[Objective]To discuss the anatomy and etiology of cubital tunnel syndrome.[Method]The clinical data and surgical findings of sixty five cubital tunnel syndrome cases were analyzed,and the per-operative electromyogram results of twenty five cases were studied.[Result]Hypertrophy of arcuate ligament resulted in compression and abrasion of ulnar nerve in sixty patients;we found that the ulnar nerve conduct velocity decreased(the average speed was 27.97 m/s),motional amplitude also decreased(the average voltage was 1.95 mv),and latent period prolonged(the average time was 5.41 ms)after pre-operative electromyogram.[Conclusion]The major etiology of cubital tunnel syndrome is chronic injury with sustained compression of ulnar nerve around elbow joint.Careful physical examination of ulnar nerve function and pre-operative electromyogram will help us to diagnose the cubital tunnel syndrome.Cubital tunnel syndrome should be differentiated from tardy ulnar nerve palsy of other sites.

Objective To investigate the effects of osteogenic growth peptide (OGP) in combination with extracorporeal shock waves (ESWs) on osteoblast proliferation.Methods Passaged cells were divided into four groups for different treatments:a control group,an OGP + ESW group,an ESW group,and an OGP group.After the respective treatments,the cells were cultured for 24 h,48 h and 72 h and counted using methylthiazdy tetrazolium (MTT) and an inverted fluorescence microscope. Immunohistochemical examination was used for detecting protein kinase A (PKA)activity,and a reverse transcription-polymerase chair reaction (RT-PCR) was used for examining PKA mRNA expression at 24 and 48 hours.Results Cell counting revealed that cell proliferation in the OGP + ESW,ESW and OGP groups was significantly promoted compared with the control group.Cell proliferation was greatest in the OGP + ESW group.The immunohistochemical examination showed positive staining intensities in the OGP + ESW,ESW and OGP groups significantly higher than in the control group.The positive staining intensity in the OGP + ESW group was again the highest.PKA activity was also significantly higher in the OGP + ESW,ESW and OGP groups than in the control group with the level in the OGP + ESW group the highest.Conclusion OGP in combination with ESW has a synergistic effect in stimulating osteoblast proliferation and growth.

BACKGROUND:Carboxymethylated chitosan is shown to promote some kinds of cells proliferation, but its effects on proliferation of Schwann cells need further studies.
OBJECTIVE:To investigate the effects of carboxymethylated chitosan on proliferation of Schwann cells and expression of nuclear factor-κB in cultured Schwann cells.
METHODS:Schwann cells from Sprague-Dawley rats at logarithmic growth phase were seeded in 96-wel plates, and cultured respectively with PBS, 0, 10, 50, 100, 200, 500, 1 000 mg/L carboxymethyl chitosan for 24 hours. cellproliferation was detected using the cellcounting kit-8 assay. After trypsin digestion, Schwann cells from Sprague-Dawley rats at logarithmic growth phase were used to prepare cellsuspensions, which were seeded in 6-wel cellculture plates and cultured respectively with 50, 100 and 200 mg/L carboxymethyl chitosan and PBS for 24 hours. Then, 5-bromo-2-deoxyuridine, real-time PCR and western blot assay were performed.
RESULTS AND CONCLUSION:cellcounting kit-8 and 5-bromo-2-deoxyuridine detection results showed that carboxymethyl chitosan at 50-1000 mg/L, especial y at 200-500 mg/L, could promote Schwann cellproliferation. Real-time PCR and western blot results showed 50-200 mg/L carboxymethyl chitosan could promote nuclear factorκB mRNA and protein expression in Schwann cells in a dose-dependent manner, suggesting carboxymethyl chitosan can promote Schwann cellproliferation and expression of nuclear factor-κB in Schwann cells cultured in vitro.

Objective To investigate the incidence of dental fluorosis,urinary fluoride level and intelligence of children who lived in the coal-burning-borne endemic fluorosis areas and to reveal the effects of comprehensive control measures on intelligence of children in this area.Methods Children aged 8-12 who lived in coal-burning-borne endemic fluorosis areas in Bijie City of Guizhou Province were selected and divided into two groups according to the duration of comprehensive treatments given:long treatment group (Xiaba Village and Zhongtun Village,furnace stovewas changed and comprehensive control measure of health education was carried out for more than 3 years) and short treatment group(Chadi Village and Maoliping Village,stoves were improved and health education time ＜ 1 year).The children who lived in a non-fluorosis area were selected as controls in 2012.Dental fluorosis was diagnosed by the method of Dean; urinary fluoride was analyzed by the method of fluoride-ion selective electrode; and the intelligence quotient (IQ) was measured by Raven's Standard Progressive Matrices Test.Results The number of children surveyed in control group was 104,long treatment group was 298,short treatment group was 339,and the incidence rates of dental fluorosis were 0 (0/104),725％(216/298) and 85.2％ (289/339),respectively,and the incidence rates of dental fluorosis in children lived in the endemic fluorosis areas were significantly increased compared with that of control group; the difference of incidence rates between long treatment group and short treatment group was statistically significantly(x2 =15.736,P ＜ 0.01).Urinary fluoride content were (2.33 ± 0.18) and (3.03 ± 0.16)mg/L,respectively,compared with the control group[(1.34 ± 0.64) mg/L],the values in endemic fluorosis areas were significantly higher(F =306.53,P ＜ 0.01).Above average IQ of children in the control group was 97.1％ (101/104),which was significantly higher than that of long and short treatment groups; after a lengthy treatment,mental retardation detection rate was significantly lower in the low-age group,8-10 year-old ehildren(x2 =7.542,P ＜ 0.01).Urinary fluoride content was negatively correlated with the level of IQ (r =-0.553,P ＜ 0.01).Conclusions The intelligence development of children in coal-burning-borne endemic fluorosis area is significantly delayed.After a certain period of comprehensive treatment,the decreased level of cognition is inhibited and the mental retardation in the low-age group is improved.

OBJECTIVETo investigate the effects of Pyrroloquinoline quinine (PQQ) on hydrogen peroxide-induced apoptosis of Schwann cells (SCs) and its mechanism.

METHODSSCs were isolated and cultured in vitro, and identified by S-100 immunofluorescence staining. The cultured SCs were divided into control group, hydrogen peroxide-treated group, hydrogen peroxide and PQQ treated groups. The intracellular superoxide dismutase (SOD) and malondialdehyde (MDA) content was detected; the apoptotic rate of SCs induced by hydrogen peroxide was determined by flow cytometry assay. The Hoechst33342 staining was used to detect the nuclear fragmentation and apoptotic nuclear condensation of SCs; the Rhodamine123 staining was used to detect the changes of mitochondrial membrane potential in SCs, the Western blot analysis was used to detect the expression of Bcl-2 in hydrogen peroxide induced SCs.

RESULTSThe SOD activity was significantly decreased and MDA level was increased in H2O2 induced SCs (P < 0.05), after addition of PQQ, the SOD content increased and MDA content decreased (P < 0.05). Flow cytometry results showed that the early apoptotic rate was 58.8% in H2O2 induced SCs, which has significant difference compared with the control group (P < 0.05), after addition of 10, 50, 100 nmol/L PQQ, the apoptotic rates were reduced to 33.7%, 18.7%, 3.9% respectively, showing significantly different with injured group (P < 0.05). Hoechst 33342 staining showed that H2O2 induced SCs had typical morphological characteristics, such as uptake of nuclear chromatin, nuclear shrinkage, nuclear fragmentation phenomenon. The proportion of apoptotic cells after PQQ treatment reduced. Rhodamine staining results showed that the H2O2 induced mitochondrial membrane potential reduction in SCs, which was reversed by addition of PQQ. Western blot analysis showed that the expression of Bcl-2 was decreased in H2O2 induced SCs, while it increased significantly after addition of PQQ (P < 0.05).

CONCLUSIONPQQ has a protective effect on oxidative stress-induced apoptosis of SCs.

Apoptosis ; drug effects ; Benzimidazoles ; Cell Nucleus ; drug effects ; DNA Fragmentation ; Fluorescent Dyes ; Humans ; Hydrogen Peroxide ; pharmacology ; Malondialdehyde ; metabolism ; Oxidants ; pharmacology ; Oxidative Stress ; Pyrroles ; pharmacology ; Quinine ; pharmacology ; Quinolines ; pharmacology ; Schwann Cells ; cytology ; drug effects ; Superoxide Dismutase ; metabolism

Objective To study the effects of carboxymethylated chitosan (CMCS) to nitric oxide (NO)-induced apoptosis on rat chondrocytes,and explore p38MAPK signal transduction pathway in the process and its mechanism.Methods The rat articular cartilage cells were cultured in vitro,collagen type-2 (collagen-2) immunohistochemical staining was used to identify the cartilage cells.The model of chondrocyte apoptosis was built by different concentrations of sodium nitroprusside (SNP) induction.The cells were divided into the control group,the SNP treated group SNP+CMCS treated group,and the SNP+p38 MAPK inhibitor SB203580 treated group.The apoptotic rate of chondrocytes was calculated by FCM,apoptotic nuclei was identified by Hoechst33342 stain,the mitochondrial membrane potential changes was detected by Rhodamine123 (Rho123) stain,the expression of p38 and p-p38 were detected by Western blotting analysis.Results 1-3 mmol/L SNP could induce chondrocyte apoptosis,the apoptotic rate was increased with the SNP increasing,the most obvious apoptosis was occurred in 3 mmol/L SNP treated chondrocytes,which was 69.8％ (P＜0.05).SNP could increase the nuclear fragmentation of chondrocytes,the cells with nuclear fragmentation was significantly higher than that in the control group.SNP could reduce mitochondrial membrane potential in chondrocytes,which decreased significantly compared with the control group.SNP could increase the p-p38 expression in chondrocytes,which was 4.3 times compared to the control group.CMCS of different concentrations could reduce the apoptotic rate of SNP-induced chondrocytes,which was 51.0％,29.9％ and 15.2％,which was decreased significantly (P＜0.05) when compared with 3 mmol/L SNP induced group,CMCS decreased the cells number of SNP-induced nuclear fragmentation.CMCS increased the mitochondrial membrane potential in SNP-induced chondrocytes.CMCS reduced the expression levels of p-p38 in SNP-induced chondrocytes.Conclusion CMCS has protective effect on SNP-induced apoptosis of chondrocytes.This process is completed by inhibiting the activity of p38 MAPK signal pathway.

Objective To explore the difference of DNA methylation levels between normal Schwann cells (NSCs) and activated Schwann cells (ASCs) in rats. Methods The adult Wistar rats were received sciatic nerve ligation and fed for 7 days. The ASCs and NSCs were separated from ligated sciatic nerves and brachial plexus respectively. Immunocytochemical staining of S-100 antibody was used to identify the cells. The growth condition of cells was detected by CCK-8 method. Methylated DNA immunoprecipitation sequencing (MeDIP-Seq) was applied to filter the differentially methylated regions in ASCs and NSCs. The distribution of differentially methylated genes related with axonal regeneration in chromosome was analyzed, and Gene ontology(GO)and PATHWAY analysis were also conducted. Results High purity of ASCs and NSCs were obtained successfully, which were both positive for S-100 antibody. In the same culture condition, ASCs showed a faster proliferation than that of NSCs. A total of 177 176 differentially methylated regions were found by MeDIP-Seq. Among them, 1 097 were located in the promoter (≤1 kb), 1 136 in the promoter (1-2 kb) and 567 on the CpG. After functional annotation of differentially methylated genes, 214 differentially methylated genes related with axonal regeneration were found in ASCs and NSCs. Compared with NSCs, 191 genes were up-regulated and 23 genes were down-regulated in ASCs. These genes were located on different chromosomes, most of which on chromosome 12 (22 genes) and the least on chromosomes M (2 genes). GO analysis indicated that the differential methylated genes were involved in axon growth, axon formation, axon elongation and axon guidance. The MAPK, cell adhesion molecules, Ras signaling pathway may be related with the differential methylated genes. Conclusion The methylation levels between ASCs and NSCs are significantly different, which are probably related with axon regeneration.

Objective To investigate the situation of medical waste management in medical institutions of Hubei Prov-ince,and put forward the improvement strategies.Methods The questionnaires were designed according to the relevant standards,situation of medical waste management in 75 hospitals in Hubei Province was investigated by stratified sampling, 73 available questionnaires were got.Results The construction of medical waste management software and hardware in 73 hospitals were basically met the requirements of the standards,the qualified rates in organization and system management, classification and disposal of medical waste in departments were all >90%;83.56% (61/73)of the hospitals carried out the best environmental practice(BEP)for medical waste;application of more than 40 kinds of disposable medical devices and supplies were reduced;76.71% (56/73)of hospitals’soft infusion bags were collected and recycled by designated company;only 21.54%(14/65)of hospitals send pathological chemical waste liquid to hazardous waste disposal center;disposal ways of orthopedic stainless steel plates were different,56.16% (41/73 )of hospitals treated plates as medical waste,only 35.62%(26/73)of hospitals informed patients how to deal with it,and signed informed consent with patients. Conclusion Medical waste management in medical institutions in Hubei Province has been paid more and more attention, but for special categories of medical waste disposal,such as soft infusion bags(bottles),orthopedic stainless steel plates, and pathological chemical waste liquid,there are some problems,training still needs to be strengthened,the classification and disposal of medical waste needs to be standardized further.

Objective To investigate the phototoxicity effects of the nanocompound of upconversion nanoparticles (UCNPs) on rat astrocytes in vitro.Methods The spinal astrocytes cells were cultured successfully in vitro and then incubated with the UCNPs-MC540 of various concentrations and exposured 980 nm infrared laser irradiation of different energy densities.The cell survival rates of each group were detected by MTT assay.The cellular morphology was observed via transmission electron microscope after photodynamic therapy.Results UCNPs-MC540 of different concentrations without laser irradiation or laser of different energy had no significant effects on cell survival rates.when cells incubated with 100 μg/ml UCNPs-MC540 for 12 h underwent laser irradiation of different energy,the cellular survival rates significantly decreased with the increased energy densities.when the cells incubated with UCNPs-MC540 of various concentrations for 12 h underwent laser irradiation of 2 000 J/cm2,the cellular survival rates significantly decreased with the increased concentrations.Compared with controls,the TEM show the apoptosis sign in the cells incubated with 200 μg/ml UCNPs-MC540 after laser irradiation of 2 000 J/cm2.Conclusion The UCNPs-MC540 mediated photodynamic therapy have effective killing effect on astrocytes by the mechanism of induction the apoptosis.

Objective To investigate the protective effects of carboxymethylated chitosan (CMCS) on nitric oxide (NO) induced apoptosis in rat chondrocytes, and the probable roles and mechanisms of PI3K/Akt signaling pathway in these process.Methods Rat knee articular cartilage was used as the source of chondrocytes, the cells were identified by immunohistochemical staining against collagen type Ⅱ, odium nitroprusside (SNP, 3 mmol/L) was used to establish the apoptotic models of chondrocytes.Cells were divided into four groups: the control group, the SNP-induced group, the SNP+CMCS treated group, the SNP+CMCS+PI3K inhibitor Wortmannin treated group.Cell proliferation were assessed by cell proliferation assay kit (CCK-8), the apoptotic rate of chondrocytes was determined by FCM with Annexin V-FITC/PI double staining, the expression levels of MMP-13 and TIMP-1 mRNA were detected by real-time polymerase chain reaction (PCR) analysis, the expression of Akt and p-Akt protein levels was detected by Western blotting analysis.One-way analysis of variance (ANOVA) statistical analysis was used to calculate the data.Results Three mmol/L SNP can inhibit proliferation (0.221±0.023), and the proliferation was reduced by 70％ compared with the control group (0.736±0.032, F=8.203, P=0.021);and the induced apoptosis in cultured chondrocytes could be observed.The apoptotic rate was (68.8±5.2)％.Increased MMP-3 and decreased TIMP-1 mRNA expression were observed in SNP-induced cells.After adding CMCS to SNP-induced chondrocytes, the proliferation was increased while apoptotic rate was decreased, the apoptotic rate decreased to (14.7±2.3)％.CMCS could promote the activation of p-Akt in SNP-induced chondrocytes and restore SNP-induced MMP-13 and TIMP-1 mRNA expression.Conclusion CMCS could protect apoptosis in SNP induced chon-drocvtes via activation of PI3K/Akt pathwav.