OBJECTIVE:To study the effect of paroxetine combined with low dose of olanzapine on sleep process and architec-ture of depression patients with insomnia. METHODS:84 depression patients with insomnia were randomly divided into control group and observation group. Control group was given 20 mg Paroxetine tablet,once every morning;observation group was addi-tionally given 2.5 mg Olanzapine tablet,once before going to bed. Sleep quality [Pittsburgh Sleep Quality Index(PSQI)],depres-sion scores [Hamilton Depression Scale (HAMD)],sleep process [sleep latency (SL),awakening times (AT),the actual total sleep time (TST),sleep efficiency (SE),rapid eye movement (REM) sleep latency (RL)] and sleep architecture [sleep stage 1 (S1),2(S2),3(S3)and the proportion of REM to sleep] in 2 groups before and 3,6 months after treatment and the incidence of adverse reactions(ADR)were observed. RESULTS:After treatment,PSQI and HAMD scores in 2 groups were significantly lower than before,and gradually decreased by time,and observation group was lower than control group;TST in observation group was significantly higher than before and control group,S1 in observation group was significantly lower than before,SE,S3 and REM in 2 groups were significantly higher than before,and observation group was higher than control group,SL,AT,RL and S2 were significantly lower than before,and observation group was lower than control group,the differences were statistically significant (P<0.05). There were no obvious ADR in 2 groups. CONCLUSIONS:Paroxetine combined with low dose of olanzapine can sig-nificantly relieve depression,optimize sleep process and sleep architecture,then impove sleep quality.

Background:Chronic atrophic gastritis(CAG)is a common disease of digestive system and is a precancerous lesion of the intestinal type gastric cancer. Serum pepsinogens(PGs)and gastrin 17(G17)are biological markers of gastric mucosal lesions,which have a prominent role in diagnosis of CAG and screening of early gastric cancer. Aims:To study the correlation of serum PGs and G17 with age in patients with CAG. Methods:A total of 582 CAG patients admitted from Jan. 2016 to Sep. 2017 at the Baoding First Central Hospital were enrolled. The levels of serum PGⅠ,PGⅡ and G17 were determined by ELISA,and the PGⅠ/ PGⅡ ratio(PGR)was calculated. The correlations of these indices with the clinical data of CAG patients were analyzed. Results:The levels of serum PGⅠ and PGⅡ were increased with age(P<0.01),and the levels of PGR and G17 were decreased with age(P <0.05). Spearman rank correlation coefficient analysis showed that the levels of PGⅠ and PGⅡ were positively correlated with age(rs=0.374,P<0.01;rs=0.559, P<0.01),and the levels of PGR and G17 were negatively correlated with age(rs= -0.649,P<0.01;rs= -0.141, P<0.05). Conclusions:The levels of serum PGⅠ,PGⅡand G17 in patients with CAG were correlated with age. When serum PGs and G17 are used as serological indicators for diagnosis of CAG and screening of early gastric cancer,the impact of age on these indices should be taken into account.

Objective:To investigate a large Chinese family in which 9 patients over 4 generations were diagnosed with a form of autosomal dominant spondyloepimphyseal dysplasia(SEMD).Mothods:X-Ray radiograph of proand at 18-month showed absence of secondary ossification centra of femoral heads.His father at 24-year presented severe spondyloepiphyseal changes that principally involved the vertebral bodies,the femoral necks and femoral heads and characterized by generalized platyspondyly with thoracolumbar scoliosis,irregular femoral necks,absent ossification of femoral heads,flat acetabular roofs and coxa vara.The other patients had similar clinical and radiological features.Haplotyping was performed with leukocyte DNA for 5 micosatellite repeat markers from chromosome 12 and the result showed COL2A1 gene as a candidate gene.A total of 54 exons and promoter of COL2A1 gene were amplified and sequenced from all patients and available normal relatives.In addition,exon 23 of COL2A1 gene was amplified and sequenced from 10 controls simultaneously.Results:All patients were identified a 1510(G→A) transition in exon 23 of COL2A1 gene that caused a change from a COL2A1 coding region in available glycine to serine at amino acid position 504.No mutation was found in the normal relatives and 10 controls. Conclusion:The mutation of COL2A1 gene is responsible for this form of SEDC of the family.This is the first familial report of SEDC relating to 1510G→A mutation of COL2A1 gene.The detailed clinical radiogram data will be useful for extending the phenotypic spectrum of type Ⅱcollagenopathies.

Objective To observe the initial mechanism investigation in immune escaping correlated T cell proportion of Lewis lung cancer by Fuzheng-Peiyuan formula. To provide a theoretical basis for the application of the Chinese medicine of strengthening the body resistance in clinics. Methods The healthy C57BL/6J mice were divided into six groups by the random number table: the Chinese medicine group, the Chinese medicine plus chemotherapy group, the chemotherapy group, the model group and the normal control group. There were 6 mice in each group. All the groups expect the normal control group were inoculated subcutaneously with Lewis lung cancer cell suspension 0.2 ml. The medicine given to the Chinese medicine group were orally Fuzheng-Peiyuan formula with 8.17 g/kg. The combination group was given intraperitoneal injection of cyclophosphamide 60 mg/kg and orally Fuzheng-Peiyuan formula 8.17 g/kg. The chemotherapy group received the injection of cyclophosphamide 60 mg/kg and intragastric administration of normal saline. The model group and normal control group were administered with saline. After continuous administration for 13 days, the expressions of CD4, Foxp3, CD8 and CD28 in spleen cells of tumor bearing mice were observed by flow cytometry. Results Compared with the model group, the chemotherapy group and the chemotherapy combined with Chinese traditional medicine group showed that tumor weight (1.76 ± 0.42 g, 1.40 ± 0.43 g vs. 4.37 ± 0.59 g) significantly decreased (P<0.01); and the CD4+ Foxp3+ cells of mouse spleen cells in the Chinese medicine group and Chinese medicine plus chemotherapy group (11.25% ± 1.69%, 9.30% ± 2.68% vs. 14.21% ± 1.50 %) significantly decreased (P<0.05 or P<0.01). Conclusions The result initial proved that the Chinese medicine could strengthen the body resistance, adjust the proportion of Treg and CTL in spleen T cell in tumor-bearing mouse.

Objective To investigate the prevalence of nutritional risk (NRS2002) and malnutrition inhospitalized stroke patient and their nutritional intervention. Methods The stroke patients admitted to three de-partments of vascular neurology ward including cerebral hemorrhage, cerebral infarction and subarachnoid hemor-rhage in Beijing Tiantan Hospital from January 2018 to January 2019 were recruited using cluster sampling. Nutri-tional risk screening 2002 ( NRS 2002) was used to screen the nutritional risk of inpatients Malnutrition was as-sessed by criteria:(1) body mass index (BMI) <18. 5 kg/m2 with poorer general condition from January 2018 to January 2019;(2) Global leadership initiative on malnutrition ( GLIM) criteria were used except whole body muscle mass measurement from October 2018 to January 2019. The nutritional intervention for patients were closely observed during hospitalization. Results A total of 1532 patients were registered and1036 patients were included in the final analysis considering the inclusion and exclusion criteria. The prevalence of nutritional risk was 33. 0％ ( 342/1036) . The prevalence of malnutrition based on BMI and GLIM criteria was 0. 9％( 9/1036) and 2. 5％ (10/393) respectively. Among the 342 patients with nutritional risk, 112 patients received nutritional support therapy by tube feeding, but only 29 patients received nutritional support that met guideline standards. 81 patients received not standard nutritional support, and 2 patients received highly unregulated nutritional sup-port. No patients received sugar and electrolyte infusion, oral nutritional supplements ( ONS) , oral nutritional a-gents and compound nutrition intervention. The other 230 patients took hospital diet. Conclusion The prevalence of nutritional risk in hospitalized patients with cerebral hemorrhage, cerebral infarction or subarachnoid hemorrhage was high, and the prevalence of malnutrition was extremely low. There was a low proportion of nutri-tional support. High quality of large sample cohort studies will be conducted to show whether reasonable applica-tion of nutritional support therapy in patients with nutritional risk can improve patient outcome.

Whether and how garlic-derived -allylmercaptocysteine (SAMC) inhibits hepatocellular carcinoma (HCC) is largely unknown. In the current study, the role of low-density lipoprotein receptor (LDLR)-related protein 6 (LRP6) in HCC progression and the anti-HCC mechanism of SAMC was examined in clinical sample, cell model and xenograft/orthotopic mouse models. We demonstrated that SAMC inhibited cell proliferation and tumorigenesis, while induced apoptosis of human HCC cells without influencing normal hepatocytes. SAMC directly interacted with Wnt-pathway co-receptor LRP6 on the cell membrane. LRP6 was frequently over-expressed in the tumor tissue of human HCC patients (66.7% of 48 patients) and its over-expression only correlated with the over-expression of -catenin, but not with age, gender, tumor size, stage and metastasis. Deficiency or over-expression of LRP6 in hepatoma cells could partly mimic or counteract the anti-tumor properties of SAMC, respectively. administration of SAMC significantly suppressed the growth of Huh-7 xenograft/orthotopic HCC tumor without causing undesirable side effects. In addition, stable down-regulation of LRP6 in Huh-7 facilitated the anti-HCC effects of SAMC. In conclusion, LRP6 can be a potential therapeutic target of HCC. SAMC is a promising specific anti-tumor agent for treating HCC subtypes with Wnt activation at the hepatoma cell surface.