4-Methyl-anilinium nitrate.

In the crystal structure of the title compound, C(7)H(10)N(+)·NO(3) (-), N-H⋯O hydrogen bonds involving the ammonium group and the nitrate O atoms result in the formation of zigzag chains propagating in [100].

4-Methyl-anilinium 3,5-dinitro-benzoate.

The crystal structure of the title compound, C(7)H(10)N(+)·C(7)H(3)N(2)O(6) (-), displays N-H⋯O hydrogen bonding between the ammonium groups and the O atoms of the 3,5-dinitro-benzoate anions. Inter-molecular C-H⋯O inter-actions further stabilize the packing. An O atom of each of the nitro groups is disordered over two sites with site occupancy factors of 0.59 (5) and 0.41 (6).

4-Methyl-anilinium p-toluene-sulfonate.

The crystal structure of the title compound, C(7)H(10)N(+)·C(7)H(7)O(3)S(-), displays strong N-H⋯O and N-H⋯S hydrogen bonding between the ammonium group and the p-toluene-sulfonate anion, linking the cations and anions into chains along the b axis.

4-Meth-oxy-anilinium iodide.

The crystal structure of the title compound, C(7)H(10)NO(+)·I(-), displays N-H⋯I hydrogen bonds between the 4-meth-oxy-anilinium cations and the iodide anion together with weaker C-H⋯π contacts.

Efficacy and safety of sotagliflozin adjuvant therapy for type 1 diabetes mellitus: A systematic review and meta-analysis.

BACKGROUND: To systematically evaluate the efficacy and safety of sotagliflozin (SOTA) adjuvant therapy for type 1 diabetes mellitus (T1DM). METHODS: Through April 2019, the Web of Science, PubMed, Cochrane Library, Embase, and China National Knowledge Infrastructure databases were electronically searched to identify randomized controlled trials exploring SOTA adjuvant therapy for T1DM. Strict screening and quality evaluations of the obtained literature were performed independently by 2 researchers. Outcome indexes were extracted, and a meta-analysis of the data was performed using Revman 5.3 software. RESULTS: A total of 7 randomized controlled trials were included. The meta-analysis results showed that compared with the patients in the placebo group, the patients in the SOTA group had a lower hemoglobin A1c (mean difference [MD] = -0.28, 95% confidence interval [CI] [-0.34, -0.22], P < .01), lower total daily insulin use (MD = -8.89, 95% CI [-11.64, -6.13], P < .01), faster weight loss (MD = -3.03, 95% CI [-3.79, -2.26], P < .01), better fasting blood glucose and 2-hour postprandial blood glucose control (MD = -0.75, 95% CI [-1.04, -0.45], P < .01; MD = -2.42, 95% CI [-3.17, -1.67], P < .01), and a higher rate of well-controlled glucose levels (relative risk = 1.75, 95% CI [1.55, 1.99], P < .01), while no significant difference in the incidence of severe hypoglycemic events was found between the SOTA and placebo groups (risk difference [RD] = -0.01, 95% CI [-0.02, 0.00], P = .13). The incidence of diabetic ketoacidosis was higher in the SOTA group than in the placebo group (RD = 0.03, 95% CI [0.02, 0.04], P < .01). The incidence of genital mycotic infection was higher in the SOTA group than in the placebo group (RD = 0.06, 95% CI [0.05, 0.08], P < .01). No significant difference in the incidence of urinary tract infections was detected between the SOTA group and the placebo group (RD = 0.00, 95% CI [-0.01, 0.01], P = 0.97). CONCLUSIONS: SOTA is a potential drug for the treatment of T1DM and is effective for controlling blood sugar. The main adverse reactions to SOTA are genital mycotic infections and diabetic ketoacidosis. We must further assess the severity of diabetic ketoacidosis caused by SOTA.

1,1'-{[1,1'-(Pyridinium-2,6-di-yl)diethyl-idyne]diimino}diguanidinium penta-chloridocadmate(II) monohydrate.

In the title organic-inorganic hybrid salt, (C(11)H(20)N(9))[CdCl(5)]·H(2)O, the crystal structure is stabilized by intermolecular hydrogen bonds between the organic cation, the complex inorganic anion and the uncoordinated water molecule, forming a three-dimensional network.

Effectiveness and safety of sotagliflozin adjuvant therapy for type 1 diabetes mellitus: A protocol for Systematic review and Meta-analysis.

BACKGROUND: Type 1 Diabetes Mellitus (T1DM) has long required insulin treatment. Sotagliflflozin (SOTA), as a dual SGLT-1/2 inhibitor, has the potential to be the first oral antidiabetic drug (OAD) to be approved for T1DM in the US market. It is important to evaluate the effectiveness of SOTA for T1DM. METHODS: Web of Science, PubMed datebase, Cochrane Library, Embase, Clinical Trials, and CNKI will be searched to identify randomized controlled trials (RCTs) exploring SOTA adjuvant therapy for T1DM. Strict screening and quality evaluation will be performed on the obtained literature independently by 2 researchers; outcome indexes will be extracted. The bias risk of the included studies will be evaluated based on Cochrane assessment tool. Meta-analysis will be performed on the data using Revman 5.3 software. RESULT: We will provide practical and targeted results assessing the efficacy and safety of SOTA for T1DM patients, to provide reference for clinical use of SOTA. CONCLUSION: The stronger evidence about the efficacy and safety of SOTA for T1DM patients will be provided for clinicians. TRIAL REGISTRATION NUMBER: PROSPERO CRD42019133099.

Ubiquitin specific peptidase 49 inhibits non-small cell lung cancer cell growth by suppressing PI3K/AKT signaling.

Ubiquitin specific peptidase 49 (USP49) has been reported as a tumor suppressor in several tumors, but its function and molecular mechanism in non-small cell lung cancer (NSCLC) are still unknown. In this study, USP49 was found downregulated in NSCLC primary tissues and cell lines, and high USP49 predicted a positive index for the overall survival of NSCLC patients. Overexpression of USP49 downregulated the expression levels of Cyclin D1, and upregulated p53 expression. Further flow cytometry analysis showed that overexpressed USP49 induced cell cycle arrest at G0/G1 phase. As a result, overexpression of USP49 significantly inhibited cell growth of NSCLC cells. In mechanism, overexpression of USP49 inhibited PI3K/AKT signaling, but knockdown of USP49 enhanced this signaling. Further studies indicated that USP49 deubiquitinated PTEN and stabilized PTEN protein, which suggested that USP49 inhibited PI3K/AKT signaling by stabilizing PTEN in NSCLC cells. In conclusion, we demonstrated that USP49 was functional in NSCLC cells, and inhibited NSCLC cell growth by suppressing PI3K/AKT signaling, suggesting that USP49 could be as a novel target for NSCLC therapy.

Alteration of circulatory platelet microparticles and endothelial microparticles in patients with chronic kidney disease.

OBJECTIVE: To compare plasma platelet microparticles (PMPs), P-selectin, endothelial microparticles (EMPs), and von Willebrand factor (vWF) between a normal control group and patients with chronic kidney disease (CKD) and to explore the significance of PMPs and EMPs in CKD. METHODS: Levels of plasma PMPs, P-selectin, EMPs and vWF in 122 CKD patients and 20 normal controls were detected by flow cytometry and enzyme-linked immunosorbent assay (ELISA). Relationships between PMPs, EMPs and blood pressure, creatinine clearance rate, 24-hour urine protein, hemoglobin, and cholesterol were analyzed. RESULTS: (1) Plasma PMPs, P-selectin, EMPs and vWF levels in CKD patients were significantly higher than those of the control group. Plasma PMPs and P-selectin levels for nephrotic syndrome (NS) were significantly higher than for other CKD groups. No significant difference was found between other CKD groups. Plasma EMPs and vWF in NS, lupus nephritis (LN) and hypertensive nephropathy groups were significantly higher than that of diabetic nephropathy (DN) and chronic glomerulonephritis (CGN) groups. (2) Plasma PMPs, P-selectin, EMPs and vWF in stage I-II CKD patients were significantly higher than those of stage III-V CKD patients, no significant difference was found within stage I-II CKD patients or stage III-V CKD patients. (3) PMPs and EMPs were positively correlated with blood pressure and 24-hour urinary protein, but no significant correlation was found with the creatinine clearance rate, hemoglobin or cholesterol. P-selectin and vWF were positively correlated with PMPs and EMPs respectively. CONCLUSION: CKD patients have significant platelet activation and endothelial dysfunction, which was involved in CKD's occurrence and development; high blood pressure and proteinuria are important reasons for platelet activation and endothelial dysfunction in patients with CKD; PMPs and EMPs can be used as new markers for dysfunctional platelet activation and endothelium.