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E Y Wang

Publications and source records attributed to E Y Wang.

At least 19 recordsLinked to original sources
PubMed2003

Activin signal transduction in the fetal rat adrenal gland and in human H295R cells.

The presence of activin A and its effects have previously been documented in the adrenal gland, particularly in the human fetal adrenal gland and the rat adrenal gland. The primary signaling pathway of activin involves interactions between receptor and intracellular (Smad) proteins that have not been completely described in the adrenal gland. In this study, we demonstrate that the components of the activin signaling cascade are present in two complementary models, the fetal rat adrenal gland and the human adrenocortical cell line, H295R, by means of RT-PCR, western analysis, and immunoprecipitation techniques. Using the cell line, activin signaling was analyzed using an activin-responsive reporter gene, p3TP-luc, and luciferase assays to assess transcriptional activity with co-expression of the different activin receptors and Smads to demonstrate the functionality of the signaling cascade. In the fetal rat adrenal gland, the relative amounts of mRNA of the type II receptors, RII and RIIB, were regulated by gestational age, such that the RIIB levels increased after birth while RII levels fell. Using immunodetection techniques, the activin receptors and the different Smad proteins were detected in the rat fetal adrenal glands. Notably, the presence of Smad4 protein is significantly increased after birth in the rat adrenal gland. RT-PCR established a similar profile in the H295R cells. Using p3TP-luc, the H295R cells show transcriptional activation of this activin-responsive reporter in the presence of activin A. Co-expression of type I and type II receptors as well as Smads, results in ligand-independent transcriptional activity in addition to an activin-stimulated response. In determining activin's effects on adrenal function, adrenal steroid production was evaluated by incubation of the H295R cells with increasing doses of activin A and inhibin A, resulting in a detectable increase in P450c17 expression. Co-incubation of activin A with follistatin diminishes this response. These results are consistent with a role for activin A in the adrenal gland by demonstrating that the elements of the activin signaling pathway are present, intact, and functional. This suggests that in the adrenal gland the components of the activin receptor/Smad pathway are dynamically changing in the transition from fetal to neonatal life, and are important to the function of this organ.

Activin Receptors, Type II↗
PubMed2001

Definition of the supraclavicular and infraclavicular nodes: implications for three-dimensional CT-based conformal radiation therapy.

PURPOSE: To delineate with computed tomography (CT) the anatomic regions containing the supraclavicular (SCV) and infraclavicular (IFV) nodal groups, to define the course of the brachial plexus, to estimate the actual radiation dose received by these regions in a series of patients treated in the traditional manner, and to compare these doses to those received with an optimized dosimetric technique. MATERIALS AND METHODS: Twenty patients underwent contrast material-enhanced CT for the purpose of radiation therapy planning. CT scans were used to study the location of the SCV and IFV nodal regions by using outlining of readily identifiable anatomic structures that define the nodal groups. The brachial plexus was also outlined by using similar methods. Radiation therapy doses to the SCV and IFV were then estimated by using traditional dose calculations and optimized planning. A repeated measures analysis of covariance was used to compare the SCV and IFV depths and to compare the doses achieved with the traditional and optimized methods. RESULTS: Coverage by the 90% isodose surface was significantly decreased with traditional planning versus conformal planning as the depth to the SCV nodes increased (P < .001). Significantly decreased coverage by using the 90% isodose surface was demonstrated for traditional planning versus conformal planning with increasing IFV depth (P = .015). A linear correlation was found between brachial plexus depth and SCV depth up to 7 cm. CONCLUSION: Conformal optimized planning provided improved dosimetric coverage compared with standard techniques.

Clavicle↗
PubMed2000

Serum levels of activin A and inhibin A and the subsequent development of preeclampsia.

OBJECTIVE: To determine whether serum levels of activin A and inhibin A are altered in patients before development of preeclampsia. METHODS: Blood samples were collected from patients during the second trimester of prenatal care. We identified patients who subsequently developed preeclampsia and matched them with patients who had no evidence of preeclampsia during their gestation. Matching criteria included gestational age at blood sampling, gestational age at delivery, and birth weight. Assays were then performed to assess the levels of activin A and inhibin A in the control and study groups. A power calculation determined that 12 patients who subsequently developed preeclampsia, if matched with controls in a 1:2 ratio, would allow the detection of differences in analyte levels that were 60% as large as those previously reported between patients already diagnosed with preeclampsia and matched controls. RESULTS: Twelve patients with preeclampsia were identified and matched with 24 controls. No differences in serum levels of activin A or inhibin A were detected between the two groups. Because of the significant overlap of analyte levels between the two groups, no cutpoint that would allow identification of patients destined to become preeclamptic could be determined. CONCLUSION: These data suggest that activin A and inhibin A cannot be used as markers for later development of preeclampsia in a low-risk population.

Activins↗
PubMed1999

Implications of decidualization-associated protease expression in implantation and menstruation.

During progesterone-induced decidualization of estradiol (E2)-primed human endometrial stromal cells (HESCs), the interstitial-type extracellular matrix (ECM) of the follicular phase endometrium is transformed in the luteal phase to a mixture of residual interstitial- and new basal laminar-type components. This transformation is accelerated by reduced proteolytic activity of HESCs undergoing decidualization (DZ). In cultured HESCs, progestins, but not E2, induce the expression of several DZ markers, and E2 enhances these effects despite the lack of response to E2 alone. Using this well-characterized in vitro DZ model we evaluated the expression of plasminogen activators (PAs), which degrade ECM components that undergo rapid turnover, and matrix metalloproteinases (MMPs), which degrade the bulk of ECM components. Medroxyprogesterone acetate (MPA) inhibited the catalytic activity of urokinase-type PA (uPA) and tissue-type PA (tPA) as well as the expression of such MMPs as interstitial collagenase (MMP-1) and stromelysin-1 (MMP-3). Moreover, E2 + MPA elicited greater inhibitory effects on the expression of all of these proteases. Progestin inhibition of PA activities reflected reciprocal upregulation in the output of the PA inhibitor PAI-1, which produced large molar excesses of PAI-1 compared with the PAs in HESC-conditioned medium. By contrast, the tissue inhibitor of the MMPs, TIMP1, as well as gelatinase A (MMP-2), was constitutively expressed by the HESCs. In the absence of implantation, menstruation-associated degradation of the functional endometrial ECM is triggered by withdrawal of circulating ovarian steroids. This process was evaluated in cultured HESCs that were first decidualized during 10 days of exposure to E2 + MPA, and then withdrawn to steroid-free medium with and without the antiprogestin RU 486. As expected, steroid withdrawal reversed progestin-inhibited PA activity as well as the expression of MMP-1 and MMP-3 and progestin-enhanced PAI-1; much greater reversal was observed in medium supplemented with RU 486. Unlike the changes in PAI-1, neither TIMP1, nor MMP-2 expression was affected by withdrawal to steroid-free or to RU 486-medium. By altering the composition of the ECM of the luteal phase endometrium, progestin-elicited inhibition of the PAs, uPA and tPA, as well as that of the MMPs, MMP-1 and MMP-3, modulates trophoblast adhesion, migration and differentiation. Conversely, steroid withdrawal elicited increases in uPA, MMP-1 and MMP-3 activities would promote endometrial sloughing by degrading the mixture of decidual cell-derived basement membrane-like proteins and interstitial components that comprise the stromal ECM of the perimenstrual endometrium.

Decidua↗
PubMed1999

Identification of naturally occurring follistatin complexes in human biological fluids.

Follistatin (FS) binds activin and inhibin proteins. Many organs are sensitive to activin and inhibin; thus the formation of FS-activin/inhibin complexes is important to our understanding of ligand activity. Other investigators studying FS have detected large molecular weight immunoreactive FS bands (greater than the expected molecular weight of FS alone) that have not been well characterized. The goal of this study was to identify naturally occurring FS monomers and FS-activin/inhibin complexes in several organ systems. The pituitary, ovary, kidney, and urine were chosen for this investigation. Molecular masses were assigned to in vitro assemblies of complexes containing recombinant inhibin or activin with FS for comparison with naturally occurring FS forms. The recombinant complex of FS-activin was primarily 97-kDa size, while FS-inhibin complexes were detected in a range of molecular sizes from 66 kDa to 97 kDa, 133 kDa, and > 220 kDa. FS-containing complexes of 66-kDa, 97-kDa, and 133-kDa were identified in the tissues examined and in pregnant urine. Our study points to the assembly of a series of FS-activin/inhibin complexes in a variety of organ systems that may impact upon the available amount of free versus bound (or "complexed") ligand, which must be considered when investigating the biology of activin- or inhibin-responsive cells. In addition, urine may be an important biological fluid that can be used to measure significant changes in circulating FS complexes.

Activins↗
PubMed1998

Chronic antagonism of nuclear factor-kappaB activity in cytotrophoblasts by dexamethasone: a potential mechanism for antiinflammatory action of glucocorticoids in human placenta.

Circulating glucocorticoids are present in increasing quantities as human gestation progresses, peaking during labor whether it occurs before or at term. Although the precise role of glucocorticoids in pregnancy is not well defined, it is clear that glucocorticoids suppress inflammation in many cell types by antagonizing the acute stimulatory actions of members of the Rel/nuclear factor-kappaB (NF-kappaB) family on cytokine gene expression. In the present study we tested the hypothesis that during pregnancy, glucocorticoids chronically suppress inflammation in the human placenta. Cytotrophoblasts obtained from human term placentas were maintained for 48 h in culture medium supplemented with 10% charcoal-stripped calf serum with and without 100 nmol/L dexamethasone (DEX). Enzyme-linked immunosorbent assay studies revealed that cytotrophoblasts constitutively express interleukin-8 (IL-8), a known mediator of placental inflammation, between 24-96 h of culture. A 48-h treatment of cytotrophoblasts with 100 nmol/L DEX significantly reduced the production of IL-8 to 24+/-1% of control levels (P < 0.01). DEX and cortisol mediated a dose-dependent inhibition of IL-8 expression, with ED50 values of 5 and 50 nmol/L, respectively. DEX treatment also significantly reduced levels of IL-6 and tumor necrosis factor-alpha in culture medium, suggesting that glucocorticoids coordinately reduce cytokine levels in cytotrophoblasts. As cytokine expression is regulated by NF-kappaB and activator protein-1 (AP-1) transcription factors, electrophoretic mobility shift assays (n = 4) were used to determine whether DEX treatment altered the binding of nuclear proteins from cytotrophoblasts to labeled oligonucleotides corresponding to the kappaB and AP-1 response elements. We observed that a 48-h treatment of cytotrophoblasts with 100 nmol/L DEX markedly reduced binding of nuclear extracts from cytotrophoblasts to the kappaB response element. DEX treatment promoted a relatively smaller reduction of binding to the AP-1 response element. Northern blotting experiments revealed that DEX treatment did not alter the level of IkappaB, p50, or p65 messenger ribonucleic acid, suggesting that the antiinflammatory action of glucocorticoid in cytotrophoblasts did not directly involve alterations in the level of NF-kappaB proteins. Our results demonstrate a novel chronic suppressive action of glucocorticoid on cytokine production and nuclear binding of NF-kappaB and AP-1 proteins in cytotrophoblasts, providing a potential mechanism through which glucocorticoids may suppress inflammation at maternal-fetal interfaces across gestation.

Anti-Inflammatory Agents↗
PubMed1997

Decidual cell regulation of hemostasis during implantation and menstruation.

Progesterone stimulation of the estradiol (E2)-primed human endometrium initiates DZ of the stromal cells around the spiral arterioles. Under continued steroid stimulation, DZ spreads wave-like to establish the decidual cell as a major cell type of the luteal phase and pregnant endometrium. Because of their widespread distribution throughout the endometrium and concentration at perivascular sites, decidual cells are spatially and temporally positioned to mediate the opposing requirements of maintaining hemostasis during endovascular trophoblast invasion, yet promoting menstrual hemorrhage in the absence of implantation. The experimental results summarized in this review indicate that the paradoxical properties manifested by endometrial stromal/decidual cells are controlled by several proteins with either hemostatic or ECM-degrading or vasoactive activity, and that their expression is altered in response to changes in levels of circulating ovarian steroids during the menstrual cycle. These conclusions are drawn primarily from studies with a well-characterized in vitro model of DZ using monolayers of stromal cells derived from specimens of predecidualized endometrium. Thus, progestins modify the expression of several DZ-related markers in the cultured stromal cells, and E2 enhances these effects despite the lack of response to E2 alone. These responses are consistent with the differential actions displayed by E2 and progesterone in vivo, by which E2 primes the endometrium for the decidualizing effects of progesterone by elevating progesterone receptor levels. Accordingly, during steroid-induced in vitro DZ, a marked increase in the expression of stromal cell TF and PAI-1 and reciprocal inhibition of tPA activity suggest mechanisms to account for the absence of hemorrhage during invasion of the endometrial vasculature by implanting trophoblasts. In contrast to steroid-induced DZ, the events of menstruation are initiated in response to a decline in circulating levels of ovarian steroids. Accordingly, subjecting in vitro decidualized stromal cells to steroid withdrawal results in pronounced reversal in the expression of all of the end points listed above. Consequently, the local hemostatic environment is transformed into a hemorrhage-promoting milieu. Taken together with vascular injury resulting from ischemia induced by spiral artery vasoconstriction, the net effect is attainment of two prerequisites for menstrual hemorrhage, vascular injury and inadequate hemostasis.

Decidua↗
PubMed1995

Tepoxalin, a novel dual inhibitor of the prostaglandin-H synthase cyclooxygenase and peroxidase activities.

Prostaglandin-H synthase-1, the rate-limiting enzyme in prostaglandin synthesis, has both cyclooxygenase (CO) and peroxidase (PO) activities. While most nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit only the CO activity, we describe an inhibitor, tepoxalin, that inhibits both the CO (IC50 = 0.1 microM) and the PO (IC50 = 4 microM) activities. Unlike many NSAIDs which are competitive inhibitors of CO, tepoxalin is a noncompetitive inhibitor of CO and its inhibitory effect on PO but not CO is reversed by excess heme. Moreover, inhibition of the PO activity by tepoxalin is not dependent on the enzymatic turnover of the CO activity. The hydroxamic acid of tepoxalin is responsible for the PO inhibition since a carboxylic acid derivative of tepoxalin retains full CO but not PO inhibition. We postulated that the hydroxamic group might confer the ability to inhibit PO on conventional CO inhibitors. This idea was supported by the observation that naproxen hydroxamic acid, but not naproxen showed PO inhibition. Furthermore, tepoxalin's carboxylic acid analogue and naproxen each competitively relieved PO inhibition by their respective hydroxamic acids. The intracellular activity of PO as monitored by the release of reactive oxygen species was also inhibited by both tepoxalin and naproxen hydroxamic acid. These observations suggest a strategy for design of novel compounds to inhibit prostaglandin synthase PO. The therapeutic implications of these novel PO inhibitors are discussed.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1995

Novel intracellular signaling function of prostaglandin H synthase-1 in NF-kappa B activation.

Many potent nonsteroidal antiinflammatory drugs (NSAIDs) exert their effects by inhibiting the cyclooxygenase activity of prostaglandin H synthase-1 (PGHS1, thus disrupting prostaglandin biosynthesis. However, these drugs do not block the activation of NF-kappa B, an inducible transcription factor which regulates numerous inflammation-related genes. Here we demonstrate that PGHS1 peroxidase, a NSAID-insensitive activity of PGHS1, mediates NF-kappa B activation through an intracellular reactive oxygen signaling pathway. Overexpression of PGHS1 strongly potentiated NF-kappa B activation by phorbol esters and dramatically elevated the generation of intracellular reactive oxygen species (ROS) in response to low concentrations of t-butyl peroxide. Both functions were dependent on PGHS1 peroxidase activity and could be suppressed by the potent antioxidant pyrrolidine dithiocarbamate. In contrast, elimination of PGHS1 cyclooxygenase activity by NSAIDs or site-directed mutagenesis failed to block ROS production or NF-kappa B activation. Thus, PGHS1 peroxidase serves an intracellular signaling function leading to NF-kappa B activation, separable from its role in prostaglandin synthesis.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1994

Tepoxalin, a novel immunosuppressive agent with a different mechanism of action from cyclosporin A.

Tepoxalin, a compound previously identified as a dual cyclooxygenase/lipoxygenase (CO/LO) inhibitor, is a potent inhibitor of T cell proliferation. Comparing the suppressive effects of tepoxalin and cyclosporin A (CsA) on OKT3-, PMA-, IL-2-, and PMA+ionomycin-induced T cell proliferations revealed marked differences in the mechanism of action between the two compounds. Whereas CsA was most effective in suppressing OKT3-stimulated proliferation, tepoxalin was more potent in inhibiting PMA-, PMA+ionomycin-, and IL-2-induced proliferation. Quantitative PCR (QPCR) assays used to detect cytokine messages showed that tepoxalin blocked IL-2 mRNA transcription in PMA- and PMA+ionomycin-, but not OKT3-stimulated T cells whereas CsA was most potent in inhibiting OKT3-induced IL-2 mRNA induction in these cells. Both tepoxalin and CsA did not inhibit the expression of IL-2R; however, only tepoxalin, but not CsA, inhibited the proliferation of IL-2-dependent blasts and the transcription of IFN-gamma, an IL-2-dependent target gene. Moreover, addition of exogenous IL-2 restored OKT3-induced proliferation to CsA- but not tepoxalin-treated cells. These data suggest that tepoxalin, but not CsA, suppressed T cell proliferation by inhibiting IL-2-induced signal transduction. Consistent with these findings, tepoxalin, unlike CsA, which was most potent when added at the initiation of OKT3 stimulation, was equally active, regardless of whether it was added at the beginning or 48 h after culture initiation. The difference in mechanism of action between tepoxalin and CsA was confirmed further by the synergistic suppressive effects on T cell proliferation upon co-administration of the two compounds.

Base Sequence↗
PubMed1994

The role of progestationally regulated stromal cell tissue factor and type-1 plasminogen activator inhibitor (PAI-1) in endometrial hemostasis and menstruation.

The physiologic mechanisms whereby the human endometrium maintains hemostasis during endovascular trophoblast invasion, yet permits menstrual hemorrhage, are unknown. This paradoxical relationship was investigated by evaluating endometrial expression of tissue factor (TF), the primary initiator of hemostasis, and plasminogen activator inhibitor-1 (PAI-1), the primary inhibitor of fibrinolysis. We observed increased immunostaining for TF and PAI-1 in sections of decidualized stromal cells from luteal phase and gestational endometrium. To determine whether TF and PAI-1 expression are directly linked to decidualization, both endpoints were monitored in a well described in vitro model of decidualization. Thus, confluent stromal cell cultures were exposed to vehicle control, 10(-8) M estradiol (E2), 10(-8) to 10(-6) M medroxyprogesterone acetate (MPA) or both E2 + MPA for 2-24 days in serum-containing or defined media. The progestin enhanced the content of stromal cell-associated immunoreactive and functionally active TF and PAI-1 released into the medium and elevated levels of stromal cell TF and PAI-1 mRNA. While E2 alone was ineffective, it greatly augmented MPA-enhanced TF and PAI-1 protein and mRNA content. Dose-dependent effects on TF and PAI-1 content were observed between 10(-8) to 10(-6) M MPA +/- E2. Similar results were observed for decidual cells derived from first trimester endometrium and cultured in type 1 collagen gels. Following optimal induction of TF and PAI-1 expression by E2 + MPA in stromal cell cultures, removal of these steroids greatly reduced levels of both TF and PAI-1 protein and mRNA within 4 days. These studies suggest a mechanism whereby endometrial hemostasis is maintained during trophoblast invasion yet reduced at the end of nonfertile cycles to permit menses.

Cells, Cultured↗
PubMed1994

Four-year cross-lagged associations between physical and mental health in the Medical Outcomes Study.

This article provides an application of structural equation modeling to the evaluation of cross-lagged panel models. Self-reports of physical and mental health at 3 different time points spanning a 4-year interval were analyzed to illustrate the cross-lagged analysis methodology. Data were collected from a sample of 856 patients with hypertension, diabetes, heart disease, or depression (or any combination of these) participating in the Medical Outcomes Study. Cross-lagged analyses of physical and mental health constructs revealed substantial stability effects across time. A structural model with standard effects revealed positive effects of physical health on mental health but negative (suppression) effects of mental health on physical health. The effects of mental health on physical health became nonsignificant when the model was revised by adding nonstandard effects (direct effects of measured variable residuals on latent variables). Recommendations for structural equation modeling of cross-lagged panel data are provided.

Adult↗
PubMed1994

Developmental regulation of glucocorticoid-mediated effects on extracellular matrix protein expression in the human placenta.

The extracellular matrix (ECM) protein fibronectin (FN) is a critical regulator of uterine-placental adherence. In the present report we compared the effects of glucocorticoids on FN expression in cytotrophoblast cultures isolated from human first trimester and term placentas to elucidate potential steroid-dependent cellular mechanisms associated with human parturition. Based on immunoassays, treatment of first trimester cytotrophoblasts with 10(-7) M dexamethasone (DEX) for 2 cr 4 days reduced medium levels of oncofetal FN (onfFN; i.e. FNs bearing an oncofetal epitope) to approximately 80% of control levels. Conversely, treatment of cytotrophoblasts isolated from term placentas with DEX dramatically reduced medium levels of onfFN to approximately 12% of control values. Treatment of both first trimester and term cells with 10(-6) M progestin, mineralocorticoid, or estrogen had no significant effect on onfFN expression in either cell type. Glucocorticoids specifically down-regulated medium levels of onfFN in term cells, but not in first trimester cells. In contrast, DEX treatment promoted an approximately 3- to 7-fold increase in levels of hCG in both first trimester and term cytotrophoblasts, suggesting that the effects of glucocorticoid on FN and hCG expression are elicited through independent cell-signaling pathways. In first trimester cells, DEX promoted a reduction in rates of FN and laminin synthesis to 60-70% of control levels. In term cells, DEX treatment reduced levels of FN and laminin synthesis to approximately 10% of control levels. Similarly, DEX treatment down-regulated levels of FN mRNA to approximately 60% and 10% of control values in first trimester and term cells, respectively. The first trimester of human pregnancy is associated with low levels of glucocorticoids and reduced glucocorticoid responsiveness. These conditions would favor high levels of placental ECM protein synthesis, thus stabilizing uterine-placental adherence. Conversely, elevated levels of glucocorticoids near parturition and increased glucocorticoid responsiveness would inhibit placental ECM protein synthesis, reducing uterine-placental adherence and promoting the separation of placenta from uterus.

Cells, Cultured↗
PubMed1993

Steroid regulation of oncofetal fibronectin expression in human cytotrophoblasts.

Oncofetal fibronectin (onfFN) is a uniquely glycosylated form of FN suggested to play a critical role in uterine/placental adherence during pregnancy. In the present study we have examined steroid regulation of onfFN in highly purified preparations (> or = 95%) of cytotrophoblasts isolated from human term placentas. Based on immunoassays, relative to controls, treatment of cytotrophoblasts with 10(-6) M medroxyprogesterone acetate (MPA) down-regulated media levels of onfFN 25, 53, 59, and 62% on days 1, 2, 3 and 4, respectively. The pattern of steroid regulation and levels of total FN were nearly identical to that of onfFN suggesting that chronic steroid treatment regulates synthesis of FN and not its oncofetal glycosylation. MPA treatment induced a 2-fold stimulation in media levels of hCG indicating that increased placental function was associated with steroid-mediated changes in FN expression. Steroid specificity experiments demonstrated that MPA, cortisol, and dexamethasone were potent inhibitors of onfFN expression whereas estradiol (E2), deoxycorticosterone, testosterone, progesterone, and the synthetic progestin OD-14, were not. This suggested that glucocorticoids and not progestins may be the physiologic regulators of placental FN expression and that MPA may mediate its matrix-modifying activity through a glucocorticoid-like mechanism. Treatment of cells with dexamethasone (10(-7) M) did not affect the levels of total protein synthesis or the release of human placental lactogen to the culture medium. This indicated that steroid-mediated down-regulation of onfFN expression in cytotrophoblasts did not result from a general reduction of protein synthesis. Based on densitometric scanning of Western blots, MPA and dexamethasone treatments down-regulated media levels of onfFN 70% relative to control levels. Northern blotting revealed that MPA and dexamethasone mediated a 60-90% reduction in steady state levels of FN mRNA in the presence or absence of E2. Our in vitro model may provide a unique system to evaluate steroidal effects on extracellular matrix (ECM) protein expression. In addition, we suggest that steroids may critically regulate placental ECM protein synthesis, and thus affect trophoblast/uterine adherence throughout pregnancy and expulsion of the placenta and membranes following delivery of the fetus.

Amino Acid Sequence↗
PubMed1991

Mediating mechanisms in a school-based drug prevention program: first-year effects of the Midwestern Prevention Project.

Describes (a) the effects of a social-influences-based drug prevention program (the Midwestern Prevention Project) on the mediating variables it was designed to change and (b) the process by which the effects on mediating variables changed use of drugs (tobacco, alcohol, and marijuana). Students in 42 middle schools and junior high schools in Kansas City, Missouri, and Kansas City, Kansas, were measured in the fall of 1984 (N = 5,065) and again 1 year later (N = 5,008) after 24 of the schools had been through the program. Compared to students in control schools, students in program schools became less likely to express belief in the positive consequences of drug use, less likely to indicate that they would use such drugs in the future, more likely to report that their friends were less tolerant of drug use, and more likely to believe that they were better able to communicate with their friends about drug or school problems. Change in perceptions of friends' tolerance of drug use was the most substantial mediator of program effects on drug use. There was evidence that intentions to use and beliefs about the positive consequences of use may also mediate program effects on drug use.

Adolescent↗
PubMed1991

[Surgical correction of congenital cryptotia].

From 1983 to 1988, we have operated on eight cases of cryptotia. The method of operation was to deepen the cephalo-auricular sulcus and to obtain a normal position of the ear. 1. The local flap usually used is either a V-Y advancement flap or a rotated flap. The author designs two V flaps, the upper one near the auricle is rotated to provide tissue between the upper part of the auricle and temporal region which should be dissected deep enough. The other V-Y advancement flap is used to increase the transverse length of the auricle. 2. The contracted transverse, oblique and superior auricular muscular fibres are dissected. In children the insertion of the superior auricular muscle is transposed and sutured to the eminentia fossae. 3. The repair of the cartilagenous deformity of the auricle includes placing two to three parallel incisions on the back of the superior part and elevating and suturing the angulated superior third helix to the cut edge of the back of the auricle. Good results were obtained in all cases.

Adolescent↗
PubMed1990

[Corrective rhinoplasty for post-traumatic deformity of nose].

From 1981 to 1986 the author has used osteotomy technique for corrective rhinoplasty in 15 cases. They were localized depression or deviation of the nose. The depression deformity was treated by osteotomy and elevating by making cuts along the midline of the nose and on each lateral cartilage. Then the dorsum of the nose was repositioned. All 15 cases obtained satisfactory cosmetic result without any complication.

Adolescent↗