ObjectiveTo investigate the association between the Clock T3111C and T257G gene polymorphisms and sleep epilepsy patients in Han population of Hunan province.MethodsThree hundred and eleven subjects with epilepsy ( sleep epilepsy group ( n =112 ),aperiodic group ( n =95 ),awakening epilepsy group ( n =104 ) ) and 300 sex- and age-matched healthy controls were enrolled in the study.Genomic DNAs were extracted from peripheral blood leucocytes by phenol-chloroform methods.The Clock T3111C and T257G polymorphisms were detected by polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP).Results(1) Two genotypes(TT and TC) were detected in Clock T3111C.The frequency of Clock site T3111C genotypes in all of the people was 86.09％ (TT,526/611),13.91％(TC,85/611),0( CC),T allele gene frequency was 93.04％ (1134/1222) and C allele gene frequency was 6.96％ (85/1222).There was no significant difference in genotype and gene distribution of Clock gene T3111C polymorphism between sleep epilepsy group,aperiodic group,awakening epilepsy group and control group.(2)Two genotypes(TT and TG) were detected in Clock T257G.The frequency of Clock site T257G genotypes in all of the people was 85.92％ (TT,525/611 ),14.08％ (TG,86/611 ),0( GG),T allele gene frequency was 92.96％ (1136/1222) and G allele gene frequency was 7.04％ (86/1222).There was no significant difference in genotype and gene distribution of Clock gene T257G polymorphisms between sleep epilepsy group,aperiodic epilepsy group,awakening epilepsy group and control group.(3)There was an almost complete correspondence (complete linkage disequilibrium) of bases between the positions 257 and 3111.ConclusionClock gene T3111C and T257G polymorphisms are not associated with sleep epilepsy in Han population of Hunan province.

Anti-cancer drug bleomycin (BLM) can cause acute lung injury (ALI) which often results in pulmonary fibrosis due to a failure of resolving acute inflammatory response. The aim of this study is to investigate whether toll-like receptor (TLR) 2 mediates BLM-induced ALI, inflammation and fibrosis. BLM-induced dendritic cells (DCs) maturation was analyzed by flow cytometry and cytokine secretion was detected by the ELISA method. The expression and activity of p38 and ERK MAPK were determined with Western blotting. The roles of TLR2 in ALI, inflammation and fibrosis were investigated in C57BL/6 mice administered intratracheally with BLM. The results demonstrated that BLM-administered mice had higher expression of TLR2 (P<0.001) and its signaling molecules. Blocking TLR2 significantly inhibited the maturation of DCs and reversed BLM-stimulated secretion of cytokines in DCs, such as IL-6 (P<0.001), IL-17 (P<0.05) and IL-23 (P<0.05). TLR2 inhibition attenuated BLM-induced increase of inflammatory cells in bronchoalveolar lavage fluid (BALF), and reversed the immunosuppressive microenvironment by enhancing TH1 response (P<0.05) and inhibiting TH2 (P<0.001), Treg (P<0.01) and TH17 (P<0.01) responses. Importantly, blocking TLR2 in vivo significantly protected BLM-administered mice from pulmonary injury, inflammation and fibrosis and subsequently increased BLM-induced animal survival (from 50% to 92%). Therefore, TLR2 is a novel potential target for ALI and pulmonary fibrosis.

Objective To study the clinical features of paroxysmal sympathetic hyperactivity (PSH).Methods The clinical data,imaging and electroencephalography (EEG) of 10 patients with PSH was analyzed retrospectively.Results Of the 10 patients with PSH,9 were males and 1 was a female.The overall age of all the patients was (37.6 ± 19.1) years,ranging from 15 to 78 years.The primary diseases included traumatic brain injury 5 cases,intracranial hemorrhage 1 case,cerebral infarction 1 case,hypoxic ischemic encephalopathy 1 case,arachnoid cyst 1 case and cryptococcal meningoencephalitis 1 case.All patients developed at least 5 of 7 features which contained paroxysmal agitation,hyperthemia,diaphoresis,tachypnea,tachycardia,hypertension and dystonia.PSH occurred within 24 hours after brain injury in 3 patients; 24 hours to 3 weeks in 5 patients ; 5 months in 1 patient; 9 years in 1 patient.The frequency varied from one time in several days to several times in one day.The duration varied from 1 minute to 3 hours.The episodes in 4 patients occurred more often at night,1 around palinesthesia and the frequency of other 5 patients showed no differences between day and night.There were 2 cases appeared sober-minded,and the states of consciousness of the other 8 cases were hard to judge during PSH.The Glasgow Coma Scale scores of 8 cases were 3 to 8 points and the other 2 cases were 15 points.No epileptic-form activity was detected by EEG and no particular lesions were responsible.Neuro-imaging examinations suggested frontal lobe,temporal lobe,parietal lobe,occipital lobe,basal ganglion,pons and lateral ventricle were damaged.And 9 patients received an ineffective antiepileptic drug treatment.The efficacy in the management of PSH with dopamine agonists combining with β-blockers was observed.Two patients achieved complete remission,6 patients had a reduction in episode frequency,1 patient showed no response to the therapy and 1 patient discharged and could not be connected.Conclusions PSH can occur after various types and different degrees of brain injury.PSH is often misdiagnosed as epilepsy,and anticonvulsant therapies are useless.PSH receives good responses to β-blockers and dopamine agonists.

Objective To explore the clinical and neuroimaging features of a frontotemporal dementia with parkinsonism linked to chromosome 17 ( FTDP-17 ) pedigree caused by mutation of microtubule-associated protein tau ( MAPT) gene.Methods The proband and one patient from a FTDP-17 pedigree were assessed through standardized clinical evaluation , neuropsychology assessment , video-electroencephalogrom ,MRI, genetic sequencing , as well as 18 F fludeoxyglucose ( FDG) SPECT for brain metabolism and 11 C 2β-carbomethoxy-3β-( 4-fluoro ) tropane ( CFT ) PET for dopamine transporter ( DAT ) distribution, respectively.Results A FTDP pedigree with 15 patients (6 still alive) was recruited to this study.The proband and one affected patient were genotyped and confirmed as MAPT c .1788T>G mutation. Parkinsonism was the first symptom for both two patients . Personality, speech changes and dementia accompanied with brain atrophy were developed at the later stage in one patient .The 18 F FDG SPECT studies illustrated asymmetric hypometabolism of the temporal , frontal lobes and basal ganglia in two patients . Regarding to the 11 C CFT PET, one affected patient showed asymmetric decreased uptake of tracer in basal ganglia regions.Conclusions FTDP-17 can display a confusingly broad clinical phenotype , with the parkinsonism as the first symptom . Brain glucose metabolism and DAT distribution could be potential biomarkers in early diagnosis of FTDP-17.

Objective. This study characterized the activation of platelet integrin aⅡbβ3 induced by two anti-human platelet te-traspanin monoclonal antibodies(mAbs),HI117 and SJ9A4. Methods. Using 125I-labeled human fibdnogen(Fg), specific Fg binding to human platelets induced by HI117 and SJ9A4 was measured as indication of activation of platelet integrin αⅡbβ3 by the two mAbs. Results. H1117 and SJ9A4( 10μg/ml and 20μg/ml) induced evident specific Fg binding to human platelets, sug-gesting that the two mAbs evoked activation of platelet integrin αⅡbβ3. Further study indicated that HI117 and SJ9A4 induced integrin t Ⅱ 1β3 activation independent of platelet Fc-receptors, and that HI117 and SJ9A4-induced integrin αⅡbβ3 activation was inhibited by sphingosing, aspirin, apyrase, and/or PGI2. Conclusion. The anti-platelet tetraspanin(CD9)mAbe,HI117 and SJ9A4, can induce platelet integrin αⅡbβ3 act-vation independent of Fc-receptors. Three signaling pathways,i.e.thromboxane,secreted ADP, and cAMP pathways may be involved in the process, with protein kimse C activation presumably being the comtmon step of the three pathways.

Objectives　To characterize the activation of platelet integrin αⅡbβ3 induced by two anti-human platelet tetraspanin monoclonal antibodies (mAbs), HI117 and SJ9A4, and investigate their potential mechanism of action. Methods　Using 125　　I-labeled human fibrinogen (Fg), specific Fg binding to human platelets induced by HI117 and SJ9A4 was measured. Results　HI117 and SJ9A4 (10?μg/ml and 20?μg/ml) induced specific Fg binding to human platelets, suggesting that the two mAbs evoked activation of platelet integrin αⅡbβ3. Further study indicated that HI117 and SJ9A4 induced integrin αⅡbβ3 activation independent of platelet Fc-receptors, and that HI117 and SJ9A4-induced integrin αⅡbβ3 activation was inhibited by pretreatment of platelets with sphingosine, aspirin, apyrase, and/or PGI2. Conclusions　Anti-platelet tetraspanin (CD9) mAbs, HI117 and SJ9A4, can induce platelet integrin αⅡbβ3 activation independent of Fc-receptors. Three signaling pathways, namely thromboxane, secreted ADP, and cAMP pathways, may be involved in the process, with protein kinase C activation presumably being the common step of the three pathways.

Based on the principle of magnetic anastomosis technique, the design of magnetic anastomosis system for endoscopic tissue clamping is proposed. The system includes a semi-ring magnet, a special structure transparent cap and a detachable push rod. With the help of the existing digestive endoscopy and endoscopic tissue gripper, the endoscopic close clamping and anastomosis of the bleeding or perforated tissue can be completed. After the anastomosis, the magnet falls off and is discharged through the digestive tract. Animal experiments showed that the system was easy to use, the fistula was clamped firmly, the magnet was discharged for 7~21 days, and there was no magnet retention and digestive tract obstruction. Further safety verification, optimization of endoscopic operation, the system can be used in clinical trial.
Anastomosis, Surgical ; Animals ; Constriction ; Endoscopy, Gastrointestinal ; Magnetics ; Magnets

Objective: To investigate the changes of microorganisms and metabolites in joint effusion of patients with Rheumatoid arthritis(RA), Osteoarthritis(OA) and Urarthritis(UA). To provide new ideas for the study of the effect of microbiota on the pathogenesis of arthritis. Methods: Joint effusion samples were collected from 20 patients with RA, 20 patients with OA, and 20 patients with UA. 16S rRNA gene sequencing and untargeted ultra-high performance Liquid chromatography-mass spectrometry(LC-MS) were used to explore the differences in microorganisms and metabolites among the three groups. Pearson correlation analysis was used to detect the correlation between effusion microbiota and metabolites. Results: There were differences in microbial diversity and microbiota composition among the three groups. Combined with VIP>1 from OPLS-DA andP<0.05 from two-tailed Students t-test, 45 differential metabolites(Between RA and OA groups), 38 differential metabolites(Between UA and OA groups) and 16 differential metabolites(Between RA and UA groups), were identified. GO analysis and KEGG pathway analysis showed that the differential metabolic pathways among the three groups were mainly concentrated in citric acid cycle(TCA cycle), nucleotide metabolism, amino acid metabolism and glycolysis pathway. Correlation analysis of joint effusion microbiota and metabolites suggested that bacteria enriched in the three groups of joint effusion, such asPrevotella,Clostridium ruminosus,Prevotellaceae＿UCG-001, were related to many key metabolites such as lysozyme, uric acid, glucose, and L-glutamine. Conclusion This study shows that there are a variety of bacterial flora in joint cavity effusion of RA, OA, and UA patients, and the differential metabolites produced by them are involved in the pathogenesis of the three types of arthritis by affecting a variety of metabolic pathways.

Objective To investigate the incidence of Holmes tremor (HT) after stroke and its outcome after medication and rehabilitation. Methods Patients diagnosed as HT after stroke in the ward of neurorehabilitation department from October, 2019 to September, 2021 were reviewed the clinical features, imaging manifestations, drug treatment plan, rehabilitation evaluation scales scores, rehabilitation plan and outcome. Results There were five inpatients with HT (0.7%, 5/715), and all were hemorrhagic stroke, accounting for 1.7% of hemorrhagic stroke. The lesions were located in the midbrain and pons in three cases, cerebellum in one case and thalamus in one case. The tremor appeared 1.5 to seven months after stroke, limited on head and limbs, with other neurological dysfunction. After the comprehensive treatment of drugs and rehabilitation, tremor improved in four cases, and ineffective in one case. The motor and balance function improved less, and the activities of daily living improved somehow. Conclusion The incidence of Holmes tremor is low in stroke patients. The tremor might respond to the treatment, but motor function would not.