Objective To study the relationship of peripheral vascular disease(PVD) with gender and serum uric acid in patients with type 2 diabetes.Methods Lower extremities of 82 male and 70 female patients with type 2 diabetes were screened for PVD by color Doppler uhrasonography,and the levels of serum uric acid,fasting blood glucose,glycosylated hemoglobin and serum lipid were examined.Results In male,serum uric acid(328.12?107.30) ?mol/L,age(65.00?9.66) yrs,durations of diabetes(7.38?6.17) yrs, HBA_1Cc(7.74?1.83)% were significantly higher in the diabetic patients with PVD than those in patients without PVD.And these changes were not shown in female patients.In male,the detectable rate of PVD(82.14%)in diabetics with high level uric acid was also increased than that in normal uric acid group(53.70%).Conclusion The higher level of serum uric acid in type 2 diabetics was closely related with the occurrence of peripheral vascular disease in male.So we should actively control the level of serum uric acid in male.

The clinical data of one case of laryngeal neuroendocrine carcinoma in our hospital were respectively analyzed. The patient was a 61-year-old male, and complained of progressive pain of right ear for 7-year, it was misdiagnosed as glossopharyngeal neuralgia and larynx hemangioma. This patient was achieved total laryngectomy and bilateral cervical lymph nodes dissection. As of 12 months after surgery, the patient remains under follow-up observation, and no findings indicating obvious recurrence or metastasis has been observed. This disease is a rare and highly malignant tumor that is lack of specific feature in clinical performances. Recognition at larynx is essential so that proper patient management can be initiated.
Carcinoma, Neuroendocrine ; diagnosis ; therapy ; Humans ; Laryngeal Neoplasms ; diagnosis ; therapy ; Male ; Middle Aged

Objective To investigate the inhibitory effects and mechanism of ginsenoside Rg3 on vasculogenic mimicry of human breast cancer MCF-7 cell line. Methods The MCF-7 cells at logarithmic growth phase were obtained, and were cultured with different concentrations (0, 20, 50, 100, 150 and 300 mg/L) of ginsenoside Rg3. Cells cultured without Rg3 were served as controls. The IC50 were determined by CCK8 assay and anti-angiogenic effects were performed for testing the potential of tube-like structure (TLSs) formation. The expression levels of VEGF-A, MMP 9 and HIF-1αwere detected by Western blotting and real-time PCR. The secreted contents of VEGF-A and MMP9 were detected by enzyme linked immunosorbent assay (ELISA). Results The ginsenoside Rg3 suppressed the proliferation of MCF-7 cells in a dose-dependent manner, in which IC50 was (115.34±8.50) mg/L. The formation numbers of TLSs in MCF-7 cells were significantly inhibited by Rg3 in concentration dependent manner in 50 mg/L, 100 mg/L and 150 mg/L for (19.0 ± 1.0), (15.0 ± 1.5), and (10.0±1.7) vs. controls (22.0±1.8, F=150.805, P<0.05). The mRNA and protein expression levels of VEGF-A, MMP9 and HIF-1αprotein were inhibited by 50 mg/L,100 mg/L and 150 mg/L Rg3 vs. controls (P<0.05). Meanwhile, the contents of VEGF-A in MCF-7 cell supernatant was down-regulated by 50 mg/L,100 mg/L and 150 mg/L Rg3 vs. controls (P<0.05). The contents of MMP-9 in MCF-7 cell supernatant was down-regulated by 100 mg/L and 150 mg/L Rg3 vs. controls (P<0.05). There was no significant difference in MMP-9 expression between 50 mg/L group and control group. Conclusion The ginsenoside Rg3 is able to inhibit the vasculogenic mimicry of MCF-7 cells, which may be related with the down-
regulation of VEGF-A, MMP9 and HIF-1α.

Vectors used to carry foreign genes play an important role in gene therapy, among which, the adeno-associated virus (AAV) has many advantages, such as nonpathogenicity, low immunogenicity, stable and long-term expression and multiple-tissue-type infection, etc. These advantages have made AAV one of the most potential vectors in gene therapy, and widely used in many clinical researches, for example, Parkinson's disease. This paper introduces the biological characteristics of AAV and the latest research progress of AAV carrying neurotrophic factor, dopamine synthesis related enzymes and glutamic acid decarboxylase gene in the gene therapy of Parkinson's disease.
Animals ; Aromatic-L-Amino-Acid Decarboxylases ; genetics ; Dependovirus ; genetics ; Gene Transfer Techniques ; Genetic Therapy ; Genetic Vectors ; Glial Cell Line-Derived Neurotrophic Factor ; genetics ; Glutamate Decarboxylase ; genetics ; Humans ; Nerve Growth Factors ; genetics ; Neurturin ; genetics ; Parkinson Disease ; therapy

China ; Humans ; Laparoscopy ; education ; Mentors ; Urology ; education

Objective To investigate the molecular mechanism of bone marrow mesenchymal stem cells (BM-MSCs) in repairing cisplatin-induced acute renal injury.Methods The rats were injected 6 mg/kg of cisplatin intraperitoneally,and bone marrow mesenchymal stem cells (BM-MSCs group) or PBS (PBS group) were injected respectively via tail vein after 24 hours.The rats without injecting cisplatin were selected as a normal control group.The repair effect of BM-MSCs on renal injury was observed by HE staining and immunohistochemistry.In addition,NRK-52E cells were cultured in vitro and treated with cisplatin for 6 hours.Then,NRK-52E cells were continued to culture for 48 hours or co-cultured with BM-MSCs for 48 hours,and NRK-52E cells untreated with cisplatin were used as a control.The expression levels of miR-92b and its target gene PTEN were detected by qRT-PCR,and the expression level of p-Akt by western blot.Results HE staining showed that the tubular protein casts in BM-MSCs group were significantly less than that in PBS group,and that the renal tubular structure was significantly improved in BM-MSCs group.Immunohistochemical staining indicated that the number of cells expressing proliferating cell nuclear antigen (PCNA) in BM-MSCs group (131.0 ± 14.4) was significantly higher than that in PBS group (42.2 ±6.1,t =11.28,P ＜0.01).qRT-PCR results showed that in the vivo experiment,compared with the expression level of miR-92b and PTEN in the normal control group (1.11 ± 0.78,1.01 ± 0.21),PBS group were (4.64 ± 1.06) and (0.61 ± 0.2),respectively (all P ＜ 0.05);BM-MSCs group were (2.27 ± 0.81) and (1.1 ± 0.1),respectively (all P ＜ 0.05).In vitro experiment,compared with the expression level of miR-92b and PTEN in the negative control group (1.12 ± 0.77,1.02 ± 0.13),cisplatin group were (7.64 ± 0.72) and (0.58 ± 0.2),respectively (all P ＜ 0.05),cell group were (4.38 ± 0.50) and (1.15 ± 0.23),respectively (all P ＜ 0.05).Western blot results showed that compared with the expression level of p-Akt in cisplatin group (0.96 ± 0.18),p-Akt expression in cell group was (2.11 ± 0.11,P ＜ 0.01).Conclusion BM-MSCs may repair the cisplatin-induced acute renal injury via down-regulating the expression level of miR-92b.

OBJECTIVE:To determine serum concentrations of western medicines in patients treated with "traditional Chinese antiepileptic medicine" alone and to evaluate the curative effects.METHODS:A total of 60 epileptic patients who visited our hospital between Feb.1997 and June 2006 were subjected to plasma drug level monitoring and during which the patients were treated with "traditional Chinese antiepileptic drugs" alone.Plasma concentrations of 4 kinds of western medicin-es were determined by FPIA.RESULTS:Of the 60 cases,valproic acid,carbamazepine,phenytoin and phenobarbitone were detected in 18,40,41,and 47 cases/times,respectively.On average,more than two kinds of western medicines were detected in every patient,and the blood concentrations were mostly beyond effective plasma drug concentration.The total curative effects were unsatisfactory.CONCLUSION:The fact that western medicine ingredients detected in these traditional Chinese antiepileptic medicines is inconformity with medication principle of epilepsy.Traditional Chinese antiepileptic medicines should be used with caution in the clinic in the treatment of epileptic patients.

T, p.R394W in exon 9.

OBJECTIVE: Investigate common deafness gene mutations in patients with severe and profound non-syndromic hearing loss in Liaoning in order to understand their hereditary etiologies and characteristics at the molecular level. METHOD: Peripheral blood samples were obtained and the DNA templates were extracted from 128 non-syndromic hearing loss patients who are sporadic in clinics. The deafness gene chip was applied to detect hot-spot deafness gene mutations including GJB2, GJB3, SLC26A4 and mitochondrial 12S rRNA. Deafness etiology questionnaires, pure tone audiometry, auditory brainstem response, tympanometry and temporal bone CT were also applied. RESULT: Various types of gene locus mutations were seen in 52 of the 128 patients (40.6%); (1) GJB2 gene mutations (n=22) included c. 235 del C homozygous mutation (n=10), c. 235 del C heterozygous mutation (n=5); c. 176_191 del 16 heterozygous mutation (n=l); c 35 del G heterozygous mutation (n=l); c. 235 del C/c. 299_300 del AT mutation (n=l), c. 235 del C/c. 176_191 del 16 mutation (n=l), c. 35 del G/c. 176_191 del 16 mutation (n=l); c. 299_300 del AT/c. 919-2 A>G mutation (n=l), c. 235 del C/c. 919-2 A>G mutation (n=l). (2) SLC26A4 gene mutations (n=30) included c. 919-2 A>G homozygous mutation (n=6), c. 919-2 A>G heterozygous mutation (n=17), c. 2168 A>G homozygous mutation (n=l), c. 2168 A>G heterozygous mutation (n=2), c. 2168 A>G/c. 919-2 A>G mutation (n=2), c. 919-2 A>G/GJB2 c. 235 del C mutation (n=2); (3) No GJB3 and mitochondrial 12S rRNA mutation. Genetic deafness was confirmed at the gene level in 24 cases (18.8%) and 28 patients (21.9%) were diagnosed as carriers of genetic deafness gene mutations. CONCLUSION Genetic deafness occupies a large population in deaf community in Liaoning. Molecular genetic screening for these mutations and genetic counseling are effective methods to prevent the occurrence of hereditary hearing loss and provide theoretical guidance.
Adolescent ; Child ; Child, Preschool ; China ; Connexins ; DNA Mutational Analysis ; Deafness ; genetics ; Female ; Genetic Testing ; Humans ; Infant ; Male ; Mutation

Objective To explore the effect of lysophosphatidic acid(LPA)on blood-brain barrier(BBB) permeability and its possible mechanism.Methods LPA or LPA+suramin(L+S)were stereotaxically injected into the right eaudate nucleus in SD rats in vivo.Evans blue(EB)was used to quantitatively measure the permeability of BBB at different time points.The expression of matrix metalloproteinase-9 was detected by immunohistochemistry technique.The pathological ultrastruetural changes of BBB were assessed by transmission electron microscopy.Results The BBB permeability began to increase after LPA administered into ipsilateral eaudate nucleus,and reached the peak at 24h.Then the permeability of BBB gradually lowered after 48h.In comparison with the same time points of control group,there were quite significant differences(P＜0.01).After L+S was injected,the change of BBB permeability had differences in comparison with those of LPA group in the same time points,(P＜0.05).MMP-9 positive cells were mainly vascular endothelial cells.The numbers of MMP-9 positive blood vessels grew at 6h in LPA group,and the expression of it reached maximum at 24h,then the number of it decreased at 48h,showing significant statistical differences in comparison with the L+S group(P＜0.01),It was observed microscopically that ultrastrueture of BBB of the LPA group was changed sharply,such as basement membrane roughed and fragmented,astroeyte end-feet swolled markedly and perivaseular space enlarged obviously.But there were no remarkable changes in BBB in L+S group.Conclusion LPA can induce increase of BBB permeability and its possible mechanism is the strong expression of MMP-9 protein produeted by endothelial cells through the mediation of LPA receptor,leading to degradation of basement membrane.