Objective To establish a new and convenient assay for whole blood lead concentration. Methods Whole blood sample was digested by nitric acid-perchloric. Under the condition of pH 0.8～1.0, lead concentration was examined by Hydridegeneration Atomic Fluorescence Spectrometry.Results The method had good linearity when lead concentration were between 0 to 600 ?g/L, r =0.999. The within-run CV of the method for high, middle and low lead level were 4.1%, 3.6% and 3.5% respectively. The between-run CV were 4.9%, 4.6% and 4.7% respectively. The recovery rates were 105.4%, 98.5% and 94.8% respectively. The single-blind test result of series standard lead samples provided by Chinese Academy of Preventive Medicine were within the acceptable range. The detecting Limit of this method was 0.3 ng. There was no significant interference from main two-valence positiveion. The sample can be storage at lest for 1 months at 4℃. Samples of 869 children from Tianjin were tested by this method. The mean value was 91.9 ?g/L, median was 83.8 ?g/L, all data were within 23.1～386.3 ?g/L. The result showed out positive skewness distribution.Conclusion This method were sensitive, accurate, precise, quick and low-cost. It was suitable for use in clinical laboratories.

The antibody against AT1-EC2 plays a role in some kinds of inflammatory vascular diseases including malignant hypertension, preeclampsia, and renal-allograft rejection, but the detailed mechanisms remain unclear. In order to investigate the changes of NADPH oxidase and reactive oxygen species in the aorta in a mouse model which can produce AT1-EC2 antibody by active immunization with AT1-EC2 peptide, 15 mice were divided into three groups: control group, AT1-EC2-immunized group, and AT1-EC2-immunized and valsartan-treated group. In AT1-EC2-immunized group and AT1-EC2-immunized and valsartan-treated group, the mice were immunized by 50 μg peptide subcutaneously at multiple points for 4 times: 0, 5, 10, and 15 days after the experiment. In AT1-EC2-immunized and valsartan-treated group, valsartan was given at a dose of 100 mg/kg every day for 20 days. After the experiment, the mice were sacrificed under anesthesia and the aortas were obtained and frozen in liquid nitrogen for the preparation of frozen section slides and other experiments. The titer of AT1-EC2 was assayed by using ELISA. The level of NOX1 mRNA in the aorta was determined by using RT-PCR. The expression of NOX1 was detected by using Western blotting. Confocal scanning microscopy was used to assay the α-actin and NOX1 expression in the aortic tissue. The O(2)∸ production was detected in situ after DHE staining. The mice produced high level antibody against AT1-EC2 in AT1-EC2-immunized group and AT1-EC2-immunized and valsartan-treated group, and the level of NOX1 mRNA in the aortic tissues was 1.6±0.4 times higher and the NOX1 protein expression was higher in AT1-EC2-immunized group than in control group. There were no significant differences in the level of NOX1 mRNA and protein expression between control group and AT1-EC2-immunized and valsartan-treated group. The expression and co-localization of α-actin and NOX1 in AT1-EC2-immunized group increased significantly as compared with those in control group, and the O(2)∸ production increased about 2.7 times as compared with control group. There were no significant differences between control group and AT1-EC2-immunized and valsartan-treated group. It is concluded that active immunization with AT1-EC2 can activate NOX1-ROS, and increase vascular inflammation, which can be inhibited by AT1 receptor blocker valsartan. This may partially explain the mechanism of the pathogenesis of inflammatory vascular diseases related to antibody against AT1-EC2.

Objective To investigate the relationship between the promoter of IL-12B gene polymorphism and the susceptibility and clinical features of chronic gastritis and duodenal ulcer with or without Helicobacter pylori(Hp) infection in children and adolescent.Methods Mucosal biopsies were obtained from 132 children and adolescent (patient group),including 100 children with chronic gastritis and 32 children with duodenal ulcer,undergoing an upper gastrointestinal endoscopy for dyspeptic symptoms.Biopsy specimens were stained with hematoxilin and eosin (HE),and gastritis was graded according to the Sydney system.Serology,urease test and histology were taken to assess Hp status.Genomic DNA was obtained from peripheral blood or gastric biopsies of patients and 102 healthy children as normal control group.The promoter of IL-12B +1188A/G gene polymorphism was genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and sequencing.The genotype distributions and allele frequencies were compared between the study group and the normal control group,and the association of genotypes with clinicopathological features was studied.IL-12B mRNA level expressions in gastric mucosa were confirmed by reverse transcription PCR biopsy-based tests.Results The genotype distributions and allele frequencies of IL-12B +1188A/G gene polymorphisms were similar in gastric upper gastrointestinal diseases and healthy subjects.The IL-12B +1188A/G gene polymorphisms were not associated with Hp status.IL-12B+1188A/G gene polymorphisms did not affect IL-12B mRNA level expressions and were not associated with the degree of antrum chronic inflammation.Conclusions These data suggest that IL-12B+1188A/G gene polymorphisms are not associated with susceptibility to chronic gastritis and duodenal ulcer in children and adolescent.

BACKGROUND: Hypothermia is associated with poor outcome in trauma patients; however, hemorrhagic shock (HS) model with anesthetized swine was different from that of clinical reality. To identify the effects of environmental hypothermia on HS, we investigated hemodynamics and oxygen dynamics in an unanesthetized swine model of HS under simulating hypothermia environment.METHODS: Totally 16 Bama pigs were randomly divided into ambient temperature group (group A) and low temperature group (group B), 8 pigs in each group. Venous blood (30 mL/kg) was continuously withdrawn for more than 15 minutes in conscious swine to establish a hemorrhagic shock model. Pulmonary arterial temperature (Tp), heart rate (HR), mean arterial pressure (MAP), pulmonary arterial pressure (PAP), pulmonary arterial wedge pressure (PAWP), central venous pressure (CVP), cardiac output (CO), hemoglobin (Hb), saturation of mixed venous blood (SvO2) and blood gas analysis were recorded at the baseline and different hemorrhagic shock time (HST). The whole body oxygen delivery indices, DO2I and VO2I, and the O2 extraction ratio (O2ER) were calculated.RESULTS: Core body temperature in group A decreased slightly after the hemorrhagic shock model was established, and environmental hypothermia decreased in core body temperature. The mortality rate was significantly higher in group B (50％) than in group A (0％). DO2I and VO2I decreased significantly after hemorrhage. No difference was found in hemodynamics, DO2I and VO2I between group A and group B, but the difference in pH, lactic acid and O2ER was significant between the two groups.CONCLUSION: Environmental hypothermia aggravated the disorder of oxygen metabolism after hemorrhagic shock, which was associated with poor prognosis.

OBJECTIVETo explore the feasibility and safety of abdominosacral resection for patients with locally advanced primary low rectal cancer.

METHODSA total of 97 low rectal cancer patients were amenable to surgery but not anal sphincter preservation were included in this study and divided into the abdominoperineal resection group(n=49) and abdominosacral resection group(n=48) according to the order of alternative admission time between June 2010 and January 2012. Intraoperative and postoperative parameters were compared between the two groups.

RESULTSThe surgery went well and no perioperative mortality in the two groups. Compared with abdominoperineal resection group, the operative time of abdominosacral resection group(including the 2nd position adjustment time) was longer[(188±45) min vs. (143±48) min, P=0.000], the unexpected prostate or vagina injury incidence was lower [0 vs. 14.3%(7/49), P=0.032), and the perineal wound infection rate was lower [2.1% (1/48) vs. 18.4% (9/49), P=0.040].

CONCLUSIONAbdominosacral excision is feasible and safe for patients with locally advanced primary low rectal cancer.

Abdomen ; surgery ; Digestive System Surgical Procedures ; Humans ; Perineum ; Rectal Neoplasms ; surgery ; Treatment Outcome

OBJECTIVETo assess the reaction of cytokines induced killer (CIK) cells treatment in hematopoietic injury at different levels on patients with benzene poisoning and seek a novel, safe and effective immunotherapy for benzene poisoning.

METHODSCIK cells were in vitro activated by interleukin-2 (IL-2) and granulocyte-macrophage-colony-stimulating factor (GM-CSF) from the peripheral blood mononuclear cells (PBMC). Thirty-two patients with benzene poisoning were treated with CIK cells. Nineteen patients with mild or moderate benzene poisoning in the control group were treated with VitB4, batilol, leucogen, inosine and stanozolol. The results for treatment of 12 patients with aplastic anemia induced by severe benzene poisoning (the efficacy rate and the case fatality rate) were analyzed. The change of T-lymphocyte subset analyzed by flow cytometry was also observed before and after treatment.

RESULTSFor mild or moderate benzene poisoning, the increase of WBC and RLT in CIK group was higher than that in the control group (P < 0.05). The CD(4)/CD(8) levels were significantly increased after CIK treatment. And for severe benzene poisoning, the effective rate of the CIK group was 91.7% and the mortality rate was 0%.

CONCLUSIONCIK treatment is safe and effective for hematopoietic injury caused by benzene poisoning. The mechanism may be related with the immune modulation of CIK treatment on immunodeficiency of patients with benzene poisoning.

Adult ; Benzene ; poisoning ; Cytokine-Induced Killer Cells ; immunology ; Female ; Follow-Up Studies ; Humans ; Immunotherapy ; Male ; Middle Aged ; Treatment Outcome ; Young Adult

Objective: Schizophrenia is one of the most devastating neuropsychiatric disorders. Genetic epidemiological studies have confirmed that schizophrenia is a genetic disease. Genes promoting neurodevelopment may be potential candidates for schizophrenia. As an adaptor linking a number of tyrosine kinase receptors in multiple intracellular signaling cascades, Src homology 2 domain containing transforming protein 3 (SHC3) is a member of the Shc-like adaptor protein family, and expressed predominantly in the mature neurons of the central nervous system (CNS). In the present study, we aimed to investigate the association of SHC3 and schizophrenia. Methods: An independent case-control association study was performed in a sample including 710 schizophrenia patients and 1314 healthy controls from a Northeast Chinese Han population. Results: The allelic and genotypic association analyses showed that four SNPs in SHC3 significantly associated with schizophrenia (rs2316280, rs4877041, rs944485 and rs7021743). The haplotype composing of these four SNPs also showed significantly individual and global association with schizophrenia. Conclusion Our present results suggest SHC3 as a susceptibility gene for schizophrenia.

The threshold hypothesis of attenuated lentiviral vaccine considers that the type of host response to infections of lentiviruses depends on the viral load. To evaluate the correlation between viral loads of the attenuated vaccine strain of equine infectious anemia virus (EIAV) and their effects to induce protective immunity, longitudinal plasma viral loads in groups of horses inoculated with either an attenuated EIAV vaccine strain (EIAV(DLV125)) or sub-lethal dose of an EIAV virulent strain (EIAV(LN40)) were compared. Similar levels of plasma viral loads ranging from 10(3)-10(5) copies/mL were detected from samples of these two groups of animals (P > 0.05) during 23 weeks post the inoculation. However, different responses to the challenge performed thereafter with lethal dose of the EIAV virulent strain were observed from the groups of horses inoculated with either EIAV(DLV125) or sub-lethal dose of EIAV(LN40). The protective efficiency was 67% (3 of 4 cases) and 0 (none of 2 cases), respectively. Our results implicate that the viral load of EIAV attenuated vaccine is not the primary factor, or at least not the solo primary factor, to determine the establishment of immune protection.
Animals ; Equine Infectious Anemia ; blood ; immunology ; prevention & control ; Horses ; Immunization ; methods ; Infectious Anemia Virus, Equine ; immunology ; pathogenicity ; RNA, Viral ; blood ; genetics ; Random Allocation ; Reverse Transcriptase Polymerase Chain Reaction ; Time Factors ; Vaccines, Attenuated ; administration & dosage ; immunology ; Viral Load ; Viral Vaccines ; administration & dosage ; immunology ; Virulence ; immunology

The antibody against AT1-EC2 plays a role in some kinds of inflammatory vascular diseases including malignant hypertension, preeclampsia, and renal-allograft rejection, but the detailed mechanisms remain unclear. In order to investigate the changes of NADPH oxidase and reactive oxygen species in the aorta in a mouse model which can produce AT1-EC2 antibody by active immunization with AT1-EC2 peptide, 15 mice were divided into three groups: control group, AT1-EC2-immunized group, and AT1-EC2-immunized and valsartan-treated group. In AT1-EC2-immunized group and AT1-EC2-immunized and valsartan-treated group, the mice were immunized by 50 μg peptide subcutaneously at multiple points for 4 times: 0, 5, 10, and 15 days after the experiment. In AT1-EC2-immunized and valsartan-treated group, valsartan was given at a dose of 100 mg/kg every day for 20 days. After the experiment, the mice were sacrificed under anesthesia and the aortas were obtained and frozen in liquid nitrogen for the preparation of frozen section slides and other experiments. The titer of AT1-EC2 was assayed by using ELISA. The level of NOX1 mRNA in the aorta was determined by using RT-PCR. The expression of NOX1 was detected by using Western blotting. Confocal scanning microscopy was used to assay the α-actin and NOX1 expression in the aortic tissue. The O(2)∸ production was detected in situ after DHE staining. The mice produced high level antibody against AT1-EC2 in AT1-EC2-immunized group and AT1-EC2-immunized and valsartan-treated group, and the level of NOX1 mRNA in the aortic tissues was 1.6±0.4 times higher and the NOX1 protein expression was higher in AT1-EC2-immunized group than in control group. There were no significant differences in the level of NOX1 mRNA and protein expression between control group and AT1-EC2-immunized and valsartan-treated group. The expression and co-localization of α-actin and NOX1 in AT1-EC2-immunized group increased significantly as compared with those in control group, and the O(2)∸ production increased about 2.7 times as compared with control group. There were no significant differences between control group and AT1-EC2-immunized and valsartan-treated group. It is concluded that active immunization with AT1-EC2 can activate NOX1-ROS, and increase vascular inflammation, which can be inhibited by AT1 receptor blocker valsartan. This may partially explain the mechanism of the pathogenesis of inflammatory vascular diseases related to antibody against AT1-EC2.
Animals ; Aorta ; metabolism ; Disease Models, Animal ; Mice ; Mice, Inbred C57BL ; NADPH Oxidases ; genetics ; Reactive Oxygen Species ; metabolism ; Vaccination ; methods

Mutation in any of five key amino acid residues (at positions 26, 27, 30, 31 and 34) within the M2 protein of influenza A viruses leads to resistance against the amantodine class of anti-influenza drugs. In this study, a pyrosequencing method was described to rapidly detect established five molecular markers of resistance to M2 blockers, amantadine. The residues L26, V27, A30, S31 and G34 in the M2 protein were targeted for pyrosequencing, and 94 avian influenza viruses were used to perform the amantadine resistance analysis. Our results showed that most of avian influenza viruses were amantadine resistant, Mutations V27I and S31N were founded in these isolates.
Amantadine ; therapeutic use ; Animals ; Antiviral Agents ; therapeutic use ; Chickens ; Drug Resistance, Viral ; genetics ; Influenza A virus ; drug effects ; genetics ; Influenza in Birds ; drug therapy ; virology ; Reverse Transcriptase Polymerase Chain Reaction