In this work, a colorimetric aptamer-based method for detection of cadmium using gold nanoparticles modified MoS2 nanocomposites as enzyme mimic is established. In short, biotinylated Cd2+ aptamers are immobilized by biotin-avidin binding on the bottoms of the microplate, the complementary strands of Cd2+ aptamers are connected to the Au-MoS2 nanocomposites which have the function of enhanced peroxidase-like activity. The csDNA-Au-MoS2 signal probe and target Cd2+ compete for binding Cd2+ aptamer, the color change can be observed by addition of chromogenic substrate, thereby realizing visual detection of Cd2+. The absorbance of the solution at 450 nm has a clear linear relationship with the Cd2+ concentration. The linear range is 1-500 ng/mL, and the limit of detection is 0.7 ng/mL. The assay was used to test white wine samples, the results are consistent with those of atomic absorption spectrometry; which prove that this method can be used for detection of Cd2+ in real samples.Capsaicin (CAP) is a spice-derived substance of the genus Capsicum, which has high pungency and therapeutic potential. For many years, it has been considered only as an agonist of the transient receptor potential vanilloid member 1 (TRPV1), a member from the family of transient potential receptors (TRPs). Capsaicin can lead to a variety of effects on cells, acting in specific organelles, and promoting different responses. Such studies, however, point the capsaicin acting independently of the TRPV1 channel, being able to alter membrane fluidity, ion flux, and reactive oxygen species levels on cells. In this context, capsaicin has been used as a therapeutic alternative for the treatment of some diseases, such as disorders related to pain and inflammation. Further, researchers have investigated the involvement of capsaicin in cancer. Thus, this review aims to examine the ways that capsaicin can act on cells independently of the vanilloid receptor activation and demonstrate the therapeutic uses of capsaicin as an alternative tool for some disorders.Coronavirus Disease 2019 (COVID-19) caused by a Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) was first reported in Wuhan, China at the end of December 2019. SARS-CoV-2 is a highly pathogenic zoonotic virus and closely related to the Severe Acute Respiratory Coronavirus (SARS-CoV) and Middle East Respiratory Syndrome Coronavirus (MERS-CoV). The COVID-19 was declared as a global pandemic due to its high infectiousness, and worldwide morbidities and mortalities. The Chinese scientists at the start of the outbreak reported genome sequences, which made the characterization of glycoproteins and other structural proteins possible. Moreover, researchers across the world have widely focused on understanding basic biology, developing vaccines, and therapeutic drugs against the COVID-19. However, until now, no promising treatment options, as well as vaccines, are available. In this review, we have described SARS-CoV-2's genome, transmission, and pathogenicity. We also discussed novel potential therapeutic agents that can help to treat the COVID-19 patients.Stress-induced cardiomyopathy (SIC) is associated with high mortality rates, potentially due to a lack of available therapies. To facilitate the identification of therapeutic targets for SIC, we explored the detailed mechanisms of disease onset and progression using a mouse model. Over-activation of the β-adrenergic receptor (β-AR) upon stress leads to inflammasome activation, cytokine cascades, macrophage infiltration, and pathological cardiac remodeling in mice, mimicking SIC. However, the detailed mechanisms by which acute β-AR stimulation induces cardiac inflammation remain elusive. We found that resveratrol (RSV) could attenuate isoproterenol-induced cardiac inflammation in mice, suggesting that RSV might be a promising therapeutic option in SIC. Mechanistically, we revealed that the SIRT1/NRF2 signaling pathway is the bona fide target of RSV and plays a significant role in the RSV-induced protective effect in cardiac inflammation.Metformin administration has been reported to influence the carotid intima-media thickness (CIMT) in humans. However, since previously conducted studies have yielded inconsistent results, the exact effect of metformin on CIMT remains unclear. Causes that could lead to inconsistency in reported research could be the duration and dose of the intervention, as well as the sample size. To address this inconsistency, we conducted a systematic review and meta-analysis to evaluate the influence of metformin on CIMT in human subjects.  https://www.selleckchem.com/products/Cytarabine(Cytosar-U).html  We identified eligible studies by searching several electronic databases (EMBASE, PubMed-MEDLINE, Web of Science and Google Scholar) up to December 12, 2019. Data were pooled using the random-effects model. Combining data from 1087 participants (9 studies), our meta-analysis revealed that the administration of metformin resulted in a significant reduction in CIMT (WMD = -0.049 mm; 95% CI -0.095, -0.004). Stratified analyses showed that an intervention lasting ≥12 months (WMD -0.084 mm, 95% CI -0.145, -0.024) and an intake of metformin ≤1500 mg/day (WMD -0.081 mm, 95% CI -0.132, -0.029) resulted in a significantly greater reduction in CIMT. However, an intervention duration of less than 12 months and an intake of metformin ˃1500 mg/day yielded no significant effects on CIMT. The results of the current study confirm that metformin administration is associated with a significant reduction in CIMT. Taking into account that CIMT reflects the burden of atherosclerosis, the clinical utility of metformin might also be related to its anti-atherogenic effects.Bombyx mori antimicrobial peptides (BmAMPs) are important effectors in silkworm immune system. They can inhibit and kill a variety of bacteria and fungi. Recent studies have shown that some kinds of BmAMPs exert strong inhibitory effects on a variety of tumor cells. In the present study, the antitumor activity of BmAMP Cecropin A (BmCecA) and BmAMP Cecropin D (BmCecD) was investigated against human esophageal cancer cells and their antitumor mechanism preliminary explored. Cell Counting Kit-8 and colony formation assays indicated that BmCecA and BmCecD suppressed cell proliferation and reduced colony formation of both Eca109 and TE13 cells in a dose-dependent manner, but exhibited no inhibitory effect on normal human embryonic kidney 293T cells. Wound healing and invasion experiments indicated that both BmCecA and BmCecD inhibited migration and invasion of Eca109 and TE13 cells in vitro. Annexin V/propidium iodide staining and flow cytometry detection suggested that BmCecA induced the apoptosis of Eca109 cells in a dose-dependent manner.