Objective To observe the effect of monochromatic infrared energy(MIRE)on diabetic periphe- ral neuropathy(DPN).Methods Seventy-four subjects with diabetic peripheral neuropathy who were tested by Semmes-Weinstein monofilaments(SWM)were randomized into 2 groups:a conventional management group and a conventional management plus MIRE group.Then the patients'sensory function and other DPN symptoms were evalu- ated by the SWME and the score of Michigan Neuropathy Screening Instrument.Results After treatments,there was a decrease(P＜0.01)in the number of the sites insensitive to SWME(grade 5.07),and MNSI scores were sig- nificantly decreased(P＜0.01).The MIRE management was more effective than conventional management.Con- clusion Monochromatic infrared energy is perhaps a safe,non-pharmaceutical and non-invasive method for the treat- ment of diabetic peripheral neuropathy.

Cardiovascular Diseases ; Follistatin-Related Proteins ; physiology ; Humans

Objective To compare the advanced non -small cell lung cancer (NSCLC)patients before and after chemotherapy peripheral blood EGFR mutation status,we understand whether the chemotherapy drug impacts the EGFR mutation status of the advanced NSCLC patients,so as to improve the precision of EGFR TKIs -drug use. Methods To collect the peripheral blood of 30 cases of advanced NSCLC before chemotherapy and after chemotherapy for 6 cycles.DHPLC technique was used to detect the EGFR mutation states of EGFR exon 19 and in exon 21.Results In 30 patients,chemotherapy prior EGFR mutation positive rate was 53.3% (16 /30).After 6 cycles of chemotherapy, the EGFR mutation positive rate was 36.6% (11 /30),the consistent rate was 56.6 (17 /30)before and after chemo-therapy,inconsistent rate was 53.4% (13 /30).10 cases from positive to negative before chemotherapy,3 cases from negative into positive before chemotherapy with statistical significance (P =0.046).Six EGFR19 exons changed, change rate of 20%,8 EGFR21 exons shift changed at a rate of 26%.EGFR19,21 shift in 1 case,with no statistical significance(P =0.39,P >0.05).Conclusion (1)The late NSCLC patients before and after peripheral blood of EGFR mutation status change,so before starting the targeted therapy we must recive real -time detection of peripheral blood EGFR mutation status,so as to decide whether to choose EGFR TKIs targeted drug therapy.(2)EGFR21 exons transformation rate is higher than EGFR19 exons conversion rate,but with no statistical difference,this phenomenon may be related to EGFR19 exons patients who with EGFR mutations -TKIs treatment efficiency is higher.

0bjective: To observe the effects of parotid saliva(PARS), extraparotid saliva(EPS) and purified high molecular weight mucin(MG1) on the aggregation of streptococcus mutans . Methods: PARS, EPS and MG1 were prepared routinely and applied in the cultures of S. mutans Inbritt, S.mutans LM and S.sobrinus OMZ 176 respectively for 2 h. The aggregation of the bacteria was measured spectrophotometrically.Results: The aggregation (%) of S.mutans Inbritt, S.mutans LM and S.sobronus OMZ 176 induced by EPS was 32.80 , 57.87 and 35.46 , that by MGI 25.68, 32.77 and 24.16 , that by PARS 13.52, 22.23 and 16.00, respectively. Conclusion: The effect of MGI on the aggregation of streptoccus mutans is weaker than that of EPS and stronger than that of PARS. The aggregation may be primarily induced by mucins.

Acetamides ; metabolism ; toxicity

Objective By using multi detector row spiral CT (MDCT) to investigate the CT imaging findings of gallbladder abnormalities caused by hepatic parenchymal diseases and those of inflammatory cholecystitis. Methods CT and clinical data of 80 patients with gallbladder abnormalities were retrospectively reviewed. Fifty patients were in hepatic disease group, including 20 chronic hepatitis, 25 liver cirrhosis, and 5 cirrhosis with hepatocellular carcinoma. Thirty patients were in inflammatory group, including 19 chronic cholecystitis, 6 acute cholecystitis, 3 cholecystitis with acute pancreatitis, 1 gangrenous cholecystitis, and 1 xanthogranulomatous cholecystitis. All patients underwent MDCT plain scan and contrast enhanced dual phase scanning of upper abdomen. Results In hepatic disease group, 48 cases had evenly thickened gallbladder wall (96%) with mean thickness of (3.67?0.49) mm; 38 cases had clear gallbladder outlines (76%); 38 cases had gallbladder wall enhancement of various degree (76%); 14 cases had gallbladder bed edema and localized non dependant pericholecystic fluid collection (28%). In inflammatory cholecystitis group, 28 cases had obscuring gallbladder outlines (93%) ; 26 cases had gallbladder wall evenly thickened (87%), 4 cases showed unevenly thicked wall (13%), the mean thickness being (4.54?1.14) mm; 30 cases had inhomogenous enhancement of the gallbladder wall (100%); 9 cases had high attenuation bile (30%); 4 cases had dependant pericholecystic fluid collection (13%); 5 cases had transient enhancement of adjacent hepatic bed in arterial phase (17%); micro abscess and gas in the gallbladder wall was observed in 1 case respectively. Conclusion MDCT can offer imaging findings useful for differentiating abnormal gallbladder changes caused by hepatic parenchymal diseases from those due to inflammatory cholecystitis.

Objective To characterize and quantify the CD4 +CD25 + regulatory T (Treg) cell population in peripheral blood of patients with ankylosing spondylitis (AS) and to determine the influence of treatment with tumor necrosis factor (TNF)-a inhibitors on them.Methods Peripheral blood mononuclear cells (PBMC) were isolated from 25 patients with active AS,in which 10 patients were treated with 12 weeks of etanercept,and 21 healthy subjects.CD4+CD25high T cells were analyzed using flow cytometry,and mRNA expression of FOXP3 was determined by real-time polymerase chain reaction (PCR).Proliferation of T cells to PHA was measured by WST-1 assay using depleted CD25+ cells by immunomagnetic sorting.Results There was no significant difference in the percentage of CD4+CD25high cells in peripheral blood between patients with active AS and controls (P＞0.05).However,PBMC from patients with active AS expressed reduced levels of FOXP3 mRNA (P＜0.01) which were inversely correlated with C-reactive protein (CRP)(P＜0.01).CD4+CD25+ cells in peripheral blood of both active AS patients and controls exhibited suppressive capacity on the proliferation of effector T cells in vitro (both P＜0.01).Treatment with etanereept increased significantly CD4+CD25high cells and FOXP3 mRNA expression (both P＜0.01),with negative correlations between these increases and decrease in CRP levels (P＜0.05 and P＜0.01,respectively).Conclusion In AS patients,peripheral FOXP3-expressing CD4 +CD25 + Treg cells are abnormal,and are up-regulated by etanercept treatment.This suggests a possible pathogenesis of AS and a potential mechanism for clinical efficacy of TNF-α inhibitors.

Objective To investigate the effect of electro-acupuncture on the spinal nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) signal pathway in a rat model of neuropathic pain (NP). Methods Forty-eight pathogen-free male SD rats weighing 190-210 g were randomly divided into 3 groups (n = 16 each):group Ⅰ sham operation (group S); group Ⅱ group NP and group Ⅲ electro-acupuncture + NP (group E). NP was induced by chronic constrictive injury (CCI). Right sciatic nerve was exposed and 4 loose ligatures were placed on the sciatic nerve at 1 mm intervals with 4-0 chromic catgut. In group E Huantiao and Weizhong points on the operated side were stimulated with electric stimulator (frequency 2 Hz, wave length 0.6 ms, starting at a voltage of 1mA and increasing by 1 mA every 10 min) for 30 min once a day at 11-17 d after CCI. Pain threshold to mechanical and thermal nociceptive stimuli was measured before (T0 , baseline) and at 10 and 16 d after CCI (T1, T2). The animals were sacrificed at 17 d after CCI and the lumbar segment (L4-6) was removed for determination of the activities of total NO synthase (tNOS), induced and neural NOS (iNOS, nNOS) (by spectrophotometry), NO content (by nitrate reductase method) and cGMP content (by immuno-histochemistry) in the spinal cord in 8 animals and the expression of iNOS and nNOS in the dorsal horn of the spinal cord (by immuno-histochemistry) in another 8 animals in each group. Results CCI significantly decreased the mechanical and thermal pain threshold at T1 and T2 as compared with the baseline at T0 in group NP and E. Hyperalgesia induced by CCI was significantly attenuated by electro-acupuncture at T2 in group E as compared with group NP.CCI significantly increased tNOS and nNOS activities, NO and cGMP content in the spinal cord and up-regulated nNOS expression in the spinal dorsal horn. Electro-acupuncture significantly attenuated the CCI-induced increases in tNOS and nNOS activities, NO and cGMP content in the spinal cord and nNOS expression in the spinal dorsal horn. There was no significant difference in the iNOS activity among the 3 groups. Conclusion NO-cGMP signal pathway in the spinal cord is involved in the acupuncture analgesia.

objective To examine nuclear transIocation of peroxisome proliferator-activated receptor γ(PPARγ)in rats following focal cerebral ischemia/reperfusion(I/R),and to explore the significance of altered PPARγ,nuclear translocation in ischemic brain injury.Methods Healthy adult male SD rats underwent 60-min cerebral artery occlusion followed by reperfusion of 4,8,or 24 h,respectively.The cytoplasmic-to-nuclear shuttling of PPARγ was characterized by Western blot,immunohistochemical and immunofluoreseence staining.The effects of PPARγ agonist rosiglitazone (Ros) and antagonist GW9662 on I/R-induced PPARγ nuclear translocation were also examined in the present study. Furthermore,TTC staining war adopted to determine the change in cerebral infarction volume. Results (1)Western blot analysis revealed an increase of PPARγ in the nucleus and a simultaneous reduction in the cytosol following ischemia and reperfusion for 4 h(tcytosol=9.03,tmuclear=27.19,P=0.00).Prolonged the reperfusion further enhanced this I/R induced PPARγ translocation in a time-dependent manner.Using immunohistochemistry and immunofluorescence,nuclear PPAR γ positive staining increased from 48.3%in the sham control to 80.3% following ischemia and reperfusion for 24 h.(2)Western blot analysis revealed that PPARγ agonist Ros further increased I/R-induced nuclear enrichment of PPARγ,whereas PPARγ antagonist GW9662inhibited I/R-stimulated change in PPARγ.(3)When compared to the L/R group using TTC staining,Ros treatment significantly decreased the infarction volume by 48.40%(15.46±4.94 versus 29.96±3.39,t=5.93.P=0.00),whereas GW9662 increased by 58.95%(47.62±4.93 versus 29.96±3.39,t=7.23,P=0.00).Conclusions Cerebral I/R injury induces PPARγ translocation from the cytosol to the nucleus.This change may represent an intrinsic neuroprotective response against brain I/R injury.