ObjectiveTo observe the clinical efficacy of warming-unblocking Yin Heel Vessel plus rehabilitation training in treating post-stroke strephenopodia, for seeking the optimal treatment protocol.MethodNinety eligible subjects withpost-stroke strephenopodia were randomized into an acupuncture group, a rehabilitation group, and a united group, to respectively receive warming-unblocking Yin Heel Vessel, rehabilitation treatment, and warming-unblocking Yin Heel Vessel plus rehabilitation training. ResultTwo treatment courses later, there was no significant difference in comparing the strephenopodia score between the acupuncture group and rehabilitation group (P>0.05); the strephenopodia score in the united group was significantly different from that in the acupuncture group and rehabilitation group (P<0.05), and the improvement in strephenopodia in the united group was superior to that in both acupuncture group and rehabilitation group.ConclusionWarming-unblocking Yin Heel Vessel plus rehabilitation can produce a content efficacy in treating post-stroke strephenopodia.

Objective To study the effect of morin on LPS induced acute lung injury mouse model and its mechanism .Meth‐ods Thirty male C57B/L mice were randomly divided into control group ,LPS group and LPS+ morin group ,with 10 in each group .5 mg/kg LPS was instilled into the lung from an trachea intubation in LPS group and LPS+morin group .Then the mice in LPS+morin group received an intraperitoneal injection of morin (40 mg/kg) every day for the next 3 d .Others received an equal a‐mount of saline .After 72 h ,the mice were sacrificed .The bronchoalveolar lavage fluid (BALF) was collected and centrifuged;the sediments were stained with Wright‐Giemsa for total cell and neutrophil count and the supernates were prepared for ELISA .The wet and dry weight of lung was weighed to calculate the wet/dry weight ratio .HE staining was performed to examine the pathologi‐cal change of lung .Western blot was used to determined the expression of TLR4 ,IKK and NF‐κB .Results Intratracheal instillation of LPS successfully established ALI model in mouse .LPS caused significant pathological changes including inflammatory cells infil‐tration ,alveolar septa thickness ,hemorrhage and edema .The wet/dry weight ratio ,the total cell count ,neutrophil count ,TNF and IL‐1βlevel in BALF ,and the expression of TLR4 ,NF‐κB ,and IKK were all increased significantly (P<0 .05) ,which were allevia‐ted by intraperitoneal injection of morin .Conclusion Morin can dampen the inflammatory response during LPS induced ALI in mouse ,which is potentially attributed to its inhibitory effect on the activation of NF‐κB .

OBJECTIVE To evaluate the role of forkhead transcription factor p3(Foxp3) in the pathogenesis of allergic rhinitis(AR).METHODS Nasal tissues and peripheral blood mononuclear cells(PBMCs) were obtained from 17 patients with AR and 11 controls.Foxp3 was detected in nasal tissues by immunohistochemisry and real-time reverse transcription polymerase chain reaction(RT-PCR).Foxp3 and CD4+CD25+T cells were evaluated in PBMCs by using ? ow cytometry.RESULTS The numbers of Foxp3+ cells was(44.2?20.5)cells/mm2 and(129.5? 35.6)cells/mm2 in nasal mucosa of two groups(P

Objective To explore effect of ginkgetin injection on brain damage factor in patients with acute cerebral infarction.Methods 180 cases of acute cerebral infarction patients were selected from June 2014 to February 2015, and divided into experiment group and control group.88 cases in control group were treated with clinical routine therapy, 92 cases in experimental group were treated on base of the control with ginkgetin injection, 2 weeks for a course.The clinical efficacy, MESS and serum HIF-1α, TNF-α, Caspase-3, were detected and compared.Results The clinical efficacy of the experiment group was better than that of control group(P<0.05),and the MESS of the experiment group was lower than the control group(P<0.05).Serum HIF-1α, Caspase-3, TNF-αlevels were lower than the control group(P<0.05).Conclusion Ginkgetin injection can effectively improve the patient’s neurological symptoms, it is of great significance to the clinical treatment of cerebral infarction.

OBJECTIVETo investigate the density and distribution of nerve endings and neuropeptide Y (NPY) in lumbar facet joints of patients with low back pain.

METHODSFifteen patients without low back pain were selected as control group (group A). Facet joint samples in group A were obtained during the operation or lumbar spinal canal tumor they suffered from. Those patients with low back pain were divided into three groups according to their different origins of pain, such as not from facet joint (group B, 15 patients) ,from facet joint only (group C, 20 patients), or from facet joint partially (group D, 20 patients). Different origins were determined by VAS after facet joint block. The density and distribution of nerve ending and neuropeptide in the capsular tissues were analyzed by a modified gold chloride staining and immunochemistry respectively.

RESULTSCompared with the ones in group A and B, the fact joints in group C and D were more inclined to be degenerated and got more nerve endings. NPY was expressed mainly in the facet joint of patients with low back pain in group C and D. In addition, there was a significant relationship between the distribution of nerve endings and NPY expression,while none of them were related with MRI Fujiwara grade of facet joint.

CONCLUSIONThese results suggest that the number of mechanoreceptors, neural sprouting and secreted peptides in the facet joint capsules vary with the change of mechanical or nociceptive stimulation, which may promote the development of low back pain in return.

Adult ; Aged ; Case-Control Studies ; Chronic Pain ; etiology ; metabolism ; pathology ; Female ; Humans ; Low Back Pain ; etiology ; metabolism ; pathology ; Male ; Mechanoreceptors ; physiology ; Middle Aged ; Nerve Endings ; pathology ; Neuropeptide Y ; analysis

Objective To investigate the pathological types and features of lymph nodes in human immunodeficiency virus(HIV)/acquired immune deficiency syndrome(AIDS)patients with superficial lymphadenectasis.Methods The tissues of lymph nodes were obtained from 151 HIV/AIDS patients with superficial lymphadenectasis for pathological examination.The pathological results were observed by light microscope after Hematoxylin-Eosin(HE),acid-fast,periodic acid-Schiff (PAS),and digested-PAS(D-PAS)staining.The pathological results of lymph nodes were described and the correlation between pathological changes and CD4+T lymphocyte count was analyzed.Chisquare test was used for the statistic analysis.Results The benign lesions were found in 145 patients (96.0%),while the malignant tumors were found in 6 patients(4.0%).The pathological findings in the 151 HIV/AIDS patients included tuberculosis(72 patients),lymph node reactive hyperplasia(34patients),lymphatic fungal infections(23 patients,including penicillium diseases in 19 cases),AIDSrelated lymphadenectasis(14 cases),non-Hodgkin lymphoma(5 cases),benign fibrous histiocytoma (1 case).In addition,there were 83 patients(55.0%)with CD4+T lymphocyte count lower than 100×106/L.The frequency of penicillium diseases was higher in patients with lower CD4+T lymphocyte count(x2=7.757,P=0.021).Conclusions The major reasons for superficial lymphadenectasis in HIV/AIDS patients are infectious diseases,such as tuberculosis and fungal infections,which are common in patients with lower CD4+T lymphocyte counts.Non-Hodgkin lymphoma is the most common malignant tumor in this patient population.

Objective To access the long-term efficacy and safety of immunosuppression on the progression of IgA nephropathy (IgAN) by Meta analysis.Methods Databases EMBASE,Pubmed,Elsevier Science Direct,Scopus,Web of Science,Google Scholar,Cochrane Library,China National Knowledge Infrastructure,WanFang and VIP Data were retrieved to collect the randomized controlled trials (RCTs) at least 3 years follow-up on immunosuppression for IgAN published before May 2014.The literatures were screened independently by two reviewers according to the inclusion and exclusion criteria,and the methodological quality was assessed.Statistic software Stata 12.0 was used to conduct analysis.Results Nine articles were included in this study with a total of 568 patients.Immurnosuppression could lowered the risk for the progression to ESRD (RR=0.32,95％CI:0.20-0.49,P ＜ 0.01).As far as the efficacy of immunosuppression,subgroup analysis indicated that three studies with more than 7 year follow-up (RR=0.28,95％CI:0.13-0.59,P ＜ 0.01) were similar with 7 studies followed by for less than 7 years (RR=0.34,95％ CI:0.19-0.59,P＜0.01); six adopted immunosuppressor monotherapy (RR=0.29,95％ CI:0.15-0.58,P＜ 0.01) were similar to two used corticosteroids plus other immunosuppression (RR=0.33,95％CI:0.18-0.59,P ＜ 0.01); There were no significant differences between four studies from Europe (RR=0.27,95％CI:0.14-0.53,P ＜ 0.01) and five from Asia (RR=0.35,95％ CI:0.19-0.65,P＜0.01).Immunosuppression was associated with an increased risk for adverse events (RR=2.33,95％ CI:1.33-4.09,P＜0.01).Conclusion Immunosuppression for IgAN may reduce long-term risk of progression to ESRD,but increase the risk of adverse events to some extent.

Objective To investigate the molecular characteristics of immune response signaling molecules induced by transfection of coxsackievirus B2 ( CVB2 ) structural proteins into epithelial cells. Methods Recombinant eukaryotic expression plasmids containing the coding regions of CVB2 structural proteins VP1-VP4 were constructed and then transfected into 16HBE cells. Culture supernatants and cell ly-sates of the transfected 16HBE cells were collected. Expression of signaling molecules involved in innate im-mune responses in transfected 16HBE cells at mRNA level was detected by RT-Q-PCR. The proliferation of T cells co-cultured with culture supernatants and cell lysates of the transfected 16HBE cells was analyzed by ELISPOT. Results Expression of innate immunity-related signaling molecules such as TGF-β-activated ki-nase ( TAK) , NF-κB-inducing kinase ( NIK) , IκB kinase α ( IKKα) and IFN-β at mRNA level was up-regulated in 16HBE cells transfected with CVB2 structural proteins VP1-VP4. Both culture supernatants and cell lysates of the transfected 16HBE cells enhanced the proliferation of T cells. Conclusions CVB2 struc-tural proteins VP1-VP4 could enhance the expression of innate immunity-related signaling molecules to var-ying degrees and promote the activation of adaptive immunity.

OBJECTIVETo investigate the role of neuronal apoptosis in organophosphorus poisoning-induced delayed neuropathy (OPIDN) and its dynamic pathological changes.

METHODSTo establish OPIDN animal model, triorthocresyl phosphate (TOCP)was given to hens with a single dose (1 000 mg/kg, im). Changes of neuropathology, number of neurons and apoptotic cells in the third lumbar spinal cord were observed by HE, Nissl and TUNEL methods 3, 5, 7, 10, 14, 18 days after injection.

RESULTSThe hens showed OPIDN typical signs (progressive ataxia and hypotonia) about 9 days after TOCP exposure. HE staining revealed dark red nucleus in neurons of anterior horn of lumbar spinal cord 5 days after exposure, but this phenomenon disappeared 18 days later. Nissl method showed that the number of neurons in anterior horn of spinal cord decreased [from (82 +/- 4) cell/mm(2) to (66 +/- 6) cell/mm(2)]. TUNEL positive cells began to appear [(22 +/- 2) cell/mm(2)] 5 days after TOCP exposure, and reached the peak [(27 +/- 3) cell/mm(2)] 7 days later, and disappeared 18 days later.

CONCLUSIONNeuronal apoptosis in anterior horn of spinal cord of hens appeared in OPIDN, suggesting that cellular apoptosis may play an important role in the pathogenesis of OPIDN.

Animals ; Apoptosis ; drug effects ; Chickens ; Female ; In Situ Nick-End Labeling ; Insecticides ; toxicity ; Models, Animal ; Neurons ; drug effects ; Spinal Cord ; drug effects ; Tritolyl Phosphates ; toxicity