Objective:To observe influence of qingzhifugan pellet on mixed-type animal model of fatty liver with chronic hyperlipemia and alcoholized hepatic damage. Methods:The mixed-type animal model of fatty liver was established by administering with high lipids and alcohol feeds. Therapeutic experiments were conducted with a self-made new drug the qingzhifugan pellet. The efficacy of the tested drug was evaluated comprehensively by such measures as sero-level of lipids and ferments,as well as the histological pathology of liver. Results:It was shown that the tested drug can decrease the sero-level of lipids,promote the metabolism of lipids in liver,recover the alcoholized hepatic damage,and relieve the liver fat denaturation. Conclusion:It suggested that the tested drug possessed certain effect for treating or improving chronic hyperlipemia and alcoholized hepatic damage in the animal model.

OBJECTIVE:To investigate the current situation of unreasonable prescriptions in outpatient and emergency depart-ments of our hospital,and to provide reference for rational drug use in the clinic. METHODS:The evaluation of outpatient and emergency prescriptions in our hospital during 2013-2015 were summarized and analyzed. Irrational prescriptions were divided into 3 categories,involving 19 items. The main,secondary and general factors of irrational prescriptions were analyzed by Pareto chart. RESULTS:Among 19 types of irrational prescriptions,main factors included unsuitable drug selection,inappropriate usage and dosage,inappropriate drug combination,prescribing not in accordance with the antibiotics management regulations,incomplete di-agnosis. No indications of medication,drug dosage beyond the regulations ofthree urgent seven slowwere treated as the second-ary factors. Other 12 items were general factors. CONCLUSIONS:According to the main and secondary irrational drug use types, clinical pharmacists should carry out effective intervention and pharmaceutical care to improve the level of rational drug use and en-sure the safety of clinical drug use.

OBJECTIVETo probe into effective surgical procedures and improve the outcome of treatment for patients with severe hepatic injury.

METHODSA retrospective study involving 113 patients with severe hepatic trauma (AAST grade IV and V) during the past 12 years was carried out. Ninety-eight patients underwent surgical treatment. Surgical interventions including hepatectomy or direct control of bleeding vessels by finger fracture technique with Pringle maneuver, selective ligation of hepatic artery, retrohepatic caval repair with total hepatic vascular occlusion, and perihepatic packing were mainly used.

RESULTSIn the 98 patients treated operatively, the survival rate was 69.4% (68/98). Among 40 patients with juxtahepatic venous injury (JHVI), 15 were cured with the maximum blood transfusion of 12,000 ml. Eight cases of Grade IV injury treated nonoperatively were cured. The percentage of failure of nonoperative management was 42.9% (6/14). The overall mortality rate was 32.7% (37/113), and 57% of the deaths were due to exsanguination.

CONCLUSIONSReasonable surgical procedures based on classification of hepatic injuries can increase the survival rate of severe liver trauma. Accurate perihepatic packing is effective in dealing with JHVI.

Adolescent ; Adult ; Age Factors ; Aged ; Female ; Hemostasis, Surgical ; methods ; Hepatectomy ; methods ; mortality ; Humans ; Injury Severity Score ; Laparotomy ; methods ; Liver ; injuries ; surgery ; Liver Diseases ; etiology ; mortality ; surgery ; Male ; Middle Aged ; Prognosis ; Retrospective Studies ; Risk Assessment ; Sex Factors ; Survival Rate ; Treatment Outcome

OBJECTIVETo detect mutations of the NF1 gene in two sporadic cases with neurofibromatosis type 1 (NF1) and explore their molecular mechanisms.

METHODSClinical data of the two patients was collected. Genomic DNA was extracted from peripheral blood samples. Specific primers were designed to exclude pseudogenes. PCR was performed to amplify all coding exons of the NF1 gene. PCR products were directly sequenced.

RESULTSTwo novel mutations of the NF1 gene (c.1019-1020delCT in exon 9 and c.7189G to A in exon 48) were respectively identified in the two patients but not among their unaffected parents or 100 healthy controls.

CONCLUSIONMutations of the NF1 gene may have predisposed to the NF1 in the two patients.

OBJECTIVETo investigate the different effects of an angiotensin II type 1 (AT(1)) receptor antagonist, losartan, and an angiotensin converting enzyme (ACE) inhibitor, fosinopril, on cardiomyocyte apoptosis, myocardial fibrosis, and angiotensin II (Ang II) in the left ventricle of spontaneously hypertensive rats (SHRs).

METHODSSHRs of 16-week-old were randomly divided into 3 groups: SHR-L (treated with losartan, 30 mg.kg(-1) x d(-1)), SHR-F (treated with fosinopril, 10 mg x kg(-1) x d(-1)), and SHR-C (treated with placebo). Each group consisted of 10 rats. Five rats, randomly selected from each group, were killed at the 8th and 16th week after treatment. Cardiomyocyte apoptosis, collagen volume fraction (CVF), perivascular collagen area (PVCA) and Ang II concentrations of plasma and myocardium were examined.

RESULTSCompared with the controls at the 8th and 16th week, systolic blood pressures were similarly decreased in both treatment groups. Left ventricular weight and left ventricular mass indexes were significantly lower in both treatment groups. However, the latter parameter at the 16th week was reduced to a less extent in the fosinopril group than that in the losartan group. Compared with the controls, cardiomycyte apoptotic index was significantly reduced at the 8th week only in the fosinopril group, and at the 16th week in both treatment groups. The index of the fosinopril group was lower than that of the losartan group at the latter endpoint examined. Compared with the controls, the left ventricular collagen volume fraction and perivascular collagen area at the 8th and 16th weeks were significantly reduced in the SHRs treated with either fosinopril or losartan. However, the collagen volume fraction at the latter endpoint in the fosinopril group was lower than that in the losartan group. Compared with the controls at endpoints, plasma and myocardium Ang II levels were significantly increased in the losartan group. However, plasma Ang II concentrations were not altered, and myocardium Ang II concentrations at the 8th and 16th weeks were significantly reduced in the fosinopril group.

CONCLUSIONSBoth losartan and fosinopril could effectively inhibit cardiomyocyte apoptosis and myocardial fibrosis and reverse heart hypertrophy. Fosinopril may be more effective in these cardioprotective effects, suggesting that the effects of both drugs are related to the inhibition of myocardium renin-angiotension-aldsterone system.

Angiotensin II ; analysis ; Animals ; Antihypertensive Agents ; therapeutic use ; Apoptosis ; drug effects ; Blood Pressure ; drug effects ; Fibrosis ; Fosinopril ; therapeutic use ; Hypertension ; complications ; drug therapy ; Hypertrophy, Left Ventricular ; drug therapy ; Losartan ; therapeutic use ; Myocardium ; chemistry ; pathology ; Rats ; Rats, Inbred SHR

Objective To investigate the incidence of insomnia and its influencing factors in the outpatients with cardiovascular diseases in a general hospital.Methods A total of 956 consecutive cases of the outpatients was collected from March 2016 to September in the department of cardiology patients in this general hospital.Insomnia was diagnosed with the 2012 Chinese adult insomnia diagnosis and treatment guidelines.All subjects underwent clinical examination,generalized anxiety scale (GAD-7),patient health questionnaire depression scale (PHQ-9),and self-made demographic sociology information questionnaire.Results A total of 925 patients with completed data was included in the analysis data.The insomnia incidence rate was 51.4％.The insomnia incidence rates were 57.8％ and 37.6％ in the patients with and without cardiovascular diseases.The difference was statistically significant (P ＜ 0.01) between both groups.The insomnia incidence rates in the patients with hypertension,coronary heart disease,arrhythmia,hypertension combined with coronary heart disease and other cardiovascular diseases were 50.8％,56.3％,53.2％,63.0％,and 54.3％,respectively.There were significant differences between the groups (P ＜ 0.05).The incidence of anxiety or depressive symptoms was 44.5％ in all investigators.Insomnia incidence rates were 75.6％ and 32.0％ in the subjects with and without anxiety or depressive symptoms.The difference was statistically significant (P ＜ 0.01) between both groups.Multivariate logistic regression analysis showed that gender,type A personality,family income satisfaction,cardiovascular diseases and anxiety/depression were independent factors to affect the occurrence of insomnia.Conclusions The insomnia incidence rates was high in the outpatients from the department of cardiology of general hospital.The main factors that affect the occurrence of insomnia include psychological,social aspects,and cardiovascular diseases.

OBJECTIVE: To explore the genetic basis for a sporadic case with neurofibromatosis type 1 (NF1). METHODS: Peripheral blood samples were collected from the patient, his unaffected parents and 100 healthy controls. The NF1 gene was detected by PCR and direct sequencing. RESULTS: The patient was found to carry a novel nonsense variant c.4339C>T (p.Q1447X) in exon 33 of the NF1 gene. The same variant was not found in his unaffected parents and the 100 healthy controls. CONCLUSION The c.4339C>T (p.Q1447X) variant probably underlies the pathogenesis of NF1 in this patient.

OBJECTIVETo analyze the clinical and genetic features of 9 ethnic Han Chinese patients with disseminated superfacial actinic porokeratosis (DSAP).

METHODSGenomic DNA was extracted from peripheral blood samples collected from the patients. PCR and direct sequencing were carried out for five patients from a family, 4 sporadic cases, and 120 healthy controls to identify potential mutations of four genes (MVK, MVD, PMVK, FDPS) involved in the mevalonate pathway as well as SLC17A9, SSH1, and SART3 genes. Pathogenecity of suspected mutations were assessed with SIFT, and Polyphen-2 scores.

RESULTSA c.746T>C mutation was identified in the family and two sporadic cases, while a c.875A>G mutation was identified in another sporadic case. No mutation was identified in the remainder genes among all patients. Scoring has suggested that the c.746T>C and c.875A>G mutations of the MVD gene are probably pathogenic.

CONCLUSIONc.746 T>C and c.875A>G of the MVD gene are most common mutations. Skin rashes of the patients have a strong connection with the sunlight, albeit a significant difference among patients was discovered.

Aged, 80 and over ; Case-Control Studies ; Female ; Humans ; Male ; Middle Aged ; Mutation ; genetics ; Pedigree ; Porokeratosis ; genetics

OBJECTIVETo screen for KIT gene mutations in two Han Chinese pedigrees affected with Piebaldism.

METHODSClinical data of the pedigrees was collected. Genomic DNA was extracted from blood samples collected from the pedigrees and 120 unrelated healthy controls. All coding exons of the KIT gene were subjected to PCR amplification and direct sequencing.

RESULTSTwo missense mutations, c.1861G>A(p.Ala621Thr) and c.1872G>A(p.Met624Ile), were identified respectively in the two pedigrees. Neither mutation was found among healthy members from the respective pedigree and the 120 unrelated healthy controls. c.1872G>A is a novel mutation.

CONCLUSIONMutations of the KIT gene may affect the structure and function of the transmembrane receptor KIT, which lead to the disease.

Ubiquitination is one of the most important post-translational modification processes in eukaryotic cells,in which the ubiquitin molecules and/or ubiquitin chains are covalently transferred to the substrate after a series of enzymatic cascade reactions involving the activating (E1),conjugating (E2) and ligating (E3) enzymes.Coupling to the 26S proteasome complex to form the Ubiquitin-Proteasome System (UPS),ubiquitination plays an essential role in controlling protein stability,thereby maintaining the dynamic balance of the key cellular proteins.Besides,ubiquitination is also involved in a wide range of protein degradation-independent events,such as gene transcription and translation,signal transduction,DNA repair and endocytoais,exerting a key function in response to exogenous stimuli and the cellular homeostasis.Similar to kinases,components of the ubiquitination system are often dysregulated,leading to a variety of diseases,such as cancer.Recently,accumulating evidence has shown an increasing number of dysregulated ubiquitination processes in osteosarcoma (OS).Herein,this review briefly provides current perspectives on the aberrance of ubiquitination-associated factors and their roles in OS,providing novel insight into potential therapeutic targets of OS.