Unveiling Sb3+ Doping and Tricolor Luminescence from Intrinsic Self-Trapped Excitons in Cs2ZnCl4 Crystals.

Zero-dimensional (0D) lead-free halide perovskites have lately received significant interest owing to their captivating broadband emissions. An in-depth understanding of the luminescence mechanism of self-trapped excitons (STEs) and realization of effective regulation of luminescence properties have become a major challenge in the research of lead-free metal halides. Herein, we have synthesized the Cs2ZnCl4 and Sb3+-doped Cs2ZnCl4 crystals and conducted a comprehensive investigation into their distinct electronic structures and optical characteristics. The findings from both experimental and theoretical investigations indicate that the tricolor luminescence in Cs2ZnCl4 and blue emission in Sb3+-doped Cs2ZnCl4 stem from intrinsic STEs, and the near-infrared emission originates from extrinsic STEs associated with the Sb3+ ion in Sb3+-doped Cs2ZnCl4. Sb3+ doping increases the quantum yield of Cs2ZnCl4 to a large extent. In addition, intersystem crossing, exciton self-trapping, and lattice relaxation are the main reasons for the large Stokes shift. The present study is expected to provide a novel perspective for researchers in comprehending the luminescent mechanism of STEs and advancing the utilization of 0D lead-free metal halides in optoelectronic applications.

An outbreak of acute GII.17 norovirus gastroenteritis in a long-term care facility in China: The role of nursing assistants.

More than 30 residents and nursing assistants in a geriatric nursing hospital developed acute gastroenteritis from December 7th to December 18th, 2014 in Shanghai, China. An immediate epidemiological investigation was conducted to identify the etiological agent of the outbreak, mode of transmission and the risk factors. Cases were investigated according to an epidemiological questionnaire. Samples from cases, highly transmissible environmental surfaces and drinking water were collected for pathogens detection. A retrospective cohort study was conducted to explore the transmission mode. A total of 34 cases were affected in this acute gastroenteritis outbreak, including 23 residents, 9 nursing assistants and 2 doctors. 13 out of 30 samples were positive for GII.17 norovirus, no other pathogen was detected. Nursing assistants who developed gastroenteritis symptoms had a higher attack rate in residents they cared than those who did not develop any gastroenteritis symptoms (p<0.001). The acute gastroenteritis outbreak was caused by GII.17 norovirus. Person-to-person close contact and contaminated environmental surfaces were the probable transmission route. Nursing assistants were considered to play an important role in the secondary spread of norovirus. The poor medical skill and personal hygiene habits of nursing assistants in China should be paid attention and improved urgently which is critically important to prevent hospital infections.

Hepatic insulin gene therapy prevents diabetic enteropathy in STZ-treated CD-1 mice.

Depending on the population examined, from 6 to 83% of people with diabetes mellitus exhibit symptoms of altered gut motility, manifesting as dysphagia, reflux, early satiety, nausea, abdominal pain, diarrhea, or constipation. Hyperglycemia-induced cell loss within the enteric nervous system has been demonstrated in both diabetic rodents and patients with diabetes. Glycemic control is recommended to prevent diabetic gastroenteropathy but is often difficult to achieve with current treatment modalities. We asked if hepatic insulin gene therapy (HIGT) could inhibit the development of diabetic gastroenteropathy in mice. Bowel length, bowel transit, colonic muscle relaxation, and the numbers of both stimulatory and inhibitory neurons in the colonic myenteric plexus were compared in groups of diabetic mice (DM), control nondiabetic mice (Con), and diabetic mice treated with HIGT (HIGT). Delivery of a metabolically responsive insulin transgene to the liver of STZ-diabetic mice with an adeno-associated virus, sero-type 8 (AAV8) produced near-normal blood sugars for over 1 month and prevented anatomic, functional, and neurohistologic changes observed in diabetic mice. We conclude that in addition to normalizing oxidative metabolism in diabetic rodents, HIGT is sufficient to prevent the development of diabetic gastroenteropathy.

Fisetin inhibits the activities of cyclin-dependent kinases leading to cell cycle arrest in HT-29 human colon cancer cells.

Fisetin, a natural flavonol present in edible vegetables, fruits, and wine, was reported to exert anticarcinogenic effects. The objective of the current study was to examine the effect of fisetin on the cell cycle progression of the human colon cancer cell line HT-29. HT-29 cells were cultured in serum-free medium with 0, 20, 40, or 60 micromol/L fisetin. Fisetin dose dependently inhibited both cell growth and DNA synthesis (P < 0.05), with a 79 +/- 1% decrease in cell number observed 72 h after the addition of 60 micromol/L fisetin. Perturbed cell cycle progression from the G(1) to S phase was observed at 8 h with 60 micromol/L fisetin treatment, whereas a G(2)/M phase arrest was observed after 24 h (P < 0.05). The phosphorylation state of the retinoblastoma proteins shifted from hyperphosphorylated to hypophosphorylated in cells treated with 40 micromol/L fisetin. (P < 0.05). Fisetin decreased the activities of cyclin-dependent kinases (CDK)2 and CDK4; these effects were likely attributable to decreases in the levels of cyclin E and D1 and an increase in p21(CIP1/WAF1) levels (P < 0.05). However, fisetin also inhibited CDk4 activity in a cell-free system (P < 0.05), indicating that it may directly inhibit CDk4 activity. The protein levels of cell division cycles (CDC)2 and CDC25C and the activity of CDC2 were also decreased in fisetin-treated cells (P < 0.05). These results indicate that inhibition of cell cycle progression in HT-29 cells after treatment with fisetin can be explained, at least in part, by modification of CDK activities.

[Yixintong tablet's protection against experimental myocardial ischemia].

OBJECTIVE: Various models of experimental myocardial ischemia were set up to ovbserve the Yixinton's protection against ischemia. METHOD: Models of experimentally acute myocardial ischemia were made by ligature or medication (pituitrin or isoprenaline) to check the indices of ECG, hemodynamics, and morphology. RESULT: A dosage of Yixintong tablets 100 mg/kg, 200 mg/kg was given to rats by gavage; the rats had undergone a thirty-minute ligatute of coronary lef anterior descending branch, and used as a model of ischemic reperfusion. The observations showed that Yixintong tablets exerted a recovery effect on heart rate, blood pressure, internal pressure of left ventricule and its peak/trough rate (+/- dp/dtmax), and ST segment (electrocardiogram). The tablet markedly reduced the myocardial infarct size of the coronary-ligatured rats. The tablet benefited the rats with pituitrin(iv)- or isoprenaline(ip)-induced acute myocardial ischemia to reverse any ST deviation and T-wave fall. CONCLUSION: Yixintong has a protective and therapeutic action to the experimental myocardial ischemia.