Objective To investigate the situations of close contacting with MDR-TB in family and analysis the necessity and urgency of family protection.Methods Nine typical primary MDR-TB cases in our hospital that close contacted with family pulmonary TB patients.their relatives contacted with them and their treatment prognosis were retrospectively analyzed.Results All of the 9 cases were transmitted by lineal MDR-TB relatives.In one case,3 generations were pumonary TB patients.All of 4 family members were pulmonary TBpatients in another case.3 cases were treated with operations:2 cases with pulmonary lobectomy and 1 case with intestinal resection.Treatment prognosis:3 cases cured,2 cases not cured,4 cases dead.Conclusions Family close contacting with MDR-TB patients should be intervened earlier:including health education,effective protection and health examination regularly et al.

Metastasis is a multistep process involving modification of morphology to suit migration, reduction of tumor cell adhesion to the extracellular matrix, increase of cell mobility, tumor cell resistance to anoikis, and other steps. MicroRNAs are well-suited to regulate tumor metastasis due to their capacity to repress numerous target genes in a coordinated manner, thereby enabling their intervention at multiple steps of the invasion-metastasis cascade. In this study, we identified a microRNA exemplifying these attributes, miR-124, whose expression was reduced in aggressive MDA-MB-231 and SK-3rd breast cancer cells. Down-regulation of miR-124 expression in highly aggressive breast cancer cells contributed in part to DNA hypermethylation around the promoters of the three genes encoding miR-124. Ectopic expression of miR-124 in MDA-MB-231 cells suppressed metastasis-related traits including formation of spindle-like morphology, migratory capacity, adhesion to fibronectin, and anoikis. These findings indicate that miR-124 suppresses multiple steps of metastasis by diverse mechanisms in breast cancer cells and suggest a potential application of miR-124 in breast cancer treatment.
Anoikis ; Breast Neoplasms ; genetics ; metabolism ; pathology ; Cell Adhesion ; Cell Line, Tumor ; Cell Movement ; Connective Tissue Growth Factor ; metabolism ; DNA Methylation ; Down-Regulation ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs ; genetics ; metabolism ; Neoplasm Metastasis ; rho GTP-Binding Proteins ; metabolism ; rho-Associated Kinases ; metabolism

【Objective】 To observe the expression of PKCε and μ opioid receptor(MOR) and explore their relationship in the spinal cord of rats with remifentanil-induced hyperalgesia(RIH) . 【Methods】 Eighteenadult male SD rats were randomly divided into control group, saline group and remifentanil group with 6 rats in each group. Hyperalgesia was induced by continuous infusion of 4 μg/(kg·min) remifentanil for 2 hours via vein tail. Pain sensitivity was assessed by the Hargreaves test to determine paw withdrawl latency to a thermal stimulus at 6 h and 24 h after remifentanil administration. Real-time fluorescent quantitative PCR and Western blot analysis were used to measure the expression levels of PKCε and MOR in the spinal cord of rats and their distribution was detected by immunofluorescence. In order to observe the effect of inhibitors on RIH and the protein expression of MOR in the spinal cord of rats, we injected different PKC inhibitors including Bisindolylmaleimide I(BIS, inhibiting PKCε) and Gö6983(not inhibiting PKCε) intrathecally 30 mins prior to remifentanil infusion. 【Results】 The results of behavioral experiment showed that the paw withdrawal thermal latency was significantly reduced at 24 h after remifentanil infusion [PWTL=(5.31 ± 0.87) s, P < 0.01] . Western blot and Real time PCR results revealed upregulated PKCε expression(P<0.001) and downregulated MOR expression(P<0.001). Immunofluorescence results indicated that PKCε and MOR were colocalized with neurons in the dorsal horn of rat spinal cord. Preemptive intrathecal injection of BIS alleviated the hyperalgesia in rats and inhibited MOR expression(P<0.001), but injection of Gö6983made no difference(P>0.05) . 【Conclusion】 PKCε and MORin spinal dorsal horn neurons may be involved in RIH, and PKCε may regulate the expression levels of MOR. This research provides a new theoretical mechanism for the prevention and treatment of RIH.

Carcinoma, Hepatocellular ; virology ; Hepacivirus ; Hepatitis B ; Hepatitis B virus ; Hepatitis C ; Humans ; Liver Neoplasms ; virology

This study is to investigate the protection effect of schisandrin B (Sch B) against oxidation stress of HK-2 cells induced by cisplatin and the mechanisms involved. HK-2 cells were cultured and divided into different groups: solvent control group, cisplatin exposure group, positive group, Sch B treatment group. Cell viability and toxicity were evaluated by MTT and LDH assay. GSH level and SOD enzymes activities were also measured. DCFH-DA as fluorescence probe was used to detect ROS level by fluorescence microplate reader. Nrf2 translocation was detected by Western blotting. Real time Q-PCR was used to detect expressions of NQO1, HO-1 and GCLC mRNA level. The results showed that Sch B could significantly inhibit the decline of cell viability induced by cisplatin treatment (P < 0.05) and the protective effect was in a dose dependent manner. Furthermore, Sch B treatment significantly inhibited the increase of ROS level induced by cisplatin and reversed the decrease of GSH level (P < 0.05). When Sch B concentration was up to 5 micromol x L(-1), SOD enzyme activities were also enhanced significantly compared with that of the cisplatin group (P < 0.05). It was shown that Sch B could cause nuclear accumulation of Nrf2 in association with downstream activation of Nrf2 mediated oxidative response genes such as GCLC, NQO1 and HO-1. These results suggested Sch B could protect against the oxidative damage of HK-2 cells induced by cisplatin via the activation of Nrf2/ARE signal pathway.
Antineoplastic Agents ; toxicity ; Antioxidants ; isolation & purification ; pharmacology ; Cell Line ; Cell Survival ; drug effects ; Cisplatin ; toxicity ; Cyclooctanes ; isolation & purification ; pharmacology ; Glutamate-Cysteine Ligase ; genetics ; metabolism ; Glutathione ; metabolism ; Heme Oxygenase-1 ; genetics ; metabolism ; Humans ; Kidney Tubules, Proximal ; cytology ; metabolism ; L-Lactate Dehydrogenase ; metabolism ; Lignans ; isolation & purification ; pharmacology ; NAD(P)H Dehydrogenase (Quinone) ; genetics ; metabolism ; NF-E2-Related Factor 2 ; genetics ; metabolism ; Polycyclic Compounds ; isolation & purification ; pharmacology ; RNA, Messenger ; metabolism ; Reactive Oxygen Species ; metabolism ; Schisandra ; chemistry ; Signal Transduction ; Superoxide Dismutase ; metabolism

OBJECTIVETo observe the expressions of caspase-8 and caspase-9 mRNA, and explore the changes of apoptosis of bone marrow hematopoietic cells in patients with chronic mountain sickness (CMS).

METHODSOf 18 CMS patients and 16 controls were enrolled in this study. The apoptotic index (AI) of bone marrow mononuclear cells (BMMNC) was measured by TUNEL technique, the levels of caspase-8 and caspase-9 mRNA in BMMNC of CMS patients and controls were determined by RT-PCR. Results (1)The AI of BMMNC in patients with CMS (8.51 ± 3.35)% was lower than that in controls (16.00 ± 4.28)% (P < 0.01); (2) The values of caspase-8 and caspase-9 mRNA were (0.28 ± 0.07) and (0.23 ± 0.08) respectively, in CMS patients, which were significantly lower than those of (0.45 ± 0.09) and (0.41 ± 0.09) respectively, in the controls (both P < 0.01); (3) Hemoglobin (Hb) value was negatively correlated with levels of caspase-8 and caspase-9 mRNA (r values were -0.52 and -0.61 respectively, both P < 0.05) in CMS patients. There was a negative correlation between AI and Hb (r value was -0.89, P < 0.01) in CMS patients. However, the significant relationship was not found between AI and level of caspase-8 or caspase-9 mRNA (P > 0.05).

CONCLUSIONSThe results showed a decrease apoptosis of BMMNCs and reduced levels of caspase-8 and caspase-9 mRNA in CMS patients, the latter might be involved in the change of BMMNCs apoptosis.

Adult ; Altitude Sickness ; metabolism ; pathology ; Apoptosis ; Bone Marrow Cells ; metabolism ; Case-Control Studies ; Caspase 8 ; metabolism ; Caspase 9 ; metabolism ; Humans ; Male ; Middle Aged

Objective To observe and study the efficacy and the impact on memory of alzheimer′s disease patients treated with perception of enhancing intelligence and treating dementia.Methods A total of 114 cases of alzheimer′s patients were randomly divided into treatment group (57 cases) and control group (57 cases).Patients in control group were treated with piracetam, oral 0.8 -1.6 g, 4 times a day.Patients in treatment group were taken perception of enhancing intelligence and treating dementia on the basis of control group, 2 times a day, 4 weeks for a course of treatment.Before and after three months treatment, MMSE, BI, and cognitive function, memory and Blessed dementia scale were assess.Clinical efficacy and adverse reactions of the two groups were observed.Results Total effective rate in treatment group was 94.74%, significantly higher than that in control group, which was 63.15%( P<0.05 ).After treatment, MMSE score ( 17.5 ±2.1 ) and BI score (74.9 ±5.7) in control group were significantly lower than that in treatment group, which were ( 22.2 ±2.3 ) , ( 85.8 ±5.9 ) , ( P<0.05).After treatment, cognitive function, vocabulary and memory in treatment group were significantly higher than that in control group.The Blessed dementia scale score in treatment group (4.6 ±2.4) was lower than that in control group (5.8 ±2.5).The incidence of adverse reactions in treatment group(7.01%), was lower than that in control group(28.07%, P<0.05).Conclusion Perception of enhancing intelligence and treating dementia combined piracetam can effectively improve the clinical symptoms, memory and life skills of alzheimer′s patients.

ObjectiveTo observe the changes in the expression and distribution of G protein-gated inwardly rectifying potassium channel subunit 2 （GIRK2） in the dorsal root ganglion （DRG） and spinal cord dorsal horn of rats with remifentanil-induced hyperalgesia. MethodsHyperalgesia was induced by intravenous infusion of remifentanil 4 μg/kg/min for 2 h in adult male SD rats. At 6th hour and on days 1， 3 and 5 following remifentanil treatment， we used immunofluorescence to examine the changes in the GIRK2 distribution and expression. Immunoblotting was used to detect GIRK2 expression of the total protein and membrane protein in DRG and spinal dorsal horn of rats. Behavioral testing was applied to evaluate the effect of intrathecal injection of GIRK2-specific agonist ML297 on thermal nociceptive threshold on day 1 after remifentanil infusion. Resultsmmunofluorescence results showed that GIRK2 was mainly co-localized with IB4-positive small neurons in DRG and nerve fibers in spinal dorsal horn. GIRK2 expression was significantly downregulated following remifentanil treatment. Immunoblotting results revealed that on day 1 following intravenous infusion of remifentanil， compared with those in the control group， GIRK2 expression levels of the total protein and membrane protein in DRG （0.47 ± 0.10 vs. 1.01 ± 0.17， P < 0.001； 0.47 ± 0.11 vs. 1.06 ± 0.12， P < 0.001） and spinal dorsal horn （0.52 ± 0.09 vs. 1.10 ± 0.08， P < 0.001； 0.54 ± 0.10 vs. 1.01 ± 0.13， P < 0.001） were all significantly decreased. The behavioral results showed that intrathecal ML297 effect on thermal withdrawal latency was significantly reduced following remifentanil treatment （P < 0.001）. ConclusionsRemifentanil might induce hyperalgesia via down-regulating GIRK2 expression in rat DRG and spinal cord dorsal horn.

BACKGROUNDThere are no reports on exnografting cultured human fetal neocortical cells in this infracted cavities of adult rat brains. This study was undertaken to observe whether cultured human cortical neurons and astrocytes can survive and grow in the infarcted cavities of adult rat brains and whether they interconnect with host brains.

METHODSThe right middle cerebral artery was ligated distal to the striatal branches in 16 adult stroke-prone renovascular hypertensive rats. One week later, cultured cells from human embryonic cerebral cortexes were stereotaxically transferred to the infarcted cavity of 11 rats. The other 5 rats receiving sham transplants served as controls. For immunosuppression, all transplanted rats received intraperitoneal injection of cyclosporine A daily starting on the day of grafting. Immunohistochemistry for glial fibrillary acidic protein (GFAP), synaptophysin, neurofilament, and microtubule associated protein-2 (MAP-2) was performed on brain sections perfused in situ 8 weeks after transplantation.

RESULTSGrafts in the infarcted cavities of 6 of 10 surviving rats consisted of bands of neurons with an immature appearance, bundles of fibers, and GFAP-immunopositive astrocytes, which were unevenly distributed. The grafts were rich in synaptophysin, neurofilament, and MAP2-positive neurons with long processes. The graft/host border was diffuse with dendrites apparently bridging over to the host brain, into which neurofilament immunopositive fibers protruded.

CONCLUSIONCultured human fetal brain cells can survive and grow in the infarcted cavities of immunodepressed rats and integrate with the host brain.

Animals ; Astrocytes ; transplantation ; Brain ; pathology ; Cell Proliferation ; Cell Survival ; Cells, Cultured ; Cerebral Infarction ; metabolism ; pathology ; therapy ; Fetal Tissue Transplantation ; Glial Fibrillary Acidic Protein ; analysis ; Humans ; Microtubule-Associated Proteins ; analysis ; Neocortex ; cytology ; Neurons ; transplantation ; Rats ; Synaptophysin ; analysis

remifentanil；hyperalgesia；CCL2；microglia 【Objective】To observe C-C motif chemokine ligand 2（CCL2）mediates remifentanil-induced hyperalgesia by activating microglia in rats.【Methods】Thirty-six adult male SD rats were equally and randomly divided into 6 group with 6 rats in each group：normal saline ，remifentanil，saline + intrathecal injection of phosphate buffer saline（PBS）， remifentanil + intrathecal injection of PBS，saline + intrathecal injection of CCL2 neutralizing antibody and remifentanil + CCL2 neutralizing antibody. To establish remifentanil-induced hyperalgesia model，remifentanil［4 μg/ （kg·min）2 h］ was continuously infused into rats via the tail vein. Then ，immunofluorescence and western blot were performed to examine the expression of spinal CCL2 in rats. Thirty minutes before remifentanil infusion，intrathecal injection of CCL2 neutralizing antibody was performed to observe remifentanil-induced hyperalgesia and the effect on the activation of microglial in the spinal cord of rats.【Results】Compared with the normal saline group，the thermal and mechanical pain thresholds in the remifentanil group were significantly reduced（P < 0.05）. The expression of protein（0.66 ± 0.071 vs. 0.18 ± 0.04；P < 0.001）and average immunofluorescence density of spinal CCL2（0.170 ± 0.009 vs. 0.047 ± 0.006；P < 0.001）were significantly increased on the first day after remifentanil infusion. Prior intrathecal injection of CCL2 neu⁃ tralizing antibody not only inhibited remifentanil-induced activation of microglia in the spinal cord（P < 0.001），but also mitigated remifentanil-induced thermal hyperalgesia and mechanical pain sensitivity（P < 0.05）.【Conclusion】CCL2 me⁃ diates the remifentanil-induced hyperalgesia by activating spinal microglia in rats.