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J E Benjamin

Publications and source records attributed to J E Benjamin.

5 recordsLinked to original sources
PubMed1995

Bridging the "med-ed gap" for students with special health care needs: a model school liaison program.

A successful school experience is critical to the development of all children, particularly in the areas of academic achievement, regular school attendance, and social competency. Vulnerabilities in achieving each of these three goals have been documented among students with special health care needs (SSHCN), and ascribed to the influence of their health-related disabilities. Despite recognition of these vulnerabilities, barriers still exist to successful integration of SSHCN into educational settings. A key barrier to successful integration involves poor linkages between the health and education systems. This article describes a model linkage system--the School Liaison Program at Texas Children's Hospital, developed as a U.S. Dept. of Health and Human Services Maternal and Child Health Bureau Special Project of Regional and National Significance. The program provides educational liaison services between the largest pediatric hospital in the United States and school districts in the fourth largest city. A description of the linkage system emphasizes interdisciplinary staffing by both special educators and health providers. The model for educational liaison service delivery presented includes the elements of eligibility, assessment of the educational implications of illness, plan development and referral, involvement in educational placement, and monitoring. Resources for integrating SSHCN into educational settings are suggested.

Adolescent↗
PubMed1995

Health services delivery to students with special health care needs in Texas public schools.

A statewide survey of 2,875 Texas public school nurses was conducted to determine the characteristics, needs, and involvement of nurses in the health and education management of students with special health care needs (SSHCN). The 1,574 survey respondents (response rate = 55%) were primarily registered nurses (84%) with a mean of 8.6 years (SD = 7.1) of experience in the school setting. Respondents served 1.5 school campuses on average; the mean nurse-to-student ratio per campus was 1:728 (SD = 518). Respondents identified 106,650 SSHCN (6% of total enrollment). Asthma (47%), attention deficit disorder (26%), and seizure disorders (8%) were the most prevalent conditions encountered among SSHCN. Medication administration (54%), diapering (12%), and inhalation respiratory treatments (11%) were the most common of 48,569 health procedures delivered daily to SSHCN by nurses, clerical staff, assistants, and teachers. Parents were identified as the primary source of both child-specific health (70%) and training (68%) information in the school setting. Although nurses, of all school personnel, are likely best able to speak to the impact of a child's health impairment and needed school services, only 32% of respondents reported routine participation in special education eligibility evaluations and only 18% reported routine attendance at special education meetings for SSHCN. Moreover, 84% and 92%, respectively, reported discomfort at participating in special education eligibility evaluations and attending special education meetings.

Adolescent↗
PubMed1992

Mechanism of regulation of thyrotropin-releasing hormone receptor messenger ribonucleic acid in stably transfected rat pituitary cells.

We showed previously that the level of TRH receptor (TRH-R) mRNA in rat pituitary GH3 cells is down-regulated by TRH. Here, we study the mechanism of regulation of TRH-R mRNA in a line of GH3 cells that are stably transfected with mouse pituitary TRH-R cDNA (GH-mTRHR-1 cells). GH-mTRHR-1 cells were found to have 2.4 times the number of TRH-Rs and to stimulate a 2.5-fold greater increase in inositol phosphates in response to TRH than the parent cell line and to show TRH-induced down-regulation of TRH-R number. GH-mTRHR-1 cells contained 26 +/- 1.6 molecules of mouse TRH-R mRNA/cell and 230 +/- 31 molecules of mRNA for the neomycin resistance gene (NEO) with which it was cotransfected. In GH-mTRHR-1 cells, TRH caused a dose-dependent transient decrease in mouse TRH-R mRNA, with a nadir to 20% of control levels after 6 h. In contrast, TRH did not affect NEO mRNA or glyceraldehyde phosphate dehydrogenase (GAPDH) mRNA, an endogenous gene product. TRH stimulated the rate of transcription of mouse TRH-R DNA by approximately 2-fold, but did not affect total poly(A) RNA synthesis. Most importantly, TRH caused a 4-fold increase in the rate of degradation of mouse TRH-R mRNA, but did not affect degradation of GAPDH mRNA. The half-lives of mouse TRH-R and GAPDH mRNAs were 3 and more than 20 h in control cells and 0.75 and more than 20 h in cells treated with 1 microM TRH for 1.5 h, respectively. These data show that the predominant effect of TRH on mouse TRH-R mRNA in GH-mTRHR-1 cells is to enhance the rate of its degradation. We suggest, therefore, that down-regulation of TRH-R mRNA caused by TRH in the parent GH3 cell line is secondary to increased TRH-R mRNA degradation.

Animals↗
PubMed1992

Posttranscriptional up-regulation of thyrotropin-releasing hormone (TRH) receptor messenger ribonucleic acid by TRH in COS-1 cells transfected with mouse pituitary TRH receptor complementary deoxyribonucleic acid.

We found previously that the level of endogenous TRH receptor (TRH-R) mRNA in pituitary (GH3) cells and the level of mouse TRH-R mRNA in GH3 cells stably transfected with mouse pituitary TRH-R cDNA are down-regulated by TRH. This down-regulation is caused by TRH stimulation of TRH-R mRNA degradation via a mechanism that appears to involve protein kinase-C. In this report we study regulation of TRH-R mRNA in monkey kidney (COS-1) cells transiently transfected with mouse pituitary TRH-R cDNA. In transfected COS-1 cells, TRH and phorbol 12-myristate 13-acetate (PMA) caused increases in the level of TRH-R mRNA. In contrast, TRH caused only a small transient increase in the level of the mRNA for the neomycin resistance gene, which was cotransfected with TRH-R, and did not affect the level of the mRNA for glyceraldehyde phosphate dehydrogenase, an endogenous gene. The increases in TRH-R mRNA caused by TRH and PMA were inhibited to similar extents by H-7 (1-[5-isoquinolinesulfonyl]2-methyl piperazine dihydrochloride), an inhibitor of protein kinases. The effect of TRH was observed in cells transfected with expression vectors in which TRH-R cDNA was controlled by cytomegalovirus or Rous sarcoma virus promoters. There was no effect of TRH or PMA on the rate of transcription of the transfected TRH-R cDNA. In contrast, TRH caused the rate of degradation of TRH-R mRNA to decrease from 8.0% to 5.1%/h. Hence, TRH, most likely via a protein kinase-C-mediated mechanism, up-regulates TRH-R mRNA levels in transfected COS-1 cells by decreasing the rate of TRH-R mRNA degradation. Since TRH and PMA down-regulate TRH-R mRNA in GH3 cells, posttranscriptional regulation of TRH-R mRNA is a cell-type specific process.

Animals↗