hamim Sadewa. "Variation of Resistin Gene Is Correlated with Insulin Resistance in Obese People of Indonesia." Open Access Macedonian Journal of Medical Sciences 7, no. 12 (June 18, 2019): 1891–95. http://dx.doi.org/10.3889/oamjms.2019.456.

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BACKGROUND: Obesity is considered associated with an increase of resistin levels that plays a role in the regulation of energy and maintaining fasting blood glucose. Polymorphism of resistin is thought to be correlated with the levels of resistin and insulin resistance.AIM: This study aimed to examine the association of +299G > A and -420C > G resistin (RETN) gene with resistin level and insulin resistance in obese people of Indonesia.METHODS: We examined 142 healthy unrelated subjects consisting of 71 obese and 71 controls. Fasting blood glucose was measured by the enzymatic method while the resistin and insulin levels were measured by Elisa method. Insulin resistance was calculated by HOMA-IR index. Polymorphisms of RETN genes were examined by the Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) method, and the data was tested. The data were correlated with Kruskal Wallis continue logistic regression and simple linear regressionRESULTS: In the obese group, there was an increased level of insulin (17.74 vs 11.27 mU/L) and insulin resistance (HOMA-IR 3.9 vs 1.46) compared to the control group. Polymorphism of +299G > A was associated with insulin resistance (GA and GA + AA genotype significantly different compare GG genotype with P < 0.001). Resistin level was negatively correlated with insulin level (P = 0.017). CONCLUSION: In this study, polymorphism of +299G > A was identified as a risk factor for insulin resistance, and there was a significant association of serum resistin level with insulin level in the population of Indonesia.

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Menzaghi, Claudia, Angelo Coco, Lucia Salvemini, Ryan Thompson, Salvatore De Cosmo, Alessandro Doria, and Vincenzo Trischitta. "Heritability of Serum Resistin and Its Genetic Correlation with Insulin Resistance-Related Features in Nondiabetic Caucasians." Journal of Clinical Endocrinology & Metabolism 91, no. 7 (July 1, 2006): 2792–95. http://dx.doi.org/10.1210/jc.2005-2715.

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Abstract Context: Serum levels of resistin are believed to modulate insulin resistance in humans. Objective: The aim of this study was to investigate whether serum resistin levels are genetically controlled and whether this control is shared with other insulin resistance traits. Design and Methods: The study cohort included 264 nondiabetic probands, Caucasian from Italy, and their 473 adult family members. Phenotypic characterization included anthropometric variables, blood pressure, fasting glucose and insulin, lipid profile, and resistin levels. Genotypes were determined at position g.−420C→G (rs1862513), IVS2+181G→A (rs3745367), and GAT(n) polymorphisms of the resistin (RETN) gene. Results: In the 264 unrelated probands, resistin levels were significantly (P < 0.01) correlated with adiposity, blood pressure, C-reactive protein, and the metabolic syndrome score. In a variance component analysis of the 264 probands and their 473 relatives, about 70% of the observed variation of serum resistin levels was heritable (P < 0.0001). A small, but significant (P = 0.004) proportion of this variance was explained by the G→A variation at position IVS2+181 of the RETN gene. Significant genetic correlations (P < 0.05) were observed between resistin and body mass index (ρg = 0.30), waist circumference (ρg = 0.32), the insulin resistance index HOMAIR (ρg = 0.28), and the metabolic syndrome score (ρg = 0.35). Conclusions: These data indicate that serum resistin is highly heritable and has some common genetic background with traits related to insulin resistance, reinforcing the hypothesis that this adipokine may play a pathogenic role in insulin resistance-related abnormalities, including type 2 diabetes and cardiovascular disease.

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Beckers, Sigri, Fenna de Freitas, Doreen Zegers, An Verrijken, Armand V. Peeters, Frida Peiffer, Stijn L. Verhulst, et al. "Identification and functional characterization of a missense mutation in resistin in two patients with severe obesity and insulin resistance." European Journal of Endocrinology 164, no. 6 (June 2011): 927–36. http://dx.doi.org/10.1530/eje-10-1080.

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ObjectiveIn this study, we hypothesized that mutations in the resistin encoding gene, RETN, may cause a monogenic form of obesity.Design/methodsWe screened the coding region of RETN in 81 morbidly obese adults, 263 overweight and obese children/adolescents, and 116 healthy lean subjects. In vitro experiments include qPCR, ELISA, and western blot for WT and mutant resistin transfected into 3T3-L1 adipocytes.ResultsMutation analysis identified five sequence variants in our patient populations: 3′-UTR +87 G/A, 3′-UTR +100 A/G, T73T, IV3-61 C/A, and C78S. In our control population, we only found the 3′-UTR +87 G/A variant. We started functional experiments for the C78S mutation that was found in a 20-year-old obese male (body mass index (BMI)=39.7 kg/m2) and his obese mother (BMI=31.9 kg/m2). In vitro testing demonstrated that the mutation does not impair mRNA expression. We identified a 100-fold lower extracellular protein concentration for mutant resistin compared with WT levels using a resistin ELISA on cell culture medium (P=4.87×10−6). We also detected a decreased intracellular concentration for the mutant protein (tenfold lower relative levels, P=0.007). The plasma resistin levels of the proband and his mother, however, did not differ significantly from lean control individuals.ConclusionsIn conclusion, we identified the first missense mutation in resistin in a morbidly obese proband and his obese mother. Functional testing of the mutant protein suggests that the C78S mutant protein is degraded, possibly resulting in a decreased extracellular concentration, which may predispose to obesity.

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Abd-Elmonsef, Marwa M. E., Naglaa F. Ghoname, Abeer Shahba, Maha M. Hagras, Lamees M. Dawood, and Mohamed M. E. Abd-Elmonsef. "Association of the RETN –420C˃G Polymorphism with Rheumatoid Arthritis in an Egyptian Population." International Journal of Current Microbiology and Applied Sciences 5, no. 11 (November 10, 2016): 183–95. http://dx.doi.org/10.20546/ijcmas.2016.511.021.

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Utami, Rizki Fajar, Pramudji Hastuti, and Ahmad Hamim Sadewa. "RETN rs3745368 polymorphism and resistin level in Javanese ethnic Indonesian obese: a case control study." Jurnal Teknologi Laboratorium 8, no. 1 (June 23, 2019): 41–49. http://dx.doi.org/10.29238/teknolabjournal.v8i1.164.

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Obesity has become a global public health problem. It occurs due to a positive energy balance leading to adipose tissue expansion. White adipose tissue was an endocrine organ which secreted resistin. Resistin also produced by immune cells due to low chronic level inflammation might cause higher resistin level in obese people. Polymorphism +62G>A RETN gene was reported has a relationship with low resistin level and A allele as a protective allele. This study aimed to determine genotype and allele frequency distribution concerning resistin level. Another objective aimed to know the correlation between resistin level with body mass index. The design of the research was a case-control study with 122 people (18-40 y.o.), divided equally in the case group (BMI ≥ 27 kg/m2) and control group (BMI 18.5-24.9 kg/m2) without diabetes mellitus. Blood was taken after fasting a minimal 8 hours. Plasma was used to measure the resistin level. DNA genotyping was analyzed using PCR-RFLP. Genotyping result showed three genotypes of RETN gene +62G>A polymorphism (GG, GA, AA). There was no significant difference in genotype and allele frequency distribution related to obesity status (p=0.680; p=1) and resistin level (p=0.537) between case and control group. There was no significant difference in resistin level between case and control group (p=0.770). Resistin level was correlated with BMI in obese group (p= 0.05; r= -0.25). The present study concludes that there is no significant difference in genotype and allele frequency distribution related to obesity status and resistin level. Resistin level has a negative correlation with BMI.

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Cieslak, Jakub, Joanna Nowacka-Woszuk, Magdalena Bartz, Honorata Fijak-Nowak, Maria Grzes, Maciej Szydlowski, and Marek Switonski. "Association studies on the porcine RETN, UCP1, UCP3 and ADRB3 genes polymorphism with fatness traits." Meat Science 83, no. 3 (November 2009): 551–54. http://dx.doi.org/10.1016/j.meatsci.2009.07.001.

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Li, Yahui, Huaixing Li, Shiyuan Dong, Chao Yu, Yu Jiang, and Shuhan Sun. "Influence and related mechanism of Retn gene expression on glucose uptake in 3T3-L1 cells." Frontiers of Medicine in China 1, no. 3 (July 2007): 269–73. http://dx.doi.org/10.1007/s11684-007-0051-1.

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Chi, Shuguang, Cailian Lan, Sizhong Zhang, Hekun Liu, Xizhen Wang, Yuanzhong Chen, Xuexiang Chen, Suyun Chen, and Wei Zhang. "Association of −394C>G and −420C>G polymorphisms in the RETN gene with T2DM and CHD and a new potential SNP might be exist in exon 3 of RETN gene in Chinese." Molecular and Cellular Biochemistry 330, no. 1-2 (April 21, 2009): 31–38. http://dx.doi.org/10.1007/s11010-009-0097-2.

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Hernández-Romero, D., E. Orenes-Piñero, A. García-Honrubia, V. Climent, A. I. Romero-Aniorte, C. M. Martínez, M. García-Bautista, et al. "Involvement of the −420C>G RETN polymorphism in myocardial fibrosis in patients with hypertrophic cardiomyopathy." Journal of Internal Medicine 278, no. 1 (January 5, 2015): 50–58. http://dx.doi.org/10.1111/joim.12334.

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Joyce, Brian T., Huikun Liu, Leishen Wang, Jun Wang, Yinan Zheng, Drew Nannini, Alex Drong, et al. "Novel epigenetic link between gestational diabetes mellitus and macrosomia." Epigenomics 13, no. 15 (August 2021): 1221–30. http://dx.doi.org/10.2217/epi-2021-0096.

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Background & objectives: Examine maternal gestational diabetes mellitus (GDM), macrosomia and DNA methylation in candidate genes IGF1, IGF2, H19, ARHGRF11, MEST, NR3C1, ADIPOQ and RETN. Materials & methods: A total of 1145 children (572 GDM cases and 573 controls) from the Tianjin GDM study, including 177 with macrosomia, had blood DNA collection at median age 5.9 (range: 3.1–10.0). We used logistic regression to screen for associations with GDM and model macrosomia on 37 CpGs, and performed mediation analysis. Results: One CpG was associated with macrosomia at false discovery rate (FDR) <0.05 (cg14428359 in MEST); two (cg19466922 in MEST and cg26263166 in IGF2) were associated at p < 0.05 but mediated 26 and 13%, respectively. Conclusion: MEST and IGF2 were previously identified for potential involvement in fetal growth and development ( Trial Registration number: NCT01554358 [ClinicalTrials.gov] ).

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Hivert, M. F., A. K. Manning, J. B. McAteer, J. Dupuis, C. S. Fox, L. A. Cupples, J. B. Meigs, and J. C. Florez. "Association of Variants in RETN With Plasma Resistin Levels and Diabetes-Related Traits in the Framingham Offspring Study." Diabetes 58, no. 3 (December 15, 2008): 750–56. http://dx.doi.org/10.2337/db08-1339.

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Onuma, Hiroshi, Yasuharu Tabara, Ryoichi Kawamura, Jun Ohashi, Wataru Nishida, Yasunori Takata, Masaaki Ochi, et al. "Dual Effects of a RETN Single Nucleotide Polymorphism (SNP) at –420 on Plasma Resistin: Genotype and DNA Methylation." Journal of Clinical Endocrinology & Metabolism 102, no. 3 (December 8, 2016): 884–92. http://dx.doi.org/10.1210/jc.2016-2417.

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Kumar, Vikas, Jaswinder Singh, Ashish Aneja, and Jasbir Singh. "Association of RETN gene polymorphism at +299 G>A with type 2 diabetes mellitus: a meta-analysis." International Journal of Diabetes in Developing Countries 40, no. 1 (June 10, 2019): 12–20. http://dx.doi.org/10.1007/s13410-019-00746-x.

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Kartodihardjo, Hariadi, and Chalid Muhammad. "Mengatasi Persoalan Institusional Pengelolaan Sumber Daya Alam (PSDA): Pembelajaran dari Kasus Revitalisasi Ekosistem Tesso Nilo (RETN) di Provinsi Riau." Jurnal Hukum Lingkungan Indonesia 5, no. 2 (July 27, 2019): 253. http://dx.doi.org/10.38011/jhli.v5i2.95.

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UCHIYAMA, TOMOKO, ASAKO ITAYA-HIRONAKA, AKIYO YAMAUCHI, MAI MAKINO, SUMIYO SAKURAMOTO-TSUCHIDA, RYOGO SHOBATAKE, HIROYO OTA, MAIKO TAKEDA, CHIHO OHBAYASHI, and SHIN TAKASAWA. "1771-P: Upregulation of RETN, TNFα, and CCL2 mRNAs in Adipocytes by Intermittent Hypoxia and Its MicroRNA-Mediated Mechanism." Diabetes 68, Supplement 1 (June 2019): 1771—P. http://dx.doi.org/10.2337/db19-1771-p.

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Arráiz, Nailet, Carolina Escalona, Carem Prieto, Valmore Bermúdez, Endrina Mújica, María Patricia Sánchez, and Andrea Mújica. "Polimorfismo 3’UTR +62G>A del gen RETN codificante de resistina y asociación con componentes del síndrome metabólico." Medicina Clínica 141, no. 8 (October 2013): 325–31. http://dx.doi.org/10.1016/j.medcli.2012.07.020.

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Saleh, Razwa, Zahidul Islam Zahid, Mohammad Atikur Rahman, Preeti Jain, Ashraful Alam, Masashi Kawaichi, and Hasan Mahmud Reza. "Prevalence of PPAR-γ2 (rs1801282), RETN (rs3745367) and ADIPOQ (rs2241766) SNP markers in the Bangladeshi type 2 diabetic population." Meta Gene 10 (December 2016): 100–107. http://dx.doi.org/10.1016/j.mgene.2016.08.002.

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Gao, L., E. Coe, M. Campbell, M. Yang, T. Hand, N. M. Rafaels, A. Poloczek, H. Watson, G. Dunston, and N. Hansel. "Polymorphisms in Resistin (RETN) and Resistin-like Beta (RETNLB) and Risk of Asthma in Independent Populations of African Descent." Journal of Allergy and Clinical Immunology 123, no. 2 (February 2009): S166. http://dx.doi.org/10.1016/j.jaci.2008.12.623.

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NAWAZ, Yasar, Sumbla GHAZANVI, Nadia RASHEED, Shah JAHAN, and Muhammad Ikram ULLAH. "Association of Serum Resistin Level and Resistin (RETN) Gene (-420C>G) Polymorphism in Pakistani Women with Polycystic Ovarian Syndrome." Turkish Journal of Endocrinology and Metabolism 24, no. 1 (2020): 16–22. http://dx.doi.org/10.25179/tjem.2019-66784.

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Xia, Qing Lin, Liu Xian Pan, Yuan Dong Peng, Li Ya Li, Hong Zhong Wang, Rui Bao, and Jian Hong Yi. "First Principles Investigation of Electronic Structure, Chemical Bonding, Elastic and Optical Properties of Novel Rhenium Nitrides." Key Engineering Materials 512-515 (June 2012): 883–89. http://dx.doi.org/10.4028/www.scientific.net/kem.512-515.883.

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we investigate the electronic structure, chemical bonding, optical and elastic properties of the novel rhenium nitrides, hexagonal phase re3n and re2n by using density-functional theory (dft) within generalized gradient approximation (gga). the calculated equilibrium lattice constants of both re3n and re2n are in reasonable agreement with the experimental results. the band structure along the higher symmetry axes in the Brillouin zone, the density of states (dos) and the partial density of states (pdos) are presented. the calculated energy band structures and dos show that re3n and re2n are metal compounds. The dos and pdos show that the dos at the fermi level (ef) is located at the bottom of a valley and originate mainly from the 5d electrons of re. population analyses suggest that the chemical bonding in re3n and re2n has predominantly covalent character with mixed covalent and ionic characteristics. the dielectric function, reflectivity, absorption coefficient, refractive index, electron energy-loss function and optical conductivity are presented in an energy range for discussing the optical properties of re3n and re2n. basic mechanical properties, such as elastic constants cij, bulk modulus b and shear modulus g are calculated. The young’s modulus e, poisson's ratio ν and bh/gh are also predicted. results conclude that the hexagonal phase re3n and re2n are mechanical stable and behaves in a ductile manner. polycrystalline elastic anisotropy is also derived from polycrystalline bulk modulus b and shear modulus g.

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López-Quintero, A., A. G. García-Zapién, S. E. Flores-Martínez, Y. Díaz-Burke, C. E. González-Sandoval, R. I. Lopez-Roa, E. Medina-Díaz, M. L. Muñoz-Almaguer, and J. Sánchez-Corona. "Contribution of polymorphisms in the LEP, LEPR and RETN genes on serum leptin and resistin levels in young adults from Mexico." Cellular and Molecular Biology 63, no. 8 (August 30, 2017): 10. http://dx.doi.org/10.14715/cmb/2017.63.8.3.

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Zhou, Qiang, Bo Chen, Tianxing Ji, Miaoshan Luo, and Jiandong Luo. "Association of genetic variants in RETN, NAMPT and ADIPOQ gene with glycemic, metabolic traits and diabetes risk in a Chinese population." Gene 642 (February 2018): 439–46. http://dx.doi.org/10.1016/j.gene.2017.10.084.

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Wang, Li, Zhou, Gao, Liu, Li, Niu, et al. "Association of Twelve Candidate Gene Polymorphisms with the Intramuscular Fat Content and Average Backfat Thickness of Chinese Suhuai Pigs." Animals 9, no. 11 (October 23, 2019): 858. http://dx.doi.org/10.3390/ani9110858.

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The present study aimed to identify the molecular markers for genes that influence intramuscular fat content (IFC), but not average backfat thickness (ABT). A total of 330 Suhuai pigs were slaughtered, and measurements of IFC and ABT were obtained. Phenotypic and genetic correlations between IFC and ABT were calculated. Thirteen single nucleotide polymorphisms (SNPs) among 12 candidate genes for IFC were analyzed, including FABP3, LIPE, IGF1, IGF2, LEP, LEPR, MC4R, PHKG1, RETN, RYR1, SCD, and UBE3C. Associations of the evaluated SNPs with IFCIFC and ABT were performed. Our results showed that the means of IFC and ABT were 1.99 ± 0.03 % and 26.68 ± 0.28 mm, respectively. The coefficients of variation (CVs) of IFC and ABT were 31.21% and 19.36%, respectively. The phenotypic and genetic correlations between IFC and ABT were moderate. Only the FABP3 (rs1110770079) was associated with IFC (p < 0.05) but not with ABT. Besides, there was a tendency for associations of RYR1 (rs344435545) and SCD (rs80912566) with IFC (p < 0.1). Our results indicated that the FABP3 (rs1110770079) SNP could be used as a marker to improve IFC without changing ABT in the Suhuai pig breeding system.

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Yang, Wei-Hung, Shoou-Jyi Wang, Yung-Sen Chang, Chen-Ming Su, Shun-Fa Yang, and Chih-Hsin Tang. "Association of Resistin Gene Polymorphisms with Oral Squamous Cell Carcinoma Progression and Development." BioMed Research International 2018 (October 14, 2018): 1–8. http://dx.doi.org/10.1155/2018/9531315.

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Oral squamous cell carcinoma (OSCC) accounts for over 90% of malignant neoplasms of the mouth. In Taiwan, OSCC is the fourth most common male cancer and the fourth leading cause of male cancer death. Resistin (RETN) is an adipokine that is associated with obesity, inflammation, and various cancers. Here, we examine the association between four single nucleotide polymorphisms (SNPs) of theRETNgene (rs3745367, rs7408174, rs1862513, and rs3219175) and OSCC susceptibility as well as clinical outcomes in 935 patients with OSCC and in 1200 cancer-free healthy controls. We found that, in 1465 smokers,RETNpolymorphisms carriers with the betel-nut chewing habit had a 6.708–10.882-fold greater risk of having OSCC compared toRETNwild-type carriers without the betel-nut chewing habit. Patients with OSCC who had A/A homozygous ofRETNrs3219175 polymorphism showed a high risk for an advanced tumor size (> T2), compared to those patients with G/G homozygotes. In addition, A/T/G/G haplotype significantly increased the risks for OSCC by 1.376-fold. This study is the first to examine the risk factors associated withRETNSNPs in OSCC progression and development in Taiwan.

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Elkhattabi, L., I. Morjane, H. Charoute, R. Saile, and A. Barakat. "Computational screening and analysis of the functional and structural impact of SNPS of the human RETN gene associated to type 2 diabetes." Atherosclerosis 315 (December 2020): e199-e200. http://dx.doi.org/10.1016/j.atherosclerosis.2020.10.622.

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Butera, Federico, and Fernando Alberti. "Il governo delle reti inter-organizzative per la competitivitŕ." STUDI ORGANIZZATIVI, no. 1 (December 2012): 77–111. http://dx.doi.org/10.3280/so2012-001004.

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I policy maker sono costantemente alla ricerca delle forme e degli strumenti per contribuire ad aumentare la prosperitŕ economica e sociale del proprio territorio. Gli studi a livello internazionale ci dicono che la prosperitŕ di un territorio č direttamente riconducibile alla sua competitivitŕ, e quindi in primis al livello di produttivitŕ e innovazione del sistema delle imprese. Come verrŕ ampiamente illustrato in questo articolo, le reti inter-organizzative - nella varietŕ di forme che l'evidenza empirica ci suggerisce - attraverso una flessibilitŕ senza precedenti, una piů veloce circolazione delle informazioni, la condivisione di visioni, saperi e conoscenza, l'efficiente e rapido scambio di risorse e competenze per competere, assicurano al tempo stesso specializzazione, efficienza e alti livelli di produttivitŕ. La configurazione e la natura di tali reti č in via di continua ridefinizione ed espansione e l'uso del termine rete č spesso generico o inappropriato. Anche i confini delle reti vanno continuamente ridefiniti, in un continuum che va dalle imprese tradizionali che esternalizzano e delocalizzano parte della loro produzione fino al puro networking di varia natura. Noi ci concentreremo solo su quelle reti interorganizzative che rappresentano forme nuove di impresa, di quasi impresa, di sistemi di imprese che consentono una gestione competitiva e innovativa della catena del valore e dei processi fondamentali, conseguendo risultati economici e sociali, in una parola prosperitŕ. Ci occuperemo in particolare del fenomeno piů nuovo che caratterizza l'Italian way of doing industry, ossia lo sviluppo e i successi delle medie imprese, nodi di reti inter-organizzative che coinvolgono non solo imprese piccole, ma anche imprese grandi, in una proiezione spesso globale. Su queste nuove forme di reti inter-organizzative, si apre uno spazio di intervento straordinario per i policy maker in azioni di attivazione, incentivazione e supporto, capaci di condurre a superiori livelli di competitivitŕ le imprese componenti le reti, le reti stesse e i territori da cui esse muovono, ovvero capaci di favorire una maggiore prosperitŕ. Tali spazi di governo delle reti inter-organizzative possono avere natura infrastrutturale (trasporti, edilizia, tecnologie, credito, servizi, ecc.), relazionale (governo della catena del valore, dei processi, dei flussi, delle architetture d'impresa, dei sistemi informativi e di comunicazione, dei sistemi professionali ecc.) e cognitiva (capitale umano, capitale intellettuale, sistema di valori e norme, ecc.). Tutte e tre queste dimensioni sono importantissime e vanno gestite congiuntamente in nuove forme di management assicurate dalle imprese "pivotali" e nell'ambito di quello che nell'articolo č definito come meta-management, ovvero quelle posizioni di attori pubblici e privati - spesso in raccordo fra loro - che assicurano supporto e guida strategica alle reti. Nuovi modelli di management e di meta-management implicano una conoscenza profonda della rete e, di conseguenza, una visione d'insieme attuale e futura sicura e convincente e una capacitŕ di execution che sappia consolidare o riorientare la rete; valorizzare le risorse, materiali e personali, lě racchiuse e soprattutto perseguire obiettivi e misurare risultati. Meta-management non significa favorire il mero networking tra imprese, ma attivarsi come agenzie strategiche e provvedimenti concreti capaci di disegnare politiche di accompagnamento e sostegno alla creazione e alla valorizzazione di robusti network tra imprese e tra imprese e istituzioni, che trascendano le consuete filiere e agglomerazioni locali. Una economia e una societŕ fatta di reti inter-organizzative non č uguale a quella fatta prevalentemente di singole imprese "castello". Sulle reti di impresa e sull'impresa rete incombono alcune rilevanti questioni a cui il nostro lavoro tenta di dare alcune risposte Vediamole qui di seguito. 1. Diagnosi. L'organizzazione a rete č oggi scarsamente riconoscibile. Come diagnosticarla, come identificarne le caratteristiche strutturali e comprenderne i problemi critici? 2. Sviluppo e progettazione. L'organizzazione a rete si puň supportare con adeguati servizi, sviluppare intenzionalmente o addirittura progettare, come qui si sostiene? E se sě, in che modo? I metodi da adoperare per gestire questo sviluppo sono certo diversi da quelli adottati da strutture accentrate, sono meno top-down e meno razionalistici: ma quali possono essere? 3. Stabilitŕ e mutamento. Ogni nodo o soggetto della rete fa parte di reti diverse, in alcuni casi abbandona in rapida successione le une per legarsi ad altre. Come combinare l'estrema mutevolezza di queste multiple appartenenze con l'esigenza di stabilitŕ e crescita di ogni singolo nodo, come far sě che l'intera rete si comporti come un "attore collettivo" capace di un governo? 4. Risultati. Se e come definire obiettivi o ri-articolarli velocemente nel tempo? Come valutare i risultati delle diverse dimensioni economiche e sociali? 5. Decisioni e misura. L'organizzazione a rete - come e piů dell'impresa tradizionale - cambia per repentine innovazioni, per adattamento, per micro-decisioni, per miglioramento continuo, č il risultato di scelte su cosa fare dentro e cosa comprare, su quali funzioni accentrare e quali decentrare, su quando acquisire o vendere unitŕ aziendali e su quando fare accordi, dove allocare geograficamente le attivitŕ. Vi sono criteri e metodi da adottare, per operare in questi contesti di agilitŕ, velocitŕ e rapiditŕ di processi decisionali? 6. Sistemi. Quali tecniche o sistemi operativi adatti all'impresa rete dovranno essere sviluppati? Quali sistemi di pianificazione e controllo di gestione dell'impresa rete, if any? Č possibile stabilire standard di qualitŕ per la rete? Come sviluppare dimensioni quali linguaggi, culture, politiche di marchio e di visibilitŕ, come potenziare le comunitŕ, come promuovere formazione e apprendimenti? 7. Strutture. Le reti di impresa includono una grande varietŕ di forme, come vedremo. La rete di imprese puň includere una parte di gerarchia: quali modelli di organigrammi sono compatibili? Quali sistemi informativi, di telecomunicazioni, di social network sono adatti per la rete di imprese? Quali sistemi logistici? Quali regole e contratti formali? Quali flussi finanziari? Le risorse umane si possono gestire e sviluppare lungo la rete? E in che modo? E che dire dei sistemi di controllo della qualitŕ? 8. Nascita e morte. La rete di imprese e soprattutto i suoi "nodi" hanno un tasso di natalitŕ/ mortalitŕ piů elevato dell'impresa tradizionale. Gestire la nascita e la morte delle imprese diventerŕ ancora piů importante che gestire le imprese. Chi lo farŕ e come? 9. Vincoli e opportunitŕ. La legislazione, le relazioni industriali, la cultura manageriale sono oggi vincoli e opportunitŕ allo sviluppo di forme di rete di imprese. La globalizzazione dell'economia, lo sviluppo dei servizi, le nuove tecnologie, la cultura dei giovani, invece, sembrano operare piů come fattori facilitanti quando addirittura non cogenti. Come gestire (e non subire) vincoli e opportunitŕ? Cosa puň fare l'impresa, e cosa possono fare le istituzioni pubbliche? Vi sono nuovi programmi e regole nazionali e regionali per la costituzione delle reti di impresa: quale č la loro efficacia e impatto? In tale quadro, un'Agenzia Strategica (una grande impresa, una media impresa, un ente governativo, una Camera di commercio, un'associazione imprenditoriale, un istituto di credito) puň esercitare un ruolo centrale nella promozione e governo delle reti inter-organizzative per la competitivitŕ dei territori, mettendo a fuoco i propri interventi di policy avendo come oggetto prioritario queste nuove forme di impresa, quasi-impresa, sistemi di impresa usando diverse leve: - innanzitutto, fornendo o favorendo l'accesso a risorse chiave, come credito, finanziamenti, sgravi fiscali, servizi per l'internazionalizzazione, conoscenze, marketing ecc.; - agendo da fluidificatore delle reti tra imprese, che sappia rimuovere ostacoli nelle strutture relazionali e irrobustire nodi, processi, strutture di governance laddove necessario; inserendosi direttamente nelle strutture relazionali come ponte per connettere nodi disconnessi; - esercitando a pieno il ruolo di meta-manager di reti inter-organizzative ossia imprimendo al sistema un indirizzo strategico di fondo, governando i processi "politici" interni alla rete ossia la distribuzione di potere e risorse e creando le condizioni culturali, strategiche organizzative e tecnologiche; - facendo leva sull'essere un policy maker cross-settoriale e multi-territoriale. Le reti di impresa hanno successo se si integrano entro "piattaforme industriali" (ad es. IT, Green economy, portualitŕ e logistica), entro cluster territoriali (es. distretti, economie regionali, etc.), sistemi eterogenei interistituzionali (che includono imprese pubbliche, amministrazioni, istituzioni e associazioni). La nostra tesi č che azioni di governo della rete attraverso nuove forme di management e di meta-management sono tanto piů efficaci quanto piů contribuiscono a supportare e strutturare reti organizzative robuste o che tendono a diventare tali, ossia imprese reti e reti di impresa governate; sono tanto meno efficaci o quanto meno misurabili quanto piů supportano solo processi di networking poco definiti destinati a rimanere tali. Nei termini di Axelsson, policy e management hanno effetto su reti che esprimono a) modelli di relazione fra diverse organizzazioni per raggiungere fini comuni. Hanno un effetto minore o nullo quando le reti di cui si parla sono solo b) "connessioni lasche fra organizzazioni legate da relazioni sociali" o c) un insieme di due o piů relazioni di scambio.

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Deligoz, E., K. Colakoglu, H. B. Ozisik, and Y. O. Ciftci. "Vibrational properties of Re2N and Re3N compounds." Solid State Communications 151, no. 17 (September 2011): 1122–27. http://dx.doi.org/10.1016/j.ssc.2011.05.028.

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Alberti, Fernando G. "Il contratto di rete: una rassegna." STUDI ORGANIZZATIVI, no. 2 (April 2013): 176–97. http://dx.doi.org/10.3280/so2012-002007.

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Il presente articolo intende essere una breve nota tesa a fare il punto dello stato di adozione e di elaborazione dei contratti di rete. Con il contratto di rete, il Legislatore ha voluto introdurre una nuova fattispecie giuridica finalizzata a favorire l'aggregazione tra imprese di minore dimensione, aumentando cosě le dimensioni aziendali per meglio competere nei mercati internazionali e supportare l'innovazione. Il contratto di rete si differenzia nella ratio da altre forme burocratiche di reti inter-organizzative esistenti, per maggiore flessibilitŕ sia nella definizione degli scopi e dei confini della rete stessa sia nel livello di coinvolgimento dei partner. I contratti di rete stanno assumendo una diffusione tale da essere spesso utilizzati come sinonimi di rete tra imprese. Come ampiamente illustrato e chiarito in un articolo apparso sul numero precedente di Studi Organizzativi, le reti tra imprese si caratterizzano per una varietŕ di forme, assetti, obiettivi, meccanismi operativi e composizione, tale per cui l'appiattimento del fenomeno ai soli contratti di rete, che si registra nella retorica quotidiana di policy makers, giuristi e media, risulta essere non solo immotivato ma anche ontologicamente fallace. Emerge, quindi la necessitŕ anche per gli studiosi di strategia e organizzazione, e non solo per i giuristi, di chiarire questo fenomeno, comprenderne la natura, le potenzialitŕ e i limiti, analizzarne la diffusione e gli strumenti a supporto, ma anche metterlo in relazione con il piů ampio fenomeno delle reti inter-organizzative di cui i contratti costituiscono solo una delle possibili forme. Dagli elementi riportati in questo articolo si evince come il fenomeno dei contratti di rete, per quanto nascente, abbia vissuto nell'ultimo periodo sia un forte incremento quantitativo nell'ultimo anno sia un forte incremento sul fronte qualitativo. L'affinamento della fattispecie giuridica, la crescente casistica e l'ampio dibattito accademico, istituzionale e professionale creatosi attorno al fenomeno hanno stimolato molti a ragionare attorno al tema delle reti di imprese, anche se ancora con poca distinzione tra il concetto di rete di imprese - e le sue variegate forme - e quello di contratto di rete, che rappresenta solo un possibile inquadramento burocratico per la formalizzazione di una rete.

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Wang, Juanjuan, Mengsi Xu, Xinhua Wang, Jinquan Yang, Lei Gao, Yan Zhang, Xin Huang, Mengli Han, Rui Gao, and Shangquan Gan. "Comparative Proteome Analysis Reveals Lipid Metabolism-Related Protein Networks in Response to Rump Fat Mobilization." International Journal of Molecular Sciences 19, no. 9 (August 28, 2018): 2556. http://dx.doi.org/10.3390/ijms19092556.

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Altay is a typical fat-tailed sheep breed displaying the unique ability to rapidly mobilize fat, which is vital for maintaining a normal metabolism that facilitates its survival in lengthy winter conditions. However, the physiological, biochemical, and molecular mechanisms underlying fat mobilization remain to be elucidated. In this study, the monitoring of rump fat adipocyte sizes disclosed a positive correlation between cell size and fat deposition ability. In addition, we subjected sheep to persistent starvation to imitate the conditions that trigger rump fat mobilization and screened 112 differentially expressed proteins using the isobaric peptide labeling approach. Notably, increased secretion of leptin and adiponectin activated the key fat mobilization signaling pathways under persistent starvation conditions. Furthermore, the upregulation of resistin (RETN), heat-shock protein 72 (HSP72), and complement factor D (CFD) promoted lipolysis, whereas the downregulation of cell death-inducing DFFA-like effector C (CIDEC) inhibited lipid droplet fusion, and the increase in HSP72 and apolipoprotein AI (Apo-AI) levels activated the body’s stress mechanisms. The synergistic actions of the above hormones, genes, and signaling pathways form a molecular network that functions in improving the adaptability of Altay sheep to extreme environments. Our findings provide a reference for elucidating the complex molecular mechanisms underlying rump fat mobilization.

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Vashi, Neeti, Carolina Stryjecki, Jesus Peralta-Romero, Fernando Suarez, Jaime Gomez-Zamudio, Ana I. Burguete-Garcia, Miguel Cruz, and David Meyre. "Genetic markers of inflammation may not contribute to metabolic traits in Mexican children." PeerJ 4 (June 23, 2016): e2090. http://dx.doi.org/10.7717/peerj.2090.

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Background:Low-grade chronic inflammation is a common feature of obesity and its cardio-metabolic complications. However, little is known about a possible causal role of inflammation in metabolic disorders. Mexico is among the countries with the highest obesity rates in the world and the admixed Mexican population is a relevant sample due to high levels of genetic diversity.Methods:Here, we studied 1,462 Mexican children recruited from Mexico City. Six genetic variants in five inflammation-related genes were genotyped: rs1137101 (leptin receptor (LEPR)), rs7305618 (hepatocyte nuclear factor 1 alpha (HNF1A)), rs1800629 (tumor necrosis factor alpha (TNFA)), rs1800896, rs1800871 (interleukin-10 (IL-10)), rs1862513 (resistin (RETN)). Ten continuous and eight binary traits were assessed. Linear and logistic regression models were used adjusting for age, sex, and recruitment centre.Results:We found that one SNP displayed a nominal evidence of association with a continuous trait: rs1800871 (IL-10) with LDL (beta = −0.068 ± 1.006, P = 0.01). Subsequently, we found one nominal association with a binary trait: rs7305618 (HNF1A) with family history of hypertension (odds-ratio = 1.389 [1.054–1.829], P = 0.02). However, no P-value passed the Bonferroni correction for multiple testing.Discussion:Our data in a Mexican children population are consistent with previous reports in European adults in failing to demonstrate an association between inflammation-associated single nucleotide polymorphisms (SNPs) and metabolic traits.

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Geraci, Salvatore, and Chiara Bodini. "Rete di reti per la salute degli immigrati." SALUTE E SOCIETÀ, no. 2 (November 2011): 129–40. http://dx.doi.org/10.3280/ses2011-002010.

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TIMIRCI-KAHRAMAN, OZLEM, UMIT YILMAZ, NESIBE YILMAZ, AYDIN CEVIK, CEM HOROZOGLU, FARUK CELIK, MUHAMMED OGUZ GOKCE, ARZU ERGEN, ABDULLAH MELEKOGLU, and UMIT ZEYBEK. "A Study of Short- and Long-term mRNA Levels of the Retn, Iapp, and Drd5 Genes in Obese Mice Induced with High-fat Diet." In Vivo 32, no. 4 (2018): 813–17. http://dx.doi.org/10.21873/invivo.11312.

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Martínez-Paz, Pedro, Marta Aragón-Camino, Esther Gómez-Sánchez, Mario Lorenzo-López, Estefanía Gómez-Pesquera, Rocío López-Herrero, Belén Sánchez-Quirós, et al. "Gene Expression Patterns Distinguish Mortality Risk in Patients with Postsurgical Shock." Journal of Clinical Medicine 9, no. 5 (April 28, 2020): 1276. http://dx.doi.org/10.3390/jcm9051276.

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Nowadays, mortality rates in intensive care units are the highest of all hospital units. However, there is not a reliable prognostic system to predict the likelihood of death in patients with postsurgical shock. Thus, the aim of the present work is to obtain a gene expression signature to distinguish the low and high risk of death in postsurgical shock patients. In this sense, mRNA levels were evaluated by microarray on a discovery cohort to select the most differentially expressed genes between surviving and non-surviving groups 30 days after the operation. Selected genes were evaluated by quantitative real-time polymerase chain reaction (qPCR) in a validation cohort to validate the reliability of data. A receiver-operating characteristic analysis with the area under the curve was performed to quantify the sensitivity and specificity for gene expression levels, which were compared with predictions by established risk scales, such as acute physiology and chronic health evaluation (APACHE) and sequential organ failure assessment (SOFA). IL1R2, CD177, RETN, and OLFM4 genes were upregulated in the non-surviving group of the discovery cohort, and their predictive power was confirmed in the validation cohort. This work offers new biomarkers based on transcriptional patterns to classify the postsurgical shock patients according to low and high risk of death. The results present more accuracy than other mortality risk scores.

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Journal articles on the topic 'RETN'

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