On August 24 2024, Xiaoshan District Center for Disease Control and Prevention, Hangzhou City, received a report of two cases of varicella infection among staff in the intensive care unit (ICU) of a hospital in its jurisdiction. The center immediately organized personnel to conduct an epidemiological investigation of the cases and their close contacts. The index case was a patient admitted to the ICU who had large areas of red rash and pustules on the chest, back, and right axilla. This case was diagnosed with herpes zoster by a dermatology consultation within the hospital. The other nine secondary cases were all nursing staff in the ICU, who were clinically diagnosed with varicella between August 21 and September 1, with an attack rate of 14.06%. All secondary varicella cases had a history of contact with the herpes zoster case and no history of varicella infection. Their varicella vaccination history was unknown. Based on the results of the on-site epidemiological and sanitary investigations, it was determined that this was an outbreak of varicella in the hospital caused by a herpes zoster case. After the last case was diagnosed, no new cases were reported within the longest incubation period (21 days), and the outbreak was declared over on September 21. Close contact with the herpes zoster case was likely the main cause of the outbreak. This highlights the need for early identification and isolation of suspected herpes zoster cases in hospitals in the future, as well as enhanced protective measures to prevent nosocomial infections.

Objective To evaluate the therapeutic effect of Huangqin Decoction(HQD)on ulcerative colitis(UC)in mice and explore its mechanism.Methods Male Balb/c mice were randomly divided into normal control group,model group,mesalazine group(5-ASA,200 mg/kg),and low-,medium-and high-dose HQD groups(2.275,4.55 and 9.1 g/kg,respectively).With the exception of those in the normal control group,all the mice were exposed to 3%DSS solution in drinking water for 7 days to establish UC models.After treatment with the indicated drugs,the mice were assessed for colon injury and apoptosis using HE,AB-PAS and TUNEL staining,and the expression levels of inflammatory factors were detected with ELISA.Western blotting,immunohistochemistry and qRT-PCR were used to detect the changes in protein expressions associated with the intestinal chemical barrier,mechanical barrier and endoplasmic reticulum stress(ERS).Results HQD treatment significantly reduced DAI score and macro score of UC mice,decreased colonic epithelial cell apoptosis,lowered expressions of IL-6,TNF-α,IL-1β and IL-8,and enhanced the expressions of MUC2 and TFF3.HQD treatment also upregulated the protein expressions of claudin-1,occludin and E-cadherin,reduced the expressions of GRP78,CHOP,caspase-12 and caspase-3,decreased the phosphorylation levels of PERK,eIF2α and IRE1α,and increased the Bcl-2/Bax ratio in the colon tissues of UC mice.Conclusion HQD inhibits colonic epithelial cell apoptosis and improves intestinal barrier function in UC mice possibly by reducing ERS mediated by the PERK and IRE1α signaling pathways.

Objective To evaluate the therapeutic effect of Huangqin Decoction(HQD)on ulcerative colitis(UC)in mice and explore its mechanism.Methods Male Balb/c mice were randomly divided into normal control group,model group,mesalazine group(5-ASA,200 mg/kg),and low-,medium-and high-dose HQD groups(2.275,4.55 and 9.1 g/kg,respectively).With the exception of those in the normal control group,all the mice were exposed to 3%DSS solution in drinking water for 7 days to establish UC models.After treatment with the indicated drugs,the mice were assessed for colon injury and apoptosis using HE,AB-PAS and TUNEL staining,and the expression levels of inflammatory factors were detected with ELISA.Western blotting,immunohistochemistry and qRT-PCR were used to detect the changes in protein expressions associated with the intestinal chemical barrier,mechanical barrier and endoplasmic reticulum stress(ERS).Results HQD treatment significantly reduced DAI score and macro score of UC mice,decreased colonic epithelial cell apoptosis,lowered expressions of IL-6,TNF-α,IL-1β and IL-8,and enhanced the expressions of MUC2 and TFF3.HQD treatment also upregulated the protein expressions of claudin-1,occludin and E-cadherin,reduced the expressions of GRP78,CHOP,caspase-12 and caspase-3,decreased the phosphorylation levels of PERK,eIF2α and IRE1α,and increased the Bcl-2/Bax ratio in the colon tissues of UC mice.Conclusion HQD inhibits colonic epithelial cell apoptosis and improves intestinal barrier function in UC mice possibly by reducing ERS mediated by the PERK and IRE1α signaling pathways.

Objective:To explore the characteristics of T lymphocyte subsets and cytokines in hyperlipidemia-induced acute pancreatitis (HLAP) and its prognostic value.Methods:This study included 184 patients with acute pancreatitis (AP) admitted to the First Affiliated Hospital of Xiamen University from January 2018 to May 2021. Based on disease etiology, there were 92 HLAP cases and 92 non-hyperlipidemia-induced AP (NHLAP) cases. Stratified by disease severity according to 2012 Atlanta classification criteria, the patients were divided into the severe subgroup (SAP) and non-severe subgroup (NSAP). Peripheral venous blood samples were taken from all patients on day 1, 3, and 5 after admission. T lymphocyte subsets were determined by flow cytometry, and cytokines were detected by flow fluorometry. The number of CD4 +% and CD8 +% and the expression of cytokines were compared by Student’s t test or Mann-Whitney U analysis. Logistic regression analyses were performed to identify risk factors for severe AP, and a receiver operating characteristic (ROC) curve was constructed to predict severe AP. Statistical significance was taken as P<0.05. Results:Compared with the NHLAP group, patients in the HLAP group had lower CD4 +%, while higher levels of IL-2 on day 1 ( P<0.05), and had also lower CD4 +%, while higher levels of IL-4, IL-6, and IL-10 on day 3 ( P<0.05). Furthermore, IL-6 and IL-10 levels of the HLAP group were significantly increased compared to the NHLAP group on day 5 ( P<0.05). IL-10 levels in the SAP subgroup were significantly higher than those in the NSAP subgroup on day 1 ( P<0.05). Compared with the NSAP subgroup, the SAP subgroup had elevated levels of IL-2, IL-4, IL-6, IL-10 and IFN-γ on day 3 (all P<0.05), and had lower CD4 +%, while increased levels of IL-6 and IL-10 on day 5 (all P<0.05). Multivariate Logistic regression analysis showed that IL-10 was an immune indicator of independent risk factor for severe AP in the HLAP group on day 1 ( OR=1.139, 95% CI: 1.038-1.251, P<0.05). Finally, ROC analysis showed that the area under the curve of IL-10 to assess HLAP with severe AP was 0.772, and the best cut-off value for predicting severe AP was 5.6 pg/mL, with a sensitivity of 83.3% and a specificity of 68.8%. Conclusions:Changes of CD4 +% and cytokines are different between the HLAP and NHLAP groups. IL-10 can be used as a predictor of early disease severity in patients with HLAP.

The clinical manifestation, laboratory findings, and imaging examination of a baby with familial glucocorticoid deficiency were summarized. The patient presented achypnea, cyanosis, and pigmentation of the whole body skin, no convulsion and hypoglycemia found. Laboratory findings revealed low blood cortisol and high blood ACTH levels. A 1-bp homozygous deletion(c.106+ 1delG) in intron 3 of melanocortin 2 receptor accessory protein(MRAP) gene in the patient was found. His parents were found to be heterozygous carrier for the same mutation, without any clinical manifestation.

Objective:To explore the clinical and genetic characteristics of a Chinese baby with perinatal hypophosphatasia (HPP) and his parents for better understanding of the disease.Methods:The clinical data of the patient with HPP was carefully collected. The laboratory and radiographic examination data were taken for this baby patient. Sequencing for all the twelve tissue-nonspecific alkaline phosphatase(ALPL) exons and the flanking exon-intron junctions were performed in the proband and his parents with their genomic DNA from peripheral blood.Results:The blood level of alkaline phosphatase was decreased in this patient while serum calcium level was increased. His bone revealed chondrodysplasia-like change. Compound heterozygous mutations were found in the proband, with c. 346G>A(p.A116T) in exon 5 and c. 1171C>T(p.R391C) in exon 10. His father and mother were without clinical manifestation while respectively carried c. 346G>A(p.A116T and c. 1171C>T(p.R391C) missense mutations, suggesting an autosomal recessive inheritance in this family.Conclusion:Perinatal HPP has a high mortality rate. Skeletal deformities, hypercalcemia, and low level of ALP are important in the differential diagnosis of perinatal HPP.

The outbreak of COVID-19 has spread quickly across 114 countries/territories/areas in six continents worldwide and has been announced as a pandemic by WHO. This study analyzed global COVID-19 epidemiological trends, examined impact of the pandemic on global health security, diplomacy, and social environment in China, and provided short- and long-term strategic policy recommendations for China’s subsequent preparedness and responses.

OBJECTIVE: To detect potential variant in a male neonate affected with congenital nephrogenic diabetes insipidus (CNDI). METHODS: Clinical data of the patient was collected. Genomic DNA was extracted from peripheral blood samples from the child and his parents. The whole coding regions of the arginine vasopressin V2 receptor (AVPR2) gene were amplified by PCR and subjected to Sanger sequencing. RESULTS: The patient presented recurrent fever and polyuria after birth. Multiple blood gas analyses indicated hypernatremia. Ultrasound showed bilateral hydronephrosis and hydroureter. The patient was partially responsive to hydrochlorothiazide. DNA analysis identified a hemizygous frameshift variant c.890-899delACCCGGAGGC in exon 2 of the AVPR2 gene in the proband. His mother was heterozygous for the same variant. CONCLUSION The c.890-899delACCCGGAGGC variant of the AVPR2 gene probably underlies the CNDI in the child. Above discovery has enriched to spectrum of CNDI associated variants.
Adult ; Diabetes Insipidus, Nephrogenic/genetics* ; Exons ; Female ; Frameshift Mutation ; Humans ; Hydrochlorothiazide/therapeutic use* ; Infant, Newborn ; Male ; Pedigree ; Receptors, Vasopressin/genetics*

Public Health Emergency Operation Center (PHEOC) was conceptualized and established for coordinating information and resources towards goal-oriented response in large scale public health emergency. Yet, the activities undertaken by PHEOCs and their intended goals have not been fully optimized in current scenario. This paper revisited the collective efforts invested in PHEOC conceptualization and development, identified the opportunities and challenges in compliance with standards and framework, demonstrated the accountability of PHEOC network, thereby promoted best practice guidance for global public health emergency preparedness and response. This review will help navigate emergency response complexities leveraging PHEOC partnerships and advance the ability to detect and respond to public health emergencies in low resource settings. The review shows that the information on how to adapt best practice guidance to local circumstances could incentivize the full implementation of prevention, early detection and response to outbreaks. Identifying and correcting deficiencies in effectiveness evaluation will provide the basis for continuous PHEOC improvement. With the gradually reopening economies and public services in some countries, there is an urgent need to emphasize and validate the collective efforts undertaken by PHEOCs for tackling the COVID-19 pandemic.

RING finger protein 152 (RNF152) is a novel RING finger protein and has not been well characterized. We report here that RNF152 is a canonical RING finger protein and has E3 ligase activity. It is polyubiqitinated partly through Lys-48-linked ubiquitin chains in vivo and this phenomenon is dependent on its RING finger domain and transmembrane domain. RNF152 is localized in lysosomes and co-localized with LAMP3, a lysosome marker. Moreover, over-expression of RNF152 in Hela cells induces apoptosis. These results suggest that RNF152 is a lysosome localized E3 ligase with pro-apoptotic activities. It is the first E3 ligase identified so far that is involved in lysosome-related apoptosis.
Amino Acid Sequence ; Apoptosis ; HeLa Cells ; Humans ; Lysosomes ; metabolism ; Molecular Sequence Data ; Phylogeny ; Proteasome Endopeptidase Complex ; metabolism ; RING Finger Domains ; Sequence Alignment ; Ubiquitin-Protein Ligases ; metabolism ; Ubiquitination