Objective To explore the effect of rotenone exposure on the metabolic homeostasis of nicotinamide adenine dinucleotide(NAD+)in dopaminergic neurons of the rat mid-brain striatum,and investigate the effect of exogenous NAD+intervention on the cellular damage response of dopaminergic neurons induced by rotenone.Methods Male SD rats(8 weeks old,200～250 g)were divided into a control group using a table of random numbers,a rotenone exposure group,an NAD+-intervention group,and an NAD+group.An intoxication model was established in the rotenone exposure group.NAD+(250 mg/kg)was administered simultaneously with rotenone exposure in the NAD+-intervention group.The NAD+group was only given NAD+,while the control group received no intervention.After modeling,open field test was performed to evaluate behavioral changes.After scarification,serum samples and mid-brain striatal tissues were collected.HE staining was used to observe the morphology of dopaminergic neurons in the striatum.The NAD+content in the tissues was detected with NAD+/NADH kit.Western blotting was employed to determine the contents of tyrosine hydroxylase(TH),nicotinamide phosphoribosyltransferase(NAMPT),nicotinamide mononucleotide adenylyltransferase(NMNAT),and solute carrier family 25 member A51(SLC25A51).ELISA was utilized to measure the content of dopamine in the striatal tissues.Immunohistochemical staining was applied to observe the distribution and contents of TH proteins in the striatal tissues of each group.Results Rotenone exposure significantly affected the vital signs and motor abilities of rats,induced disorderly-arranged,atrophy and deformed neurons in the striatal tissue,decreased the content of TH,rate-limiting enzyme for dopamine synthesis,by approximately 29%(P<0.01),the content of dopamine by about 42%,and that of NAD+by almost 50%(P<0.01),while increased the NADH/NAD+ratio(P<0.01).After exposure,the content of NAMPT,an enzyme related to NAD+synthesis,was decreased by 26%(P<0.05),the contents of NMNAT1-3 and SLC25A51,mitochondrial transporters of NAD+by approximately 21%,38%,43%,and 21%,respectively(P<0.01).Exogenous NAD+intervention improved the motor function of exposure rats and the morphology of dopaminergic neurons in the mid-brain striatal tissue,and restored the content of TH in the striatal tissue significantly by 12.8%(P<0.05),and the content of dopamine by 20.9%(P<0.05).Conclusion Rotenone disrupts the NAD+homeostasis in dopaminergic neurons by inhibiting the NAD+synthesis and transport pathways in the mid-brain striatal tissues,while exogenous NAD+intervention can effectively alleviate the dopaminergic neuron damage induced by rotenone exposure.

AIM: To explore the clinicopathological and immunohistochemistry(IHC)characteristics of meibomian gland carcinoma(MGC).METHODS: Patients who were pathologically diagnosed as MGC from January 1, 2015 to December 31, 2020 in our hospital were enrolled, and their clinicopathological information was retrospectively analyzed. Cancer tissues from all the cases were IHC stained. En Vision two-step method, DAB staining, as well as hematoxylin re-staining were applied in the IHC assay.RESULTS: A total of 50 patients with 21 males and 29 females(1:1.38)were enrolled in the study, ranging from 26 to 80 years old, with a median age of 60 years. The upper eyelid, which was the predilection site, accounting for 66%(33/50). Histopathologically, moderately or poorly differentiated was in the majority(35/50, 70%). The expression rates of IHC parameters of MGC patients were as follows: GATA-3(49/50, 98%), EMA(49/50, 98%), CAM5.2(42/50, 84%), AR(41/50, 82%), MSH2(50/50, 100%), MSH6(50/50, 100%), MLH1(50/50, 100%), PMS2(50/50, 100%), Ki67(positive, 50%-90%). All the patients were followed up for 12 to 72 mo, with 5 cases of recurrence and 0 deaths.CONCLUSION: Pathological diagnosis of MGC should focus on observing cancer cells' cytoplasm to find relevant clues for cortical gland differentiation. Comprehensive analysis of multiple indicators is required when using IHC to assist diagnosis. For most MGC cancer cells, positive expressions of GATA-3, EMA, AR, CAM5.2 and a high Ki67 proliferation index could be always found. In addition, screening for Muir-Torre syndrome related IHC indicators could be also performed in diagnosing MGC simultaneously.

Objective To investigate the mechanism and protective effect of Humanin(HN)on rotenone(Rot)-induced toxic damage for dopamine neurons.Methods The Rot-poisened PC12 cell model was constructed,and the control group,the Rot poisening group,the HN pretreated Rot poisening group,and the HN treatment group were set up.ELISA was used to detect the content of HN inside and outside of Rot-infected cells,CCK-8 assay was used to detect cell viability,and ATP detection kit was used to detect the intracellular ATP content.Dichloro-dihydro-fluorescein diacetate(DCFH-DA)assay was used to detect the level of reactive oxygen species(ROS)in cells.Western blotting was performed to detect the expression level of mitochondrial autophagy regulatory proteins Pink1,Parkin,p62,LC3,mitochondrial biogenesis regulatory protein PGC1α,division/fusion regulatory proteins OPA1,MFN2,DRP1,p-DRP1 and antioxidant stress regulatory proteins Keap1 and Nrf2.HBAD-mcherry-EGFP-LC3 adenovirus transfected cells was used to observed the number of autophagosomes and autophagolysosomes.Results The results showed that the intracellular concentration of HN in PC12 in the Rot poisening group was significantly higher than that in the control group(P＜0.05);Compared with the control group,the Rot poisening group had significantly decreased activity of PC12 cells,decreased ATP content and increased production of ROS.After the poisen of Rot in PC12 cells,the expression of Pink1 and p-Parkin,the ratio of LC3Ⅱ/LC3Ⅰ and the expression of p-DRP1 in mitochondrial fusion protein was increased,while the expression of p62,the expression of mitochondrial biogenesis protein PGC1 α,mitochondrial fusion proteins MFN2 and OPA1,and antioxidant stress proteins Keap1 and Nrf2 were decreased(all P＜0.05).The number of autophagosomes and autophagolysosomes in PC12 cells in the Rot poisening group was higher than that in the control group(P＜0.05),and HN pretreatment(20 μmol/L)could significantly improve the changes mentioned above caused by Rot poisening(P＜0.05).Conclusion HN ameliorates Rot-induced toxic damage for dopamine neurons by inhibiting mitophagy and mitochondrial division and promoting mitochondrial biogenesis and fusion,and anti-oxidative stress.

COVID-19 ; Coronavirus Nucleocapsid Proteins ; Humans ; Nucleocapsid Proteins ; Phosphoproteins ; SARS-CoV-2

Objective To investigate the effect of home-based motor imagery training on the lower extremity motor function,balance ability and activities of daily living in post-stroke patients. Methods Fifty-six stroke survivors were divided into the control group and the intervention group by random number table method.All the patients got the conventional nursing, rehabilitation booklets and the video tapes which contained physical therapy and occupational therapy. Furthermore, the patients in the intervention group received 6 weeks motor imagery (MI) therapy through an instant messaging client (Tencent QQ), three times a week, 30mins per time. The outcomes were measured before discharge (T0), immediately after the intervention (T1), and 6 weeks (T2) after the intervention using the Fugl-Meyer Motor Assessment Scale (FMA), Berg Balance Scale (BBS), Barthel Index (BI). Results At baseline, the scores of FMA、BBS、BI in the intervention group were (15.12 ± 4.19), (24.50 ± 2.72), (54.04 ± 17.44) points, while in the control group were (14.23 ± 3.67), (23.92 ± 2.82), (49.46 ± 15.09) points. There were no differences on any scale between the two groups at baseline (t=0.810, 0.750, 1.012, P>0.05). At 6 weeks,the scores of FMA, BB, BI in the control group were (14.81 ± 3.50), (29.31 ± 2.43), (50.77 ± 14.47) points, and were significantly lower than (17.38 ± 4.10), (37.38 ± 4.30), (74.62 ± 11.22) pointsin the interventiongroup (t=2.438, 8.326, 6.641, P<0.05 or 0.01). At 12 weeks, the scores of FMA, BB, BI in the control group were (15.54±3.44), (32.35±1.98), (59.08±13.85) points, and were significantly lower than (18.58±4.19), (41.19±3.96), (86.54± 9.88) points in the intervention group (t=2.858, 10.189, 8.233, P<0.01). A main effect of intervention (F=4.158, 63.716, 30.379, P < 0.05) and an interactive effect of time and intervention (F=47.941, 61.029, 29.685, P=0.000) were observed in the model of FMA, BBS, BI using ANOVA of repeated measures. The factors were compared with each other and the difference was statistically significant (P=0.000). Conclusions The home-based MI training can improve the lower extremity motor function, balance ability and activities of daily living in patients with stroke.

Self-efficacy is the extent or strength of one′s belief in one′s own ability to complete tasks and reach goals. Self-efficacy affects every area of human endeavor. By determining the beliefs a person holds regarding his or her power to affect situations, it strongly influences both the power a person actually has to face challenges competently and the choices a person is most likely to make. In this paper, the factors affecting self-efficacy, the effects of self-efficacy, the application range and interventions of self-efficacy in clinical disease management are reviewed. It has great significance in the improvement of ability of disease management,disease prognosis and quality of life by lifting the self-efficacy.

Objective To investigate the influence of a multifaceted stroke telehome-care (THC) on extremities function, activities of daily living (ADL) and quality of life in stroke patients with hemiplegia. Methods A total of 52 stroke survivors in department of neurology were randomized to the THC intervention or usual care. The patients in the control group received conventional care, while those in the intervention group were additionally given a THC program over 3 months. The THC intervention includes motor imagery and adaptive strategies. Data collection was undertaken using the Fugl-Meyer Motor Assessment Scale (FMA), the Barthel Index (BI), the Stroke Impact Scale (SIS) at baseline, 3 months, and 6 months. Results At baseline, the scores of FMA, BI, and SIS in the intervention group were 53.62 ± 23.52, 54.04 ± 17.44, 179.96 ± 28.51, and while the scores of the control group were 50.96 ± 19.52, 49.46 ± 15.09, 169.23 ± 28.48. There were no pre-existing differences on any scale between the two groups (t=0.443, 1.012, 1.358, P > 0.05). At 3 months, the scores of FMA, BI, SIS in the control group were 53.54 ± 17.45, 50.77 ± 14.47, 76.19 ± 27.78, and were significantly lower than 78.38 ± 12.54, 74.62 ± 11.22, 228.54±22.63 in the THC group (t=5.895, 6.641, 7.449,P<0.01). At 6 months, the scores of FMA, BI, SIS in the control group were 57.88±17.89, 59.08±13.85, 183.92±26.56, and were significantly lower than 90.58 ± 9.60, 86.54 ± 9.88, 252.19 ± 20.10 in the THC group (t=8.211, 8.233, 10.451, P < 0.01). Conclusions A telehome-care program that provide distance training and education of disabled persons resulted in greater improvements in physical functioning, ADL and quality of life.

Objective To investigate the status of anxiety,depression and self-efficacy, social support among patients with severe burns and analyze their correlation. Methods Eighty-four patients with severe burns were selected by convenience sampling. They were evaluated by Hospital Anxiety and Depression scale (HADS), General Self-efficacy Scale (GSES) and Social Support Assessment Scale (SSAS) and the correlation of two scales was analyzed. Results The anxiety score was 6.62 ± 3.98, depression score was 7.63 ± 4.36, self-efficacy score was 20.94 ± 4.96 and the social support score was 41.40±6.47;Self-efficacy was negatively correlated with the anxiety (r=-0.356, P<0.05) and depression (r=-0.362, P<0.05). Social support was also negatively correlated with the anxiety (r=-0.305, P<0.05) and depression (r=-0.320, P<0.05). Conclusions There is a medium level of anxiety and depression among patients with severe burns. Psychological interventions via increasing the self- efficacy are suggested for the patients with severe burns in the future.

Limbic encephalitis is a new type of autoimmune encephalopathies.The clinical manifestation is primarily defined by the subacute onset of short-term memory loss,seizures,confusion and psychiatric symptoms.The diseases usually have a variety of clinical manifestations,and are very serious,occurring with or without tumor association.Routine detection of serum and cerebrospinal fluid (CSF) and imaging tests show no specificity,but associated antibodies can be detected in serum and (or) CSF.Early identification,tumor resection and immunotherapies are helpful in improving the prognosis of patients.This article aims to study the pathogenesis,classification,clinical features and treatment of antibody-associated limbic encephalitis and to improve the diagnosis and prognosis of the disease.

Nerve agent not only inhibit acetylcholinesterase ( AChE) at an early stage, but also induce prolonged and progressive neuroinflammation and delayed neurodegeneration.Recently, the US National Institute of Health ( NIH) has sponsored some major programs of toxic mechanisms and treatment of nerve agents, which aims at the development of quick and effective treatment to acute intoxication and delayed effect.The experimentally effective new antidotes mainly include AChE-targeting drugs, broad-spectrum reactivators and scavengers, antiinflamatory and nerve protection drugs.