The viral infection due to the new coronavirus or coronavirus disease 2019 (COVID-19), which was reported for the first time in December 2019, was named by the World Health Organization (WHO) as Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV2), because of the very similar genome and also its related symptoms to SARS-CoV1. The ongoing COVID-19 pandemic with significant mortality, morbidity, and socioeconomic impact is considered by the WHO as a global public health emergency. Since there is no specific treatment available for SARS-CoV2 infection, and or COVID-19, several clinical and sub-clinical studies are currently undertaken to find a gold-standard therapeutic regimen with high efficacy and low side effect. Based on the published scientific evidence published to date, we summarized herein the effects of different potential therapies and up-to-date clinical trials. The review is intended to help readers aware of potentially effective COVID-19 treatment and provide useful references for future studies.

The global impact of the new coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), infection that caused COVID-19 has been evident in the last few months from the unprecedented socioeconomic disruption to more than 600,000 deaths. The lack of vaccine and effective therapeutic agents for the disease prompted world-wide effort to test those antiviral therapeutics already in use for other diseases. Another interesting approach has been based on the pathological sequel of the disease that involve severe inflammatory reaction (or the cytokine storm) associated with pneumonia in critically ill patients. This article outlines the prophylaxis therapeutic potential of supplements vitamins and micronutrients in COVID-19. By ameliorating the inflammatory and oxidative stress associated with the disease and some direct antiviral effects, the application of these agents as adjuvants and other alternative approaches are discussed. Available clinical trials including those currently registered on these supplements are scrutinized.

Background Insulin resistance (IR) and fat accumulation in visceral adipose tissue are key players in developing type 2 diabetes (T2D). Several adipose tissue derived-gene polymorphisms are related to higher body mass index (BMI), insulin resistance and T2D. The association of omentin rs2274907 (Val109Asp) and fat-mass and obesity-associated (FTO) rs9939609 gene polymorphisms with overweight/obesity and T2D is controversial. The aim of this study was to determine the association between omentin Val109Asp and FTO rs9939609 polymorphisms and insulin resistance in newly-diagnosed T2D patients. Methods The case-control study included 83 newly-diagnosed T2D patients and 85 healthy matched controls, aged 20–80 years. Fasting blood glucose and insulin levels were measured by the enzymatic method and enzyme-linked-immunosorbent assay, respectively. Insulin resistance was calculated using the homeostasis model assessment (HOMA) index. Genotyping was examined using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Results There are significant differences between both omentin Val109Asp and FTO rs9939609 polymorphisms and studied individuals ( P = 0.011 and P = 0.0001, respectively). Both genetic polymorphisms of omentin Val109Asp and FTO rs9939609 (T/A) are significantly related to higher HOMA index ( P = 0.030 and P = 0.046, respectively). However, omentin Val109Asp polymorphism was only related to individuals who were overweight/obese. Additionally, both omentin Val109Asp and FTO rs9939609 polymorphisms were significantly positively correlated to familial history of diabetes ( P = 0.046 and P = 0.024, respectively). Conclusions Omentin V109D and FTO rs9939609 genetic variations may change insulin metabolism and have key roles in developing T2D through insulin resistance. Thus, the evaluation of these polymorphic regions may be helpful for predicting type 2 diabetes.

Background Omentin, releasing by adipose-tissue may be related to glucose metabolism. The omentin circulating levels and the related mRNA expression in visceral adipose-tissue are different in types of diabetes and the exact function of this molecule is still unknown. The aim of this study was to examine omentin gene expression in adipose-tissues of type-1 and type-2 diabetic mice for the investigation of the effects of fat-mass and insulin–glucose metabolism. Methods In this study, 36 C57BL/6 mice were divided into four experimental groups, including control, type-1 diabetes (inducted by streptozotocin), type-2 diabetes with obesity (high-fat diet + low-dose-streptozotocin [HFD + STZ]), and type-2 with normal weight (normal-pellet diet + low-dose-streptozotocin [NPD + STZ]). The present study involved the measurements of oral-glucose-tolerance-test and the levels of biochemical parameters, including blood glucose, omentin, insulin, lipid-profile, as well as aminotransferases. In addition, the omentin mRNA expression was evaluated by real-time polymerase-chain-reaction. Results The results of omentin gene expression analysis showed a significant difference between mRNA expressions in the experimental groups. The plasma omentin levels were significantly higher in type-1 diabetes group and lower in type-2 diabetes with NPD + STZ; however, the plasma omentin levels were not changed in the HFD + STZ group. In addition, the findings of serum-biochemical analysis revealed significant differences, compared to the control-group. Conclusions The omentin expression may be affected by insulin and glucose levels in different types of diabetes more than fat-mass, and due to the local activity, the serum omentin may not comply with its gene expression.

In late 2019, an outbreak of respiratory disease named COVID-19 started in the world. To date, thousands of cases of infection are reported worldwide. Most researchers focused on epidemiology and clinical features of COVID-19, and a small part of studies was performed to evaluate the genetic characteristics of this virus. Regarding the high price and low availability of sequencing techniques in developing countries, here we describe a rapid and inexpensive method for the detection of D614G mutation in SARS-CoV-2. Using bioinformatics databases and software, we designed the PCR-RFLP method for D614G mutation detection. We evaluated 144 SARS-CoV-2 positive samples isolated in six months in Northeastern Iran. Our results showed that the prevalent type is S-D in our isolates, and a small number of isolated belongs to the S-G type. Of 144 samples, 127 (88.2%) samples have belonged to type S-D, and 13 (9%) samples typed S-G. The first S-G type was detected on 2020 June 10. We have little information about the prevalence of D614G mutation, and it seems that the reason is the lack of cheap and fast methods. We hope that this method will provide more information on the prevalence and epidemiology of D614G mutations worldwide.

BackgroundAlpha-synuclein (SNCA) as the presynaptic protein is expressed in different tissues and prevents insulin-resistance (IR) through increasing glucose-uptake by adipocytes and muscles. However, the effect of insulin metabolism on SNCA expression has scarcely elucidated. In present study we assessed the probable effect of insulin resistance on SNCA expression in muscle C2C12 cells and also skeletal muscle tissues of type 2 diabetic mice.Materials and methodsSixteen male C57BL/6 mice were divided into two experimental groups, including control and type 2 diabetic mice with IR (induced by high-fat diet + low-dose streptozotocin). The animals of the study involved the measurements of fasting blood glucose, oral-glucose-tolerance-test, as well as fasting plasma insulin. Moreover, insulin-resistant and insulin-sensitive muscle C2C12 cells were prepared. The insulin-resistance was confirmed by the glucose-uptake assay. Comparative quantitative real time PCR was used to assess the SNCA expression.ResultsThe obtained results have showed a significant ~ 27% decrease in SNCA expression level in muscle tissue of diabetic mice (P = 0.022). Moreover, there was a significant change of SNCA expression in insulin-resistant C2C12 cells (P < 0.001).ConclusionType 2 diabetes due to insulin-resistance can decrease SNCA gene expression in muscles. In addition to the role of SNCA in cell susceptibility to insulin and glucose uptake, the SNCA expression can also be affected by insulin metabolism.

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ObJeCTIVe: Subclinical hypothyroidism (SCH) is defined as high levels of TSH in the presence of normal levels of serum FT4. Since thyroid peroxidase (TPO) plays a key role in thyroid hormone synthesis, variations in the TPO gene can change the enzyme structure and result in the production of anti-TPO antibodies. The aim of this study was to examine the relationship between the Asn698Thr (A2095C) and Thr725Pro (A2173C) polymorphisms of the TPO gene and anti-TPO levels in patients with SCH. DESIGN: In this study, 150 individuals (75 cases and 75 controls), aged 19-75 years, were selected randomly by a clinician. The thyroid function tests included were FT3, FT4, TSH and anti-TPO antibodies using elISA. The TPO gene polymorphisms were examined by PCR-RFlP. ReSUlTS: Anti-TPO levels in the experimental group was significantly increased (P=0.020). The A2095C genotype frequency in the experimental and control groups were 37.3% vs 34.7% for the AA healthy genotype, 20% vs 46.7% for AC and 42.7% vs 18.6% for CC, respectively (P=0.001). The A2173C genotype frequency in the experimental and control groups were 22.6% vs 68% for healthy AA, 40% vs 25.3% for AC and 37.4% vs 6.7% for CC, respectively (P <0.001). The increased anti-TPO antibodies were significantly associated with the A2173C polymorphism (P=0.035). The findings showed that the chance (odds ratio) of developing subclinical hypothyroidism in individuals who had C alleles was 1.5 and 5.6-fold higher than in individuals without these alleles in the A2095C and A2173C regions, respectively. CONCLUSIONS: Determination of anti-TPO antibody levels and exon 12 TPO gene polymorphisms in patients with SCH can be helpful for prediction of overt hypothyroidism.