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83.
OBJECTIVE: To determine if sexually transmitted diseases (STDs), including human immunodeficiency virus (HIV) infection, risk assessment, and education tools provided as part of office-based primary care reduce adolescent risky sexual behaviors. DESIGN: A randomized intervention trial with 3- and 9-month follow-up. SETTING: Five staff-model managed care sites in Washington, DC (n = 19 pediatricians). PATIENTS: Consecutive 12- to 15-year-olds receiving a general health examination; 81% minority. Participation rate = 215/432 (50%). Nine-month follow-up rate = 197/215 (92%). INTERVENTION: Audiotaped STD risk assessment and education about staying safe (safer = condoms, safest = abstinence). MAIN OUTCOME MEASURES: Adolescent-reported sexual intercourse and condom use. RESULTS: More intervention adolescents reported pediatrician discussion on 11/13 sexual topics. Although more vaginal intercourse (odds ratio [OR] = 2.46, 95% confidence interval [CI] = 1.04-5.84) was reported in the intervention group at 3 months, this was not true of overall sexual intercourse (OR = 1.55, 95% CI =.73-3.32). More sexually active adolescents reported condom use in the intervention group at 3 months (OR = 18.05, 95% CI = 1.27-256.03). At 9 months, there were no group differences in sexual behaviors; however, more signs of STD were reported by the control (7/103) than the intervention group (0/94). CONCLUSIONS: STD risk assessment and education tools administered in a single office visit facilitated STD/HIV prevention education. Any impact on sexual activity and condom use was short-lived. Further research is needed to develop brief, office-based sexual risk reduction for young adolescents. 相似文献
84.
目的:确定塞来昔布对于经常服用稳定剂量甲氨喋呤(MTX)治疗类风湿性关节炎(RA)患者的肾脏清除率和血浆药代动力学方面的影响。方法:选取14例至少已服用MTX3个月,且每个星期的剂量稳定在5-15mg,有类风湿关节炎的成年妇女,随机给予塞来昔布(200mg.bid)或安慰剂单盲治疗,每一阶段7,分二阶段交叉试验,研究MTX的药代动力学和肾脏平均清除率。结果:当MTX和塞来昔布或安慰剂合用时,MTX 相似文献
85.
Relationship between skin fold thickness and insulin resistance in the essential hypertensive patients in Vietnam 总被引:2,自引:2,他引:0
Toan C Nguyen Khoa TA Pham Quyen TL Do Cuong T Nguyen Diep D Nguyen Vinh G Le Cong D Nguyen 《老年心脏病学杂志》2005,2(4):228-232
Background Previous studies reported a close relationship between obesity and insulin resistance in the essential hypertensive patients. Objective In this study, we examined the relationship between the skin fold thickness and insulin resistance then developed a formula to estimate the insulin resistance index according to the skin fold thickness in the essential hypertensive patients. Subjects and Methods Medical records of 80 patients (37 males, 43 females) were reviewed and the data were tabulated. Anthropometric indexes (including height, weight, waist circumference, hip circumference, and skins fold thickness at 5 fatty difference points on the Erdheim diagram), fasting plasma glucose and insulin concentration were recorded. The mean age was 57.0 ?9.2 years. The insulin resistance index was calculated following the Homeostasis Model Assessment (HOMA) formula. Results Compared with the group with BMI < 23 kg/m2, the group with BMI≥23 kg/m2 had higher fasting insulin concentration (8.85±4.97 pmol/L vs 15.60±8.70 pmol/L, P<0.001 ) and higher insulin resistance index in ( 2.15±1,24 vs 3.76±2.22, P<0.001). No significant difference in fasting plasma insulin concentration, insulin resistance index between male and female was observed (P > 0.05). There was a positive correlation between skin fold thickness and the fasting insulin concentration and insulin resistance index. The skin fold thickness at point A8 had the best coefficient correlated with fasting plasma insulin(r=0.79, P < 0.001) and insulin resistance index (r= 0.79, P < 0.001). A formula to estimate the insulin resistance index by skin fold thickness at point A8 as: Insulin resistance index = 0.12×[skin fold thickness at A8 point (mm)] - 1. Conclusion: In the essential hypertensive patients, the formula to estimate insulin resistance index as 0.12×[skin fold thickness at A8 point (mm)]-1 may predict accurately the level of insulin resistance. (J Geriatr Cardiol 2005; 2(4):228-232 ) 相似文献
86.
Jeffrey I. Everitt Cheryl L. Walker Thomas W. Goldsworthy Douglas C. Wolf 《Molecular carcinogenesis》1997,19(3):213-219
Transforming growth factor-α (TGF-α) is a multifunctional cell regulatory protein with a wide range of effects on cell growth and differentiation and has been implicated in the neoplastic transformation of a variety of cell types. Altered expression of TGF-α and its cognate receptor (epidermal growth factor receptor) is enhanced in human and rat renal cell carcinomas. The objective of the study reported here was to determine whether altered TGF-α expression is an early or late event in renal tubular oncogenesis. The immunohistochemical expression of TGF-α was studied in preneoplastic renal tubular lesions in a rat model of hereditary renal cell carcinoma. Strong TGF-α immunoreactivity was present at all stages of renal cell tumor development, including the earliest detectable dysplasias. In contrast, the non-neoplastic regenerating tubular epithelium of rat degenerative nephropathy did not stain for TGF-α, although this tissue exhibited a proliferative capacity similar to that observed in the dysplastic and neoplastic lesions. This study indicated that altered TGF-α expression was detectable early in the development of renal cell tumors and may be an important feature of the transformed phenotype. Mol. Carcinog. 19:213–219, 1997. © 1997 Wiley-Liss, Inc. 相似文献
87.
88.
The feasibility of in vitro interleukin 2 (IL-2) activation and expansion of mononuclear cells (MNCs) derived from adult patients with acute myelogenous leukemia (ANLL) was studied. Patients' natural killer (NK) and lymphokine-activated killer (LAK) cell activity was compared with that of normal donors in terms of: (a) cytolytic activity (four- hour 51Cr release assay) against an NK-sensitive target (K562), NK- resistant targets (Raji/Daudi), and fresh/cryopreserved autologous and allogeneic leukemic blasts; (b) proliferation and expansion in culture with 1,000 U/mL recombinant IL 2 (rIL 2); and (c) the cell surface phenotype of the cultured cells. In 21 of 24 patients with active disease (AP) MNCs derived from the peripheral blood (PBL) or bone marrow (BM) could be cultured and expanded in the presence of rIL 2. These cultures initially contained between 30% and 50% blasts, and during 2 to 4 weeks of culture destruction of blasts and enrichment of up to 60% in cells with the morphology of large granular lymphocytes (LGLs) was observed. Expansion in culture varied between two- and 100- fold. MNCs from all patients in remission (RP) could be activated by rIL 2 and expanded up to 30-fold after 1 to 3 weeks in culture. NK activity of fresh PBLs from AP was significantly lower than in normal controls, whereas NK activity of RP was within the normal range. High levels of postactivation NK and LAK activity on K562/Raji/Daudi and on fresh/cryopreserved leukemic blasts was generated in approximately 50% of cases of AP and in most RP. Cell surface phenotype studies showed that cultured cells derived from ANLL patients were significantly enriched (up to 40%) in NKH-1 (Leu 19) positive cells, with RP LAK cells also expressing a high proportion of CD16 positive cells (up to 40%). This study has shown that it is feasible to activate and significantly expand killer cells derived from active disease and remission ANLL patients during 1 to 3 weeks culture with IL 2 with good maintenance of cytolytic activity. Both initial NK activity and LAK generation was optimal in remission patients. Based on data from this study, a clinical protocol has been developed for treatment of early relapse ANLL patients with LAK cells cultured for 1 to 3 weeks and systemic IL 2. 相似文献
89.
Chaperonin-mediated assembly of wild-type and mutant subunits of human propionyl-CoA carboxylase expressed in Escherichia coli 总被引:1,自引:0,他引:1
We developed a bacterial expression system for the human alpha and beta
cDNAs of propionyl-CoA carboxylase (PCC). These cDNAs (less the putative
mitochondrial matrix targeting presequences) were co-expressed in
Escherichia coli on one plasmid vector with each cDNA having its own
IPTG-inducible promoter. Only negligible amounts of active PCC were
measured despite the presence of both alpha and beta subunits as indicated
by Western blot analysis and the almost complete biotinylation of the alpha
subunit. Co-expression of this plasmid with a second plasmid vector
over-expressing the E. coli chaperonin proteins, groES and groEL, resulted
in a several hundred-fold increase in PCC specific activity, to a level
comparable with that found in crude human liver extracts. PCC was partially
purified on monomeric avidin affinity resin and the presence of both alpha
and beta subunits was demonstrated, thereby confirming the assembly of both
subunits into an active enzyme. Deficiency of either alpha PCC or beta PCC
results in propionic acidemia, an autosomal recessive disorder. We used
this expression system to characterize one missense mutation previously
described in five Japanese alleles, namely C1283T (Thr428lle) in beta PCC.
This mutation, when expressed in E.coli under the same conditions as that
of wild-type PCC, had null activity, despite the presence of assembled
alpha PCC and beta PCC subunits. This bacterial expression system can be
useful for analysis of either alpha PCC or beta PCC mutations. Our findings
indicated that the groES and groEL chaperonin proteins were essential for
folding and assembly of the human PCC heteromeric subunits.
相似文献
90.
Schuler PJ Trellakis S Greve J Bas M Bergmann C Bölke E Lehnerdt G Mattheis S Albers AE Brandau S Lang S Whiteside TL Bier H Hoffmann TK 《European journal of medical research》2010,15(8):337-344