Objective To analyze the characteristics of viral hepatitis mortality and life loss among residents in Pudong New Area from 2003 to 2023, and to provide a basis for related prevention and control work. Methods Viral hepatitis mortality data were obtained from the Pudong New Area mortality monitoring system. The crude mortality rate (CMR), standardized mortality rate (SMR), potential years of life lost (PYLL), average years of life lost (AYLL), and standardized potential years of life lost (SPYLL) were calculated to analyze viral hepatitis deaths. The average annual change (AAPC) and annual percentage change (APC) of the mortality rate were calculated by Joinpoint regression analysis to analyze the trend of mortality. Results The CMR and SMR of viral hepatitis among residents in Pudong New Area from 2003 to 2023 were 3.89/100000 and 1.98/100000, respectively. Both CMR and SMR of viral hepatitis showed a decreasing trend over time (CMR:APC=-5.476, t=-13.581, P<0.001; SMR:APC=- 7.624, t= -21.253, P<0.001). The CMR for males was 4.75/100000 and the SMR for males was 2.65/100000; the CMR for females was 3.04/100000 and the SMR for females was 1.32/100000, with a higher mortality rate for males than for females（Z_CME=12.094，P<0.001; Z_SMR=-14.718，P<0.001). Deaths were concentrated in the age groups of 45-64 years old and 65 years old and above, accounting for 91.62% of the total deaths. The PYLL of deaths due to viral hepatitis among residents in Pudong New Area from 2003 to 2023 was 26912 person-years, with a PYLLR of 0.45% and an AYLL of 8.88 years per person. Conclusion The mortality rate of viral hepatitis among the residents of Pudong New Area in 2003-2023 shows a decreasing trend over time. The mortality rate of males is higher than that of females, and the deaths of middle-aged and elderly people account for a large proportion of the total deaths. Chronic hepatitis B is the main cause of death.

Antimicrobial resistance (AMR) poses a critical global health threat. This review systematically examines AMR surveillance technology advances, from conventional culture methods to modern molecular diagnostics (e.g., whole-genome sequencing) and artificial intelligence-assisted approaches. It focuses on the current application of mass spectrometry, machine learning predictive models, and real-time surveillance networks. To address challenges including inadequate technical standardization, clinical translation barriers, and data-sharing limitations, we propose integrated ^"genotype-phenotype^" strategies and global standardization framework, while exploring future applications of CRISPR-based portable detection, single-cell sequencing, and blockchain technologies.

ObjectiveTo investigate the urate-lowering effect of Shenling Qushi prescription in the mouse model of hyperuricaemia. MethodsSixty-three C57BL/6N mice were randomly assigned to the following groups （n=9）： Control， model， low-dose （6 g·kg^-1） Shenling Qushi prescription， medium-dose （12 g·kg^-1） Shenling Qushi prescription， high-dose （24 g·kg^-1） Shenling Qushi prescription， medium-dose Shenling Qushi prescription plus febuxostat （12+0.003 g·kg^-1）， and febuxostat （3 mg·kg^-1）. A mouse model of persistent hyperuricaemia was established via intraperitoneal injection of potassium oxazolamide （250 mg·kg^-1） combined with oral administration of allopurinol （300 mg·kg^-1） over a 28-day period. Concurrently， the prescription was administered orally at the specified doses once daily for 21 consecutive days. Throughout the experiment， mouse body weight， food intake， water consumption， and urine output were measured and recorded. Kidney and liver indices were calculated. Renal histopathological changes were observed by haematoxylin and eosin staining. Serum uric acid （SUA） and urinary uric acid （UUA） levels， along with xanthine oxidase （XOD） and adenosine deaminase （ADA）， alanine aminotransferase （ALT） and aspartate aminotransferase （AST） activities， were determined. Real-time PCR was employed to assess the mRNA levels of urate anion transporter 1 （URAT1） and glucose transporter 9 （GLUT9） in the renal tissue， alongside those of XOD and ADA in the liver tissue. The protein levels of URAT1 and GLUT9 in the renal tissue were determined by Western blot. ResultsCompared with the normal group， model mice exhibited reduced food intake and body weight （P<0.01）， decreased water consumption yet increased urine output， no significant change in the liver index but increased kidney index （P<0.01）. Pathological findings revealed renal tissue damage including glomerular atrophy， epithelial cell detachment， and inflammatory cell infiltration. Furthermore， the model group exhibited elevated UUA and SUA levels （P<0.01）， enhanced activities of ALT， AST， XOD， and ADA in the liver tissue （P<0.05， P<0.01）， upregulated mRNA and protein levels of URAT1 and GLUT9 in the renal tissue （P<0.05）， alongside markedly elevated mRNA levels of XOD and ADA in the liver （P<0.01）. Compared with the model group， the Shenling Qushi prescription groups showed no significant changes in body weight or food intake， with water consumption and urine output remaining within normal ranges， alleviated glomerular atrophy， with reduced pathological damage such as inflammatory infiltration， declined UUA and SUA levels （P<0.01）， and increased activities of ALT， AST， XOD， and ADA in the serum （P<0.01）. Real-time PCR results demonstrated that Shenling Qushi prescription downregulated the mRNA levels of URAT1 and GLUT9 in the renal tissue （P<0.05， P<0.01） and XOD and ADA in the hepatic tissue （P<0.05， P<0.01）. Western blot results demonstrated Shenling Qushi prescription reduced the protein levels of URAT1 and GLUT9 （P<0.05， P<0.01）. ConclusionShenling Qushi prescription modulates fluid balance and reduces uric acid levels， thereby alleviating renal injury in hyperuricaemic mice. This effect is highly likely mediated through inhibition of uric acid synthesis and reabsorption.

Background The crude mortality rate of sudden death has shown a steady upward trend. Pudong New Area, Shanghai, is a highly urbanized and densely populated district that is substantially affected by the urban heat island effect and has experienced frequent extreme temperature events in recent years. However, evidence on the association between ambient temperatures and sudden death among local residents remains limited. Objective To examine the association between daily mean temperature and sudden death in Pudong New Area, and to provide evidence for reducing temperature-related risks of sudden death. Methods Data on sudden death, meteorological factors (daily average temperature, daily average relative humidity, and daily average air pressure), and air pollutants [inhalable particulate matter (PM₁₀), sulfur dioxide (SO₂), and nitrogen dioxide (NO₂)] in Pudong New Area from 2016 to 2021 were collected. A distributed lag non-linear model was used to examine the associations of daily mean temperature with total sudden death and sudden death due to cardiovascular and cerebrovascular diseases, including lagged and cumulative effects (lag0, 0-3, 0-7, 0-14, and 0-21 d). Stratified analyses were performed by sex, age, and education level to identify vulnerable populations. The temperature attributable burden of sudden death was assessed by calculating attributable number (AN) and attribute fraction (AF). Results A total of 19458 sudden deaths were reported in Pudong New Area from 2016 to 2021, of which 11082 (56.95%) were due to cardiovascular and cerebrovascular diseases. Both low (P₅, 4.6 ℃) and high (P₉₅, 30.2 ℃) temperatures were associated with increased risks of sudden death. The cumulative risks associated with low temperature peaked at lag 0-21 d for both total sudden death and sudden death due to cardiovascular and cerebrovascular diseases. In contrast, the cumulative risks associated with high temperature peaked at lag 0-7 d for total sudden death and at lag 0-3 d for sudden death due to cardiovascular and cerebrovascular diseases. Stratified analyses showed that females, individuals aged ≥65 years, and those with primary school education or below were more sensitive to low temperature; whereas females, individuals aged <65 years, and those with secondary school education or above were more sensitive to high temperature. Using 21.5 ℃ as the minimum mortality temperature, the AN of total sudden deaths attributable to non-optimal temperature was 3791 (95%CI: 1853, 5587), with an AF of 20.41% (95%CI: 9.47%, 28.94%); the AN attributable to low temperature was 3358 (95%CI: 1087, 5062), with an AF of 17.26% (95%CI: 5.89%, 26.01%), whereas the AN attributable to high temperature was 225 (95%CI: −274, 655), with an AF of 2.03% (95%CI: −2.53%, 5.78%). For sudden deaths due to cardiovascular and cerebrovascular diseases, the AN attributable to non-optimal temperature was 2721 (95%CI: 1747, 5575), with an AF of 24.55% (95%CI: 9.59%, 28.65%); the AN attributable to low temperature was 2496 (95%CI: 988, 3562), with an AF of 22.53% (95%CI: 8.97%, 32.41%), whereas the AN attributable to high temperature was 614 (95%CI: −15, 1176), with an AF of 3.15% (95%CI: −0.08%, 6.02%). Conclusions Both low (P₅, 4.6 ℃) and high (P₉₅, 30.2 ℃) temperatures are associated with increased risks of sudden death in Pudong New Area, Shanghai. High temperature shows a relative short-term effect, whereas low temperature shows a stronger cumulative effect. Females, people ≥65 years, and individuals with primary school educational attainment or below are more vulnerable to low temperature, while females, people <65 years, and those with secondary school educational attainment or above are more vulnerable to high temperature. The attributable burden of low temperature is greater than that of high temperature. Targeted health protection measures should be strengthened for vulnerable populations during extreme temperature events.

Increasing evidence shows that the early lesions of Parkinson's disease (PD) originate from gut, and correction of microbiota dysbiosis is a promising therapy for PD. FLZ is a neuroprotective agent on PD, which has been validated capable of alleviating microbiota dysbiosis in PD mice. However, the detailed mechanisms still need elucidated. Through metabolomics and 16S rRNA analysis, we identified glycoursodeoxycholic acid (GUDCA) was the most affected differential microbial metabolite by FLZ treatment, which was specially and negatively regulated by Clostridium innocuum, a differential microbiota with the strongest correlation to GUDCA production, through inhibiting bile salt hydrolase (BSH) enzyme. The protection of GUDCA on colon and brain were also clarified in PD models, showing that it could activate Nrf2 pathway, further validating that FLZ protected dopaminergic neurons through promoting GUDCA production. Our study uncovered that FLZ improved PD through microbiota-gut-brain axis, and also gave insights into modulation of microbial metabolites may serve as an important strategy for treating PD.

Although enteric glial cell (EGC) abnormal activation is reported to be involved in the pathogenesis of Parkinson's disease (PD), and inhibition of EGC gliosis alleviated gut and dopaminergic neuronal dysfunction was verified in our previous study, the potential role of gut microbiota on EGC function in PD still need to be addressed. In the present study, fecal microbiota transplantation revealed that EGC function was regulated by gut microbiota. By employing 16S rRNA and metabolomic analysis, we identified that 3-indolepropionic acid (IPA) was the most affected differential microbial metabolite that regulated EGC gliosis. The protective effects of IPA on PD were validated in rotenone-stimulated EGCs and rotenone (30 mg/kg i.g. for 4 weeks)-induced PD mice, as indicated by decreased inflammation, improved intestinal and brain barrier as well as dopaminergic neuronal function. Mechanistic study showed that IPA targeted pregnane X receptor (PXR) in EGCs, and inhibition of IL-13Rα1 involved cytokine-cytokine receptor interaction pathway, leading to inactivation of downstream JAK1-STAT6 pathway. Our data not only provided evidence that EGC gliosis was critical in spreading intestinal damage to brain, but also highlighted the potential role of microbial metabolite IPA in alleviating PD pathological damages through gut-brain axis.

[Purpose]To analyze the trends in pancreatic cancer mortality and disease burden among residents in Shanghai Pudong New Area from 2002 to 2022,and to investigate the effects of age,period,and birth cohort on mortality risk.[Methods]Data on pancreatic cancer deaths among residents of Pudong New Area from 2002 to 2022 were collected through the Shanghai Population Cause of Death Registration System.The crude mortality rate,age-standardized mortality rate by Chinese standard population(ASMRC),potential years of life lost(PYLL),potential years of life lost rate(PYLLR),and average years of life lost(AYLL)were calculated.Joinpoint regression was applied to calculate the average annual percentage change(AAPC)for analyzing the changing trend of the mortality rate of pancreatic cancer.The age-period-cohort model was applied with R 4.4.1 to analyze the age,period,and cohort effects on the mortality risk of pancreatic cancer.[Results]The crude mortality rate of pancreatic cancer among residents in Pudong New Area increased from 10.42/105 in 2002 to 18.73/105 in 2022,showing a significant upward trend(AAPC=2.90％,P＜0.001);the ASMRC was generally stable(AAPC=-0.05％,P=0.775).The crude mortality rate of males(17.09/105)was higher than that of females(13.75/105),and both showed an upward trend(AAPC=3.05％and 2.75％respectively,both P＜0.001).After the age of 40,the mortality rate of pancreatic cancer increased significantly with the growth of age in both sexes.The PYLL was 31 347 person-years,showing an upward trend(AAPC=1.83％,P＜0.001),and the AYLL was 3.59 years,showing a downward trend(AAPC=-2.45％,P＜0.001).The age effect showed that the mortality risk of pan-creatic cancer was increased with age;the period effect showed that the mortality risk decreased from 2002 to 2016 and then increased;the cohort effect showed that the mortality risk increased with the advancement of the birth cohort.[Conclusion]From 2002 to 2022,the crude mortality rate of pancreatic cancer in Pudong New Area showed an upward trend,and the mortality rate of males was higher than that of females.The mortality risk of pancreatic cancer increases with age,and the later the birth year of the residents,the higher the mortality risk.Early screening should be strengthened for men and the elderly,environmental and lifestyle risk factors should be paid attention to in combination with the characteristics of cohort effect,and the prevention and control strategy for the whole population should be optimized.

Spine fracture and dislocation are common traumatic spinal conditions that often require surgical intervention due to compromised spinal stability. Surgical approaches include anterior, posterior, and combined anterior-posterior spinal procedures. According to the specific surgical requirements, patients may be placed in the prone position or repositioned between prone and supine positions during surgery. Intraoperative repositioning has become an essential step in patient positioning. However, during repositioning, patients with spinal fracture and dislocation are at increased risk for complications such as hemodynamic instability, nerve injury, and pressure injuries to the skin and soft tissue. Notably, due to the instability of the spinal cord, even minor manipulations can further exacerbate the damage, potentially leading to severe outcomes like paraplegia. Although the current clinical guidelines provide instructive recommendations for standard position, there remains no specific protocols for intraoperative repositioning in patients with spine fracture and dislocation. With a concern for the lack of clinical studies on positioning techniques, risk prevention, and operational norms for special patients, no applicable guidelines or standards are available. A consensus was required to provide clinical reference, meet the requirements of surgical treatment, and minimize the safety risks of patients caused by improper placement of positions. Professional Committee of Operating Room Nursing of Shaanxi Nursing Association organized experts in nursing management and operating room nursing from major hospitals across China to formulate Expert consensus on intraoperative repositioning for patients with spinal fracture and dislocation ( version 2025). The consensus provides 11 recommendations covering pre-repositioning preparation, intraoperative maneuvers, and post-repositioning observation, aiming to provide references for clinical standardization of the intraoperative repositioning process and protection of patients′ safety.

ObjectiveTo investigate the alleviating effect of calcium cyanamide （CaCN₂） soil fumigation on replanting problems of Rehmannia glutinosa. MethodsNewly soil （NP） was used as the control group， while three treatment groups were established： replanted soil （RP）， newly soil treated with CaCN₂ （120 g·m²， tillage depth 25 cm） （NPCC）， and replanted soil treated with CaCN₂ （RPCC）. R. glutinosa was cultivated in all groups. At harvest， the tuber agronomic traits （number of enlarged roots， maximum root diameter， fresh weight， dry weight） were measured. The content of catalpol and rehmannioside D was quantified by ultra-high-performance liquid chromatography （UPLC） to evaluate medicinal quality. Rhizosphere soil available nutrients and enzyme activities were analyzed by assay kits. The community structure and composition of fungi and bacteria in rhizosphere soil were assessed via internal transcribed spacer 2 （ITS2） sequencing and 16S rDNA sequencing， respectively. ResultsCompared with NP， the RP group showed obviously reduced in tuber agronomic traits and quality indicators （P0.05）. However， the RPCC group showed significant improvement in agronomic traits and a notable increase in rehmannioside D content compared to RP （P0.05）. The contents of available phosphorus and potassium in RPCC and NP groups were obviously lower than those in RP （P0.05）. The polyphenol oxidase soil （S-PPO） activity in RP was obviously lower than in NP （P0.05）， while sucrose soil （S-SC）， acid phosphatase soil （S-ACP）， and S-PPO activities in RPCC were obviously higher than in RP （P0.05）. Microbial richness and diversity in RP were obviously higher than in NP （P0.05）， whereas no significant differences were observed between the RPCC and NP. The relative abundances of fungal genera Nectria， Myrothecium， Tomentella， and bacterial genus Skermanella were obviousl lower in RPCC and NP than in RP （P0.05）. Correlation analysis that S-ACP activity was positively correlated with the content of rehmannioside D （P0.05）. Fungal genera Engyodontium and Alternaria， and bacterial genera Pir4 lineage， Pirellula， Methyloversatilis， Brevundimonas， Ralstonia， and Acidibacter were obviously positively correlated with tuber dry weight （P0.05）. Conversely， fungal genera Pseudaleuria， Nectria， Haematonectria， Ceratobasidium， and bacterial genera Streptomyces， Skermanella， RB41， Gemmatimonas， and Bacillus were obviously negatively correlated with dry weight （P0.05）. The fungal genus Alternaria and bacterial genera Brevundimonas， Ralstonia， Acidibacter， and Dongia showed positive correlations with medicinal quality of R.glutinosa tuber， while fungal genera Pseudaleuria， Nectria， Stachybotrys， Fusarium， Gibberella， Ceratobasidium， and bacterial genera Sphingomonas， Skermanella， RB41， Gemmatimonas， and Bacillus were obviously negatively correlated （P0.05）. ConclusionCaCN₂ soil fumigation can significantly improve enzyme activities in replanted Rehmannia rhizosphere soil， enhance the utilization of available nutrients， reshape microbial community structure of replanted R.glutinosa at the family and genus level， and notably improve tuber agronomic traits and medicinal quality. This study provides a novel approach to alleviating replanting problems and offers insights for the integrated development of standardized cultivation techniques， including soil disinfection， nutrient-targeted regulation， and microbial inoculant application.

Objective : To explore whether chrysophanol(CHR) affects macrophage polarization by promoting mitochondrial biosynthesis through AMPK/PGC-1α pathway. Methods : The molecular docking and binding ability of CHR with AMPK and PGC-1α were predicted by Autodock vina software. Human monocytes(THP-1) were induced to M0 macrophages by phorbol myristate acetate(PMA), and to M1 macrophages by lipopolysaccharide(LPS) combined with interferon-γ(IFN-γ), which were set as Control group. M1 macrophages treated with CHR were set as CHR group. M1 macrophages treated with CHR combined with AMPK inhibitor(Compound C) were set as CHR+Compound C group. The mRNA expression levels of M1 macrophage markers(iNOS, CD86) and mitochondrial biosynthesis related genes(PGC-1α, NFR-1, TFAM) were detected by Quantitative real time polymerase chain reaction(qRT-PCR). The expression level of M1 macrophage marker iNOS was detected by immunofluorescence. The protein expression levels of AMPK, p-AMPK and PGC-1α were detected by Western blot. Results : The docking results showed that the binding energies of CHR with AMPK and PGC-1α were-8.4 kcal/mol and-7.4 kcal/mol, respectively. qRT-PCR results showed that the in vitro model of M1 macrophages was successfully established. Compared with the Control group, CHR treatment significantly increased the mRNA expression of mitochondrial biosynthesis-related genes PGC-1α, NFR-1, and TFAM(P<0.001). Compared with CHR treatment group, CHR combined with Compound C treatment significantly decreased the mRNA expression levels of mitochondrial biosynthesis-related genes PGC-1α, NFR-1, and TFAM(P<0.05). Immunofluorescence results showed that CHR treatment inhibited the protein expression of iNOS compared with the Control group(P<0.001). Compared with CHR treatment group,CHR combined with Compound C treatment reversed the inhibitory effect of CHR on i NOS protein expression(P<0.05). Western blot results showed that compared with the Control group,the CHR treatment group had significant increase in the protein expression levels of p-AMPK and PGC-1α(P<0.001).Compared with CHR treatment group,CHR combined with Compound C treatment significantly decreased the protein expression levels of p-AMPK and PGC-1α(P<0.05). Conclusion Chrysophanol may inhibit macrophage polarization to M1 by activating AMPK/PGC-1α signaling pathway to promote mitochondrial biosynthesis.