0.05).Conclusion GH improves FAH of children with GHD.Height at the initiation of puberty is the most significant determining factor for the long-term efficacy.Hence,it is important that the diagnosis should be made and treatment be initiated as early as possible to afford children with GHD the opportunity to make up much of their height deficit before puberty.Adequate dosage of GH should be used for the children taking initial treatment at puberty to attain satisfactory FAH.

Objective To examine the impact of psychosocial factors on physical activity,so as to provide guidance for the development of an effective physical activity intervention program for individuals with hypertension.Methods This study used a baseline data from an intervention study on regular physical activity among hypertensive individuals.A multi-stage,stratified random sampling was utilized and finally 12 communities from 6 urban districts were chosen.Questionnaires were administrated through face-to-face interviews.A total of 586 participants were recruited and finally 559 completed the interviews with the response rate as 95.4％.Descriptive statistics and Cronbach' sα coefficients were used to test the reliability.General Linear Model analysis was used to analyze the relationship between stages of physical activity and psychological factors.Results Psychosocial measures on physical activity demonstrated good reliability with Cronbach α coefficient from 0.7 to 0.9.The scores for each psychological measures increased by increasing the scores of stages of physical activity.General Linear Model analysis revealed self-efficacy (β=0.379) while enjoyment of physical activity (β =0.234) was significantly correlated with physical activity (P＜0.05).The behavioral processes and family support marginally increased the physically activity (β =0.069 for behavioral processes and β=0.163 for family support,P＜0.10).Conclusion Our findings were informative for the development of community-based intervention programs on physical activity among hypertensive individuals.It indicated that physical activity intervention programs should be psychosocial theory-based,especially increasing their self-confidence and enjoyment,as well as with family support,in order to adopt and maintain the physical activities.

Chronic myeloproliferative disease (CMPD) is a group of malignant blood disorders including polycythemia vera, essential thrombocythemia, primary myelofibrosis, chronic myeloid leukemia, and so on. CMPD is characterized by proliferation of one or several lineages in hematopoietic system. The pathogenesis of CMPD is not clear except chronic myeloid leukemia associated with the bcr/abl fusion gene. In recent years, more studies demonstrated that CMPD have a higher mutation rate of gene jak2. In this review, the association of jak2 gene mutation with clinical diagnosis, clinical feature and molecular target therapy in CMPD and other hematological disease were summarized.
Chronic Disease ; Humans ; Janus Kinase 2 ; genetics ; Mutation ; Myelodysplastic-Myeloproliferative Diseases ; genetics

OBJECTIVETo study the changes of palate cleft gap of complete unilateral cleft lip and palate (UCLP) infants before and after presurgical orthodontic and cheiloplasty.

METHODSThe sample consisted of 18 complete UCLP infants who were treated using presurgical nasoalveolar molding (PNAM) appliance and cheiloplasty. The maxillary models were obtained at the initial visit, after PNAM treatment 1 month before cheiloplasty, and 2 months after cheiloplasty. The change of palate cleft gap were compared.

RESULTSAfter PNAM treatment and cheiloplasty, the lip profile was obviously improved, cleft gap was reduced, and the height of ala nasi fornix was recovered.

CONCLUSIONPNAM treatment can improve the lip shape and nasal deformity degree of UCLP patient. The cleft gap and upper lip tension are reduced.

Cleft Lip ; Cleft Palate ; Humans ; Infant ; Lip ; Nose ; Preoperative Care

Objective To observe the effect of stanozolol(ST) on long bone growth and maturation of pubertal female rats treated with gonadotropin releasing hormone agonist(GnRHa).Methods At 3 weeks of age,42 female Sprague-Dawley rats(brood) were divided into 7 groups(ST dosage groups,as 5 000 ?g/100 g group,200 ?g/100 g group,100 ?g/100 g group,50 ?g/100 g group,25 ?g/100 g group,solvent control group and blank control group)(n=6).Forty-eight female rats were divided into 8 groups(ST therapeutic duration)(n=6).Rats received 2.5 mg/kg im slow-released GnRHa(triptorelin,as 2 d group,3 d group,5 d group,7 d group,10 d group,13 d group,soluent control group and blank control group) which was repeated every 2 weeks for 2 times,3 days after the 2nd GnRHa(D1),ST dosage groups were subcutaneously administrated ST at the various dosage daily(D1-D13).ST therapeutic duration groups were subcutaneously administrated ST at the dosage of 100 ?g/100 g daily for different duration.All the rats were killed on the D14.On the day of sacrifice,body weight,body length and left tibial length were measured,plasma were taken for determining insulin-like growth factor-1(IGF-1),right tibia were fixed,demineralized and processed for paraffin-embedding.Paraff sections were HE stained for growth plate measurements.proliferating cell nuclear antigen(PCNA) on growth plate was analyzed with immunohistochemistry staining and image.Results 1.In the 5 000 ?g/100 g ST dosage group,the weight,Height and tibial length exceeded than those of the other dosage and control groups(Pa

OBJECTIVETo investigate the effect of cadmium (Cd) on estrogen receptor and to assess its endocrine disrupting action.

METHODSThe estrogen receptor rich supernatant was prepared from the ovariectomized Sprague-Dawley rats. The effects of cadmium on estrogen binding were performed using a sing-dose ligand-binding assay. Extract from uterus were treated with various concentrations of cadmium (0, 10(-3), 10(-5) or 10(-7) mol/L) for various pre-incubation time (0, 30, 60, 90 min) by means of orthogonal experimental design with orthogonal layout of L16(4(5)) (the experiment was repeated for 5 times). In addition to the radioinert competitor, each assay included a zero tube and a DES standard curve for quality control purpose. Data for cadmium and the DES standard curve were plotted as percent [3H]-E2 bound versus log (molar concentration), and the IC50 for cadmium was determined. The RBA for cadmium was calculated by dividing the IC50 of DES in terms of the IC50 of cadmium.

RESULTSCadmium could not block the binding of estradiol to the receptor because hormone binding did not change with increasing cadmium concentration or increasing preincubation time. The results showed that the binding of [3H]-estradiol to uterine cytosols was not significant (P > 0.05). The Bmax (its unit is pmol/mg protein) of various concentrations of cadmium (0, 10(-3), 10(-5) or 10(-7) mol/L) for pre-incubating 0 min is 203.15 +/- 75.16, 203.41 +/- 22.78, 220.82 +/- 45.35, 209.10 +/- 49.66 respectively; The Bmax of them for pre-incubating 30 min is 215.67 +/- 92.97, 139.79 +/- 53.78, 205.27 +/- 23.60, 172.63 +/- 55.09 respectively. The Bmax of them for pre-incubating 60 min is 197.11 +/- 50.68, 203.24 +/- 66.33, 183.92 +/- 31.89, 183.33 +/- 32.70, respectively. The Bmax of them for pre-incubating 90 min is 229.69 +/- 76.88, 175.70 +/- 70.28, 164.26 +/- 24.46, 150.78 +/- 65.97 respectively. Mean IC50 for cadmium is 10(-4) - 10(-3) M. If the affinities of DES binding to estrogen receptors was taken to be 100%, the relative binding affinities of cadmium was 10(-6) - 10(-7). The results indicated that cadmium had only a very poor affinity with estrogen receptor.

CONCLUSIONIn vitro assay cadmium did not have distinct disrupting effect on binding of estradiol to estrogen receptors from rat uterine.

Animals ; Cadmium ; toxicity ; Female ; In Vitro Techniques ; Rats ; Rats, Sprague-Dawley ; Receptors, Estrogen ; drug effects ; metabolism ; Uterus ; drug effects ; metabolism

This study was aimed to clarify whether valproic acid (VPA) induces apoptosis of leukemia HL-60 cell line and its possible mechanism. The effect of different concentrations and treatment time of VPA on HL-60 cell proliferation was assayed by cytotoxicity test (CCK-8 method) and fluorescence microscopy, and flow cytometry was used to detect cell apoptosis. The expressions of telomerase subunit h-tert mRNA and apoptosis-related protein as well as caspase-3 activity were detected by real time-quantitative PCR, Western blot and ELISA respectively. The results indicated that VPA inhibited proliferation of HL-60 cells and induced cell apoptosis in a dose dependent manner (r = -0.87). The expressions of anti-apoptotic protein BCL-2 and h-tert mRNA were significantly decreased while the pro-apoptotic protein BAX and caspase-3 activity increased after treatment with VPA. The apoptosis rate of HL-60 cell was negatively correlated with expression of h-tert mRNA. It is concluded that VPA can inhibit leukemia HL-60 cell proliferation and induce apoptosis. The VPA displays anti-leukemia activity possibly through reducing h-tert mRNA and BCL-2 protein expression, increasing BAX expression and activity of caspase-3.
Apoptosis ; drug effects ; Caspase 3 ; metabolism ; HL-60 Cells ; Humans ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Telomerase ; metabolism ; Valproic Acid ; pharmacology ; bcl-2-Associated X Protein ; metabolism

[Objective]To discuss the CT diagnosis and differential diagnosis of solid pseudopapillary tumor of the pancreas (SPTP).[Methods]The CT findings of 20 patients with SPTP proved by surgically pathology were retrospectively analyzed and summa?rized.[Results]SPTP were composed of solid and cystic components with surrounding capsule resulting to clear demarcation between tumor and normal pancreas without dilation of pancreatic duct. The tumor parenchyma was slightly hyperenhancement on arterial phase and showed gradual enhancement on venous and delayed phase.[Conclusions]The CT findings of SPTP have relative specifici?ty and can contribute to early diagnosis and differential diagnosis of SPTP.

OBJECTIVETo investigate the effects and the mechanisms of stanozolol (ST) on the proliferation, maturation and differentiation of in vitro cultured growth plate chondrocyte isolated from gonadotropin releasing hormone analogue (GnRHa)-treated adolescent rats, to study if ST mediates the proliferation of chondrocytes via the estrogen receptor alpha (ERalpha), androgen receptor (AR) and/or insulin-like growth factor-1 receptor (IGF-1R) and interactions of the two receptor and IGF-1R receptor signaling pathway, to investigate the mechanism of the biological effects in ST promoting bone growth/maturity at molecular level.

METHODThe rats were weaned at the end of 3 weeks and intramuscular injection of triptorelin of GnRHa preparations, qow x 2 was started. The rats were sacrificed at the end of 7 weeks, and then the tibiae growth plates were taken out with sterile procedure. The chondrocytes were obtained by two-time enzyme digestion method, and the experiments were carried out with the primary chondrocytes. Immunohistochemical staining of proliferating cell nuclear antigen (PCNA) and Western blot analysis were applied.

RESULTThe results of PCNA demonstrated that stanozolol enhanced the proliferation of the chondrocytes, time-course studies showed that the proliferation were maximally stimulated by stanozolol after 2 days of incubation and decreased again after longer periods of incubation. The expression of p-ERalpha, p-IGF-1R and p-extracellular-signal regulated kinase 1/2 (ERK1/2) increased with the incubation period of ST treatment, and reached the peak value at a certain time, and then gradually decreased. The expression of p-ERalpha, p-IGF-1R and p-ERK1/2 increased with the elevation of ST concentration, and reached the peak value at 10(-9) - 10(-8) mol/L, then gradually decreased. ST induced-p-ERalpha expression was partially blocked by ERalpha and mitogen-activated protein kinase kinase inhibitors. ST induced-p-IGF-1R expression was partially blocked by ERalpha and IGF-1R inhibitors. ST induced-p-ERK1/2 expression was partially blocked by mitogen-activated protein kinase kinase and IGF-1R inhibitors.

CONCLUSIONAs an androgen derivation, ST exerts its biological effects of promoting proliferation of the long bone growth plate chondrocytes via activating the classic ERalpha receptor pathway and mitogen-activated protein kinase pathway, and at the same time, by activation of IGF-1R. Both IGF-1R and ERalpha can promote "cross-talk" of two systems' receptor signal through mitogen-activated protein kinase signal pathway.

Androgens ; pharmacology ; Animals ; Cells, Cultured ; Chondrocytes ; cytology ; drug effects ; metabolism ; Estrogen Receptor alpha ; metabolism ; Female ; Growth Plate ; drug effects ; metabolism ; Mitogen-Activated Protein Kinase 3 ; metabolism ; Rats ; Receptor Cross-Talk ; Receptor, IGF Type 1 ; metabolism ; Signal Transduction ; drug effects ; Stanozolol ; pharmacology

OBJECTIVETo explore the effect of deltamethrin (DM) on production of free radical and transcription factor Nrf2 in rats' brain tissue.

METHODS8 male rats were randomly assigned to four groups and administered with 1% W/W tertiary butylhydroquinone (tBHQ) or olive oil for 3 days, prior to exposure to DM and then with 12.50 mg or 0mg DM/Kg BW for 5 days. The level of free radical in rats' hippocampus tissue was detected by electron spin resonance (ESR) spectroscopy. 18 male rats were randomly assigned to three groups and administered with i.p. (daily dose was respectively 0, 3.13, 12.50 mg/kg DM) for five days. After treatment, Nrf2 protein levels in the cytoplasmic and nuclear fractions of both cerebral cortex and hippocampus tissue were measured by western blot.

RESULTSThe level of free radical in hippocampus tissue of rats administered by DM and pretreatment with tBHQ prior to DM were increased to a 2.45-fold and 2.97-fold of values of control group, respectively (P < 0.05). Nrf2 protein levels in the cytoplasmic fractions of cerebral cortex of both low and high dose group were significantly increased, 1.68- fold and 1.34- fold of values of control group, respectively. Nrf2 protein levels in the nuclear fractions of cerebral cortex of both low and high dose group were increased in a dose- dependent model, 1.51-fold and 2.29-fold of values of control group, respectively (P < 0.01). Nrf2 protein levels in the cytoplasmic fractions of hippocampus tissue of both low and high dose group were increased in a dose- dependent model, 2.26-fold and 3.58-fold of values of control group, respectively. Nrf2 protein levels in the nuclear fractions of hippocampus tissue of both low and high dose group were increased, 2.42-fold and 2.45-fold of values of control group, respectively (P < 0.01).

CONCLUSIONThe studies in vivo demonstrate that DM treatment could induce free radical production and expression of Nrf2 protein in both cerebral cortex and hippocampus tissue and activate Nrf2.

Animals ; Brain ; drug effects ; metabolism ; Free Radicals ; metabolism ; Male ; NF-E2-Related Factor 2 ; metabolism ; Nitriles ; toxicity ; Pyrethrins ; toxicity ; Rats ; Rats, Sprague-Dawley