Objective To investigate the risk factors for cerebral microbleeds (CMBs) and its correlation with the 24 h microalbuminuria (mALB) in patients with small artery occlusion (SAO).Methods The patients with SAO were enrolled.CMBs were detected with susceptibility-weighted imaging.The demographic and clinical characteristics and 24 h mALB of the patients were compared.Multivariate logistic regression analysis was used to identify the independent risk factors for CMB in patients with SAO.Spearman correlation analysis was used to investigate the correlation between the 24 h mALB and the degree of CMBs.Results A total of 90 patients with SAO were enrolled and 35 patients (38.89％) had CMBs.CMBs mainly distributed in basal ganglia/thalamus and infratentorial (62％) regions.The Age (70.8 ± 5.4 vs.67.3 ± 8.1; t =2.461,P =0.016),proportion of hypertension (80.0％ vs.52.7％ ;x2 =6.851,P =0.009),and 24 h mALB levels (16.257 ± 6.031 mg/24 h vs.11.910 ±5.458 mg/24 h; t =3.536,P =0.001) in the CBM group were significantly higher than those in the non-CMB group.Spearman rank correlation analysis showed that the 24 h mALB and the severity of CMB in patients with SAO showed a significant positive correlation (rs =0.795,P =0.000).The higher the 24 h mALB level was,the more severe the CMB degree would be.Multivariate logistic regression analysis showed that only 24 h mALB was the only independent risk factor for CMBs in patients with SAO (odds ratio,1.100,95％ confidence interval 1.031-1.176; P =0.002).Conclusions The 24 h mALB is an independent risk factor for CMB in patients with SAO.The 24 h mALB level is positively correlated with the severity of CMB,and it may be used as a marker for small vascular injury.

Objective:To investigate the efficacy of Silybinin meglumine on hepatic fibrosis rats and possible mecha -nisms.Methods:The liver fibrosis rats were randomly divided into 4 groups,the model group,Silybinin meglumine 120 mg/kg group, Silybinin meglumine dose group 60 mg/kg and Silybinin meglumine low dose group 30 mg/kg,and the control group.All groups had been treated for 4 groups.Results:No deaths rat.Compared with the control group ,the reduced body weight ,less dynamic,dark hair, decreased liver and spleen indexes ,increased ALT,AST,TBIL,TG,TC and LDLC,and the decreased ALB, and the increased LXRαand SREBP1c had been observed in the model group (P<0.05).Compared with the model group ,better activity and body weight ,the in-creased liver and spleen indexs decreased ALT ,AST,TBIL,TG,TC and LDLC,and the increased ALB , and the decreased LXRαand SREBP1c had been observed in the Silybinin meglumine groups (P<0.05),in a way of dose-depended.Conclusion: The Silibinin meglumine can treat liver fibrosis ,by improving liver function,lowing lipid and decreaseing LXRαand SREBP1c expression in liver tis-sue.But the mechanism of two proteins reduced remains for further investigation .

BACKGROUND: Tendon is a fibrous tissue that connects bone and muscle. The main function is to conduct stress from the muscles to the bone during exercise. Tendinopathy is a commonly seen disease, characterized by tendon inflammation, degeneration and injury. Autophagy is widely involved in the development of many degenerative diseases. The research method based on autophagy provides a new idea for tendon repair. OBJECTIVE: To review the process and regulation mechanism of autophagy, and to analyze the pathological mechanism of autophagy involved in the tendinopathy so as to provide a reference for the prevention and treatment of tendinopathy. METHODS: The articles concerning autophagy and tendinopathy were retrieved by computer in CNKI, WanFang and PubMed databases. The keywords were "autophagy, tendon, fibroblast, tendinopathy" in English and Chinese, respectively. Finally, 54 articles were obtained through systematic induction and analysis after excluding the irrelevant and repetitive articles. RESULTS AND CONCLUSION: Autophagy can alleviate the damage to human tendon stem cells induced by oxidative stress. With the increase of the degree of extracellular matrix degradation in the tendon tissue, autophagic cell death occurs in the tendon cells due to excessive autophagy. Prostaglandin E2 significantly induces fibroblast death and autophagy in a dose-dependent manner. The muscle atrophy after the rotator cuff injury is regulated by autophagy. Rapamycin prevents peritendinous fibrosis through activation of autophagy. In conclusion, autophagy plays an important role in tendinopathy. Autophagy will become a new hotspot in tendinopathy. Further understanding of autophagy and its role in tendinopathy will contribute to finding a targeted autophagy pathway and provide new theoretical and methodological support for the intervention and treatment of tendinopathy.

OBJECTIVEThe work presented here was to research into a kind of automatic control system that would be automatically linked to the working status of electronic endoscope.

METHODSThe image video output signal and signal of negative pressure sensor were used to be a sampling signal of automatic control circuit. An electronic switch of automatic control circuit was challenged the manual control device of the negative pressure system.

RESULTSThis system simplifies the operation procedures, enhances work efficiency, reduces energy consumption and improves the service life of the machine.

CONCLUSIONThe paper concludes that this negative pressure automatic control system has many strengths like stable performance, easy installation and strong versatility. It also can be widely applied in different brand and different types of electronic endoscope in China.

Objective To assess whether propofol call induce stable psychic dependence in the rats by self-administration experiment. Methods Twenty-four male SD rats 14 weeks old weighing 240一270 mg were studied. Anesthesia was performed with intraperitoneal injection of 3%sodium pentoharbitsl 40 ms/kg and atropine 03 mg/kg.A catheter wag inserted into the right external jugular vein. Penicillin(100 000 U)0.2 ml wag injected through the external jugular vein for anti-infection and heparin sodium(50U/ml)0.1 ml for anticoagulation. The self-administration experiment of 14 days was started after the 7 days of recovery. All the rats were randomly divided into 4 groups(n=6 each):contontrol group(C),propofol 0.56 mg/kg/l group(P1),propofol 1.00 mg/kg group(P2)and pmpofol 1.70 ms/kg group(P3).The experimental events were controlled by a computer with 50 times of the maximum injection per day.The times ofactive and inactive nose-poke response and times of drug iniection were recorded per day.Results Compared with group C and P1,the times of active nosepoke response and injections were significantly increased in group P2 and P3(P<0.01).The times of active nosepoke response and injections per day were significantly increased in group P3 than in group P2(P(0.01).There was no significant difference in the times of active nose-poke response and injections between group C and P1.There was no significant difference in inactive nose-poke resporme between the 4 groups.And the total daily doses of propofol injected in the last 3 days were significantly increased in a dose-dependent manner.Conclusion Propefol can induce the development of psychological dependence in rata and it is related to the dosage.

Histone acetylation is a well-characterized epigenetic modification controlled by histone acetyltransferases (HATs) and histone deacetylases (HDACs). Imbalanced histone acetylation has been observed in many primary cancers. Therefore, efforts have been made to find drugs or small molecules such as HDAC inhibitors that can revert acetylation levels to normal in cancer cells. We observed dose-dependent reduction in the endogenous and exogenous protein expression levels of KAT8 (also known as human MOF), a member of the MYST family of HATs, and its corresponding histone acetylation at H4K5, H4K8, and H4K16 in chemotherapy drug gemcitabine (GEM)-exposed T24 bladder cancer (BLCA) cells. Interestingly, the reduction in MOF and histone H4 acetylation was inversely proportional to GEM-induced γH2AX, an indicator of chemotherapy drug effectiveness. Furthermore, pGL4-MOF-Luc reporter activities were significantly inhibited by GEM, thereby suggesting that GEM utilizes an MOF-mediated anti-BLCA mechanism of action. In the CCK-8, wound healing assays and Transwell ® experiments, the additive effects on cell proliferation and migration were observed in the presence of exogenous MOF and GEM. In addition, the promoted cell sensitivity to GEM by exogenous MOF in BLCA cells was confirmed using an Annexin V-FITC/PI assay. Taken together, our results provide the theoretical basis for elucidating the anti-BLCA mechanism of GEM.

Nasal tip hypertrophy is one of the common nasal tip morphological abnormalities in clinical practice. We make a reasonable and comprehensive treatment plan only when correctly understanding the mechanism of nasal tip hypertrophy. In this paper, the mechanism and treatment of nasal tip hypertrophywere analyzed and summarized in order to provide some guidance for rhinoplastic surgeons.

Nasal tip hypertrophy is one of the common nasal tip morphological abnormalities in clinical practice. A comprehensive treatment regimen is possible only when one can correctly understand the mechanism of nasal tip hypertrophy. In this paper, the mechanism and treatment of nasal tip hypertrophy were analyzed and summarized in order to provide some reference for rhinoplastic surgeons.

Objective To investigate the therapeutic value and possible mechanism of diammonium glycyrrhizinate (DG) in treatment of airway remodeling in a murine model of chronic asthma. Methods Thirty male BALB/C mice were randomly divided into control group, OVA+DG group and OVA group (n=10). HE staining was used to observe the pathological changes, and Masson's staining was used to detect and measure collagen deposition. Alpha-SMA and PPARγmRNA expressions were analyzed by RT-PCR, and the protein expressions ofα-SMA and PPARγwere measured by Western blotting. Results After 75 days of OVA sensitization and challenge, obvious pathological changes occurred in the lung tissues, which was more severe in OVA group than in OVA+DG group. Collagen deposition was significantly increased after OVA stimulation, but was obviously milder in OVA+DG group than in OVA group. OVA-induced up-regulation ofα-SMA was notably attenuated by DG injection. The expression of PPARγ was markedly down-regulated after OVA stimulation but was substantially enhanced after DG intervention. Conclusion DG can inhibit airway smooth muscle proliferation possibly through up-regulation of PPARγ in a murine model of chronic asthma.

Objective To investigate the therapeutic value and possible mechanism of diammonium glycyrrhizinate (DG) in treatment of airway remodeling in a murine model of chronic asthma. Methods Thirty male BALB/C mice were randomly divided into control group, OVA+DG group and OVA group (n=10). HE staining was used to observe the pathological changes, and Masson's staining was used to detect and measure collagen deposition. Alpha-SMA and PPARγmRNA expressions were analyzed by RT-PCR, and the protein expressions ofα-SMA and PPARγwere measured by Western blotting. Results After 75 days of OVA sensitization and challenge, obvious pathological changes occurred in the lung tissues, which was more severe in OVA group than in OVA+DG group. Collagen deposition was significantly increased after OVA stimulation, but was obviously milder in OVA+DG group than in OVA group. OVA-induced up-regulation ofα-SMA was notably attenuated by DG injection. The expression of PPARγ was markedly down-regulated after OVA stimulation but was substantially enhanced after DG intervention. Conclusion DG can inhibit airway smooth muscle proliferation possibly through up-regulation of PPARγ in a murine model of chronic asthma.