Objective To survey bacterium pollution state on the surface of medical equipment maintenance tools,and thenobserve the disinfection effect of ozone.Methods Totally 30 medical equipment maintenance tools including screwdriver,hexagona wrench and multimeter from certain hospital were placed in ozone disinfection cabinet,and then disinfected by ozoneup to 5 minutes.Samples on the surface of tools were collected by cotton swabs before and after disinfection,cultured for 48hours in 37 ℃,and then the bacterial colony counts were measured and analyzed,and pathogenicity bacteria were identified.The pollution couditions on kinds of tools were compared.Results The surface of the tools was polluted severely,bacterialcolony counts of which before disinfection reached (132.68±37.02) cfu/cm2,and decreased to (6.44±1.08) cfu/cm2 after 5-minutes' disinfecting.There was statistically significant difference in the bacterial counts before and after the disinfection (P＜0.01),and the inactivation ratio was up to 95.15％.Pathogenicity bacteria such as staphylococcus aureus and escherichia coliwere detected before the disinfection,and killed after that.The bacteria counts were significantly different in the three kindsof tools,and the screwdriver gained the highest count while the multimeter had the lowest one.Conclusion The surface ofmedical equipment maintenance tools is polluted by bacteria severely,including some pathogenicity bacteria,and should be disinfected regularly.Ozone can kill bacteria rapidly,and the tools can achieve sanitary standard after 5-minutes' ozone disinfecting.

Objective: To observe the clinical efficacy of mind-refreshing and balance-restoring needling method combined with Frenkel exercises in treating ataxia after cerebral stroke. Methods: The recruited 120 patients were randomized into an observation group and a control group, with 60 cases in each group. The control group was intervened by mind-refreshing and balance-restoring needling method, while the observation group was given additional lower-limb Frenkel exercises. Before and after treatment and at the follow-up, the ataxic lower-limb function was scored using Berg balance scale (BBS) and international cooperative ataxia rating scale (ICARS), and Barthel index (BI) was adopted to score the activities of daily living (ADL). Results: After treatment, the markedly effective rate was 70.2％ and the total effective rate was 96.5％ in the observation group, versus 39.7％ and 87.9％ in the control group, and the differences in the markedly effective rate and the total effective rate were statistically significant (P<0.01, P<0.05). The intra-group comparisons showed that the BBS, ICARS and BI scores after treatment and at the follow-up were significantly different from those before treatment in both groups (all P<0.01).There were significant differences in the BBS score between the two groups after treatment and at the follow-up (P<0.05, P<0.01); the between-group differences in the ICARS and BI scores were statistically insignificant after treatment (both P>0.05), while the between-group differences in the ICARS and BI scores were statistically significant at the follow-up (both P<0.05). The interaction effects between the scoring time of BBS and BI and the group factor were statistically significant (P<0.01, P<0.05). Conclusion: Mind-refreshing and balance-restoring needling can effectively improve the lower-limb ataxic symptoms and ADL after stroke; when combined with Fenkel exercises, this needling method can produce more significant efficacy.

OBJECTIVE: To observe the therapeutic effect of Bacillus acidi lactici on Helicobacter Pylori (Hp) infectious gastritis in Balb/c mouse model so as to explore a possible non-antibiotic treatment for Hp. METHODS: To establish a Balb/c mouse model with Hp infectious gastritis through inoculation of mankind Hp,32 Balb/c mice infected by Hp were randomly divided into 4 groups:Group 1(PPI trigeminy treatment group),Group 2 (Bacillus acidi lactici CL22 treatment group),Group 3 (Bacillus acidi lactici CL24 treatment group),and Group 4 (normal saline control group). Intragastric administration was given continuously for 10 days. Another 8 normal mice were chosen as Group 5(blank control group). All mice were killed after 4 weeks since last intragastric administration. Hp was detected by rapid urease test,Giemsa dying, and bacterial culture,and histopathologic changes in the gastric mucosa of mice were determined by H-E staining. RESULTS: There were significant differences in pathohistologic scores in sinus ventriculi among the 5 groups (F = 7.932, P = 0.000). The scores in Group 1, Group 2, Group 3, and Group 5 were obviously lower than those in Group 4 (P < 0.05), but there were not significant differences among Group 1, 2, and 5 (P>0.05). The pathohistologic score in Group 3 was obviously higher than that in Group 5 (P <0.05). There were significant differences in pathohistologic scores in corpus ventriculi among the 5 groups (F = 6.241, P = 0.001). The scores in Group 1,Group 2,Group 3,and Group 5 were obviously lower than those in Group 4(P <0.05), but there were not significant differences among Group 1, 2, 3,and 5 (P>0.05). There was significant difference in Hp eradication rates in sinus ventriculi among the 5 groups (chi2 = 16.923, P=0.002). The Hp eradication rates in Group 1 and 2 were obviously lower than those in Group 4 (P <0.05), but there was not significant difference between Group 1 and Group 2, Group 3 and Group 4 (P>0.05). There also were significant differences in Hp eradication rate in corpus ventriculi among the 5 groups (chi2 = 14.295, P=0.006). Of them, Group 1 and Group 2 were higher than Group 4 (P <0.05), but there were not obviously differences between Group 1 and 2,Group 3 and 4 (P>0.05). CONCLUSION Bacillus acidi lactici strain CL22 can effectively inhibit and eradicate Hp in Balb/c mouse model with Hp infectious gastritis in vivo. The therapeutic effect of Bacillus acidi lactici strain CL22 is equal to PPI + antibiotics and could be another choice of nonjantibiotic treatment for Hp.
Animals ; Antibiosis ; physiology ; Female ; Gastritis ; microbiology ; Helicobacter Infections ; microbiology ; therapy ; Helicobacter pylori ; Lactic Acid ; biosynthesis ; chemistry ; Lactobacillus ; metabolism ; physiology ; Male ; Mice ; Mice, Inbred BALB C ; Random Allocation

BACKGROUNDClinical observations have shown that the complex fractionated atrial electrogram (CFAE) associates with ganglionated plexus activity in the cardiac autonomic nervous system. This study aimed to investigate the impact of CFAE ablation on vagal modulation to atria and vulnerability to develop atrial fibrillation (AF).

METHODSTen adult mongrel dogs were involved. Cervical sympathovagal trunks were decentralized and sympathetic effects were blocked. CFAE was color tagged on the atrial 3-dimensional image and ablated during AF induced by S1S2 programmed stimulation plus sympathovagal trunk stimulation. Atrial effective refractory period (ERP) and vulnerability window (VW) of AF were measured on baseline and at vagal stimulation at 4 atrium sites. Serial tissue sections from ablative and control specimens received hematoxylin and eosin staining for microscopic examination.

RESULTSMost CFAE areas were localized at the right superior pulmonary quadrant, distal coronary sinus (CS(d)) quadrant, and proximal coronary sinus (CS(p)) quadrant (21.74%, separately). Sinus rhythm cycle length (SCL) shortening did not decrease significantly after ablation at the sites, including right atrial appendage, left atrial appendage, CS(d), and CS(p) (P > 0.05). ERP shortening during vagal stimulation significantly decreased after ablation (P < 0.01); the VW to vagal stimulation significantly decreased after ablation (P < 0.05). The architecture of individual ganglia altered after ablation.

CONCLUSIONSCFAE has an autonomic basis in dogs. The decreased SCL and ERP shortening to vagal stimulation after CFAE ablation demonstrate that CFAE ablation attenuates vagal modulation to the atria, thereby suppressing AF mediated by enhanced vagal activity. CFAE ablation could suppress AF mediated by enhanced vagal activity.

Animals ; Atrial Fibrillation ; therapy ; Autonomic Nervous System ; Catheter Ablation ; methods ; Dogs ; Electrophysiologic Techniques, Cardiac ; methods ; Electrophysiology ; Female ; Male

A boy aged 4 years and 2 months was found to have delayed language and motor development, instability of gait, poor eye contact, stereotyped behavior, and seizure at the age of 3 years. Physical examination showed special facial features, including plagiocephaly, blepharoptosis, wide nasal bridge, down-turned mouth corners at both sides, and low-set ears. There were only two knuckles at the little finger of the left hand. The anteroposterior and lateral films of the spine showed scoliosis; echocardiography showed ventricular septal defect; the Gesell Developmental Scale showed delayed language development and moderate intellectual disability; there were no abnormalities in the karyotype; genome-wide SNP arrays found a duplication in 12q24.21 region with a size of 1.03 Mb in chromosome 12, while this was not seen in his parents. The boy was diagnosed with MED13L syndrome. Point mutation, deletion, and duplication in the MED13L gene can lead to MED13L syndrome. The patients with different genotypes may have different phenotypes. Genome-wide SNP arrays may help with the diagnosis of this disease.
Child, Preschool ; Chromosome Deletion ; DNA Copy Number Variations ; Humans ; Intellectual Disability ; genetics ; Male ; Mediator Complex ; genetics ; Phenotype ; Polymorphism, Single Nucleotide ; Syndrome

BACKGROUNDPancreatic β cells are susceptible to fatty acid-induced apoptosis. The 17β-estradiol (E2) protects pancreatic β cells from apoptosis, mediated by the estrogen receptor-α (ERα). The mRNA level and promoter activity of leukemia-related protein (LRP) 16 were significantly increased by E2 in ER-α and LRP16 was a co-activator of ER-α. The aim of the study was to assess the effects of LRP16 on fatty acid-induced apoptosis in MIN6 cells.

METHODSCells with over-expressing LRP16 were obtained by lipidosome transfection. Insulin content and glucose-stimulated insulin secretion (GSIS) were examined by radioimmunoassay. Western blotting was applied to detect protein expression. Apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and flow cytometry. The forkhead boxO1 (FoxO1) subcellular localization was determined by immunocytochemical analysis.

RESULTSMIN6-LRP16 cells with overexpression of LRP16 were successfully established, and protein expression of LRP16 was 2.29-fold of that of control cells (MIN6-3.1, P < 0.05). Insulin content and GSIS in MIN6-LRP16 were substantially increased compared with those in control cells. When cells were stimulated with glucose, increased phosphorylation of extracellular signal-regulated kinase (ERK) 1/2 and serine-threonine kinase (Akt) were observed in MIN6-LRP16. When cells were under palmitate pressure, the TUNEL-positive rate in MIN6-LRP16 was (17.0 ± 0.5)%, while it in MIN6-3.1 was (22.0 ± 0.4)%. In palmitate-treated cells, attenuated Akt phosphorylation was observed, but the attenuation in Akt activity was partially restored in MIN6-LRP16 cells. Meanwhile, nuclear localization of FoxO1 in MIN6-LRP16 was apparently reduced compared with that in control cells.

CONCLUSIONSLRP16 regulated insulin content and GSIS in MIN6 cells by ERK1/2 and Akt activated way. Meanwhile, LRP16 overexpression protected MIN6 cells from fatty acid-induced apoptosis by partially restoring Akt phosphorylation and inhibiting FoxO1 nuclear redistribution. Therefore, LRP16 played important roles not only in insulin content and GSIS but also in the antilipotoxic effect mediated by Akt/FoxO1 signaling.

Animals ; Apoptosis ; drug effects ; Blotting, Western ; Cell Line, Tumor ; Fatty Acids ; pharmacology ; Forkhead Box Protein O1 ; Forkhead Transcription Factors ; genetics ; metabolism ; Mice ; Neoplasm Proteins ; genetics ; metabolism ; Phosphorylation ; drug effects ; Proto-Oncogene Proteins c-akt ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; drug effects ; genetics

OBJECTIVETo investigate the proper time of cryo-preserving tracheal allograft so as to minimize its antigenicity.

METHODSOn a dog model, this study was carried out by allografting a tracheal into a muscular flap formed with sternocephalic muscle and sternohyoid--sternothyroid muscle. The tracheal was treated with cryopreservation in defferent intervals. The viability of the graft was evaluated by the examination of fiberoptic bronchoscopy, histopathology and microangiography. The blood flow of the tracheal mucous was measured with a blood flowmeter and the survival area was decided in the calculation of the percentage.

RESULTSThere are no significant differences in the mucous membrane appearance and the mucosal blood flow one week after the surgery among the non-cryopreservation group and the groups treated with cryopreservation in 1 day, 2 weeks, 4 weeks, 6 weeks and 8 weeks. The graft was found to start necrosis 2 weeks after the transplantation with the infiltration of mononuclear cells examined under light microscope in almost all of the groups, especially in the non-cryopreservation group and the groups treated with cryopreservation in 1 day, 2 weeks. However, there was no significant difference among the autograft group and the allograft groups cryopreservated in 6 weeks and 8 weeks, and the infiltration of the mononuclear cells was not found in these groups either.

CONCLUSIONThe antigenicity of the tracheal allografts could be significantly decreased by the treatment of cryopreservation over 6 weeks.

Animals ; Bronchoscopes ; Cryopreservation ; methods ; Dogs ; Flowmeters ; Models, Animal ; Respiratory Mucosa ; blood supply ; pathology ; Trachea ; immunology ; pathology ; transplantation ; Transplantation, Homologous

Objective:To observe the efficacy and safety of two PAD regimens with different doses of bortezomib (bortezomib + Epirubicin + dexamethasone) in the treatment of patients with multiple myeloma (MM ) .Methods :The clinical data of 32 MM patients treated with PAD regimens were retrospectively analyzed .The doses of intravenous bortezomib were different in two PAD regimens .Patients in group PAD 1 (n=20) received bortezomib 1 .3 mg/m2 through intravenous injection on d 1 ,d 4 ,d 8 ,and d 11 ,epirubicin 20 mg through intravenous infusion on d 1 to d 4 ,and dexamethasone 20 mg through intravenous infusion d 1 to d 4 ,and d 8 to d 11 .Patients in group PAD 2 (n=12) received bortezomib 1 .6 mg/m2 through intravenous injection on d 1 ,d 8 ,and d 15 ,epirubicin 20 mg through intravenous infusion on d 1 ,d 8 ,and d 15 ,and dexamethasone 20 mg through intravenous infusion on d 1‐2 ,d 8‐9 ,and d 15‐16 .All patients received 3 to 6 courses of treatment and each course lasted for 28 days .Clinical efficacy and adverse reactions of two groups of MM patients were compared after the completion of 3 courses .Results:After the first three courses ,the effective rate of group PAD 1 was 80 .0% ,the effective rate of group PAD 2 was 83 .3% ,and there was no significant difference between the two groups .There were more herpes zoster patients in group PAD 1 than group PAD 2 (30% vs 0% ) ,and the difference was statistically significant (P<0 .05) .There were no statistical differences in the incidence of gastrointestinal reaction ,peripheral neuritis , granulocytopenia ,and thrombocytopenia between the two groups (20 .0% vs 16 .7% ,25 .0% vs 16 .7% ,15 .0% vs 16 .0% , and 10 .0% vs 8 .0% ,P>0 .05) .Conclusions :The PAD regimen with intravenous injection of bortezomib 1 .6 mg/m2 once a week is similar to the PAD regimen with intravenous injection of bortezomib 1 .3 mg/m2 twice a week in efficacy ,but it is safer with less adverse reactions .

Background Pancreatic β cells are susceptible to fatty acid-induced apoptosis.The 17β-estradiol (E2) protects pancreatic β cells from apoptosis,mediated by the estrogen receptor-α (Erα).The mRNA level and promoter activity of leukemia-related protein (LRP) 16 were significantly increased by E2 in ER-α and LRP16 was a co-activator of ER-α.The aim of the study was to assess the effects of LRP16 on fatty acid-induced apoptosis in MIN6 cells.Methods Cells with over-expressing LRP16 were obtained by lipidosome transfection.Insulin content and glucose-stimulated insulin secretion (GSIS) were examined by radioimmunoassay.Western blotting was applied to detect protein expression.Apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)and flow cytometry.The forkhead boxO1 (FoxO1) subcellular localization was determined by immunocytochemical analysis.Results MIN6-LRP16 cells with overexpression of LRP16 were successfully established,and protein expression of LRP16 was 2.29-fold of that of control cells (MIN6-3.1,P＜0.05).Insulin content and GSIS in MIN6-LRP16 were substantially increased compared with those in control cells.When cells were stimulated with glucose,increased phosphorylation of extracellular signal-regulated kinase (ERK) 1/2 and serine-threonine kinase (Akt) were observed in MIN6-LRP16.When cells were under palmitate pressure,the TUNEL-positive rate in MIN6-LRP16 was (17.0±0.5)％,while it in MIN6-3.1 was (22.0±0.4)％.In palmitate-treated cells,attenuated Akt phosphorylation was observed,but the attenuation in Akt activity was partially restored in MIN6-LRP16 cells.Meanwhile,nuclear localization of FoxO1 in MIN6-LRP16 was apparently reduced compared with that in control cells.Conclusions LRP16 regulated insulin content and GSIS in MIN6 cells by ERK1/2 and Akt activated way.Meanwhile,LRP16 overexpression protected MIN6 cells from fatty acid-induced apoptosis by partially restoring Akt phosphorylation and inhibiting FoxO1 nuclear redistribution.Therefore,LRP16 played important roles not only in insulin content and GSIS but also in the antilipotoxic effect mediated by Akt/FoxO1 signaling.

Objective Vasoconstriction and vascular hypersensitivity to serotonin were previously shown in animal models of adventitia injury. We investigated the contribution of angiotensin Ⅱ(Ang Ⅱ)/Ang Ⅱ receptors and oxidative stress to vascular contractility and reactivity in this model. Methods Wistar Kyoto rats were divided into 3 groups: normal(n =6, no any intervention, only for measuring the serum Ang d-1). After one week of treatment, adventitia injury was induced by positioning a silicone collar around the right carotid artery for one week. Blood flow and vascular reactivity to serotonin were determined one week after injury, the blood from left ventricle was taken to measure the serum Ang Ⅱ concentration by ELISA,and carotids were harvested for morphometry and Western blot analysis. Results Adventitia injury induced lumen cross-sectional area reduction(- 44% vs. - 5%), media diameter increase(62% vs. 10%),blood flow reduction[(2. 79 ± 0. 22)vs.(4. 33 ± 0. 84)ml/min]were significantly attenuated by valsartar. The increased vascular reactivity sensitivity to serotonin in vehicle group was also significantly reduced in valsartan group. Serum Ang Ⅱ concentration was significantly increased in vehicle group [(45.21 ± 4. 52)pg/ml vs.(19. 83 ± 0. 5)pg/ml in normal rats, P = 0. 0148]and the expression of Ang Ⅱtype 1(AT1)receptor, Ang Ⅱ type 2(AT2)receptor, as well as p22pbox in collared arteries were significantly upregulated. Valsartan did not affect the AT1 receptor expression but further increased serum Ang Ⅱ concentration[(89. 73 ±20. 44)pg/ml vs.(45.21 ±4. 52)pg/ml, P =0. 001], and AT2 receptor expression, while downregulated p22phox expressions. Conclusions Collar-induced adventitia injury resulted in chronic vsoconstriction and vascular hypersensitivity to serotonin via increased serum Ang Ⅱ level,upregulated Ang Ⅱ receptors expression in the vascular well, and activated local oxidative stress. These changes could be blocked by valsartan suggesting a crucial role of Ang Ⅱ/Ang Ⅱ receptors on vascular contractility and reactivity changes in this model.