OBJECTIVETo explore the causes of nonspecific chronic cough in children and relationship between transient receptor potential vanilloid 1 (TRPV1) gene polymorphisms and nonspecific chronic cough.

METHODSA total of 195 children with chronic cough were followed up half a month, one month and three months after their first visit to hospital. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to examine polymorphisms of the TRPV1 gene in the children. A total of 205 healthy or surgical children without chronic cough served as the control group.

RESULTSThe etiologic distribution of the 195 children with chronic cough was as follows: 96 (49.2%) cases of cough variant asthma (CVA), 48 (24.6%) cases of CVA complicated by upper airway cough syndrome (UACS), 34 (17.4%) cases of post-infectious cough, and 17 (8.7%) cases of UACS. Three genotypes were identified in both groups at positions rs222747 (CC, GC and GG), rs222748 (CC, TC and TT) and rs8065080 (CC, TC and TT). The frequencies of genotype and allele at position rs222747 did not accord with the law of Hardy-Weinberg. There was no significant difference in frequencies of genotype and allele at positions rs222748 and rs8065080 between the two groups.

CONCLUSIONSCVA, UACS and post-infectious cough are common causes of nonspecific chronic cough in children. TRPV1 gene polymorphisms at positions rs222748 and rs8065080 may be unrelated to nonspecific chronic cough in children.

Adolescent ; Alleles ; Child ; Child, Preschool ; Chronic Disease ; Cough ; etiology ; genetics ; Female ; Genotype ; Humans ; Infant ; Male ; Polymorphism, Genetic ; TRPV Cation Channels ; genetics

The hematopoietic cell phosphatase (HCP or SHP-1), the SH2 domain contain protein tyrosine phosphatase, is a crucial negative regulator in the process of hematopoietic cell development, proliferation and receptor-mediated mitogenic signaling pathways, and its mutation is responsible for the over-expansion and inappropriate activation of myelomonocytic population in motheaten mice. The aim of the study was to evaluate the role of the HCP gene in leukemogenesis. Bone marrow and/or peripheral blood from 32 acute myeloid leukemia (AML) patients, 9 acute lymphocytic leukemia (ALL) patients, 8 leukemia cell lines and 50 normal controls were analyzed by reverse transcription-polymerase chain reaction (RT-PCR) based on single strand conformation polymorphism (SSCP) and sequencing. RT-PCR showed that all samples expressed HCP gene, only one missense mutation at codon 225 (AAC to AGC, Asn to Ser) within N-terminal SH2 domain was found in an ALL patient. In addition, four polymorphic base substitutions were detected in codon 69, 85, 86 and 266, respectively. In conclusion, mutation of HCP gene is an infrequent genetic aberration which may only play a role in pathogenesis of a small part of leukemia, however, its significance needs to be further clarified.
Acute Disease ; Cell Line, Tumor ; Humans ; Intracellular Signaling Peptides and Proteins ; Leukemia ; enzymology ; genetics ; Mutation ; Polymorphism, Single-Stranded Conformational ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 ; Protein Tyrosine Phosphatases ; genetics

OBJECTIVETo investigate the prevalence of anemia and related risk factors in infants aged 6-12 months from rural areas of southern Shaanxi Province.

METHODSA questionnaire survey was used to collect the basic information on infants aged 6-12 months and their families from rural areas of southern Shaanxi Province, China. The content of hemoglobin was measured in these infants. A multivariate logistic stepwise regression analysis was performed to determine the risk factors for the development of anemia in infants.

RESULTSA total of 1 802 infants and their families participated in the survey, and there were 1 770 valid samples. A total of 865 infants (865/1 770, 48.87%) were found to have anemia. The multivariate logistic stepwise regression analysis showed that breastfeeding after birth (lack of scientific supplementary food) increased the risk of anemia in infants (OR=1.768, P<0.01). Addition of supplementary food which met the criteria for minimum feeding frequency recommended by WHO (OR=0.779, P<0.05) and formula milk feeding (OR=0.658, P<0.01) were protective factors against anemia in infants.

CONCLUSIONSIn the rural areas in southern Shaanxi Province, anemia in infants aged 6-12 months is still a serious public health problem. Improper feeding can increase the risk of anemia in infants, and scientific addition of supplementary food is the key to reducing anemia in infants.

Anemia ; etiology ; Breast Feeding ; Female ; Humans ; Infant ; Logistic Models ; Male ; Risk Factors

OBJECTIVETo investigate the effect of rosuvastatin on atherosclerosis in apoE-knockout (apoE-/-) mice.

METHODSEighteen 6-week-old apoE-/- mice fed with high fat diet were used as atherosclerosis models, twelve 6-week-old C57BL/6 mice fed with normal diet were used as control. After twelve weeks, six apoE-/- mice were used to observe the formation of atherosclerosis. Another 12 apoE-/- mice were divided into placebo treated group (n = 6) and rosuvastatin group (n = 6, 10 mg×kg(-1)×d(-1) per gavage) and treated for 12 weeks. Then, blood was collected for measuring lipid, aorta was prepared for morphologic study (HE, Oil red O, Masson) and immunohistochemical analysis (α-smooth active protein, transforming growth factor β(1), macrophage surface molecule-3).

RESULTSSerum cholesterol and low density lipoprotein levels were significantly higher in apoE-/- mice fed with high fat diet than in C57/BL6 mice(all P < 0.01)while triglyceride level was similar between the two groups, these were not affected by rosuvastatin. Similarly, atherosclerotic lesion area in apoE-/- mice fed with high fat diet was also not significantly reduced by rosuvastatin, while lipid deposition could be significantly reduced and collagen deposition could be significantly increased in the aortic atherosclerotic lesions by treatment with rosuvastatin. Upregulated TGF-β(1) and Mac-3 expression in the aortic atherosclerotic lesions in apoE-/- mice fed with high fat diet could also be significantly reduced by rosuvastatin (all P < 0.01), suggesting reduce inflammatory responses in the atherosclerotic lesion and stable atherosclerotic plaque post rosuvastatin treatment.

CONCLUSIONReducing inflammatory responses and stabilizing plaque properties might contribute to the anti-atherosclerosis effects of rosuvastatin in mice high fat diet fed apoE-/- mice.

Animals ; Antigens, Differentiation ; metabolism ; Apolipoproteins E ; genetics ; Atherosclerosis ; drug therapy ; metabolism ; pathology ; Diet, High-Fat ; Fluorobenzenes ; pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Plaque, Atherosclerotic ; pathology ; Pyrimidines ; pharmacology ; Rosuvastatin Calcium ; Sulfonamides ; pharmacology ; Transforming Growth Factor beta ; metabolism

OBJECTIVETo investigate the efficacy of Telbivudine and Entecavir for therapy of HBeAg positive chronic hepatitis B for 52 weeks.

METHODSIn this random and control study, the efficacy of Telbivudine and Entecavir treatments were compared in 180 patients with HBeAg positive chronic hepatitis B.The patients were randomly assigned to a daily 600 mg Telbivudine treatment group or daily 0.5 mg Entecavir group for 52 weeks.

RESULTSAt week 52, HBV DNA undetectable rate was better in the Entecavir-treated group than in the Telbivudine-treated group, but didn't reach statistical significance. The viral breakthrough rates were significantly lower in the Entecavir-treated group than in the Telbivudine-treated group (x2 = 4.09, P <0.05). The clearance and seroconversion of HBeAg and the mean reductions of HBeAg from baseline at week 52 were significantly greater in the telbivudine-treated group than in the entecavir-treated group (x(2) clearance = 4.63, x(2) seroconversion = 4.80, (t-mean) reductions = 2.02; P < 0.05). The HBeAg seroconversion rates were not associated with both baseline ALT and baseline HBV DNA in both groups (P more than 0.05). In Telbivudine-treated group, the HBeAg decline is more than 2 log at week 24, HBeAg decline is more than 1 log at week 12 and the HBeAg baseline were independent factors correlated to HBeAg seroconversion rates at week 52 by Binary Logistic analysis, and also in entecavir-treated group the HBeAg decline is more than 2 log at week 24, HBeAg decline is more than 2 log at week 36 and the HBeAg decline is more than 2 log at week 12 were independent factors correlated to HBeAg seroconversion rates at week 52.

CONCLUSIONSignificant difference of HBeAg seroconversion rates at week 52 existed between Telbivudine-treated group and Entecavir-treated group. Entecavir is significantly superior to Telbivudine with less resistance to nucleosides. HBeAg decline is more than 2 log at week 24 is the best predicting factor for HBeAg seroconversion at week 52.

Adolescent ; Adult ; Antiviral Agents ; therapeutic use ; DNA, Viral ; blood ; Female ; Guanine ; analogs & derivatives ; therapeutic use ; Hepatitis B e Antigens ; blood ; Hepatitis B, Chronic ; blood ; drug therapy ; Humans ; Male ; Middle Aged ; Nucleosides ; therapeutic use ; Pyrimidinones ; therapeutic use ; Thymidine ; analogs & derivatives ; Treatment Outcome ; Young Adult

The aim was to construct a prokaryotic expression plasmid encoding the fusion gene of single-chain variable fragment and monocyte chemotactic protein-3 (MCP-3). The cDNAs of immunoglobulin (Ig) VH and Ig VL were amplified by RT-PCR and assembled into the single-chain variable fragment (scFv) by recombinant PCR method. The cDNAs of Ig VH and Ig VL were connected by a (Gly4Ser)3 linker. Then, the fragments of scFv and MCP-3 were connected with a NDAQAPKS spacer, using recombinant PCR method again. The results indicated that the fusion gene of scFv-MCP-3 were constructed correctly and cloned into the prokaryotic expression plasmid successfully identified by sequencing and restriction endonucleases examination. Finally, the fusion protein was expressed in E coli DH5alpha under induction by arabinose. And the fusion protein was 65 kD and account for 30% of the total protein of the bacteria. In conclusion, a prokaryotic plasmid, encoding the fusion gene of single-chain variable fragment with MCP-3 and expressing idiotype protein vaccination against B cell lymphoma, was constructed correctly.
Amino Acid Sequence ; Animals ; Cancer Vaccines ; biosynthesis ; genetics ; immunology ; Chemokine CCL7 ; biosynthesis ; genetics ; immunology ; Genetic Vectors ; Humans ; Immunoglobulin Idiotypes ; immunology ; Immunoglobulin Variable Region ; biosynthesis ; genetics ; immunology ; Lymphoma, B-Cell ; immunology ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Plasmids ; genetics ; Prokaryotic Cells ; metabolism ; Recombinant Fusion Proteins ; biosynthesis ; genetics ; immunology ; Vaccines, DNA ; biosynthesis ; genetics ; immunology

OBJECTIVEThe SH2 domain containing inositol 5'-phosphatase (SHIP) is predominately expressed in hematopoietic cells, and is a crucial negative regulator in the development of hematopoietic cells. This paper is to evaluate the role of the SHIP gene in human leukemogenesis.

METHODSExpression of SHIP gene in bone marrow and/or peripheral blood from 32 patients with acute myeloid leukemia (AML), 9 with acute lymphoblastic leukemia (ALL), as well as human hematopoietic cell lines was analyzed by reverse transcription-polymerase chain reaction (RT-PCR), single strand conformational polymorphism (SSCP) and DNA sequencing.

RESULTSRT-PCR showed that all samples expressed SHIP gene. Mutations of SHIP gene were detected in 7 (22%) of 32 AML patients and one (12%) of 9 ALL patients. Interestingly, two missense mutations that had been observed in a AML patient at diagnosis disappeared after complete remission (CR). In addition, in vitro Akt phosphorylation was prolonged and increased following IL-3 stimulation of this patient's cells.

CONCLUSIONOur data demonstrate for the first time the mutation of SHIP gene in acute leukemia and suggest a possible role of the mutation of this gene in the development of acute leukemia. SHIP may serve as a tumor suppressor by negatively regulating the PI3K/Akt signaling pathway in hematopoietic cells.

Blotting, Western ; Cell Line, Tumor ; DNA Mutational Analysis ; HL-60 Cells ; Humans ; Inositol Polyphosphate 5-Phosphatases ; Interleukin-3 ; pharmacology ; K562 Cells ; Leukemia, Myeloid, Acute ; genetics ; metabolism ; Mutation ; Oncogene Protein v-akt ; metabolism ; Phosphoric Monoester Hydrolases ; genetics ; metabolism ; Phosphorylation ; drug effects ; Polymorphism, Single-Stranded Conformational ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; U937 Cells

The SH2 domain containing inositol 5'-phosphatase (SHIP) was initially described as a 145 kD protein phosphorylated on tyrosines upon growth factor and cytokine stimulation. SHIP is predominately expressed in hematopoietic cells, and is a crucial negative regulator in the development of hematopoietic cells. To evaluate the role of the SHIP gene in human leukemogenesis, expression and mutation of SHIP gene in bone marrow and/or peripheral blood from 32 patients with acute myeloid leukemia (AML), 9 patients with acute lymphoblastic leukemia (ALL), as well as human hematopoietic cell lines were analyzed by reverse transcription-polymerase chain reaction (RT-PCR), single strand conformational polymorphism (SSCP) and sequencing. The RT-PCR showed that all samples expressed SHIP gene. Mutations of SHIP gene were detected in 7 out of 32 AML patients (22%) and one out of 9 ALL patients (12%). Interestingly, two missense mutations that had been observed in one AML patient at diagnosis disappeared after complete remission (CR). In addition, Akt phosphorylation was prolonged and increased following IL-3 stimulation in this patient sample. In conclusion, data of this study demonstrate the mutation of the SHIP gene in acute leukemia for the first time and suggest a possible role of the mutation of this gene in the development of acute leukemia. SHIP serves as a tumor suppressor by negatively regulating the PI3K/Akt signaling pathway in hematopoietic cells.
Cell Line ; Humans ; Leukemia, Myeloid, Acute ; genetics ; Mutation ; PTEN Phosphohydrolase ; Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases ; Phosphoric Monoester Hydrolases ; genetics ; physiology ; Phosphorylation ; Polymorphism, Genetic ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; genetics ; Protein-Serine-Threonine Kinases ; metabolism ; Proto-Oncogene Proteins ; metabolism ; Proto-Oncogene Proteins c-akt ; Tumor Suppressor Proteins ; physiology

Peroral endoscopic myotomy (POEM) has emerged as a rescue treatment for recurrent or persistent achalasia after failed initial management. Therefore, we aimed to investigate the efficacy and safety of POEM in achalasia patients with failed previous intervention. We searched the MEDLINE, Embase, Cochrane, and PubMed databases using the queries “achalasia,” “peroral endoscopic myotomy,” and related terms in March 2019. Data on technical and clinical success, adverse events, Eckardt score and lower esophageal sphincter (LES) pressure were collected.The pooled event rates, mean differences (MDs) and risk ratios (RR) were calculated. A total of 15 studies with 2,276 achalasia patients were included. Overall, the pooled technical success, clinical success and adverse events rate of rescue POEM were 98.0% (95% confidence interval [CI], 96.6% to 98.8%), 90.8% (95% CI, 88.8% to 92.4%) and 10.3% (95% CI, 6.6% to 15.8%), respectively. Seven studies compared the clinical outcomes of POEM between previous failed treatment and the treatment naïve patients. The RR for technical success, clinical success, and adverse events were 1.00 (95% CI, 0.98 to 1.01), 0.98 (95% CI, 0.92 to 1.04), and 1.17 (95% CI, 0.78 to 1.76), respectively. Overall, there was significant reduction in the pre- and post-Eckardt score (MD, 5.77; p<0.001) and LES pressure (MD, 18.3 mm Hg; p<0.001) for achalasia patients with failed previous intervention after POEM. POEM appears to be a safe, effective and feasible treatment for individuals who have undergone previous failed intervention. It has similar outcomes in previously treated and treatment-naïve achalasia patients.

OBJECTIVEThe study was designed to find out the epidemic characteristics of leptospriosis and to develop effective intervention measures. The effects of floods on leptospriosis in some areas along Yangzi river and Huai river in Anhui province was also analysed.

METHODSStudy on serum epidemiology of leptospriosis was carried out from serous samples collected from native residents and animal hosts including isolation of pathogens at different phases (before,middle and after) and different monitoring spots,during the floods.

RESULTSInfection rate with leptospriosis pathogen among native residents was 13.49% during the flood-period,much higher than 2.18% at post-flood (chi2 = 22.78, P < 0.01) stage, in the flood-affected areas along Yangzi river in 1998. The average rates of infection were 2.48% and 5.35% in affected and unaffected areas along Huai river respectively, in 2003.

CONCLUSIONSThere was full evidence that floods causing the epidemics of leptospriosis. However, the transmission of leptospriosis among people would depend on affecting factors as scales of floods, lasting time, coincidence between flood happening and epidemic season, immuno-protection level against leptospriosis among people and so on to a great extent. Factors as the magnitude of pathogens carried by various kinds of infectious sources were also important determinants affecting the nature, being epidemic or pandemic of leptospriosis. It was suggested that active surveillance network on the sources of infection and risk factors of leptospriosis should be developed for the control and prevention of the disease, in the flood-hit areas.

Adolescent ; Adult ; Animals ; China ; epidemiology ; Female ; Floods ; Humans ; In Vitro Techniques ; Leptospirosis ; epidemiology ; prevention & control ; Male ; Middle Aged ; Rivers ; Young Adult