The path to intervention: community partnerships and development of a cognitive behavioral intervention for ethnic minority adolescent females

Reproductive health needs for ethnic minority adolescents are a national priority given the population growth of minority adolescents in the United States. United States census reports predict minority adolescents will comprise one-third of all young persons less than 20 years of age early in the twenty-first century. Developing culturally sensitive interventions for minority adolescents includes ecological assessments of cultural priorities, community resources, disease burden, and socioeconomic conditions. These assessments must be accomplished in partnership with the local community. Understanding reproductive health needs necessarily includes an evaluation of the absence of reproductive health, namely, the prevalence of sexually transmitted infection (STI), sexual or physical abuse, unplanned pregnancy, and the risk factors that contribute to such adverse outcomes. This article describes the methodological processes utilized to conduct an ecological assessment of a community including the health, economic, and psychosocial status of, and resources available to, a target population prior to the implementation of a community-based, cognitive behavioral intervention to reduce STI, abuse, and unplanned pregnancy.     

Prevalence of comorbid psychiatric illness and substance misuse in primary care in England and Wales

STUDY OBJECTIVE: To estimate the annual period prevalence of co-occurring psychiatric illness and substance misuse among patients in primary care. DESIGN: Analysis of the general practice research database. SETTING: England and Wales, 1993-1998. PARTICIPANTS: Registered patients at 230 general practices representing 3.1% of the population. A comorbid case was defined as one with both a psychiatric diagnosis and substance misuse diagnosis (not including alcohol or tobacco) within a calendar year. A potentially chronic comorbid case was one that met this definition and, in addition, was treated in subsequent years for either a psychiatric condition or substance misuse. MAIN RESULTS: The annual period prevalence of comorbidity increased from 50/100 000 patient years of exposure (PYE) to 80/100 000 PYE, an increase of 62% during the study period. Rates of comorbid psychoses, comorbid schizophrenia, and comorbid paranoia increased by 147%, 128%, and 144%. The average age of comorbid cases decreased from 38 years to 34 years. Over 80% of comorbid cases were newly diagnosed in each study year, although many are treated in subsequent years for either psychiatric illness or substance misuse. CONCLUSIONS: This study provides data on the nature and extent of comorbidity in primary care in England and Wales. As the comorbidity rate is increasing by about 10% each year, and as comorbid cases are becoming younger, it is probable that the comorbidity rate will have increased beyond the study end point.     

Analysis of glioma cell lines for amplification and overexpression of MDM2

Recently, amplification of the gene encoding a p53 binding protein, MDM2, was determined in 8% of the cases constituting a large series of glioblastomas. Here we have utilized Southern blot analysis to examine 30 cell lines established from such tumors, and our investigation has revealed large increases in MDM2 gene dosage in two cases, one of which showed coamplification of the CDK4 gene that resides in close proximity to MDM2 in chromosomal region 12q13–14. Northern analysis demonstrated overexpression of MDM2 mRNA in the two cell lines with gene amplification, and overexpression of MDM2 protein was evident in each of these by immunohistochemical and Western blot analysis. Analysis of TP53 cDNAs revealed normal TP53 sequences in the cell lines with MDM2 amplification; these results are consistent with those of previous studies suggesting that MDM2 amplification occurs only in tumors expressing wild-type p53. In total, these data suggest that MDM2 amplification in glioblastoma cell lines occurs at a frequency (6.7%) comparable to that determined in primary tumors; occurs in cell lines expressing wild-type p53; and can involve the coamplification of additional genes.     

Ethanol pre-exposure suppresses HIV-1 glycoprotein 120-induced neuronal degeneration by abrogating endogenous glutamate/Ca2+-mediated neurotoxicity.

The neurotoxic mechanism of HIV-1 envelope glycoprotein 120 (gp120) involves glutamatergic (NMDA) receptor/Ca2+-dependent excitotoxicity, mediated in part via glia. Pro-inflammatory cytokines also may have roles. We have reported that pre-exposure of brain cultures to 'physiological' ethanol concentrations (20-30 mM) protects against neuronal damage from HIV-1 gp120, but not from the direct receptor agonist, NMDA. Using lactate dehydrogenase assays and propidium iodide staining of rat organotypic hippocampal-entorhinal cortical slice cultures we determined that ethanol's suppression of gp120 neurotoxicity required at least 4 days of pretreatment. The gp120-induced neurotoxicity was accompanied by interleukin-6 elevations that were not affected by the pretreatment. However, gp120 induced substantial, early increases in extracellular glutamate levels that were blocked by ethanol pretreatment, conceivably abrogating excitotoxicity. Consistent with abrogation of excitotoxic pathways, fura-2 imaging showed selective deficits in gp120-dependent intracellular Ca2+ responses in ethanol-pretreated slices. Gp120 is believed to increase glutamate levels by both stimulating release and inhibiting (re)uptake. Results with a labeled glutamate analog, D-[3H]aspartate, revealed that gp120's inhibition of glutamate uptake, rather than its stimulation of release, was abolished after ethanol. Further studies indicated that two converging effects of ethanol pretreatment may underlie the abolishment of gp120-mediated glutamate uptake inhibition: (a) blockade of gp120-induced release (ostensibly from glia) of arachidonic acid, an inhibitor of astroglial glutamate reuptake, and (b) modest proliferation and activation of astroglia upon gp120 stimulation--which are likely to augment glutamate transporters. Thus, as with gp120 itself, glia and glutamate/arachidonic acid regulation appear to be important targets for ethanol.Since moderate ethanol consumption is as common among HIV-infected individuals as in the general population, this newly recognized neuroprotective (and apparently anti-excitotoxic) effect of ethanol withdrawal in vitro could be important, but it requires further study before its significance, if any, is understood.     

Altered secretion of gonadotropins and steroids resulting from delayed ovulation in the rat.

Rats were killed by decapitation at 3-h intervals during a 48-h delay of ovulation induced by sodium pentobarbital, as well as during the ensuing delayed proestrus, estrus and the first 4 days of gestation. Control animals were killed at the same intervals following injections of vehicle. Blood was collected and analyzed for LH, FSH, prolactin, progesterone and estradiol-17beta to determine if alterations in hormonal levels could account for the abnormal embryonic development which follows delayed ovulation. Hormonal concentrations in plasma were measured by radioimmunoassay except for progesterone, which was determined by competitive protein binding. Embryos were examined to verify the occurrence of abnormal development. Rate of oocyte maturation was studied in serial sections of ovaries from all animals killed at 30-min intervals on the afternoon of proestrus. Oocytes remained in meiotic arrest during the 48-h delay of ovulation, but resumed maturation at the expected time on the afternoon of the preovulatory surge of gonadotropins. Following delayed ovulation there was a significant increase in fertilized ova that were undergoing degeneration (6.5 vs 1.9%), abnormal development (3.7 vs 0.7%), and retarded development (3.1 vs 0.2%). A number of alterations in hormonal levels occurred during the prolonged preovulatory period. The proestrous surge of LH in plasma was completely suppressed on both days of treatment with Nembutal, but exhibited a normal preovulatory peak on the following day. FSH showed a small but significant rise on both days of treatment. Peak concentrations of FSH on the following day were not different in magnitude from the normal preovulatory surge, although the duration of this surge was shortened by 12 h. Prolactin and progesterone concentrations in plasma were only partially suppressed on the days of treatment, while on the following day preovulatory levels of prolactin were significantly greater than in controls. The proestrous peak levels of estradiol occurred prior to the first Nembutal injection and declined more gradually after this treatment. Plasma levels of estradiol remained above basal levels during the period of delayed ovulation with peaks of short duration at 15u0 h on the day of second treatment and the day prior to ovulation. Plasma levels of these 5 hormones during the first 4 days of gestation were not altered by delayed ovulation.     

Adult Turner syndrome associated with chylous ascites and vascular anomalies

An adult female with Turner syndrome presented with severe lymphedema and chylous ascites. In addition, the patient was found to have a right-sided aortic arch and a left-sided inferior vena cava. Although lymphedema is common in infants with Turner syndrome is previously unreported. In this patient, a peritoneo-venous shunt appeared to be beneficial.     

Analysis of T lymphocytes cloned from the synovial fluid and blood of a patient with lyme arthritis

Cloned T lymphocytes reactive with Borrella burgdorferi proteinswere isolated from a patient with chronic Lyme arthritis. Allof the T cell clones which proliferated In response to Borrellaproteins were CD3+CD4+CD8-TCRß+ and HLA-DR restricted.One T cell clone (GN30) exhibited HLA-DR-restricted cytotoxicactivity against antigen-presenting cells pulsed with Borrellaantigen. In response to Borrella antigen, the T cell clonesproduced TNF-, INF-ß, and GM-CSF. There are at leastthree distinct spirochetal proteins recognized by the four Tcell clones analyzed. Purified Borrella proteins triggered theHLA-DR-restrlcted proliferative and cytotoxic responses, aswell as lymphokine secretion by two of the T cell clones. Thespirochetal protein which triggered the HLA-DR-restrlcted proliferativeand cytotoxic activities of the T cell clone (GN30) isolatedfrom synovial fluid is the 41 kd flagellar protein.