Agonist evoked platelet activation results in intracellular Zn2+ ([Zn2+]i) fluctuations that are sensitive to the platelet redox state. Increases in [Zn2+]i correlate with activation responses, including shape change, granule release, αIIbβ3 activation and phosphatidyl-serine exposure, consistent with a role as a second messenger. This review provides insight into the numerous demonstrated and potential roles for Zn2+ in platelet function during thrombosis and hemostasis, highlighting its increasing acceptance as an intracellular and extracellular platelet regulatory agent.From Sydney Brenner’s backyard to hundreds of labs across the globe, inspiring six Nobel Prize winners along the way, Caenorhabditis elegans research has come far in the past half century. The journey is not over. The virtues of C. elegans research are numerous and have been recounted extensively. Here, we focus on the remarkable progress made in sensory neurobiology research in C. elegans. This nematode continues to amaze researchers as we are still adding new discoveries to the already rich repertoire of sensory capabilities of this deceptively simple animal. Worms possess the sense of taste, smell, touch, light, temperature and proprioception, each of which is being studied in genetic, molecular, cellular and systems-level detail. This impressive organism can even detect less commonly recognized sensory cues such as magnetic fields and humidity.

Nephrolithiasis is a major public health problem worldwide and Fu-Fang-Jin-Qian-Cao granules (FFJQC) is a traditional Chinese herbal formula that is used to treat nephrolithiasis. The main component of nephrolithiasis is calcium oxalate (CaOx) and the epithelial-mesenchymal transition (EMT) shown to play a crucial role in CaOx-induced kidney injury. However, the mechanism underlying the therapeutic effect of FFJQC on the CaOx-induced renal EMT is unknown.

This study explores the therapeutic benefits and mechanism of FFJQC in oxalate-induced kidney injury.

60 male C57BL/6 mice were used in this experiment and divided into 6 groups. A mouse kidney stone model was created by intraperitoneal injection of glyoxylate at a dose of 100 mg/kg for 6 days. The standardized FFJQC was used to treat mouse crystal kidney injury by gavage at 1.35 and 2.7 g/kg, respectively. Western blotting and immunostaining for E-cadherin, cytokeratin 18 (CK18), vimentin, smooth muscle α-actin (α-SMA) and transforming growth factor β (TGF-β)/Smad pathway were conducted on renal tissues.

Following CaOx-induced kidney injury, the levels of E-cadherin and CK18 in kidney decreased, while vimentin and α-SMA levels increased. The FFJQC treatment increased the levels of E-cadherin and CK18 and decreased vimentin and α-SMA levels in varying degrees. What’s more, the FFJQC reduced the expression of CaOx-induced fibrosis marker collagen II.

FFJQC alleviated the CaOx-induced renal EMT and fibrosis by regulating TGF-β/smad pathway. Therefore, the FFJQC is an important traditional Chinese medicine for the treatment of CaOx-induced renal injury and fibrosis.

FFJQC alleviated the CaOx-induced renal EMT and fibrosis by regulating TGF-β/smad pathway. Therefore, the FFJQC is an important traditional Chinese medicine for the treatment of CaOx-induced renal injury and fibrosis.Aim The objective of this study is to investigate the changes of UA with sitagliptin in relation to its glycemic/non-glycemic efficacies.Methods Drug naïve subjects with T2DM (n = 62) were administered 25-50 mg/day sitagliptin monotherapy for 3 months. The subjects were divided into two subgroups according to the changes in (Δ) UA (above the median [group A, n = 31] ΔUA = 23.3%, p less then 0.00001, and below the median [group B, n = 31] ΔUA = -0.9%, n.s.). Changes in glycemic/non-glycemic parameters were compared between these two groups, which acted as a control for each other.Results In the overall subjects, UA significantly increased (10.8%, p less then 0.00001). Zenidolol Significant correlations between ΔUA and ΔBMI (R = 0.252), ΔHOMA-B (R = 0.309) or ΔCPR-index (R = 0.258), and significant negative correlations between ΔUA and ΔHbA1c (R = -0.290) or ΔFFA (R = -0.271) were seen. Between group A and group B, some parameters displayed distinct regulatory patterns. HbA1c significantly decreased in both groups (group A from 9.97% to 7.65%, group B from 10.41% to 8.85%) with significant inter-group differences (higher reductions in group A, p less then 0.05). C-peptide (+10.6%) and BMI (+1.7%) significantly increased, and FFA (-20.5%) decreased in group A. HOMA-R or 20/(C-peptide x FBG) had no changes in either group, while HOMA-B (group A +85.1%, group B +38.8%) or CPR-index (group A +37.7%, group B +20.5%) increased in both groups with significant inter-group differences (both p less then 0.01). TG (-18.8%) significantly decreased, and T-C (-3.5%) and non-HDL-C (-4%) had a tendency to decrease in group B.Conclusions These results suggest that UA and beta-cell functions/glycemic efficacy are closely linked during sitagliptin therapy. Those with elevated UA had better beta-cell enhancing and glyemic efficacies. Body weights increased and FFA decreased in these populations. By contrast, those without changes in UA had favorable profiles in atherogenic lipids.

Overall survival has improved significantly in patients with human epidermal growth receptor 2 (HER2)-positive breast cancer due to the use of the monoclonal antibody trastuzumab blocking HER2. However, patients may develop trastuzumab-induced cardiotoxicity (TIC) leading to congestive heart failure. Here we assessed whether analysing NT-proBNP and assessment of electrocardiography (ECG) could detect TIC during trastuzumab therapy.

One hundred thirty-six patients undergoing adjuvant, neoadjuvant or palliative chemotherapy and HER2 blockade for HER2-positive breast cancer were prospectively assessed with echocardiography, ECG and N-terminal – pro hormone B-type natriuretic peptide (NT-proBNP) testing at baseline and at 6 and 12 months of trastuzumab therapy. TIC was defined as a left ventricular ejection fraction (LVEF) of less than 50% and a decline from baseline of ≥10 units.

Six patients developed TIC under 12 months of trastuzumab therapy (incidence 4.4%). NT-proBNP increased from 198.8 ± 64.0 pg/ml to 678.