Objective To explore the clinical effect of Jieyu Anshen decoction combined with aripiprazole tablet in the treatment of chronic schizophrenia. Methods A total of 210 patients with chronic schizophrenia who were treated in our hospital from March 2015 to March 2017 were randomly divided into two groups,with 105 cases in each group. The control group was treated with aripiprazole tablet. The observation group was treated with Jieyu Anshen decoction combined with aripiprazole tablet. The treatment effect was observed and compared. Results There was no significant difference in the clinical condition between the two groups before treatment, and the improvement was more obvious in the observation group after treatment; The effective rate in the observation group (90.47％) was significantly higher than in the control group (80.0％), the difference was statistically significant (P<0.05). There was no significant difference in the safety of the two groups. Conclusion Jieyu Anshen Decoction combined with aripiprazole tablets in the treatment of chronic schizophrenia compared to conventional methods, can improve clinical efficacy, but also has good safety, it is worth clinical reference.

[Objective]To explore the potential of a novel collagen I /chitosan /Nano?-tricalcium phosphate(?-TCP)bilayered scaffold for being used in tissue engineering(TE)of osteochondral repair.[Method]Bilayered scaffolds were produced with collagen Ⅰ,chitosan and?-TCP,using a special cross-linking and freeze drying method.The pore size,porosity and interpores of the scaffold were observed by scanning electron microscopy(SEM).Rabbit bone mesenchymal stem cells(BMSC)were isolated and amplified,then inoculated onto the scaffold.By SEM scanning,the condition of the cells adhering onto the scaffold was observed.The proliferation of the cells on the scaffolds was examined using MTT method,and the growth curve was drawn.The cell-scaffold composite were then induced to differentiate towards cartilage by 3-D culturing,and then implanted into muscle pouches 2 weeks later.The result was observed 6 weeks later by HE staining,toluidine blue staining and type Ⅱ collagen immunohistochemistry.[Result]The scaffold possessed high porosity and proper pore size,the porosity was above 95%.BMSC could adhere onto the scaffold well,and the proliferation rate of the cells on the scaffolds was perfectly good.After in vitro induction,BMSC-scaffold composite can differentiate toward cartilage ectopicly.[Conclusion]The novel collagen I /chitosan /?-TCP bilayered scaffold possesses good pore structure and biocompatibility,and will possibly become a new biomaterial of TE used for osteochondral repair.

Objective To study the liver fat content (LFC) in schizophrenia patients during olanzapine or aripipra?zol treatment, and to explore the relation between LFC and insulin resistance (IR). Methods Schizophrenia patients were randomly administered with olanzapine (10~25 mg/d, n=57) or aripiprazole (15~30 mg/d, n=47) for eight weeks. All sub?jects underwent sonographic quantification of LFC and homeostasis model assessment of insulin resistance index (HOMA-IR) once 0, 4, 8 weeks of treatment. Results Compared with baseline, the levels of HOMA-IR significantly in?creased after a 4-week and an 8-week of olanzapine treatment, and so did the LFC after an 8-week of olanzapine treat?ment (P<0.05). The levels of LFC (P>0.05) or HOMA-IR (P>0.05) did not significantly changed at week 4 and 8 in ar?ipiprazol group. The increment of LFC, HOMA-IR at week 8 was significantly higher in olanzapine group than that in ar?ipiprazol group (P<0.05). The change of LFC after 8-weeks olanzapine treatment was positively correlated with the change of HOMA-IR (r=0.298, P=0.036). Conclusion Olanzapine treatment increases whereas aripiprazol has little ef?fect on liver fat and insulin resistance in schizophrenia.

Objective To describe the clinical characteristics,and to analyze the AGXT gene mutation in three siblings with primary hyperoxaluria type I (PHI).Methods AGXT gene mutation was analyzed by direct sequencing analysis in this family,and the minor allele status was also tested.One hundred unrelated healthy subjects were also analyzed as controls.Results Three mutations in AGXT were identified in each of three patients including two novel heterozygous missense mutations and one previously reported variant.One mutation was a methionine to leucine substitution at position 49 (p.M49L,c.145A ＞ C) in exon 1,one was an asparagine to isoleucine transition at codon 72 (p.N72I,c.215A ＞ T) in exon 2,and another was a heterozygous nonsense mutation at codon 333 (p.R333*).Both p.M49L and p.R333* occured in cis configuration with the minor allele IVS1 +74 bp.Conclusions Two novel mutations are identified probably in association with PHI,however their pathogenicity and potential molecular mechanisms should be explored by further investigations.This is the first investigation on mutant gene analysis of PHI in China.

Objective To evaluate the harmful effects of olanzapine and quetiapine therapeusis on swallowing ability in patients with Alzheimer'disease (AD).Methods AD inpatients with behavioral and psychological symptoms were randomly divided into two groups,treated with olanzapine (n=42) or quetiapine (n=38) for 6 weeks.The patients were assessed with Kubota's water swallowing test and arterial oxygen saturation(SaO2) monitoring pre and pro treatment.Results After treatment,a significant higher score of water swallowing test (t =2.682,2.040;both P＜ 0.05)in either of two groups,and a significant raised degrade of SaO2 only in olanzapine group(t=4.313,P＜0.01)but not in quetiapine group (P＞0.05)were observed.There was a significant higher degrade of SaO2 in olanzapine group than that in quetiapine group (t=2.155,P＜0.05)at 6 weekend of the study.Before pharmacon,about 29％ (23/80) AD subjects were diagnosed as dysphagia.After pharmacon,more emerging dysphagia patients were surveyed in olanzapine group compared with that in quetiapine group(9/31 vs 2/26,x2=4.135,P＜0.05).No significant change (both P＞0.05) in scores of mini-mental state examination(MMSE) and a significant reduced score(t=3.019,2.867;both P＜0.01)of behavioral pathology in Alzheimer'disease rating scale (BEHAVE-AD) were found in both two groups at the end of study.There was no difference among the two groups with regard to score of MMSE or BEHAVE-AD after treatment(both P＞0.05).Conclusion Either olanzapine or quetiapine therapeutics might do some harmful effects on swallowing function in patients with AD,especially the former.

Objective To investigate the distribution and change in antimicrobial resistance of pathogens causing blood-stream infection,so as to provide reference for rational antimicrobial use.Methods The isolation and antimicrobial resistance of major pathogens from blood culture specimens from a tertiary first-class hospital in 2012-2015 were analyzed statistically.Results A total of 4 780 isolates were detected,the top five species were Escherichia coli (n = 1 008, 21.09%),Klebsiella pneumoniae (n = 624,13.05%),Acinetobacter baumannii (n = 452,9.46%),Staphylococcus aureus (n=437,9.14%),and Pseudomonas aeruginosa (n=247,5.17%).The percentage of gram-negative bacilli, gram-positive cocci,fungi,and others were 62.05%,29.31%,7.76%,and 0.88% respectively.The resistance rates of Klebsiella pneumoniae to ertapenem and imipenem increased from 4.50% in 2012 to 46.79% and 33.94% in 2015(both P<0.01).The resistance rates of Acinetobacter baumannii to cefepime,ceftazidime,tobramycin,gentamicin,and imipenem were 86.50%,80.56%,78.10%,79.87%,and 84.29% respectively;resistance rates to amikacin in 2012-2015 were 0, 10.22%,39.85%,and 21.30% respectively(P<0.01);resistance rates to minocycline in four years were 0-7.52% (P<0.01 ).Conclusion The main pathogens causing bloodstream infection are gram-negative bacilli,Acinetobacter baumannii is highly resistant to cephalosporins and carbapenems,resistance rates of Klebsiella pneumoniae to carbapenems increased rapidly.Broad-spectrum antimicrobial agents must be used cautiously to reduce the selective pressure of antimicrobial agents.

Objective To explore the molecular mechanisms involved in hypokalemic salt-losing tubulopathies ( SLTs) through genetic screening of WNK gene in patients with SLTs. Methods Forty-four kindreds of SLTs were diagnosed Batter's syndrome or Gitelman's syndrome after CLCNKB and SLC12A3 sequencing and analysis, 8 of whose phenotype can not be simply attributed to CLCNKB or SLC12A3 mutations. Primers for PCR-amplified exons of WNK4 and WNK1 gene in genomic DNA were designed, and direct sequencing was performed to analyse the PCR products. Results Two missense mutations of WNK1, Ile~(1172)→ Met (I1172M) and Ser~(2047) → Asn (S2047N), were identified. Both of these 2 mutations segregated with the disease in SLTs kindred. Conclusion Two heterozygote missense mutations of WNK1 gene (I1172 M and S2047N) were found in 8 SLTs kindreds, indicating that WNK1 might be another gene responsible for hypokalemic salt-losing tubulopathies.

Alport syndrome is a relatively common inherited kidney disease,characterized by significant clinical symptoms,which can lead to renal failure and progress to end-stage renal disease in the late stage.This disease does not only affect the renal system,but also involve other tissues and organs containing basement membranes.Recently,with the advancement of genetic engineering tech-nology,there has been a deeper understanding on the molecular pathogenesis of Alport syndrome,and the application of gene sequencing technology has provided new means for diagnosis,supplementing the traditional pathological examination method of renal biopsy.In addition,gene-based therapies are also under exploration,opening up new directions for future treatment strategies.This paper aimed to summarize the relevant knowledge of Alport syndrome based on the current progress in genetic resear-ches,with the hope of providing a theoretical basis for clinical practice.

Alport syndrome is a relatively common inherited kidney disease,characterized by significant clinical symptoms,which can lead to renal failure and progress to end-stage renal disease in the late stage.This disease does not only affect the renal system,but also involve other tissues and organs containing basement membranes.Recently,with the advancement of genetic engineering tech-nology,there has been a deeper understanding on the molecular pathogenesis of Alport syndrome,and the application of gene sequencing technology has provided new means for diagnosis,supplementing the traditional pathological examination method of renal biopsy.In addition,gene-based therapies are also under exploration,opening up new directions for future treatment strategies.This paper aimed to summarize the relevant knowledge of Alport syndrome based on the current progress in genetic resear-ches,with the hope of providing a theoretical basis for clinical practice.

The clinical data of 5 patients with autoimmune encephalitis admitted to the psychiatric department of the 904th Hospital of the Joint Logistics Service Force from January 2016 to June 2020 were retrospectively analyzed. Among 5 patients, 4 had stress psychological events within one month before the onset, and 3 had precursor symptoms such as fever and vomiting. They were all characterized by rapid progress of atypical mental and behavioral abnormalities and cognitive impairment. In terms of neurological symptoms, 1 case had faciobrachial dystonic seizures (FBDS), 3 cases had seizures, 2 cases had involuntary movement, and 4 cases had autonomic dysfunction, including central hypopnea, arrhythmia, blood pressure instability and paroxysmal facial flushing. Most neurological symptoms occur within 1 month of the onset. MRI revealed abnormalities in cerebral cortex, thalamus, temporal lobe and insular lobe in 4 cases; EEG demonstrated bilateral short-range medium amplitude θ wave in 2 cases. Abnormal cerebrospinal fluid (CSF) pressure was detected in 4 cases and 2 cases had abnormal cell number CSF. Three patients had positive anti-N-methyl-D-aspartate receptor (NMDAR) antibody, one patient had positive anti-LGI1 antibody, and one patient had positive anti-γ-aminobutyric acid B receptor (GABA BR) antibody. One case was discharged automatically, the remaining 4 patients were treated with glucocorticoid or combined with gamma globulin and cyclophosphamide, antiepileptic drugs, antipsychotic drugs and other symptomatic treatment, and their symptoms were relieved. Patients were followed up for six months, there was slightly slow residual reaction in 2 cases and personality change in 1 case. Autoimmune encephalitis characterized by mental symptoms is likely to be misdiagnosed as mental disorders. Clinicians should identify symptoms different from mental disorders, taking into account of the possibility of autoimmune encephalitis, to make early diagnosis and treatment.