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Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Diabetes resistance.'
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Journal articles on the topic "Diabetes resistance":
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Gokalp, Deniz, Alpaslan Tuzcu, Ster Irmak, Mithat Bahceci, and Ozlem Demirpence. "FREQUENCY OF ASPIRIN RESISTANCE IN PATIENTS WITH TYPE 1 AND 2 DIABETES MELLITUS AND ITS ASSOCIATION WITH METABOLIC PARAMETERS." International Journal of Surgery and Medicine 2, no. 3 (2016): 122. http://dx.doi.org/10.5455/ijsm.aspirin-resistance-diabetes.
McClain, D. A., and E. D. Crook. "Hexosamines and insulin resistance." Diabetes 45, no. 8 (August 1, 1996): 1003–9. http://dx.doi.org/10.2337/diabetes.45.8.1003.
Sceppa, Carmen Castaneda. "Resistance Training and Diabetes." Medicine & Science in Sports & Exercise 36, Supplement (May 2004): S93—S94. http://dx.doi.org/10.1249/00005768-200405001-00442.
Sceppa, Carmen Castaneda. "Resistance Training and Diabetes." Medicine & Science in Sports & Exercise 36, Supplement (May 2004): S93???S94. http://dx.doi.org/10.1097/00005768-200405001-00442.
Kraegen, E. W., P. W. Clark, A. B. Jenkins, E. A. Daley, D. J. Chisholm, and L. H. Storlien. "Development of muscle insulin resistance after liver insulin resistance in high-fat-fed rats." Diabetes 40, no. 11 (November 1, 1991): 1397–403. http://dx.doi.org/10.2337/diabetes.40.11.1397.
Mykkanen, L., D. J. Zaccaro, L. E. Wagenknecht, D. C. Robbins, M. Gabriel, and S. M. Haffner. "Microalbuminuria is associated with insulin resistance in nondiabetic subjects: the insulin resistance atherosclerosis study." Diabetes 47, no. 5 (May 1, 1998): 793–800. http://dx.doi.org/10.2337/diabetes.47.5.793.
Goran, M. I., and B. A. Gower. "Longitudinal Study on Pubertal Insulin Resistance." Diabetes 50, no. 11 (November 1, 2001): 2444–50. http://dx.doi.org/10.2337/diabetes.50.11.2444.
Wang, J., S. Obici, K. Morgan, N. Barzilai, Z. Feng, and L. Rossetti. "Overfeeding Rapidly Induces Leptin and Insulin Resistance." Diabetes 50, no. 12 (December 1, 2001): 2786–91. http://dx.doi.org/10.2337/diabetes.50.12.2786.
In our Department arrives a 75-year-old patient with hypertension, diabetes mellitus (DM) treated with hypoglycaemic drugs, dyslipidaemia and ischaemic heart disease post-acute myocardial infarction treated with triple coronary artery bypass surgery and subsequent percutaneous transluminal coronary angioplasty (PTCA). After a new PTCA and positioning of medical stent he is discharged with a double antiplatelet therapy. But after one month two thrombotic events occur in this patients almost simultaneously. Antiplatelet therapy such as clopidogrel and aspirin in combination, is the current gold standard for reducing cardiovascular events in patients with DM, providing a synergistic platelet inhibition through different platelet activation pathways, but platelets of DM patients are characterised by disregulation of several signalling pathways which may play a role not only in the higher risk of developing cardiovascular events and the worse outcome, but also in the larger proportion of DM patients with inadequate response to antiplatelet drugs compared to non DM subjects.
Dissertations / Theses on the topic "Diabetes resistance":
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Pickavance, Lucy Cecilia. "Thiazolidinedione treatment in models of insulin resistance." Thesis, University of Liverpool, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367553.
Ang, Christine W. M. "Diabetes and the maternal resistance vasculature." Thesis, University of Glasgow, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.395080.
Hale, P. J. "Insulin resistance in diabetes mellitus and obesity." Thesis, University of Oxford, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.371516.
Type 2 diabetes is an insidious disorder, with micro and/or macrovascular and nervous damage occurring in many patients before diagnosis. This damage is caused by hyperglycaemia and the diverse effects of insulin resistance. Obesity, in particular central obesity, is a strong pre-disposing factor for type 2 diabetes. Skeletal muscle is the main site of insulin-stimulated glucose disposal and appears to be the first organ that becomes insulin resistant in the diabetic state, with later involvement of adipose tissue and the liver. This study has investigated the use of novel agents to ameliorate insulin-resistance in skeletal muscle as a means of identifying intervention sites against insulin resistance and of improving glucose uptake and metabolism by skeletal muscle. Glucose uptake was measured in vitro by cultured L6 myocytes and isolated muscles from normal and obese diabetic ob/ob mice, using either the tritiated non-metabolised glucose analogue 2-deoxy-D-glucose or by glucose disposal. Agents studied included lipoic acid, isoferulic acid, bradykinin, lipid mobilising factor (provisionally synonymous with Zinca2 glycoprotein) and the trace elements lithium, selenium and chromium. The putative role of TNFa in insulin resistance was also investigated. Lipoic acid improved insulin-stimulated glucose uptake in normal and insulin resistance murine muscles, as well as cultured myocytes. Isoferulic acid, bradykinin and LMF also produced a transient increase in glucose uptake in cultured myocytes. Physiological concentrations of TNFa were found to cause insulin resistance in cultured, but no in excised murine muscles. The effect of the M2 metabolite of the satiety-inducing agent sibutramine on lipolysis in excised murine and human adipocytes was also investigated. M2 increased lipolysis from normal lean and obese ob/ob mouse adipocytes. Arguably the most important observation was that M2 also increased the lipolytic rate in adipocytes from catecholamine resistant obese subjects. The studies reported in this thesis indicate that a diversity of agents can improve glucose uptake and ameliorate insulin resistance. It is likely that these agents are acting via different pathways. This thesis has also shown that M2 can induce lipolysis in both rodent and human adipocytes. M2 hence has potential to directly reduce adiposity, in addition to well documented effects via the central nervous system.
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Reali, Federico. "Dynamical models for diabetes: insights into insulin resistance and type 1 diabetes." Doctoral thesis, Università degli studi di Trento, 2017. https://hdl.handle.net/11572/369184.
This thesis summarizes my work in systems biology as a PhD student at The Microsoft Research - University of Trento Centre for Computational and Systems Biology (COSBI) and at the University of Trento, department of Mathematics.
Systems biology is an interdisciplinary field that aims at integrating biology with computational and mathematical methods to gain a better understanding of biological phenomena [5, 6]. Among these methods, mathematical and dy- namical modeling have driven the discovery of mechanistic insights from the static representations of phenomena, that is, data. As a result, mathematical and dynamical models have now become standard tools to support new discoveries in biology and in public health issues. For example, models assist governments in determining the policies to contain the spreading of the diseases and in decisions such as vaccine purchases [7]. Similarly, complex and accurate models of the cardio-vascular systems guide surgeons during many procedures on pa- tients [8]. Furthermore, dynamical models of signaling cascades help researchers in identifying new potential drug targets and therapies for many diseases [9]. We used these modeling techniques to address biological questions related to diabetes and insulin resistance. Within this framework, this thesis contains two articles I contributed to, that focus on diabetes. These works are published in the journal of Nature Scientific Reports and are included in Chapters 3 and 4.
A significant contribution to the development of these models, and models in general, is given by optimization. Optimization is often used in modeling to determine certain unknown values or factors in a way that allow the model to optimally reproduce the experimental data. Moreover, the parameters of a model that correctly describe the undergoing dynamics may be used as diagnostic tools [10–13]. To this end, this thesis contains a methodological appendix that includes a review of optimization algorithms that has been submitted to the journal of Frontiers in Applied Mathematics and Statistics, special topic Optimization. The content of this article is reported in Appendix A.
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Reali, Federico. "Dynamical models for diabetes: insights into insulin resistance and type 1 diabetes." Doctoral thesis, University of Trento, 2017. http://eprints-phd.biblio.unitn.it/1962/1/Reali_PhDThesis.pdf.
This thesis summarizes my work in systems biology as a PhD student at The Microsoft Research - University of Trento Centre for Computational and Systems Biology (COSBI) and at the University of Trento, department of Mathematics.
Systems biology is an interdisciplinary field that aims at integrating biology with computational and mathematical methods to gain a better understanding of biological phenomena [5, 6]. Among these methods, mathematical and dy- namical modeling have driven the discovery of mechanistic insights from the static representations of phenomena, that is, data. As a result, mathematical and dynamical models have now become standard tools to support new discoveries in biology and in public health issues. For example, models assist governments in determining the policies to contain the spreading of the diseases and in decisions such as vaccine purchases [7]. Similarly, complex and accurate models of the cardio-vascular systems guide surgeons during many procedures on pa- tients [8]. Furthermore, dynamical models of signaling cascades help researchers in identifying new potential drug targets and therapies for many diseases [9]. We used these modeling techniques to address biological questions related to diabetes and insulin resistance. Within this framework, this thesis contains two articles I contributed to, that focus on diabetes. These works are published in the journal of Nature Scientific Reports and are included in Chapters 3 and 4.
A significant contribution to the development of these models, and models in general, is given by optimization. Optimization is often used in modeling to determine certain unknown values or factors in a way that allow the model to optimally reproduce the experimental data. Moreover, the parameters of a model that correctly describe the undergoing dynamics may be used as diagnostic tools [10–13]. To this end, this thesis contains a methodological appendix that includes a review of optimization algorithms that has been submitted to the journal of Frontiers in Applied Mathematics and Statistics, special topic Optimization. The content of this article is reported in Appendix A.
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Lindmark, Stina. "Neurohormonal mechanisms in insulin resistance and type 2 diabetes." Doctoral thesis, Umeå : Univ, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-225.
Hunter, Steven J. "Insulin resistance : underlying mechanisms and influence of treatment." Thesis, Queen's University Belfast, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337044.
Relton, Caroline L. "The identification and characterisation of genes associated with insulin resistance." Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.264425.
Vella, Sandro. "Pharmacological modulation of insulin resistance : benefits and harms." Thesis, University of Dundee, 2013. https://discovery.dundee.ac.uk/en/studentTheses/4428eca5-5018-4816-95d0-30c0a3043409.
Aims: Thiazolidinediones have been advocated as second or third line insulin sensitizing agents in the management of type 2 diabetes (T2DM). Their widespread use has been hampered by concerns about their cardiovascular safety, including fluid retention. Metformin is established as first-line glucose-lowering pharmacotherapy in T2DM. It has also been suggested that it may have benefits in alleviating insulin resistance in type 1 diabetes (T1DM). This thesis examined: (i) cardiovascular, renal and metabolic differences between individuals with T2DM ‘tolerant’ or ‘intolerant’ of TZDs; (ii) risk factors for TZD-associated oedema in T2DM; and (iii) the potential for metformin as adjunct therapy in T1DM. Methods: (i) A small clinical study characterising TZD tolerant and intolerant individuals with T2DM; (ii) A population-based epidemiological study of TZD induced oedema in individuals with T2DM in Tayside, Scotland (using incident loop diuretic prescription as a surrogate); (iii) A systematic review and meta-analysis of published studies of adjunct metformin in T1DM. Results (i) During a five-day high sodium diet, two known TZD-intolerant individuals with T2DM had reductions in haematocrit, aldosterone, and diastolic BP and increases in ANP and central and peripheral augmentation indices which were outwith reference ranges derived from nine TZD-tolerant individuals; (ii) Predictors of time to loop diuretic prescription included age, body mass index, systolic BP, haematocrit, ALT and macrovascular disease but rates of this outcome did not differ by therapy: 4.3% (TZDs) vs 4.7% (other agents) [unadjusted OR 0.909 (95% CI 0.690, 1.196); p = 0.493]; (iii) In meta-analysis of nine small studies in T1DM (192.8 patient-years of follow-up), metformin was associated with a reduction in total daily insulin dose (6.6 units/day; p < 0.001) but no studies examined cardiovascular surrogates or outcomes. Conclusions: Hypotheses were generated for several potential biomarkers predictive of TZD-induced oedema but the clinical importance of TZDs as a risk factor for oedema in individuals with T2DM was questioned. As there is some evidence for the safety of metformin as an adjunct therapy in T1DM but little evidence of efficacy, larger studies are warranted.
National Diabetes Information Clearinghouse (U.S.), ed. Insulin resistance and pre-diabetes. [Bethesda, MD]: National diabetes Information Clearinghouse, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, U.S. Dept. of Health and Human Services, 2003.
Korea-Japan Symposium on Diabetes Mellitus (7th 1993 Seoul, Korea). Insulin resistance in human disease: Proceedings of the 7th Korea-Japan Symposium on Diabetes Mellitus, Seoul, Korea, 13-14 April 1993. Edited by Huh Kap Bum, Shinn Soon Hyun, and Kaneko Toshio. Amsterdam: Excerpta Medica, 1993.
European Symposium on Metabolism (6th 1993 Padua, Italy). Diabetes, obesity, and hyperlipidemias, V: The plurimetabolic syndrome : proceedings of the European Symposium on Metabolism, Padova, 24-26 May 1993. Edited by Crepaldi Gaetano, Tiengo Antonio, and Manzato E. Amsterdam: Excerpta Medica, 1993.
A, Hawley John, and Zierath Juleen R, eds. Physical activity and type 2 diabetes: Therapeutic effects and mechanisms of action. Champaign, IL: Human Kinetics, 2008.
Korea-Japan Symposium on Diabetes Mellitus (9th 1997 Kyongju-si, Korea). Recent advances on the pathogenesis and management of diabetes mellitus: Proceedings of the 9th Korea-Japan Symposium on Diabetes Mellitus, Kyongju, Korea, 11-12 April 1997. Edited by Shinn Soon Hyun, Shichiri Motoaki 1935-, and Kim K. W. Dr. Amsterdam: Elsevier, 1998.
Taylor, Simeon I., and Elif Arioglu. "Diabetes Mellitus." In Hormone Resistance Syndromes, 165–84. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-698-0_8.
Bell, Patrick M. "Insulin Resistance." In Diabetes and Atherosclerosis, 27–51. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2734-9_3.
Singh, Kamalpreet, and Vasudevan A. Raghavan. "Insulin Resistance and Atherosclerosis." In Contemporary Diabetes, 41–54. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7554-5_3.
Moore, Lisa E. "Pathophysiology of Insulin Resistance." In Diabetes in Pregnancy, 1–5. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-65518-5_1.
Khaliq, Adnan, Muhammad Farhan Jahangir Chughtai, Javed Iqbal, Haq Nawaz, Samreen Ahsan, Tariq Mehmood, Atif Liaqat, et al. "Drug Resistance in Diabetes." In Biochemistry of Drug Resistance, 423–59. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-76320-6_16.
Carlberg, Carsten, Stine Marie Ulven, and Ferdinand Molnár. "Insulin Resistance and Diabetes." In Nutrigenomics: How Science Works, 131–51. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-36948-4_9.
Gartler, Stanley M., R. Scott Hansen, Vinzenz Oji, Heiko Traupe, Julia Horn, Bodo Grimbacher, Srijita Sen-Chowdhry, et al. "Insulin Resistance Related Diabetes." In Encyclopedia of Molecular Mechanisms of Disease, 1060. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6449.
Carlberg, Carsten, Eunike Velleuer, and Ferdinand Molnár. "Insulin Resistance and Diabetes." In Molecular Medicine, 633–51. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-27133-5_40.
Reissig, Federico. "Insulin Resistance and Acanthosis Nigricans." In Dermatology and Diabetes, 105–15. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-72475-1_8.
Conference papers on the topic "Diabetes resistance":
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Kherra, Sakina, Amina Chikh, Ouarda Drali, Karima Haddad, and Agnes Guichet. "39 A Donhue’s syndrome case : rare severe syndromic insuline resistance." In The 7th ASPED-ISPAD Diabetes Academy. BMJ Publishing Group Ltd, 2024. http://dx.doi.org/10.1136/bmjpo-2024-asped.39.
Elcin, Huseyn. "EARLY IDENTIFICATION OF THE NEUROLOGICAL COMPLICATIONS OF DIABETES MELLITUS." In International Trends in Science and Technology. RS Global Sp. z O.O., 2021. http://dx.doi.org/10.31435/rsglobal_conf/30032021/7474.
Diabetes mellitus is still a very common disease in the world and affects the daily lives of patients negatively. Diabetes is also known to be associated with neurological diseases such as peripheral nerve diseases, stroke and dementia. Among these, the most common disease is a peripheral nerve disease, and it has been reported that poor diabetic control increases the risk of development and can be prevented by education of the patients. Vascular dementia is more common in patients with diabetes than Alzheimer's disease, and it is thought that cerebrovascular diseases may berelated to cognitive impairment in diabetes. Although the mechanisms by which diabetes affects the brain are not clearly revealed, it is thought that changes in vascular structure, insulin resistance, glucose toxicity, oxidative stress, accumulation of glycation end products, hypoglycemic episodes and amyloid metabolism are effective.The aim of this article is to describe the neurological complications of diabetes and to emphasize the importance of patient education, good diabetes control and early diagnosis in preventing these complications.
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Leboucher, A., M. Rath, and A. Kleinridders. "Increased uremic toxins in cerebrospinal fluid of obese mice cause insulin resistance." In Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641817.
Al-Jaber, Hend Sultan, Layla Jadea Al-Mansoori, and Mohamed Aghar Elrayess. "The Role of GATA3 in Adipogenesis & Insulin Resistance." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0143.
Background: Impaired adipogenesis plays an important role in the development of obesityassociated insulin resistance and type 2 diabetes. Adipose tissue inflammation is a crucial mediator of this process. In hyperglycemia, immune system is activated partially through upregulation of GATA3, causing exacerbation of the inflammatory state associated with obesity. GATA3 also plays a role as a gatekeeper of terminal adipocyte differentiation. Here we are examining the impact of GATA3 inhibition in adipose tissue on restoring adipogenesis, reversing insulin resistance and potentially lowering the risk of type 2 diabetes. Results: GATA-3 expression was higher in insulin resistant obese individuals compared to their insulin sensitive counterparts. Targeting GATA-3 with GATA-3 specific inhibitors reversed impaired adipogenesis and induced changes in the expression of a number insulin signaling-related genes, including up-regulation of insulin sensitivity-related gene and down-regulation of insulin resistance-related genes. Conclusion: GATA3 expression is higher in differentiating adipocytes from obese insulin resistant. Inhibiting GATA3 improves adipocytes differentiation and rescues insulin sensitivity in insulin resistant cells
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"Understanding Mechanisms of Insulin Resistance in Diabetes and Obesity." In International Conference on Agricultural, Ecological and Medical Sciences. International Institute of Chemical, Biological & Environmental Engineering, 2015. http://dx.doi.org/10.15242/iicbe.c0415038.
Nikolic, A. "Genetic variation in a patient with a rare syndrome of severe insulin resistance." In Diabetes Kongress 2021 – 55. Jahrestagung der DDG. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1727543.
Tabei, S., L. Scheffler, R. Chakaroun, S. Ziesche, A. Crane, M. Stumvoll, A. Dietrich, M. Blüher, M. Gericke, and P. Kovacs. "Low-grade inflammation in insulin resistance associates with bacterial load in adipose tissue." In Diabetes Kongress 2019 – 54. Jahrestagung der DDG. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1688193.
Aldali, Sara Haitham, and Sownd Sankaralingam. "Induction of Glyoxalase 1 to prevent Methylglyoxal-Induced Insulin Resistance in Cardiomyocytes." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0230.
Background: Type 2 Diabetes mellitus is characterized by hyperglycemia and insulin resistance. Methylglyoxal (MG) a highly reactive dicarbonyl compound is also increased in diabetes. MG is detoxified by glyoxalase 1 (Glo-1) enzyme using reduced glutathione (GSH) as a co-factor. MG has been shown to have deleterious effects on cardiovascular cells and impairs insulin signaling. Insulin resistance is associated with diabetic cardiomyopathy. Trans-resveratrol (tRES) and Hesperetin (HES) combination has been shown to increase Glo-1 and improve insulin signaling in obese patients. Aim(s): The aim of this study is to investigate whether tRES-HES combination prevents MG-induced cardiac insulin resistance and the underlying mechanisms in cardiomyocytes in culture. Methodology: (H9C2) rat cardiomyocytes were treated with MG (100 µM) for 24 hours in the presence or absence of tRES-HES (10 µM). Glo-1 activity was determined by the formation of S-D lactoylglutathione; protein expression of P-Akt and P-GSK3b was determined using Western blot. In some experiments, cells were stimulated with insulin (100 nM) for 10 minutes to test insulin sensitivity. Results: MG reduced Glo-1 activity by ~25%, blunted insulin-induced phosphorylation of Akt and Gsk3b and increased the expression of beta-myosin heavy chain by ~50% (a marker of cardiac dysfunction) significantly (P˂0.05) compared to untreated control group of cells. Co-administration of tRES-HES combination restored Glo1 activity, maintained insulin-induced phosphorylation of Akt and GSK3b and prevented the increase in beta myosin heavy chain significantly (P<0.05). Conclusion: Induction of Glo1 prevents MG-induced cardiac insulin resistance and the increase in marker of cardiac dysfunction. This strategy could be helpful in preventing cardiovascular complications associated with diabetes.
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Alkhateeb, H. "Oleuropein ameliorates palmitate-induced insulin resistance by increasing Glut4 translocation through activation of AMPK." In Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641812.
Geißler, C., C. Krause, M. Kähler, I. Cascorbi, and H. Kirchner. "Longitudinal analysis of the development of hepatic insulin resistance in diet-induced obese mice." In Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641822.
Bezerra, Alexandre Sacchetti, Flavia Altheman Loureiro, Carla Maria Pasquareli Vazquez, Afonso Cesar Polimanti, and Rafi Felicio Bauab Dauar. Empiric Treatment of Foot Infection in Patients with Severe Diabetes. Science Repository, December 2021. http://dx.doi.org/10.31487/j.jicoa.2021.04.04.
Background: Despite being treated with antibiotics of broad spectrum recommended by International Consensus, severe diabetic patients with lower limb infection do not present a positive clinical evolution during empirical treatment. This study’s bacterial profile was analysed and compared with other worldwide hospital centers. Objective: To confirm the need of an individualized empirical treatment for severe diabetic patients with foot infection. Methods: Retrospective analysis of cultures and antibiograms of severe diabetic patients admitted by foot infection. Results: The results were consistent with the socioeconomic realities of developing countries. Gram-negative bacteria (52,11%) were present in most bone cultures. Results presented a high incidence of Enterococcus faecalis in both gram-positive (21,2%) and polymicrobial (34,7%) samples. Bacterial resistance with the use of ordinary antibiotics in the statistical analysis was high. Conclusion: The community infections should undergo broad spectrum empirical therapy combining amikacin (80,43%) or meropenem (72,00%) with gram-negative and vancomycin (100%) or teicoplanin (90,00%) or linezolid (74,19%) with gram-positive.
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yu, luyou, jinping yang, xi meng, and yanhua lin. Effectiveness of the gut microbiota-bile acid pathway (BAS) in the treatment of Type 2 diabetes: A protocol for systematic review and meta analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2022. http://dx.doi.org/10.37766/inplasy2022.7.0117.
Review question / Objective: To systematically evaluate the efficacy of the intestinal microbiome - bile acid pathway (BAS) in the treatment of T2DM. Condition being studied: Bile acids (BAs), an important component of bile, are also metabolites derived from cholesterol and promote intestinal absorption and transportation of dietary lipids . Studies have shown that bile acid receptor agonists can promote glP-1 secretion and improve glucose metabolism in preclinical mouse models of obesity and insulin resistance , which may become a new therapeutic target for Type 2 diabetes. However, no systematic review and meta-analysis has been found on the treatment of type 2 diabetes by intestinal microbiome - bile acid pathway. Therefore, we conducted a systematic review and meta-analysis to evaluate the safety and effectiveness of intestinal microbiome-bile acid pathway in the treatment of type 2 diabetes.
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Chen, Jiankun, Yingming Gu, Lihong Yin, Minyi He, Na Liu, Yue Lu, Changcai Xie, Jiqiang Li, and Yu Chen. Network meta-analysis of curative efficacy of different acupuncture methods on obesity combined with insulin resistance. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2022. http://dx.doi.org/10.37766/inplasy2022.8.0075.
Review question / Objective: Population：Patients diagnosed as obesity with insulin resistance. Obesity reference: Consensus of experts on the Prevention and treatment of adult obesity in China in 2011 and Consensus of Chinese experts on medical nutrition therapy for overweight/obesity in 2016 were developed by the Obesity Group of Chinese Society of Endocrinology(CSE); BMI≥28. IR reference: According to the Expert opinions on insulin resistance evaluation published by Chinese Diabetes Society, HOMA-IR≥2.68 is regarded as the standard for the diagnosis of IR. Regardless of age, gender and course of disease. Patients diagnosed as obesity with insulin resistance. Intervention：Any kind of acupuncture, moxibustion, acupuncture+moxibustion, warm acupuncture, electropuncture, auricular point, acupoint application and acupoint catgut embedding. Comparison：Other acupuncture treatments, Drug therapy or blank control. Outcome：Primary outcomes: ①Fasting blood-glucose (FBG); ②Fasting serum insulin (FINS); ③Homeostasis model assessment-IR (HOMA-IR); ④Body Mass Index (BMI). Secondary outcomes: ①Waistline; ②Waist-hip ratio;③Triglyceride (TG); ④Total cholesterol (TC); ⑤High-density lipoprotein (HDL); ⑥Low-density lipoprotein (LDL). Study: Randomized controlled trials (RCTs) of different acupuncture methods in the treatment on obesity with insulin resistance, blind method and language are not limited. Randomized controlled trials (RCTs).
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Hung, Hsuan-Yu, and Chung-Yu Chen. The impact of Sofosbuvir/Velpatasvir/Voxilaprevir treatment on serum hyperglycemia in HCV infections: A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2021. http://dx.doi.org/10.37766/inplasy2021.12.0109.
Review question / Objective: To assess the possible cause of events, the incidence of grade 3 hyperglycemia after treating Sofosbuvir/Velpatasvir/Voxilaprevir in HCV infections. Condition being studied: Sofosbuvir, velpatasvir, and voxilaprevir (SOF/VEL/VOX) is an effective, safe rescue therapy regimen for patients have previously been treated failure. Initiating Direct-Acting Antiviral (DAA) treatment for HCV infection with diabetes have experienced hypoglycemia, it could improve insulin resistance due to clean HCV. However, some studies shown that SOF/VEL/VOX has Grade 3 hyperglycemia adverse events. This finding contradicts that other DAAs studies. Information sources: Conducting a comprehensive literature search on the pubmed, Cochrane, clinicalkey, Embase, and MEDLINE electronic databases.
