Objective To study the neuropsychological behavior development of preterm infants and low birth weight infants,and to provide a reference to the early prevention and intervention on developmental retardations.Methods A total of 101 preterm infants and/or low birth weight infants received the infant development test of 0 ～ 6 year-old children intelligence developmental scale for neurological development and autism behavior checklist(ABC).Results 25 boys and 5 girls suffered from different psychological mental disorders.The occurrences were as follows:10 cases with mental retardation,9 cases with the language development delay,9 cases with motor retardation,1 case with cerebral palsy and 1 case with autism spectrum disorder.The incidence of intelligence problems were that language retardation (18.9％),the fine motor (16.8％),the adapative ability (12.6％),social action (9.5 ％) and the motor delay (3.2％).There were significant differences in the scores of social communication(x2=8.88,P=0.003),adaptive ability(x2=7.41,P=0.007),the fine motor(x2 =6.22,P=0.01) and total developmental quotient(x2 =5.58,P=0.02) between city children'and rural area.The behavioral problems more consisted in self-care ability and language retardation.Conclusion Preterm infants and low birth weight infants are exposed to language,fine motor,adaptive and communication ability problems,especially the children living in country.It is necessary to improve the early education and intervention for the rural preterm infants and low birth weight infants.

Objective: Nowadays, the power calibration methods of the microwave hyperthermia apparatus doesn't take the power loss of the radiator into account Aiming at this problem, the authors designed an equipment of measuring the actual output power of the microwave hyperthermia apparatus. A new method is proposed for calibration the output microwave power of microwave hyperthermia apparatus. Methods: The magnetron anode current was maintained at a default value by a control system. The microwave power generated by microwave source is coupled firstly to a low-power meter by the coaxial cable to measuring the power going through coaxial cable (P_(coaxial cable)). Then the microwave radiator is connected to the coaxial cable to make the microwave radiated by radiator. The radiator is assembled in the experimental device for the microwave completely absorbed by the water. The absorbed microwave energy of the water is calculated by measuring the water temperature change. The energy loss of the experimental device is calculated using the cooling rate. The output power of the radiator is equal to the ratio of the sum of the two aforementioned energy and the time. And the efficiency of the radiator η_(radiator), is equal to P_(radiator)/P_(coaxial cable) Results: The relationship between the actual output power of the microwave hyperthermia apparatus and the mag- netron anode current is P_(radiator) = 2η_(radiator) I. The efficiency of the radiator is η_(radiator)= (34±1)%. Conclusion: From the experimental results, the current method for calibration output power of microwave hyperthermia apparatus is defective, it dose not consider the conversion efficiency of radiator. Using the calibration method introduced in this paper, wecan accurately deter- mine the actual output power of microwave hyperthermia Apparatus.

OBJECTIVE: To observe the correlation between traditional Chinese medicine (TCM) syndromes ("deficiency of qi and yin" and "deficiency of liver yin and kidney yin") and A267G in 5'-untranslated region within exonal of megsin gene, and to search the substantial genetic basis for micro-differentiation of TCM syndromes in primary immunoglobulin A nephropathy (IgAN). METHODS: A total of 120 IgAN cases meeting the diagnostic criteria were enrolled. The sequence of single nucleotide polymorphism (SNP) of A267G in 5'-untranslated region within exonal of megsin gene was tested. The correlation between SNP and TCM syndromes was observed. RESULTS: There were 83 cases carrying GG genotype, 34 cases carrying GA genotype and 3 cases carrying AA genotype in 120 cases of primary IgAN. There was a high proportion of "deficiency of liver yin and kidney yin" in IgAN cases with AA and GA genotypes, and a high proportion of "deficiency of qi and yin" in IgAN cases with GG genotype (P<0.01). Odds ratio in TCM syndrome distribution between GG genotype and GA plus AA genotype was 9.800, and 95% confidence interval was 3.969-24.199. The discrepancy also resided in IgAN patients with different genders and ages. CONCLUSION: A267G in 5'-untranslated region within exonal of the megsin gene may be one of the substantial genetic basis for differentiating "deficiency of liver yin and kidney yin" syndrome and "deficiency of qi and yin" syndrome in primary IgAN.

BACKGROUND:The functions of homo heterogeneous ribonucleoprotein E1 are very wide. It can participate in the expression of skeleton proteins in the nervous system. OBJECTIVE:To construct the recombinant plasmid of homo heterogeneous ribonucleoprotein E1 and observe its expression in nerve cells for further studying the functions of it in neurocytes. METHODS:Using pcDNATM4/His C, the homo heterogeneous ribonucleoprotein E1 was subcloned into recombinant plasmid E1-pcDNATM 4/His C, fol owed by enzyming and sequencing. After SH-SY5Y cells were transfected with the recombinant plasmid, western blot analysis and real time RT-PCR were used to detect the expression of homo heterogeneous ribonucleoprotein E1 in SH-SY5Y cells. And the growth of SH-SY5Y cells was observed. RESULTS AND CONCLUSION:We successful y constructed the eukaryotic expressed vector of homo heterogeneous ribonucleoprotein E1. The recombinant plasmids were verified to express in SH-SY5Y cells correctly at mRNA and protein levels. And SH-SY5Y cells generated quickly after homo heterogeneous ribonucleoprotein E1 was over-expressed. The homo heterogeneous ribonucleoprotein E1 is an important protein in neural development. And this vector offers the premise for further studying its function in nervous system.

Humans ; Infant ; Male ; Mycobacterium tuberculosis ; Otitis Media ; microbiology ; Tuberculosis

AIM:To explore the effect of Vaccinium vitis procyanidin on the growth of glioma cells .METH-ODS:Glioma C6 cells were cultured and divided into control and 10, 20 and 40μg/L Vaccinium vitis procyanidin groups . The influence of Vaccinium vitis procyanidin on the growth of C 6 cells was measured by MTT assay and the observation un-der inverted microscope .The apoptotic rate was detected by Annexin V/PI staining .The protein expression of Bcl-2 and Bax was determined by immunocytochemistry .The protein levels of Bcl-2, Bax and caspase-3 were also examined by West-ern blotting .RESULTS:The growth of C6 glioma cells was inhibited by Vaccinium vitis procyanidin at concentrations of 10, 20 and 40 μg/L.The growth was significantly inhibited in 40 μg/L Vaccinium vitis procyanidin group at 24 h and 48 h, and in 20 and 40 μg/L Vaccinium vitis procyanidin groups at 72 h (P<0.01).The density of the cells was decreased when the concentration of Vaccinium vitis procyanidin increased .The apoptotic rate was increased when the concentration of Vaccinium vitis procyanidin increased either .The expression of Bcl-2 was decreased and Bax was increased after 10, 20 and 40 μg/L Vaccinium vitis procyanidin treatments .The ratio of Bax/Bcl-2 was increased when the dose of Vaccinium vitis pro-cyanidin increased (P<0.05 or P<0.01).The expression of Bcl-2 was decreased (P<0.01), and Bax and caspase-3 were increased after 10, 20 and 40 μg/L Vaccinium vitis procyanidin treatments .The ratio of Bax/Bcl-2 was increased when the dose of Vaccinium vitis procyanidin increased (P<0.01).CONCLUSION:Vaccinium vitis procyanidin inhibits the growth of glioma cells by down-regulating Bcl-2 protein and up-regulating Bax protein to activate caspase-3, thus indu-cing apoptosis .

Objective To analyze and determine the clinical, molecular pathology and genetic features of a Chinese family with dystrophinopathy. Methods Clinical data of the proband and his family members were collected. Immunohistochemistry staining was performed on muscular biopsy tissues with antimerosin, emerin and the N, C and central rod domains of dystrophin. Genomic DNA was extracted using standard procedures from the peripheral blood leukocytes. Multiplex ligation-dependent probe amplification (MLPA) was used to test Duchenne muscular dystrophy (DMD) gene to determine the ways and sites of genetic mutation, and analyze the relationships between genotype and phenotype. Results Patients from this family were clinically diagnosed as muscular dystrophy, and they presented serious manifestations although the immunohistochemistry analysis for the proband exhibited partial loss of dystrophin staining, and positive expression with merosin and emerin. Further test with MLPA detected the loss of exons 45--54 in DMD gene in the proband, while his mother had heterozygositic loss in exons 45--54. Conclusions The losses of exons 45--54 in the proband are all derived from his mother, who carries genetic mutation with normal phenotype. He has been diagnosed as dystrophinopathy. At the same time, his partial loss of dystrophin is not parallel to the out-of-frame mutation of the gene and his severe clinical manifestations. Abnormal expression of dystrophin is the pathological basis for dystrophinopathy phenotype. Its clinical outcome depends not only on the degree of the protein expression, but also on the function of the sites where the DMD gene less occurs.

Lymphocyte function associated antigen-1 (LFA-1) is a member of integrin family, that plays an important role in the adhesion of lymphocytes with other cells and matrix. To investigate the role of LFA-1 in collagen-induced arthritis (CIA), the incidence of CIA, histological and radiological assessments in the LFA-1 deficient (LFA-1~ -/- ) mice and control mice were examined. LFA-1~ -/- mice and control mice were immunized with 100?g collagen type II(CII) emulsified with an equal volume of Freund’s complete adjuvant (CFA), followed by the booster injection of the same amount of CII in CFA on day 21. Then, clinical, histological and radiological assessments were done. It showed that 57% control mice developed arthritis and apparently changed in the histological and radiological assessment, whereas the all of LFA-1~ -/- mice had the normal histological and radiographic response and none developed arthritis. These results suggeste that LFA-1 is indispensable for the onset of CIA.

Objective To express the plasminogen activator(Pla) of Yersinia pestis and one of its gene fragments,and to detect their immunological reactivity.Methods The pla gene and its specific gene fragment pla-c were amplified by PCR using the EV76 strain as a template.PCR products were then ligated with the plasmid pET32a (+).The recombinant plasmids pET32a (+)-pla and pET32a (+)-pla-c were subsequently trausformed into E.coli BL21 (DE3).The expressed products were purified by HIS affinity chromatography,and their immunological reactivity was detected by Western blotting.Results The recombinant Pla(52.8 × 103) was expressed as inclusion bodies,and the recombinant Pla-c protein (24.0 × 103) was expressed in the soluble form.These two recombinant proteins reacted with anti-Yersinia pestis EV76 rabbit sera.Conclusions The recombinant Pla and its specific fragments have displayed immunological reactivity,and can be served as an alternative diagnosis method for Yersinia pestis.

Objective To investigate the inhibitory effect and mechanism of rosiglitazone on chemokines secretion in renal tubular epithelial cells (HK-2) stimulated by lipopolysaccharide (LPS). Methods Cells were divided into four groups: control (CON), LPS (1 mg/L),rosiglitazone (10 μmol/L), rosiglitazone (10 μmol/L) +LPS (1 mg/L). MCP-1 and IL-8 expression was measured using real time PCR and ELISA. PPARγ was knockdown by RNAi to investigate whether the inhibitory effect of rosiglitazone was PPARγ-dependent or -independent. The NF-κB in nucleus was detected by Western blotting. The DNA binding activity of NF-κB was determined by electrophoretic mobility shift assay. Results Compared with CON group, the expressions of IL-8 and MCP-1 were increased by (4.30±0.45) and (4.80±1.29) times in mRNA level, (1.39±0.18)and (2.11 ±0.47) times in protein level, respectively, in LPS-stimulated HK-2 cells (P＜0.05).Application of rosiglitazone followed by LPS significantly reduced IL-8 and MCP-1 secretion compared with LPS group (decreasing by 66.37% and 71.88% in mRNA levels, while 41.68% and 47.87% in protein levels) (P＜0.05). In pcDNATM 6.2-GW/EmGFP-miPPARγ transfected cells, IL-8and MCP-1 only were decreased by 18.16% and 16.83% in mRNA level, while 11.39% and 11.86%% in protein level in rosiglitazone pretreated group, showing no significant difference compared with LPS group. Rosiglitazone did not block NF-κB nuclear translocation while significantly inhibiting the DNA binding activity of NF-κB. Conclusions Rosiglitazone inhibits the expressions of MCP-1 and IL-8 via a PPARγ-dependent mechanism in HK-2 cells, resulting from inhibition the DNA binding activity of NF-κB.