Objective To investigate the genetic association of complement factor B (CFB)gene polymorphisms with the susceptibility and prognosis of IgA nephropathy (IgAN).Methods Four hundreds and sixty-three Northern Han Chinese patients with IgAN and two hundreds and ninty-six geographically and ethnic matched healthy volunteers were recruited.Peripheral blood was collected from recruited individuals for DNA extracting.After amplified by plymerase chain reaction (PCR),genotyping of the four single nucleotide polymorphisms (SNPs) in CFB gene,which were rs4151667,rs12614,rs641153 and rs117314762,were performed by sequencing.Differences of allele and genotype frequencies were analyzed between IgAN patients and healthy controls.Moreover,the association between these SNPs and disease clinical manifestation,pathological features and long term renal outcome in IgAN patients were further analyzed.Results The G allele and GG genotype frequencies of rs117314762 in CFB gene were significantly higher in IgAN patients than that in healthy controls.No difference in allele and genotype frequencies of rs4151667,rs12614,rs641153 between IgAN patients and healthy controls was observed.Furthermore,no association was found between these SNPs in CFB gene and clinical manifestation,pathological features and long term renal outcome of IgAN.Conclusion Association between rs117314762 in CFB gene and IgAN susceptibility suggests that there may be functional variants in CFB gene or its linked genetic region,which needs further exploration.

Cerebral Hemorrhage ; etiology ; Cerebrospinal Fluid Rhinorrhea ; surgery ; Humans ; Male ; Middle Aged ; Postoperative Hemorrhage

Asphyxia ; etiology ; therapy ; Humans ; Male ; Middle Aged ; Retropharyngeal Abscess ; complications ; therapy ; Subphrenic Abscess ; complications ; therapy ; Treatment Outcome

Carcinoembryonic Antigen ; metabolism ; Carcinoma, Squamous Cell ; metabolism ; pathology ; surgery ; Gastrectomy ; Hodgkin Disease ; pathology ; Humans ; Lymphoma, Large B-Cell, Diffuse ; pathology ; Male ; Middle Aged ; Mucin-1 ; metabolism ; Stomach Neoplasms ; metabolism ; pathology ; surgery

Hongkong pediatric specialist training had successful experiences in the last twenty years.Hongkong hospital authority and Hongkong college of pediatricians managed pediatric specialist training together and made a series of regulations,which have strict training rotation requirements.Training hospitals all need to obtain the authentication including basic training,higher training and overseas training agencies.After 6 years strict training,the trainees have strong pediatric basic theories,procedure abilities,evidence-based practice and team work spirit.In short,the experiences of Hongkong pediatric specialist training is deserved to be learned by the standard training of pediatric resident in mainland China.

Objective:To observe the efficacy of using electroacupuncture(EA)plus stuck-needle lifting method to treat intractable facial paralysis based on the myofascial theory. Methods:Ninety patients with intractable facial paralysis were divided into a control group and an observation group using the random number table method,with 45 cases in each group.The control group was given conventional EA treatment,and the observation group received EA plus the stuck-needle lifting method based on the myofascial theory for 4 consecutive weeks,6 sessions each week.The electromyographic results,modified Portmann scale(MPS)score,facial nerve function index(FNFI),and total effective rate were compared. Results:There were no significant differences in the MPS and FNFI scores between the two groups before treatment(P>0.05).After treatment,the total effective rate and FNFI and MPS scores were notably higher in the observation group than in the control group(P<0.05).There were no significant differences in the electromyographic readings between the two groups before the intervention(P>0.05).After the intervention,the observation group had a shorter blink reflex R1 latency and a higher facial nerve compound muscle action potential compared with the control group,and the between-group differences were statistically significant(P<0.05). Conclusion:EA plus stuck-needle lifting method based on the myofascial theory can enhance treatment efficacy for intractable facial paralysis.

Objective To investigate the prevalence and its major risk factors of NAFLD among enterprises employees of Rizhao region. Methods 8 259 employees aged over 18 were selected by multi-stage stratified random cluster sampling method in the enterprises of Rizhao region. The data were analyzed, such as height, weight, blood pressure,blood lipids,blood sugar,hepatitis series,and ECG,abdominal ultrasound,chest χ ray were conducted in the fasting state. The diagnosis of NAFLD was in line with diagnostic criteria adopted by China Institute of Liver Disease and alcoholic liver disease group, and the prevalence and major risk factors of NAFLD were investigated. Results The prevalence of NAFLD was 18. 1% (male 23.0% ,female 7. 6%;the ratio of male to female:3. 03:1) ,The prevalence of NAFLD reached a peak from 40 to 50 in male and after the age of 70 in female,and there was no statistically difference after the age of 50 between male and female. The close correlation was demonstrated by Logistic regression analysis between sex, hyperuricemia, HDLC, overweight or obesity, hyperglycemia, hypertriglyceridemia and NAFLD. Conclusion The prevalence of NAFLD was high, especially in older persons in enterprises employees of Rizhao region, and sex,hyperuricemia,HDLC,overweight or obesity,hyperglycemia and hypertriglyceridemia were closely associated with NAFLD.

BACKGROUND:Finding of neural stem cells(NSCs)brings new hope for repairing central nervous system(CNS)injury.However,the influence of internal environment after brain injury on the survival and differentiation of NSCs is a complexand variable process.OBJECTIVE:To observe the survival and differentiation of human embryonic NSCs following implantation into rats with fluid percussion brain injury.DESIGN:Open experiment.SETTING:Department of Neurosurgery,Guangdong Provincial Hospital of Traditional Chinese Medicine;Beijing Institute of Neurosurgery.MATERIALS:This experiment was carried out In the Laboratory of Neural Stem Cells,Beijing Institute of Neurosurgery from September 2002 to March 2003.Twenty-four female SD rats,aged 7 weeks,with body mass of(250±10)g,were provided by the Experimental Animal lnstitute, Chinese Academy of Medical Sciences[License Nd. SCXK(Jing)2002-2003]. Cerebrum of 8-week aborted fetus was obtained (Informed consents were obtained from parturients and their relatives). Fetal survival was monitored by B ultrasonic wave during abortion. BrdU monoclonal antibody(Sigma Company),rabbit anti-nidogen polyclonal antibody(Chemicon Company),mouse anti-microtubule-associated protein 2 (MAP-2)monoclonal antibody(Neomarkers Company),rabbit anti-gliaI fibrillary acidic protein(GFAP)polyclonal antibody (Biogenex Company).METHODS:① CerebraI cortex cells of 8-week aborted human fetus was harvested and cultured in vitro for obtaining human embryronic NSCs.②Rat models of hydraulic impact injury were developed.Bone window of motor sensory area of cerebral cortex was set at 2.5mm posterior to bregma which was zero point and 3.0 mm lateral to midline.Hydraulic impact injury parameters were set as impact pressure 0.3 MPa. impact time 25 ms and impact time once. ③BrdU-labeled human embryronic NSCs were implanted into injured area al 24 hours after injury.After 1 and 4 weeks.rats were sacrificed.Adjacent sections were doubly stained bv BrdU/MAP-2 and BrdU/GFAP.MAIN OUTCOME MEASURES:①Survival and immigration of implanted human embryonic NSCs.②Differentiation of implanted human embryonic NSCs.RESULTS:①BrdU-positive cells were oval and brown.At 1 and 4 weeks after implantation,BrdU-positive cells survived and migrated,and they migrated more widely at 4 weeks after implantation. ②At 1 week after implantation,more BrdU-positive cells were found in the subcortical granular layer and subcortex,and BrdU/MAP-2-positive cells were more than BrdU/GFAP-positive cells;At 4 weeks after implantation,BrdU-positive cells were significantly reduced,and found in choroid plexus and blood capillary,and BrdU/GFAP-positive cells were more than BrdU/MAP-2-positive cells.CONCLUSION:Implanted human embryonic NSCs can survive in the region of brain injury.gradually differentiate into astrocytes during rehabilitation and are easily digested by endothelial phagocytes.It indicates that immunological rejaction possibly influences the survival of human embryonic NSCs.

Objective To investigate the effect of BPI-1095 on caspase-3 protein expression in middle artery occlusion(MCAO) rats.Methods Cerebral ischemia was induced with MCAO in adult male SD rats.Rats were randomly subjected into 6 groups with 15 rats in each group.Each rat has been given tested medication of different dosage and was sacrificed 24 h after treatment.The area of infarction was measured on each slice by image analysis system.Meanwhile,immunohistochemistry staining was used to identify caspase-3 expression in ischemic brain tissue.Results The infarcted area were significantly decreased in big and moderate dose treated rats(P<0.05,vs the placebo group).The expression of caspase-3 protein decreased in contralateral and ipsilateral hemisphere areas.The caspase-3 positive cell was significantly decreased in rats treated with big doses compared with placebo-or ASA-treated rats.Conclusion BPI-1095 shows neuroprotection in MCAO rats,which may related with the inhibition of caspase-3 expression resulting in apoptosis in penumbra.

OBJECTIVETo explore the neuroprotective effect and mechanism of picroside II on extracellular regulated protein kinases1/2 (ERK1/2) signal transduction pathway in cerebral ischemia injuryrats. METHODS The middle cerebral artery occlusion (MCAO) model was established by inserting a monofilament into middle cerebral artery. Totally 96 successfully modeled Wistar rats were divided into the modelgroup, the treatment (picroside II) group, the Lipopolysachcaride (LPS) group, and the U0126 group according to random digit table. Each group was further divided into 3 subgroups, i.e. 6, 12, and 24 h sub-groups. Picroside II (20 mg/kg) was peritoneally injected to rats in the treatment group 2 h after ischemia.LPS (20 mg/kg) and Picroside II (20 mg/kg) were peritoneally injected to rats in the LPS group 2 h after ischemia. U0126-EtOH (20 mg/kg)and Picroside II (20 mg/kg) were peritoneally injected to rats in the U0126group 2 h after ischemia. Equal volume of normal saline was peritoneally injected to rats in the control groupand the model group. The neurobehavioral function was evaluated by modified neurological severity score(mNSS) test. The structure of neurons was observed using hematoxylin-eosinstaining (HE) staining. Theapoptotic cells were detected using terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The expression of phosphorylated extracellular signal-regulated protein kinase1,2 (pERK1,2) in cortex was detected using immunohistochemistry (IHC) and Western blot.

RESULTSAfter cerebral ischemia injury neurological impairment score increased, the damage of neuron in the cortical area was aggravated, apoptotic cells increased in the model group as time went by. The expression of pERK1/2 increased more significantly in the model group than in the control group (P <0.05). The damage of neuron in the cortical area was milder, while apoptotic cells decreased, the expression of pERK1f2 obviously decreased more in the treatment group and the U0126 group (P < 0.05). The early damage of neuron in the cortical area was more severe, apoptotic cells and the expression of pERK12 were comparatively higher in early stage of the LPS group, but the expression of pERK1/2 was somewhat decreased in late stage.

CONCLUSIONSActivating ERK12 pathway could mediate apoptosis and inflammatory reactions of neurons after cerebral ischemia injury. Picroside II could protect the nerve system possibly through reducing activation of ERKI2 pathway, inhibiting apoptosis of neurons and inflammation reaction.

Animals ; Apoptosis ; Brain Ischemia ; drug therapy ; Cinnamates ; pharmacology ; Infarction, Middle Cerebral Artery ; drug therapy ; Iridoid Glucosides ; pharmacology ; MAP Kinase Signaling System ; drug effects ; Neurons ; pathology ; Neuroprotective Agents ; pharmacology ; Random Allocation ; Rats ; Rats, Wistar