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.

Chemotherapy-induced peripheral neurotoxicity (CIPN) is a severe dose-limiting adverse event of chemotherapy. Presently, the mechanism underlying the induction of CIPN remains unclear, and no effective treatment is available. In this study, through metabolomics analyses, we found that nab-paclitaxel therapy markedly increased serum serotonin [5-hydroxtryptamine (5-HT)] levels in both cancer patients and mice compared to the respective controls. Furthermore, nab-paclitaxel-treated enterochromaffin (EC) cells showed increased 5-HT synthesis, and serotonin-treated Schwann cells showed damage, as indicated by the activation of CREB3L3/MMP3/FAS signaling. Venlafaxine, an inhibitor of serotonin and norepinephrine reuptake, was found to protect against nerve injury by suppressing the activation of CREB3L3/MMP3/FAS signaling in Schwann cells. Remarkably, venlafaxine was found to significantly alleviate nab-paclitaxel-induced CIPN in patients without affecting the clinical efficacy of chemotherapy. In summary, our study reveals that EC cell-derived 5-HT plays a critical role in nab-paclitaxel-related neurotoxic lesions, and venlafaxine co-administration represents a novel approach to treating chronic cumulative neurotoxicity commonly reported in nab-paclitaxel-based chemotherapy.
Paclitaxel/toxicity* ; Animals ; Albumins/adverse effects* ; Serotonin/metabolism* ; Mice ; Humans ; Male ; Female ; Venlafaxine Hydrochloride/therapeutic use* ; Neurotoxicity Syndromes/metabolism* ; Middle Aged ; Schwann Cells/metabolism* ; Peripheral Nervous System Diseases/drug therapy* ; Antineoplastic Agents

Objective:To compare the efficacy of low-dose febuxostat and low-dose benzbromarone in lowering serum uric acid and their impact on liver function in male patients with renal underexcretion gout.Methods:This prospective cohort study enrolled 303 patients with renal underexcretion gout and normal baseline liver function. Participants were assigned to either the low-dose febuxostat group(20 mg qd) or the low-dose benzbromarone group(25 mg qd). A linear mixed-effects model was used to compare the uric acid target achievement rate(<360 μmol/L) and changes in liver enzyme levels between the two groups.Results:At week 4, the proportion of patients achieving the serum uric acid target(<360 μmol/L) was significantly higher in the benzbromarone group than that in the febuxostat group(64.2% vs 42.3%, P<0.001), with a trend toward greater efficacy at weeks 8 and 12. The incidence of alanine aminotransferase(ALT) or aspartate aminotransferase(AST) elevation above the upper limit was significantly higher in the febuxostat group compared to the benzbromarone group(35.2% vs 13.85%, P<0.001). After adjusting for baseline liver enzyme levels in the mixed-effects model, mean ALT and AST levels remained significantly higher in the febuxostat group than those in the benzbromarone group at weeks 4, 8, and 12( P<0.05). In the febuxostat group, ALT and AST levels significantly increased over time during weeks 0-4 and 4-8 ( P<0.001), peaking at week 8 followed by a decreasing trend. By week 12, the levels were not significantly different from baseline ( P>0.05). Whereas there was no significant difference at each follow-up time point in the benzbromarone group( P>0.05). Conclusions:In male patients with renal underexcretion gout, low-dose benzbromarone demonstrated superior urate-lowering efficacy and better hepatic safety compared to low-dose febuxostat.

Multimodal biometric identification technology,which combines multiple biometric methods,is being increasingly used in forensic science due to its advantages such as difficulty of forgery and great accuracy.However,the current identification mainly relies on unimodal biometrics including facial recognition,hand recognition,iris recognition,gait recognition,and voice recognition.Thus,to a large extent,the accuracy of identification depends on the quality of the unimodal data,which faces multiple challenges.In contrast,multimodal biometrics has more obvious advantages in the field of identification,which can not only effectively resist attacks,but also enrich the feature representation with complementary information from multimodal sources,mitigate the impact of environment on the identification performance,and enhance the robustness of the system.To this end,this paper combs through the relevant work in this field,and comprehensively reviews the current research status and development trend of biometric identification technology.First,based on bibliometrics,the paper combs through the relevant research results in the past ten years,analyzes,summarizes,and discusses the commonly used deep learning models in this field,respectively,from unimodal recognition to multi-modal fusion recognition.Then the paper discusses the future development direction of the multimodal biometric identification field in the light of the practical needs of court science and provides reference for identification research.

Multimodal biometric identification technology,which combines multiple biometric methods,is being increasingly used in forensic science due to its advantages such as difficulty of forgery and great accuracy.However,the current identification mainly relies on unimodal biometrics including facial recognition,hand recognition,iris recognition,gait recognition,and voice recognition.Thus,to a large extent,the accuracy of identification depends on the quality of the unimodal data,which faces multiple challenges.In contrast,multimodal biometrics has more obvious advantages in the field of identification,which can not only effectively resist attacks,but also enrich the feature representation with complementary information from multimodal sources,mitigate the impact of environment on the identification performance,and enhance the robustness of the system.To this end,this paper combs through the relevant work in this field,and comprehensively reviews the current research status and development trend of biometric identification technology.First,based on bibliometrics,the paper combs through the relevant research results in the past ten years,analyzes,summarizes,and discusses the commonly used deep learning models in this field,respectively,from unimodal recognition to multi-modal fusion recognition.Then the paper discusses the future development direction of the multimodal biometric identification field in the light of the practical needs of court science and provides reference for identification research.

Avian infectious bronchitis(IB),a rapidly spreading and acute disease in chickens,is caused by the infectious bronchitis virus(IBV).IB is characterized by its remarkable genetic varia-bility.IBV has a high degree of mutation,and the existing means of immunization often fail to a-chieve good results,seriously affecting the development of the domestic poultry industry.This ar-ticle offers a comprehensive review of the current understanding of the immune response to IBV,focusing on three key areas:non-specific immunity,mucosal immunity,and specific immunity.By dissecting these aspects,the aim is to provide a theoretical reference for the study of the immune mechanism of IBV.

Objective To investigate the effects of electroacupuncture(EA)at"Baihui(GV 20),""Pishu(BL 20),"and"Zusanli(ST 36)"on the learning and memory functions of rats with Alzheimer's disease(AD)induced by Aβ1-42.Additionally,the mechanism of EA in treating AD was explored from the perspective of the inflammatory cascade mediated by the NF-κ B/NLRP3/Caspase-1 signaling pathway.Methods A rat model of Alzheimer's disease was established by bilateral injection of Aβ1-42 solution into the C1 region of the hippocampus.According to the random number table method,32 male SPF-grade rats were divided into four groups(n=8 per group):a sham-operated group,a model group,an electroacupuncture(EA)group,and a Western medicine group(donepezil hydrochloride).The EA group received electroacupuncture at the"Baihui","Pishu",and"Zusanli"acu-points;the Western medicine group received donepezil hydrochloride via gavage.After the treatment period,Morris water maze experiments were conducted to evaluate learning and memory abilities.Hematoxylin and eosin(HE)staining was used to examine morphological changes in hippocampal tissues.Enzyme-linked immunosorbent assay(ELISA)was employed to measure serum levels of TNF-α and IL-1β.Western blotting and immunofluorescence staining were utilized to assess the co-expression levels of NF-κB p65,NLRP3,and Caspase-1 proteins in the hippocampal region.Results Compared with the sham-operated group,rats in the post-modeling group exhibited significantly prolonged escape latency(P<0.05),reduced crossings of the original platform location,and decreased time spent in the target quadrant(P<0.05).Additionally,nuclear morphology was altered,neurons surrounding the hippocampus displayed necrosis,vacuolar degeneration,and chromatin marginalization.Serum levels of TNF-α and IL-1β were elevated(P<0.05),and protein expression levels as well as fluorescent positivity for NF-κB p65,NLRP3,and caspase-1 in the hippocampus were increased(P<0.05).Compared with the model group,rats in both the EA and Western medicine groups showed a trend toward shorter escape latency(P<0.05),increased crossings of the original platform location and time spent in the target quadrant(P<0.05).Cell structures were largely intact,with only a few nuclei showing slight irregularities and some chromatin accumulation at the edges.Serum levels of TNF-α and IL-1β were reduced(P<0.05),and protein expression levels and fluorescence positivity for NF-κB p65,NLRP3,and caspase-1 in the hippocampus were also decreased(P<0.05).Conclusion EA enhances the learning and memory capabilities of AD rats,potentially by downregulating the NF-κ B/NLRP3/Caspase-1+signaling+pathway and decreasing the release of neuroinflammatory factors,thereby alleviating cognitive dysfunction in AD rats.

Avian infectious bronchitis(IB),a rapidly spreading and acute disease in chickens,is caused by the infectious bronchitis virus(IBV).IB is characterized by its remarkable genetic varia-bility.IBV has a high degree of mutation,and the existing means of immunization often fail to a-chieve good results,seriously affecting the development of the domestic poultry industry.This ar-ticle offers a comprehensive review of the current understanding of the immune response to IBV,focusing on three key areas:non-specific immunity,mucosal immunity,and specific immunity.By dissecting these aspects,the aim is to provide a theoretical reference for the study of the immune mechanism of IBV.

Objective To investigate the effects of electroacupuncture(EA)at"Baihui(GV 20),""Pishu(BL 20),"and"Zusanli(ST 36)"on the learning and memory functions of rats with Alzheimer's disease(AD)induced by Aβ1-42.Additionally,the mechanism of EA in treating AD was explored from the perspective of the inflammatory cascade mediated by the NF-κ B/NLRP3/Caspase-1 signaling pathway.Methods A rat model of Alzheimer's disease was established by bilateral injection of Aβ1-42 solution into the C1 region of the hippocampus.According to the random number table method,32 male SPF-grade rats were divided into four groups(n=8 per group):a sham-operated group,a model group,an electroacupuncture(EA)group,and a Western medicine group(donepezil hydrochloride).The EA group received electroacupuncture at the"Baihui","Pishu",and"Zusanli"acu-points;the Western medicine group received donepezil hydrochloride via gavage.After the treatment period,Morris water maze experiments were conducted to evaluate learning and memory abilities.Hematoxylin and eosin(HE)staining was used to examine morphological changes in hippocampal tissues.Enzyme-linked immunosorbent assay(ELISA)was employed to measure serum levels of TNF-α and IL-1β.Western blotting and immunofluorescence staining were utilized to assess the co-expression levels of NF-κB p65,NLRP3,and Caspase-1 proteins in the hippocampal region.Results Compared with the sham-operated group,rats in the post-modeling group exhibited significantly prolonged escape latency(P<0.05),reduced crossings of the original platform location,and decreased time spent in the target quadrant(P<0.05).Additionally,nuclear morphology was altered,neurons surrounding the hippocampus displayed necrosis,vacuolar degeneration,and chromatin marginalization.Serum levels of TNF-α and IL-1β were elevated(P<0.05),and protein expression levels as well as fluorescent positivity for NF-κB p65,NLRP3,and caspase-1 in the hippocampus were increased(P<0.05).Compared with the model group,rats in both the EA and Western medicine groups showed a trend toward shorter escape latency(P<0.05),increased crossings of the original platform location and time spent in the target quadrant(P<0.05).Cell structures were largely intact,with only a few nuclei showing slight irregularities and some chromatin accumulation at the edges.Serum levels of TNF-α and IL-1β were reduced(P<0.05),and protein expression levels and fluorescence positivity for NF-κB p65,NLRP3,and caspase-1 in the hippocampus were also decreased(P<0.05).Conclusion EA enhances the learning and memory capabilities of AD rats,potentially by downregulating the NF-κ B/NLRP3/Caspase-1+signaling+pathway and decreasing the release of neuroinflammatory factors,thereby alleviating cognitive dysfunction in AD rats.