AIM:To investigate whether total alkaloids of Cocculus orbiculatus(COTA)attenuate ulcerative colitis(UC)in mice via PINK1/parkin mitophagy pathway.METHODS:Sixty C57BL/6 mice were randomly divided into normal control group,model group,positive drug mesalazine group,and low-,medium-and high-dose(0.162,0.324 and 0.486 g/kg)COTA groups,with 10 mice in each group.Except for normal control group,the mice in all groups were given free access to 3%dextran sulfate sodium(DSS)solution for 7 consecutive days to establish a UC model in mice,and were then treated with COTA or mesalazine via oral gavage.The general condition of the mice was observed,and the colon length and disease activity index(DAI)score were determined.Colon histopathological damage was observed by HE staining.The serum levels of interleukin-1β(IL-1β),IL-6 and tumor necrosis factor-α(TNF-α)were detected by ELISA.The pro-tein levels of PINK1,parkin,microtubule-associated protein 1 light chain 3(LC3),P62 and beclin-1 in colon tissues were determined by Western blot.The protein expression of LC3 and parkin was detected by immunofluorescence.RE-SULTS:Compared with normal control group,the mice in model group showed varying degrees of soft stools or bloody stools,decreased body weight(P<0.05),increased DAI score,shortened colon length(P<0.05),and obvious pathologi-cal damage in the colon tissue.The serum levels of IL-1β,IL-6 and TNF-α were elevated(P<0.05).The protein levels of parkin,PINK1,LC3-II and beclin-1 were significantly decreased(P<0.05),while P62 protein expression was in-creased(P<0.05).Immunofluorescence showed a small number of autophagosomes in the colon tissue.In contrast,com-pared with model group,the mice in total alkaloids of Cocculus orbiculatus groups exhibited increased body weight(P<0.05),decreased DAI score,increased colon length(P<0.05),and reduced levels of IL-1β,IL-6 and TNF-α(P<0.05).The protein levels of parkin,PINK1,LC3 and beclin-1 were elevated(P<0.05),while P62 expression was re-duced(P<0.05),with numerous autophagosomes visible in the colon tissue via immunofluorescence.CONCLUSION:Total alkaloids of Cocculus orbiculatus can enhance the expression of mitophagy-related proteins PINK1,parkin,LC3 and beclin-1,activate mitophagy,and reduce the expression of inflammatory factors,thereby attenuating the inflammatory re-sponse in the colon mucosa of DSS-induced UC mice.

AIM:To investigate whether total alkaloids of Cocculus orbiculatus(COTA)attenuate ulcerative colitis(UC)in mice via PINK1/parkin mitophagy pathway.METHODS:Sixty C57BL/6 mice were randomly divided into normal control group,model group,positive drug mesalazine group,and low-,medium-and high-dose(0.162,0.324 and 0.486 g/kg)COTA groups,with 10 mice in each group.Except for normal control group,the mice in all groups were given free access to 3%dextran sulfate sodium(DSS)solution for 7 consecutive days to establish a UC model in mice,and were then treated with COTA or mesalazine via oral gavage.The general condition of the mice was observed,and the colon length and disease activity index(DAI)score were determined.Colon histopathological damage was observed by HE staining.The serum levels of interleukin-1β(IL-1β),IL-6 and tumor necrosis factor-α(TNF-α)were detected by ELISA.The pro-tein levels of PINK1,parkin,microtubule-associated protein 1 light chain 3(LC3),P62 and beclin-1 in colon tissues were determined by Western blot.The protein expression of LC3 and parkin was detected by immunofluorescence.RE-SULTS:Compared with normal control group,the mice in model group showed varying degrees of soft stools or bloody stools,decreased body weight(P<0.05),increased DAI score,shortened colon length(P<0.05),and obvious pathologi-cal damage in the colon tissue.The serum levels of IL-1β,IL-6 and TNF-α were elevated(P<0.05).The protein levels of parkin,PINK1,LC3-II and beclin-1 were significantly decreased(P<0.05),while P62 protein expression was in-creased(P<0.05).Immunofluorescence showed a small number of autophagosomes in the colon tissue.In contrast,com-pared with model group,the mice in total alkaloids of Cocculus orbiculatus groups exhibited increased body weight(P<0.05),decreased DAI score,increased colon length(P<0.05),and reduced levels of IL-1β,IL-6 and TNF-α(P<0.05).The protein levels of parkin,PINK1,LC3 and beclin-1 were elevated(P<0.05),while P62 expression was re-duced(P<0.05),with numerous autophagosomes visible in the colon tissue via immunofluorescence.CONCLUSION:Total alkaloids of Cocculus orbiculatus can enhance the expression of mitophagy-related proteins PINK1,parkin,LC3 and beclin-1,activate mitophagy,and reduce the expression of inflammatory factors,thereby attenuating the inflammatory re-sponse in the colon mucosa of DSS-induced UC mice.

Objective To analyze the current status,hotspots and trends of researches related to non-invasive brain stimulation for Parkinson's disease in the last decade. Methods Literature related to non-invasive brain stimulation for Parkinson's disease in the Web of Science Core Collec-tion was searched from January,2014,to December,2023,and CiteSpace 6.1.R3 was used to draw a knowledge map of authors,institutions,countries and keywords. Results A total of 1 351 papers were included,with a general upward trend in the number of publication,with the United States,Italy and China being the high-producing countries,and the University of London being the most prolific institution,with Alfredo Berardelli being the most prolific author.Hot keywords included deep brain stimulation,motor cortex and basal ganglia,and emergent words that have appeared in the last two years included therapy,non-invasive brain stimulation,supplementary motor areas and movement disorders. Conclusion The research hotspots related to non-invasive brain stimulation for Parkinson's disease in the last decade mainly focus on the stimulation on motor cortical areas,the combined application of non-invasive brain stimula-tion and deep brain stimulation,and non-invasive brain stimulation and non-invasive neuroimaging techniques,such as electroencephalography and functional imaging.Non-invasive brain stimulation of supplementary motor areas can be further explored to improve movement disorders in Parkinson's disease patients in the future.

In the aftermath of the pandemic,the government is accelerating the development of top-tier medical resources to broaden the supply and deliver superior healthcare services.However,during this transitional phase,hospitals are experiencing operational challenges due to concurrent construction activities.Notably,a shortage of parking facilities and increased traffic con-gestion continue to impactmedial consultation experience of patients.This paper tries to explore strategies and methods for dynam-ic parking management during hospital campus expansions,offering insights for other medical institutions into grappling with pa-tient parking issues.

Objective To investigate the protective effect of hydrogen-rich saline on systemic oxidative stress in rats with severe traumatic brain injury(STBI) .Methods Male Wistar rats(n=60) were divided into three groups randomly :sham group ,STBI+normal saline group ,STBI+ hydrogen-rich saline group .STBI model was induced by controlled cortical impact injury .Hydrogen-rich saline were intraperitoneally administered at 5 min after STBI operation .Plasma malondialdehyde (MDA ) ,Superoxide Dis-mutase(SOD) activity and glutathione peroxidase(GSH-PX) activity were measured before TBI operation ,12 ,24 h and 48 h after TBI operation .Results The level of MDA in STBI group plasma was significantly elevated from 24 h to 48 h after STBI operation (P< 0 .05) .Hydrogen-rich saline treatment significantly attenuated the increase of MDA level in STBI operation animals (P<0 .05) .The activities of SOD and GSH-PX were slightly elevated at 6 h after TBI operation ,but decreased significantly from 24 h to 48 h after STBI operation(P<0 .05) .Hydrogen-rich saline treatment significantly increased the activities of SOD and GSH-PX after STBI operation(P<0 .05) .Conclusion Hydrogen-rich saline could exert a protective effect against STBI via reducing oxidative stress .Molecular hydrogen might be a more effective therapeutic strategy for TBI patients .

AIM: To study the processing of Indigo Naturals. METHODS: Study on the microstructure of Indigo Naturals with scanning electron microscope (SEM) and X ray diffractometer (XRD) were carried out. RESULTS: Through the SEM, it is clear that Indigo attached to the surface of some white substance, and the XRD proves that the white substance in Indigo Naturals is calcium carbonate (CaCO 3). CONCLUSION: The study about the processing of Indigo Naturals indicates that Indigo Naturals consists of Indigo and other effective compositions attached the surface of calcium carbonate (CaCO 3).

Objective To study the protective mechanism of lycopene by its modulating lipid disturbance.Methods To make high fat diet model,the groups were intragastrically administered different dosage of lycopene at the same time.The lipids of serum and liver were measured.The pathological changes in liver were observed by HE staining method.Results Serum and liver TC,TG,LDL-C,AI levels in the three lycopene groups notably decreased(P

Objective To study the protective mechanism of lycopene by modulating lipid metabolic disturbance in rats. Method The hyperlipidemic rats were induced by high fat diet and were divided into groups given different doses of lycopene. The serum total cholesterd(TC), triglyceride(TG), low density lipoprotein cholesterol(LDL-C), high density lipoprotein cholesterol(HDL-C), the hepatic lipase(HL) and lipoprotein lipase(LPL)activity in liver were tested by biochemical method, and the expression of low density lipoprotein receptor(LDL-R)in liver was detected by Western blot analyses. Results Lycopene decreased serum TC, TG, LDL-C, and the activity of LPL and HL in three lycopene groups were higher than those in model group, and the high dose group was the highest. Conclusion Lycopene may increase the lipases’activity and the expression of LDL-R, and decrease the deposit of TG and LDL in liver to prevent lipid metabolic disturbance.