[Progress in health effects and measurement standards of ultraviolet radiation in the workplace].

Ultraviolet radiation affects human health. On the one hand, moderate amounts of UV radiation can promote human health and have the effect of promoting vitamin D production; but on the other hand, excessive UV radiation can also cause adverse effects on human skin and eyes, such as causing skin photoaging, skin cancer, electrophthalmia and cataracts to occur. Therefore, the measurement of ultraviolet radiation is extremely important. This paper mainly reviews the health effects of ultraviolet radiation and the progress of measurement standards in the workplace, and puts forward suggestions on the revision of the existing standards from five aspects including use new measuring instruments and methods, improve the existing measuring instruments, specify the number of measurements, expand the scope of application of the standards and consider the influence of the sun on the measurement of artificial ultraviolet radiation, so as to provide reference for the revision of new standards.

[Gastric adenocarcinoma of the fundic gland type: clinicopathological analysis of six cases].

Objective: To investigate the clinicopathological characteristics of gastric adenocarcinoma of the fundic gland(GA-FG). Methods: A total of 6 patients with GA-FG admitted from January 2014 to May 2019 were identified at Shanghai Songjiang District Central Hospital.Analyzed endoscopic findings, pathological characteristics and immunohistochemical staining of the lesions and reviewed relevant literatures. Results: Among the 6 patients, 3 were male, 3 were female, and the mean age was 66 years. The most common clinical presentation was epigastric discomfort. Gastroscopic examination revealed an elevated or flat lesion in the body of the stomach, with a diameter of 0.4 to 1.0 cm. Histopathologically, they mainly composed of main cells, but there were also scattered parietal cells, arranged in an irregular tubular or cord-like structure, and formed anastomosis branches. The tumor cells were immunohistochemically positive for MUC6 and pepsinogen 1. Conclusions: GA-FG is a rare variant of well-differentiated adenocarcinoma. It is important to understand its clinical features and histological morphology for more accurate diagnosis.

Disruption of protein complexes containing protein phosphatase 2B and Munc18c reduces the secretion of von Willebrand factor from endothelial cells.

Essentials Endothelial secretion of von Willebrand factor (VWF) promotes inflammation and thrombosis. We studied the role of protein phosphatase 2B (PP2B) and Munc18c protein complex in VWF secretion. Disruption of PP2B-Munc18c complex in endothelial cells reduced agonist-induced VWF secretion. PP2B-Munc18c complex represents a potential target for thrombotic and inflammatory conditions. SUMMARY: Background Aberrant secretion of von Willebrand factor (VWF) from endothelial cells contributes to inflammation and vascular thrombosis. Agonist-induced VWF secretion is facilitated by protein kinase and phosphatase-mediated signaling. Although the catalytic subunit of protein phosphatase 2B (PP2B-Aα) is targeted to the secretory machinery via an interaction with the vesicle trafficking protein Munc18c in endothelial cells, the functional relevance of this phosphatase complex is unclear. Objective To assess the contribution of the PP2B-Aα-Munc18c complex to endothelial VWF secretion. Results Here, we show that amino acids 120-130 of PP2B-Aα are important to support an interaction with Munc18c. A synthetic myristylated cell-permeable peptide, which is derived from amino acids 121-130 of PP2B-Aα, disrupted endogenous PP2B-Aα-Munc18c complexes in human umbilical vein endothelial cells, and decreased low-dose histamine-stimulated and thrombin-stimulated VWF secretion. Conclusion These studies indicate that PP2B-Aα-Munc18c complex supports agonist-induced VWF secretion, and suggest the potential of targeting this phosphatase complex in thrombotic and inflammatory conditions.

The ß isoform of the catalytic subunit of protein phosphatase 2B restrains platelet function by suppressing outside-in αII b ß3 integrin signaling.

BACKGROUND: Calcium-dependent signaling mechanisms play a critical role in platelet activation. Unlike calcium-activated protease and kinase, the contribution of calcium-activated protein serine/threonine phosphatase in platelet activation is poorly understood. OBJECTIVE: To assess the role of catalytic subunit of protein phosphatase 2B (PP2B) or calcineurin in platelet function. RESULTS: Here, we showed that an increase in PP2B activity was associated with agonist-induced activation of human and murine platelets. Pharmacological inhibitors of the catalytic subunit of protein phosphatase 2B (PP2B-A) such as cyclosporine A or tacrolimus (FK506) potentiated aggregation of human platelets. Murine platelets lacking the ß isoform of PP2B-A (PP2B-Aß(-/-) ) displayed increased aggregation with low doses of agonist concentrations. Loss of PP2B-Aß did not affect agonist-induced integrin αII b ß3 inside-out signaling, but increased basal Src activation and outside-in αII b ß3 signaling to p38 mitogen-activated protein kinase (MAPK), with a concomitant enhancement in platelet spreading on immobilized fibrinogen and greater fibrin clot retraction. Fibrinogen-induced increased p38 activation in PP2B-Aß(-/-) platelets were blocked by Src inhibitor. Both PP2B-Aß(-/-) platelets and PP2B-Aß-depleted human embryonal kidney 293 αII b ß3 cells displayed increased adhesion to immobilized fibrinogen. Filamin A, an actin crosslinking phosphoprotein that is known to associate with ß3 , was dephosphorylated on Ser(2152) in fibrinogen-adhered wild-type but not in PP2B-Aß(-/-) platelets. In a FeCl3 injury thrombosis model, PP2B-Aß(-/-) mice showed decreased time to occlusion in the carotid artery. CONCLUSION: These observations indicate that PP2B-Aß by suppressing outside-in αII b ß3 integrin signaling limits platelet response to vascular injury.

Nurses' self-efficacy and practices relating to weight management of adult patients: a path analysis.

BACKGROUND: Health professionals play a key role in the prevention and treatment of excess weight and obesity, but many have expressed a lack of confidence in their ability to manage obese patients with their delivery of weight-management care remaining limited. The specific mechanism underlying inadequate practices in professional weight management remains unclear. The primary purpose of this study was to examine a self-efficacy theory-based model in understanding Registered Nurses' (RNs) professional performance relating to weight management. METHODS: A self-report questionnaire was developed based upon the hypothesized model and administered to a convenience sample of 588 RNs. Data were collected regarding socio-demographic variables, psychosocial variables (attitudes towards obese people, professional role identity, teamwork beliefs, perceived skills, perceived barriers and self-efficacy) and professional weight management practices. Structural equation modeling was conducted to identify correlations between the above variables and to test the goodness of fit of the proposed model. RESULTS: The survey response rate was 71.4% (n = 420). The respondents reported a moderate level of weight management practices. Self-efficacy directly and positively predicted the weight management practices of the RNs (ß = 0.36, p < 0.01), and fully or partially mediated the relationships between perceived skills, perceived barriers, professional role identity and teamwork beliefs and weight management practices. The final model constructed in this study demonstrated a good fit to the data [χ2 (14) =13.90, p = 0.46; GFI = 0.99; AGFI = 0.98; NNFI = 1.00; CFI = 1.00; RMSEA = 0.00; AIC = 57.90], accounting for 38.4% and 43.2% of the variance in weight management practices and self-efficacy, respectively. CONCLUSIONS: Self-efficacy theory appears to be useful in understanding the weight management practices of RNs. Interventions targeting the enhancement of self-efficacy may be effective in promoting RNs' professional performance in managing overweight and obese patients.

A critical challenge: dosage-related efficacy and acute complication intracoronary injection of autologous bone marrow mesenchymal stem cells in acute myocardial infarction.

BACKGROUND: Previous studies showed improvement in heart function by injecting bone marrow mesenchymal stem cells (BMSCs) after AMI. Emerging evidence suggested that both the number and function of BMSCs decline with ageing. We designed a randomized, controlled trial to further investigate the safety and efficacy of this treatment. METHODS: Patients with ST-elevation AMI undergoing successful reperfusion treatment within 12 hours were randomly assigned to receive an intracoronary infusion of BMSCs (n=21) or standard medical treatment (n=22) (the numbers of patients were limited because of the complication of coronary artery obstruction). RESULTS: There is a closely positive correlation of the number and function of BMSCs vs. the cardiac function reflected by LVEF at baseline (r=0.679, P=0.001) and at 12-month follow-up (r=0.477, P=0.039). Six months after cell administration, myocardial viability within the infarct area by 18-FDG SPECT was improved in both groups compared with baseline, but no significant difference in the BMSCs compared with control groups (4.0±0.4% 95%CI 3.1-4.9 vs. 3.2±0.5% 95%CI 2.1-4.3, P=0.237). 99mTc-sestamibi SPECT demonstrated that myocardial perfusion within the infarct area in the BMSCs did not differ from the control group (4.4±0.5% 95%CI 3.2-5.5 vs. 3.9±0.6% 95%CI 2.6-5.2, P=0.594). Similarly, LVEF after 12 and 24 months follow-up did not show any difference between the two groups. In the BMSCs group, one patient suffered a serious complication of coronary artery occlusion during the BMSCs injection procedure. CONCLUSIONS: The clinical benefits of intracoronary injection of autologous BMSCs in acute STEMI patients need further investigation and reevaluation.

Cytotoxicity and DNA damage of five organophosphorus pesticides mediated by oxidative stress in PC12 cells and protection by vitamin E.

Previous studies have demonstrated that pesticides could induce cytotoxicity and genotoxicity in vivo and in vitro, and that oxidative stress may be an important factor involved. However, investigations comparing the capability of different organophosphorous (OP) compounds to induce cytotoxicity, genotoxicity and oxidative stress are limited. Hence, the aim of this paper was to access the cytotoxic and genotoxic effects of five OPs or metabolites, Acephate (ACE), Methamidophos (MET), Chloramidophos (CHL), Malathion (MAT) and Malaoxon (MAO), and to clarify the role of oxidative stress, using PC12 cells. The results demonstrated that MET, MAT and MAO caused significant inhibition of cell viability and increased DNA damage in PC12 cells at 40 mg L(-1). MAO was more toxic than the other OPs. ACE, MET, MAT and MAO increased the levels of intracellular reactive oxygen species (ROS) and malondialdehyde (MDA), and decreased the activity of superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) at 20 mg L(-1) and 40 mg L(-1) to different degrees. Pre-treatment with vitamin E(600 µM)caused a significant attenuation in the cytotoxic and genotoxic effect; pre-treatment reversed subsequent OP-induced elevation of peroxidation products and the decline of anti-oxidant enzyme activities. These results indicate that oxidative damage is likely to be an initiating event that contributes to the OP-induced cytotoxicity.

Purification and characterization of a superoxide dismutase from Panax ginseng.

A superoxide dismutase (SOD) with the molecular weight of 31,079 has been purified as a homodimer from Panax ginseng by employing neutral pH buffer extraction, ammonium sulfate precipitation, isoelectric point precipitation and ion exchange methods. The enzyme's specific activity determined by an improved Marklund method was 9480.43 U/mg. Metal analysis showed that the SOD contained iron with the stoichiometry of 0.9 ± 0.3 Fe/subunit and exhibited high thermal stability (70 °C) over the pH range from 4.0 to 9.0. Its maximum absorption wavelength was 278 nm and it was sensitive to hydrogen peroxide, trichloromethane-ethanol and urea. These results indicate that the enzyme is an iron SOD.

Induction of interleukin-8 in T84 cells by Vibrio cholerae.

The induction of interleukin-8 (IL-8) in vitro has been suggested to correlate with the reactogenicity of Vibrio cholerae vaccine candidates. V. cholerae vaccine candidate 638, a hemagglutinin protease/hap-defective strain, was recently reported to be well tolerated in human volunteers, suggesting a role for Hap in reactogenicity. We examined the role of hap in the induction of IL-8 in intestinal epithelial T84 cells. Wild-type V. cholerae strains 3038 and C7258 and a vaccine candidate strain, JBK70, induced levels of IL-8 similar to those of their isogenic hap mutants. Supernatant containing Hap did not stimulate IL-8 production at a variety of concentrations tested, suggesting that Hap itself does not induce IL-8 production. Furthermore, supernatant from CVD115, which had deletions of hap and rtxA (encoding repeats in toxin) and was derived from a reactogenic strain, CVD110, induced IL-8 production in T84 cells in a dose-dependent manner. The IL-8-stimulating activity of CVD115 culture supernatants was growth phase dependent and was strongest in stationary phase cultures. This IL-8 stimulator(s) was resistant to heat treatment but sensitive to proteinase. Protease activity in vitro did not correlate with the reactogenicity of V. cholerae vaccine candidates. Our data suggest that Hap is not an IL-8 inducer in T84 cells and that the IL-8 stimulator in the supernatant of V. cholerae culture may play a role in reactogenicity.

Variation in red blood cell deformability and possible consequences for oxygen transport to tissue.

Red blood cell (RBC)-plasma suspensions with a hematocrit of 10-12% were forced to flow through microchannels (equivalent diameter 6 microns, equivalent length 20 microns, 2600 in parallel) by applying a pressure difference of 20 cm H2O. Transit times for 100 microliters of fresh suspensions from 33 healthy male subjects aged between 24 and 63 ranged from 43.0 to 65.2 sec (mean +/- SD: 49.4 +/- 4.3 sec). Four measurements taken from two subjects at intervals over several weeks gave fluctuations of 45.1, 43.6, 47.6, and 45.9 sec and 52.3, 49.8, 60.1, and 50.0 sec, respectively. RBC deformability thus appeared to vary considerably between different subjects and also showed fluctuations between different days in any given subject. No correlation was obtained between the transit time and subject's age. However, higher whole blood hematocrit values were apparent in those suspensions that had longer transit times. A lower RBC deformability might be caused by dietary factors with resultant increased frequency of occasional stagnation of capillary blood flow, i.e., occasional tissue hypoxia. This would further result in an increased hematocrit.