Objective: To investigate the late identification and its influencing factors of newly reported HIV/AIDS cases in Linhai City, Zhejiang Province from 2015 to 2024, so as to provide a basis for formulating targeted AIDS prevention and control strategies. Methods: Data on newly reported HIV/AIDS cases in Linhai City from 2015 to 2024, including demographic characteristics and detection modes, were collected through the HIV/AIDS Comprehensive Control System of the Chinese Disease Prevention and Control Information System. The new identification rate and late identification proportion of HIV/AIDS cases were analyzed. The average annual percent change (AAPC) was used to assess trends in both the new identification rate and late identification proportion from 2015 to 2024. Multivariable logistic regression model was used to analyze the influencing factors for late identification among HIV/AIDS cases. Results: A total of 589 newly reported HIV/AIDS cases were documented in Linhai City from 2015 to 2024. The new identification rate declined from 5.08/105 in 2015 to 3.53/105 in 2024 (AAPC=-6.161%, P<0.05). Among them, 225 cases were late identified. After excluding 4 cases with inferred late identification, the late identification proportion increased from 24.53% in 2015 to 58.97% in 2024 (AAPC=7.595%, P<0.05). Multivariable logistic regression analysis indicated that age ≥25 years (25~<50 years, OR=3.569, 95%CI: 1.567-8.130; ≥50 years, OR=8.683, 95%CI: 3.440-21.917) and passive detection (OR=1.730, 95%CI: 1.022-2.928) were associated with a higher risk of late identification. In contrast, being married or having a spouse (OR=0.565, 95%CI: 0.332-0.960) was associated with a lower risk of late identification. Conclusions The new identification rate of HIV/AIDS cases in Linhai City from 2015 to 2024 showed a downward trend, while the proportion of late identification exhibited an upward trend. Age, marital status, and detection mode were identified as influencing factors for late identification among HIV/AIDS cases.

Acute-on-chronic liver failure (ACLF) is an acute deterioration of liver function occurring on the basis of chronic liver disease, accompanied by failure of the liver and extrahepatic organs, and is associated with a high short-term mortality rate. Liver transplantation is the only curative treatment for patients with ACLF. However, the shortage of donor livers and limitations of the organ allocation system mean that only a minority of patients can receive transplants. The current organ allocation system based on the model for end-stage liver disease (MELD) score may underestimate the urgency of liver transplantation for ACLF patients. Therefore, it is urgent to develop better assessment tools to determine which ACLF patients are most likely to benefit from liver transplantation. This article reviews the current mainstream definitions of ACLF, the selection of candidates for liver transplantation in ACLF, and the prognostic scoring systems for liver transplantation in ACLF, both domestically and internationally, in order to provide a reference for the prognostic assessment of liver transplantation in ACLF patients.

OBJECTIVE To optimize the prescription pre-review system in our hospital and evaluate its application effects. METHODS Aiming at the problems of imperfect rule base and high false positive rate in the early operation of the system， optimization measures were taken， including improving the content of the rule base， adjusting the interception level and prompt mode， refining the working model of prescription review pharmacists， and strengthening clinical communication. A retrospective cohort study was conducted， with prescription data from June to December 2023 （before optimization） as the control group and June to December 2024 （after optimization） as the observation group. Through inter group comparative analysis， the actual effect of optimizing the prescription pre-approval system was evaluated. RESULTS The prescription qualified rate increased from （82.51± 4.04）% before optimization to （90.98±1.55）% after optimization； the false positive rate decreased from （20.87±1.64）% before optimization to （7.41±2.04）% after optimization. The monthly range of prescription qualified rate narrowed from 10.24% to 4.11%， and the coefficient of variation decreased from 4.92% to 1.73%. The monthly range of false positive rate slightly increased from 4.40% to 5.34%， the coefficient of variation rose from 8.32% to 26.18%. CONCLUSIONS Through multi-dimensional optimizations of the prescription pre-review system in our hospital， its prescription review efficiency has been significantly enhanced， the quality of prescriptions has steadily improved， and the accuracy of reviews has notably improved.

Objective: To investigate the value of the Chinese visceral adiposity index (CVAI) in predicting hypertension risk, so as to provide a tool for the early assessment of hypertension risk. Methods: Health examination individuals aged ≥18 years were selected from four medical institutes in Jinhua City, Zhejiang Province in 2022. Data on basic information, lifestyle, disease history, body mass index, waist circumference, blood pressure, and blood biochemical indicators were collected through questionnaire surveys and physical examinations. CVAI was calculated to assess levels of visceral fat accumulation, divided by quartiles into Q1, Q2, Q3, and Q4 groups. The relationship between CVAI and hypertension was analyzed using a multivariable logistic regression model, and their dose-response relationship was examined using a restricted cubic spline model. The value of CVAI in predicting hypertension risk was evaluated using receiver operating characteristic (ROC) curve. Results: A total of 23 791 individuals were enrolled, with a median age of 68.00 (interquartile range, 14.00) years. Among them, 10 178 (42.78%) were males and 13 613 (57.22%) were females. The median CVAI was 111.40 (interquartile range, 48.23). Hypertension was identified in 15 563 cases, with a prevalence of 65.42%. After adjusting for lifestyle, disease history, and blood biochemical indicators, the multivariable logistic regression analysis revealed that hypertension risk in the CVAI Q2, Q3, and Q4 groups were 2.012 (95%CI: 1.865-2.170), 3.059 (95%CI: 2.826-3.311), and 5.099 (95%CI: 4.672-5.565) times that of the Q1 group, respectively. The restricted cubic spline model revealed a non-linear relationship between CVAI and hypertension risk (Pnon linearity<0.05). Hypertension risk increased more rapidly when the CVAI was ≥81.03. The area under the ROC curve for CVAI in predicting hypertension risk was 0.691, with an optimal cutoff value of 106.01, which falls within the Q2 group. Conclusions There was a nonlinear dose-response relationship between CVAI and hypertension. CVAI can predict the risk of hypertension, and 106.01 can serve as an early warning threshold for risk screening.

Objective To construct nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3)knockout mice in order to investigate the effects of NLRP3 knockout on radiation-induced acute pneumonitis and pulmonary fibrosis.Methods Nlrp3+/+and Nlrp3-/-mice were randomly divided into the control group and irradiation group.To induce radiation-caused acute pneumonitis,the control group was exposed to sham irradiation while the irradiation group was exposed to 60Co γ-rays at a dose of 22 Gy at a dose rate of 184.30 R/min.At 14 days post-irradiation,the body weight of each mouse and the wet weight of its lung tissue were measured separately using an analytical balance to calculate the lung coefficient.Quantitative real-time PCR(qPCR)and cytometric bead array(CBA)were used to detect inflammatory responses in lung tissues and serum.Hematoxylin-eosin(HE)staining and F4/80 immunohistochemical staining were used to assess pathological changes and inflammatory cell infiltration in lung tissues.Cysteinyl aspartate specific proteinase-1(caspase-1)activation was analyzed by Western blotting.To establish a model of radiation-induced pulmonary fibrosis,mice were irradiated with 60Co γ-rays at a dose of 18 Gy at a dose rate of 174.67 R/min.At 24 weeks post-irradiation,HE staining and Masson staining were performed to evaluate pulmonary fibrosis.Results NLRP3 knockout inhibited caspase-1 activation,reduced inflammatory responses in lung tissues and serum,suppressed macrophage infiltration,alleviated pulmonary edema,and thereby protected against acute radiation-induced lung injury.Additionally,NLRP3 knockout significantly ameliorated late-stage radiation-induced pulmonary fibrosis.Conclusion NLRP3 knockout can mitigate both early radiation-induced pneumonia and lateradiation-induced pulmonary fibrosis.

Objective To explore the role of dapansutrile(OLT1177)in radiation-induced intestinal injury and the mechanism.Methods C57BL/6J mice were locally irradiated in the abdomen with 60Co to induce a model of radiation-induced intestinal injury.OLT1177 was intraperitoneally injected at a dose of 100 mg/kg 2 hours before irradiation and 6 hours after irradiation before the drug was administered once a day.At 12 hours after irradiation,intestinal tissues were taken for terminal deoxynucleotidyl transferase mediated nick end labeling(TUNEL)staining to detect apoptosis in intestinal tissues.At 4 days after irradiation,mouse serum was collected to detect the levels of inflammatory factors in the serum.Hematoxylin-eosin(HE)stainingwas used for the evaluation of the damage to the intestinal villus structure.Immunohistochemical staining was adopted to detect the changes in crypt proliferation in intestinal tissues.Finally,proteins were isolated from intestinal tissues,and Western blotting was employed to evaluate the activation of nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3)inflammasome.Results After irradiation,the intestinal villi in mice were shortened.Meanwhile,there was a notable declinein the number of cells that were proliferating in the crypts,a surge in the number of apoptotic cells,and a significant spike in the overall inflammatory level.However,administration of OLT1177 inhibited the activation of the NLRP3 inflammasome,reduced apoptosis and pyroptosis,decreased the inflammatory level,and thus improved radiation-induced intestinal injury.Conclusion Administration of OLT1177 can significantly mitigate radiation-induced intestinal injury.

Objective To investigate the role of Rho/ROCK signaling pathway in mediating restraint stress-induced blood-brain barrier(BBB)injury in the amygdala of rats.Methods Sixty male SD rats were randomized equally into control group(with food and water deprivation for 6 h per day),restraint stress group(with restraint for 6 h per day),stress + fasudil treatment(administered by intraperitoneal injection at 1 mg/100 g 30 min before the 6-h restraint)group,and fasudil treatment alone group.The elevated plus-maze test was used to detect behavioral changes of the rats,serum corticosterone and S100B levels were determined with ELISA,and Evans Blue leakage in the brain tissue was examined to evaluate the changes in BBB permeability.The changes in expression levels of tight junction proteins in the amygdala were detected using immunofluorescence assay and Western blotting,and Rho/ROCK pathway activation was detected by Pull-down test and Western blotting.Ultrastructural changes of the cerebral microvascular endothelial cells were observed using transmission electron microscopy.Results Compared with those in the control group,the rats in restrain stress group and stress+fasudil group showed obvious anxiety-like behavior with significantly increased serum corticosterone level(P<0.001).Compared with those in the control group and stress+fasudil group,the rat models of restrain stress showed more obvious Evans Blue leakage and higher S100B expression(P<0.01)but lower expressions of tight junction proteins in the amygdala.Pull-down test and Western blotting confirmed that the expression levels of RhoA-GTP,ROCK2 and P-MLC 2 were significantly higher in stress group than in the control group and stress + fasudil group(P<0.05).Transmission electron microscopy revealed obvious ultrastructural changes in the cerebral microvascular endothelial cells in the rat models of restrain stress.Conclusion Restraint stress induces BBB injury in the amygdala of rats by activating the Rho/ROCK signaling pathway.

Objective To investigate the role of Rho/ROCK signaling pathway in mediating restraint stress-induced blood-brain barrier(BBB)injury in the amygdala of rats.Methods Sixty male SD rats were randomized equally into control group(with food and water deprivation for 6 h per day),restraint stress group(with restraint for 6 h per day),stress + fasudil treatment(administered by intraperitoneal injection at 1 mg/100 g 30 min before the 6-h restraint)group,and fasudil treatment alone group.The elevated plus-maze test was used to detect behavioral changes of the rats,serum corticosterone and S100B levels were determined with ELISA,and Evans Blue leakage in the brain tissue was examined to evaluate the changes in BBB permeability.The changes in expression levels of tight junction proteins in the amygdala were detected using immunofluorescence assay and Western blotting,and Rho/ROCK pathway activation was detected by Pull-down test and Western blotting.Ultrastructural changes of the cerebral microvascular endothelial cells were observed using transmission electron microscopy.Results Compared with those in the control group,the rats in restrain stress group and stress+fasudil group showed obvious anxiety-like behavior with significantly increased serum corticosterone level(P<0.001).Compared with those in the control group and stress+fasudil group,the rat models of restrain stress showed more obvious Evans Blue leakage and higher S100B expression(P<0.01)but lower expressions of tight junction proteins in the amygdala.Pull-down test and Western blotting confirmed that the expression levels of RhoA-GTP,ROCK2 and P-MLC 2 were significantly higher in stress group than in the control group and stress + fasudil group(P<0.05).Transmission electron microscopy revealed obvious ultrastructural changes in the cerebral microvascular endothelial cells in the rat models of restrain stress.Conclusion Restraint stress induces BBB injury in the amygdala of rats by activating the Rho/ROCK signaling pathway.

Objective To investigate the therapeutic effect and mechanism of NLRP3 inflammasome inhibitor-dapansutrile(OLT1177)-against acute radiation lung injury.Methods Mice were divided into the control group,OLT1177 injection group,irradiation group,and irradiation+OLT1177 injection group.A single dose of 22 Gy whole-lung 60Co radiation was used to establish a model of acute radiation lung injury.After 6 h of radiation,OLT1177(100mg/kg,once daily)was administered intraperitoneally.After 14 consecutive days of administration,lung tissues were collected and weighed while the lung coefficient was calculated.Hematoxylin-eosin(HE)staining and F4/80 immuno-histochemical staining were used to observe the pathological changes and inflammatory cell infiltration in lung tissues.Real-time quantitative PCR(qPCR)was used to detect the transcription levels of NLRP3,IL-1β,and other mRNAs in lung tissues.Serum cytokines such as TNF-α and IL-6 were measured by cytometric bead array(CBA).The activation of Caspase-1 and IL-18 was detected by Western blotting.Results Radiation caused acute inflammation in the lung tissues of mice,manifested as edema in the lung tissues and destruction of the alveolar structure,increased macrophage infiltration,and elevated expressions of inflammatory genes NLRP3,IL-1β,TNF-α,and IL-6 in the lung tissues and higher serum levels of TNF-α,IL-6.Treatment with OLT1177 significantly improved the above symptoms induced by radiation.OLT1177 inhibited the activation of NLRP3 inflammasome downstream Caspase-1 and IL-18 induced by radiation.Conclusion OLT1177 can significantly alleviate acute radiation lung injury in mice,which may be due to its inhibition of NLRP3 inflammasome activation induced by radiation.