PubMed Health⌕ Search

Biomedical subjects

J Danforth

Publications and source records attributed to J Danforth.

7 recordsLinked to original sources
PubMed2000

Expanded school mental health services: assessing needs related to school level and geography.

We surveyed 62 school administrators from three midatlantic (MD, VA, WV) and one northeastern (CT) state on factors relevant to developing school-based mental health programs. Administrators were from schools that varied on education level (elementary, middle, and high) and geographic location (urban, suburban, and rural), with equivalent numbers in each subgroup. Administrators provided ratings to questions grouped in five categories: (a) Stressful Conditions, (b) Internalizing Behavioral Problems, (c) Externalizing Behavioral Problems, (d) Substance Abuse, and (e) Barriers to Mental Health Care, and provided open-ended comments on needs of youth and mental health programs for them. They rated behavioral and substance abuse problems as progressively more serious as students advanced in school level. Urban youth were reported to encounter higher stress and present more severe internalizing problems than suburban or rural youth. Suburban and rural schools provided more health and mental health services than urban schools. Across geographic locales, physical health services far outnumbered mental health services. Findings related to barriers to mental health care, and the viability of schools as delivery sites for comprehensive mental health services, are discussed.

Adolescent↗
PubMed1992

Interleukin-6 (IL-6) gene expression and secretion by cytokine-stimulated human retinal pigment epithelial cells.

Retinal and choroidal inflammatory lesions are important causes of visual loss, but the mechanisms regulating intraocular inflammation remain poorly understood. By virtue of its position at the blood-retina barrier, the retinal pigment epithelium (RPE) cells may be critical to the initiation and propagation of ocular inflammation. Previously we showed that cytokine-stimulated RPE cells produce interleukin-8, a well-defined chemotactic factor for neutrophils and lymphocytes. In this study, we found that human RPE cells stimulated by human recombinant interleukin-1-beta (rIL-1 beta) or tumor necrosis factor-alpha (rTNF-alpha) produce interleukin-6 (IL-6). Using a plasmacytoma proliferation assay, significant levels of IL-6 were found in media of RPE cells stimulated with either rIL-1 beta or rTNF-alpha for 4 hr. Progressive accumulation of IL-6 in media overlying stimulated RPE cells occurred over the subsequent 20 hr. IL-1 beta was a significantly more potent stimulator of RPE IL-6 production than TNF-alpha, RPE IL-6 production in response to each of these cytokines was also dose-dependent over a range of 20 pg to 20 ng ml-1. Specific anti IL-6 antibody, but not control immunoglobulin, neutralized RPE-derived IL-6 activity in the plasmacytoma proliferation assays. RPE IL-6 mRNA levels were detectable 1 hr after cytokine stimulation, plateaued within 8 hr in 24-hr assays, and demonstrated dose-dependent kinetics in 6 hr assays. Lipopolysaccharide failed to induce RPE IL-6 mRNA expression or RPE IL-6 production.(ABSTRACT TRUNCATED AT 250 WORDS)

Base Sequence↗
PubMed1988

The clinical and pathophysiologic implications of pain, ST abnormalities, and scintigraphic changes induced during dipyridamole infusion: their relationships to the peripheral hemodynamic response.

In order to determine their significance during dipyridamole perfusion scintigraphy, symptomatic, ECG, and scintigraphic findings were related to each other, to the hemodynamic response, and to angiographic findings in 73 consecutive patients having coronary angiography within 3 months of scintigraphy. The group having induced "cardiac" pain differed from the group without induced pain only in their higher incidence of induced ischemic ST changes, the "marked" hemodynamic response, and their lower incidence of an "absent" hemodynamic response (all p less than 0.01). Induced ST depression was found only in patients with coronary disease. In this population, dipyridamole-induced pain was a moderately specific marker and induced ST abnormalities a more highly specific marker for coronary disease. However, both were insensitive for coronary disease diagnosis. If induced pain or ST abnormalities in the presence of significant coronary disease were accepted as indicators of ischemia, then scintigraphic abnormalities appeared to be produced by dipyridamole in roughly equal incidence by ischemic and nonischemic mechanisms. Induced ischemia related frequently to an exaggerated hypotensive response with no change in double product, suggesting its cause to be an induced increase in myocardial oxygen demand. Dipyridamole-induced image defects were noted even in the absence of a peripheral hemodynamic response. This indicates that the peripheral response does not always correlate with its central coronary effect and an absent peripheral hemodynamic response does not necessarily invalidate scintigraphic results.

Angina Pectoris↗
PubMed1985

Using beta blockers after MI in the elderly.

Data from the BHAT and the Norwegian timolol trail indicate that beta-blocking agents may provide significant benefit for the post-MI patient--regardless of the location of the infarct or the presence or absence of symptoms (ventricular arrhythmias) or risk factors (heart failure). Despite the lack of data, there is general agreement that beta blockers should be continued for at least 1 to 2 years after infarction in patients who are otherwise asymptomatic, and that these drugs should be continued indefinitely in post-MI patients with angina or hypertension who have no contraindications to beta blockers.

Administration, Oral↗