Fatal Outcome ; Humans ; Infant, Low Birth Weight ; Infant, Newborn ; Infant, Premature, Diseases ; diagnosis ; physiopathology ; Male ; Respiratory Insufficiency ; diagnosis ; physiopathology ; Syndrome

Objective_To investigate whether hUCMSCs undergo malignant transformation when exposed to MCF-7B breast cancer microenvironment and whether the abnormal activation and over expression of STAT3 play an impor-tant role in this transformation.Methods_The experiment was divided into three groups:blank group ( hUCMSCs were separately cultured),experimental group(hUCMSCs were indirectly co-cultured with MCF-7B breast cancer cells),positive control group(MCF-7B breast cancer cells were separately cultured).Morphology of cells was detec-ted by invertedmicroscope.Cell cycle was detected by flow cytometry.The mRNA expression of STAT3, c-Myc and Bcl-xL was tested by real-time PCR.The protein expression and location of p-STAT3,c-Myc and Bcl-xL were detected by immunofluorescence.The protein expressions of p-STAT3,STAT3,c-Myc and Bcl-xL were also meas-ured by Western blot.Results_The experimental group cells showed typical morphology of the tumor cells.The cells proportion of experiment group in G1 phase was significantly lower than that of the blank group(P<0.05),but which in S and G2 phase were significantly higher than those of the blank group(P<0.05).The mRNA expression levels of STAT3 ,c-Myc and Bcl-xL in experimental group was significantly higher than those in blank group ( P<0.05).p-STAT3,STAT3,c-Myc and Bcl-xL protein were significantly higher than those of the blank group(P<0.05),and they were mainly located in the nuclei.The protein expression of STATS also showed significant changes in experimental group.Conclusions_hUCMSCs trends to malignant transformations when exposed to MCF-7B breast cancer microenvironment.The abnormal activation and over expression of STAT3 are of important factors leading to the malignant transformation of hUCMSCs.

Objective To evaluate the raliability and validity of walking impairment questionnaire applied to assess the walking ability of patients with type 2 diabetes. Methods One hundred and twenty-six patients with type 2 diabetes were selected. WIQ, SF-36 and 6-minute walk test were used to collect da-ta that was conducted for reliability analysis, correlation analysis and independent-samples t test to evaluate the reliability and validity. Results The internal consistency determined by Cronhach's α was 0.867 for the total WIQ score. Significnat correlations were found between WIQ and 6MWD, also between WIQ and physical domains of SF-36. compared with patients over seventy-one years old, the score of WIQ including the distance, speed, stair climbing and total score is significantly higher than that in patients aged seventy-one or less than seventy-one years old. Conclusions The Chinese version of WIQ is a simple, valid and reliable, clinically relevant tool to assess the walking ability of patients with type 2 diabetes.

Objective To explore the expressions of autophagy-related gene Beclin-1 and LC3 in adriamycin induced eardiomyopathy rats,to prnve that autophagy might take part in the development of adriamycin induced eardiomyopathy in rats,so as to provide experimental and theoretical evidence for preventing and treating adriamycin induced cardiomyopathy.Methods Forty-five male SD rats were randomly divided into 3 groups,control groups,ADR group and ADR+3-MA group.The model of adriamycin induced cardiomyopathy rats was established.The tissue sample taken from the left ventricle wall was checked for the morphons of autophagosome by electron microscope. The expressions of Beelin-1 and LC3 of myocardium were detected.Results The morphons of autophagosome in ADR group was significantly increased compared with that in control and ADR +3-MA groups. The expression of Beclin-1 in myocardium of ADR group was significantly inereased compared with that in control and ADR +3-MA groups (P < 0.05).The level of LC3 in myocardium of ADR group was significantly increased compared with that in control and ADR+3-MA groups (P < 0.05).Conclusions Autophagy plays an important role in adriamycin induced cardiomyopathy.

Objective To observe the impacts of Kechuanning on expression of signal transducer and activator of transcription 6 (STAT 6) in CD4+, CD8+T lymphocytes of athma rats induced by virus, and analyze the mechanism of Kechuanning in treating asthma induced by RSV. Methods The PBMC was isolated from the peripheral blood, CD4+T, CD8+T lymphocyte was separated by immunomagnetic beads. The purity and activity of CD4+T and CD8+T lymphocytes were measured by using flow cytometry, trypan-blue dye exclusion test. The protein expression of STAT6 was detected by fluorescence-activated cell sorting. Results The descending progress of the trial were supported by the purity and activity of CD4+T, CD8+T lymphocyte. CD4+T lymphocyte in the asthma model group were increased (P<0.01), however the increase of CD8+T lymphocyte were not significant (P>0.05). The expression of the protein of STAT6 in the treated group with Kechuanning decoction were decreased than that in the model group (P<0.01). Compared with Dexamethasone and Salbutamol group, there were no significant differences (P>0.05). Conclusion Kechuanning decoction could decrease the protein of STAT6 in CD4+, CD8+T lymphocyte, thereby it could regulate the disorder of Th1/Th2, thus prevent and treat the asthmatic attack induced by virus.

This article systematic reviewed the recent ten years clinical research of acupuncture treatment and rehabilitation on hemiplegia after stroke.The curative effect of acupuncture treatment and rehabilitation on hemiplegia after stroke is certain,and also supported by subsequent clinical researches.At the same time,we found that there are some deficiencies.The author elaborated personal views of clinical research in the future.The main purpose is to review the clinical research progress and forecast of acupuncture treatment and rehabilitation on hemiplegia after stroke briefly.

Objective: To investigate the effects of oxLDL and HMG-CoA reductase inhibitor simvastatin on PKC activity, and level of cytosol ic free Ca 2+ in cultured human umbilical vein endothelial cells. Methods: Th e activity of PKC was determined by its ability to transfer phosphate from 32P-ATP to lysine-rich histone and level of cytosolic free calcium［Ca2+ ］i was measured by flow cytometric analysis loading with the Ca2+ dye F luo-3/Am. Results: oxLDL increased PKC total activity in a dose-de pendent manner and peaked after 12 min, then decreased slowly and maintained for at least 30 min, while oxLDL induced biphasic ［Ca2+］i responses includ ing the rapid initial transient phase and the sustained phase. Removal of extrac ellular Ca2+ did not inhibit the rapid transient phase, but abolished the sustained phase. When simvastatin was added, the activity of PKC wasmarkedly dec reased with no impairment to the initial peak response, but significantly reduce d the sustained phase. Conclusion: oxLDL can induced dynamic changes of signal transduction of PKC and level of cytosolic free Ca2+ in HUVEC, these 2 events are closely linked. The change of rapid initial transient phase i s the result of mobilization of Ca2+ from intracellular pool and the chang e of sustained phase is from the influx of extracellular Ca2+. The inhibit ion of PKC activity induced by simvastatin may contribute to the changes of ［Ca 2+］i.

AIM　To investigate the effect of OX-LDL and HMG- CoA reductase inhibitors simvastatin on PKC activity and cytosolic free Ca2+ in cultured human monocy tes. METHOD　The activity of PKC was determined by its ability to tr ansfer phosphate from ［32P］ATP to lysine-rich histone and cytosolic free calcium［Ca2+］i was measured by flow cytometric analysis loading with the Ca2+ dye fluo3/Am. RESULTS　OX-LDL increased PKC tot al activity in a dose-dependent manner with phase peaking at 12 min, then decre ased slowly and maintained for at least 20 min, while OX-LDL induced biphasic ［Ca2+］i responses including the rapid initial transient phase and the sustained phase. Removal of extracellular Ca2+ did not inhibit the rapid i nitial transient phase of OX-LDL-induced rise in ［Ca2+］i,but abolish ed the sustained phase of ［Ca2+］i response to OX-LDL. When simvastati n was added, the activity of PKC was markedly decreased and simvastatin did not impair the initial peak response to OX-LDL but significantly reduced the subseq uent plateau phase. CONCLUSION OX-LDL can significantly activate t he activity of PKC and elevate ［Ca2+］i in monocytes. The rapid initial transient phase was the result of mobilization of ［Ca2+］i from intrac ellular pool and sustained phase resulted from the influx of extracellular Ca 2+. The inhibition of PKC activity induced by simvastatin may be contribute to the changes of intracellular Ca2+.

Objective: To investigate the effects of oxLDL and HMG CoA reductase inhibitor simvastatin on PKC activity, and level of cytosolic free Ca 2+ in cultured human umbilical vein endothelial cells. Methods: The activity of PKC was determined by its ability to transfer phosphate from 32 P ATP to lysine rich histone and level of cytosolic free calcium[Ca 2+ ]i was measured by flow cytometric analysis loading with the Ca 2+ dye Fluo 3/Am. Results: oxLDL increased PKC total activity in a dose dependent manner and peaked after 12 min, then decreased slowly and maintained for at least 30 min, while oxLDL induced biphasic [Ca 2+ ]i responses including the rapid initial transient phase and the sustained phase. Removal of extracellular Ca 2+ did not inhibit the rapid transient phase, but abolished the sustained phase. When simvastatin was added, the activity of PKC wasmarkedly decreased with no impairment to the initial peak response, but significantly reduced the sustained phase. Conclusion: oxLDL can induced dynamic changes of signal transduction of PKC and level of cytosolic free Ca 2+ in HUVEC, these 2 events are closely linked. The change of rapid initial transient phase is the result of mobilization of Ca 2+ from intracellular pool and the change of sustained phase is from the influx of extracellular Ca 2+ . The inhibition of PKC activity induced by simvastatin may contribute to the changes of [Ca 2+ ]i. [

AIM To investigate the effect of OX- LDL and HMG-CoA reductase inhibitors simvastatin on PKC activity and cytosolic free Ca2+ in cultured human monocytes. METHOD The activity of PKC was determined by its ability to transfer phosphate fm [32P] ATP to lysine-rich histone and cytosolic free calcium[Ca2+]i was measured by flow cytometric analysis loading with the Ca2+ dye fluo3/Am.RE- SULTS OX-LDL increased PKC total activity in a dose-dependent manner with phase peaking at 12 min, then decreased slowly and maintained for at least 20 min, while OX-LDL induced biphasic [Ca2+ ], responses including the rapid initial transient phase and the sustained phase. Removal of extracellular Ca2+ did not inhibit the rapid initial transient phase of OX-LDL-induced rise. in [ Ca2+ ]i, but abol- abolished the sustained phase of [ Ca2+ ] i response to OX LDL. When simvastatin was added, the activity of PKC was markedly decreased and simvastatin did not impair the initial peak response to OX-LDL but sig- nificantly reduced the subsequent plateau phase. CONCLUSION OX-LDL can significantly activate the activity of PKC and elevate [Ca2+ ]i in monocytes. The rapid initial transient phase was the result of mobilization of [Ca2+ ], fm intracellular pool and sustained phase resulted from the influx of extracellular Ca2+. The inhibition of PKC activity induced by simvastatin may be contribute to the changes of intracellular Ca2+.