OBJECTIVETo determine the cause of acute poisoning occurred in a factory in Yangjiang city, Guangdong province.

METHODSIn a cross-sectional study, interviews were conducted with the administrators of the factory and the local physician. A review was conducted on the water system used for industrial purposes and a separate system used by workers for drinking water. Treatment and discharge of industrial waste water were examined. Face-to-face interview was conducted to identify risk of exposure for illness among workers.

RESULTSA total number of 36 cases were identified in the plant and the attack rate was 16.4% (36/220). The incubation period (time between drinking polluted water and the onset of symptoms) had a median of 90 minutes (range: 30 - 230 minutes). Consuming water at the factory increased the attack rate and a dose-response effect was identified (chi(2)(trend) = 79.115, P < 0.01). The nitrite content of residuals in drinking water exceeded the WHO standard (1 ppm).

CONCLUSIONSThe accident of acute poisoning was due to drinking water contaminated with sodium nitrite. The prevention of drinking water contaminated by toxic chemicals like sodium nitrite, and the design of industrial and potable water supply system need to be carefully reviewed. Regulations should be developed and enforced to minimize the impact of industrial waste water discharges to guarantee the access to clean drinking water.

Acute Disease ; Adolescent ; Adult ; Female ; Humans ; Industrial Waste ; Male ; Middle Aged ; Nitrites ; poisoning ; Water Pollutants, Chemical ; poisoning ; Water Supply ; analysis

Objective:To study the virological and serological indicators before treatment and 24 weeks after treatment to predict the partial virological response (PVR) of 48-week entecavir (ETV) treatment, and formulate early clinical adjustment treatment plans for HBeAg-positive CHB patients.Methods:HBeAg-positive CHB-na?ve patients diagnosed in the Department of Infectious Diseases, Shengjing Hospital, China Medical University, who were treated with oral ETV monotherapy from January 2018 were enrolled. The groups were divided according to the test results of HBV DNA at 48 weeks. Among them, HBV DNA < 20 IU/ml was the complete viral response (CVR) group, and HBV DNA ≥ 20 IU/ml was the PVR group. The virological and serological indexes of the two groups before treatment and 24 weeks after treatment were compared. ROC curve univariate analysis and multivariate logistic regression were performed to find out the early predictors of PVR in HBeAg-positive CHB patients receiving ETV therapy for 48 weeks.Results:As of July 2020, a total of 90 cases had completed 48 weeks of treatment, including 50 cases of CVR (55.56%) and 40 cases of PVR (44.44%). Before treatment and at 24 weeks of treatment, HBsAg, HBeAg and HBV DNA in the PVR group were significantly higher than those in the CVR group ( P < 0.001). Univariate analysis showed that HBV DNA quantification (AUC = 0.961, P < 0.001, PPV = 97.06%, NPV = 87.50%) and HBeAg quantification (AUC = 0.883, P < 0.001, PPV = 90.63%, NPV = 81.03%) had higher predictive value at 24 weeks of treatment. Multivariate analysis showed that HBeAg > 1.952 log 10 S/CO ( OR = 3.177, 95% CI: 1.261 ~ 8.267, P = 0.018) and HBV DNA > 2.205 log 10 IU / ml ( OR = 43.197, 95% CI: 6.858 ~ 272.069, P < 0.001) were independent predictors of PVR at 24 weeks of treatment, and their combination had the best predictive effect. Conclusion:In HBeAg-positive CHB patients receiving ETV treatment for 48 weeks, HBV DNA combined with HBeAg quantification can be an early predictor of PVR at 24 weeks. Additionally, patients with both HBV DNA and HBeAg > 2 log 10 at 24 weeks of treatment must wait 48 weeks to obtain CVR, so it is recommended that treatment strategies should be adjusted at this time.

Many human genetic diseases, including Hutchinson-Gilford progeria syndrome (HGPS), are caused by single point mutations. HGPS is a rare disorder that causes premature aging and is usually caused by a de novo point mutation in the LMNA gene. Base editors (BEs) composed of a cytidine deaminase fused to CRISPR/Cas9 nickase are highly efficient at inducing C to T base conversions in a programmable manner and can be used to generate animal disease models with single amino-acid substitutions. Here, we generated the first HGPS monkey model by delivering a BE mRNA and guide RNA (gRNA) targeting the LMNA gene via microinjection into monkey zygotes. Five out of six newborn monkeys carried the mutation specifically at the target site. HGPS monkeys expressed the toxic form of lamin A, progerin, and recapitulated the typical HGPS phenotypes including growth retardation, bone alterations, and vascular abnormalities. Thus, this monkey model genetically and clinically mimics HGPS in humans, demonstrating that the BE system can efficiently and accurately generate patient-specific disease models in non-human primates.
Animals ; Disease Models, Animal ; Female ; Gene Editing ; Humans ; Lamin Type A/metabolism* ; Macaca fascicularis ; Progeria/pathology*