Biomedical subjects

B Brooks

Publications and source records attributed to B Brooks.

At least 19 recordsLinked to original sources

PubMed1995

The long-term impact of urological management on the quality of life of children with spina bifida.

To evaluate the integration of children with spina bifida into adult society and identify important urological factors 20 female and 18 male spina bifida patients older than 18 years were evaluated with respect to urological management and complications. A detailed questionnaire concerning educational achievements, living arrangements, employment and interpersonal relationships was completed and compared to similar data obtained from the 1990 United States census. Educational achievement and living arrangements for most patients were comparable to age matched peers in the general population and were independent of gender or method of urinary management. The only statistically significant factor related to a positive outcome was female gender in the areas of employment (p < 0.014) and sexual relationships (p < 0.005). Female spina bifida patients adapted better to adult society than their male counterparts. Intestinal urinary conduits were detrimental to long-term renal function.

Adaptation, Psychological↗

PubMed1995

Body piercing: promoting informed decision making.

Although school nurses may be unfamiliar with adolescent body piercing, they are in a key position to assist students who are considering these procedures. Information about various types of body piercing, student experiences, and teaching strategies to talk with adolescents about this procedure are presented. Nurses can utilize the data to help students make informed decisions about body piercing.

Adolescent↗

PubMed1992

Specific activation of a tyrosine----glycine mutant of delta 5-3-ketosteroid isomerase by phenols.

A key unknown still to be explored concerning the mechanism of delta 5-3-ketosteroid isomerase from Pseudomonas testosteroni is the extent of the proton transfer between tyrosine-14 of the enzyme and the C-3 carbonyl oxygen of the steroid substrate. This report is a preliminary study of a system we are developing to allow us eventually to use a Brønsted analysis to measure this transfer. We describe the construction of an expression vector and tyrosine-14----glycine-14 mutant of the enzyme and its specific activation, in the manner of chemical rescue, by a variety of phenolic compounds. We suggest that the binding region of phenol is very tight and that the level of activation may be a result of steric constraints as well as of differences in the pKa' of the phenol.

Amino Acid Sequence↗

PubMed1992

Regulation of prostaglandin E2 production by vitamin D metabolites in growth zone and resting zone chondrocyte cultures is dependent on cell maturation.

The production of PGE2 by chondrocytes and its regulation by vitamin D metabolites was examined in this study as a function of cell maturation. Costochondral chondrocytes, derived from the resting zone and growth zone cartilage, were grown in culture to fourth passage. At confluence, they were exposed to 10(-8)-10(-11)M 1,25-(OH)2D3 or to 10(-7)-10(-10)M 24,25-(OH)2D3 for either five minutes or 3, 6, 12, or 24 hours. Indomethacin (10(-7)M) was added to one-half of the cultures to block the production of PGE2. The amount of PGE2 released into the media was determined by radioimmunoassay. Both growth zone and resting zone cells produced PGE2 in a time-dependent manner; PGE2 concentration was greater in the resting zone cell cultures. 1,25-(OH)2D3 stimulated PGE2 production by growth zone cells in a dose-dependent manner, significant at 10(-8)-10(-10)M. This effect was observed at 3 hours and remained elevated during the 24 hours of culture. 1,25-(OH)2D3 had no effect on PGE2 production by resting zone cells. However, 24,25-(OH)2D3 (10(-7)-10(-8)M) inhibited PGE2 production from 3-24 hours. No effect was noted when 24,25-(OH)2D3 was added to growth zone cells. Indomethacin reduced PGE2 production to baseline values in all groups examined. The results indicate that chondrocytes in culture produce PGE2. Production is regulated by vitamin D3 metabolites and is cell maturation-dependent.(ABSTRACT TRUNCATED AT 250 WORDS)

24,25-Dihydroxyvitamin D 3↗

PubMed1992

Biologic differences between vasodilator prostaglandins and medullipin I.

Vasodepressor prostaglandins (PGs), PGE2, PGI2, and medullipin I (Med I) are synthesized in the kidney. These vasodilator substances are thought to be involved in the antihypertensive function of the kidney. At issue is whether there are biologic differences between the vasodilator PGs and Med I. Two separate studies have shown that Med I's vasodepressor action is inhibited by four procedures: mixing with Tween 20; treatment with n-butyl boronic acid; treatment of the assay animal with SKF 525A, an inhibitor of cytochrome P-450; and removing the liver from the circulation. These same procedures were applied to the vasodilator PGs. All four failed to inhibit the vasodepressor action of the PG's. It is concluded that Med I and vasodilator PGs of the kidney are separate and distinct biologic entities.

Animals↗

PubMed1992

Peripheral low-grade mucoepidermoid carcinoma of the lung--needle aspiration cytodiagnosis and histology.

Mucoepidermoid carcinoma of the lung is a rare tumour, and is not usually considered in the differential diagnosis of a peripheral lung mass. The cytological and histological features of an intimate admixture of polygonal intermediate cells, well differentiated mucinous and squamous cells, as illustrated in this case report, serve to differentiate a well differentiated mucoepidermoid carcinoma from adenosquamous carcinoma, low grade adenocarcinoma, bronchioloalveolar carcinoma, and benign reactive changes.

Aged↗

PubMed1992

Production of 1,25-dihydroxyvitamin D3 and 24,25-dihydroxyvitamin D3 by growth zone and resting zone chondrocytes is dependent on cell maturation and is regulated by hormones and growth factors.

1,25-Dihydroxyvitamin D3 [1,25-(OH)2D3] and 24,25-(OH)2D3 have been shown to promote chondrocyte proliferation and differentiation; resting zone chondrocytes respond primarily to 24,25-(OH)2D3, whereas growth zone chondrocytes respond primarily to 1,25-(OH)2D3. This study determined whether resting zone and growth zone cells produce 24,25-(OH)2D3 or 1,25-(OH)2D3; whether this production is regulated by 1,25-(OH)2D3 (10(-8) M), 24,25-(OH)2D3 (10(-7) M), dexamethasone (10(-7) M), or recombinant human transforming growth factor-beta 1 (11 ng/ml); and whether the metabolites produced are biologically active. Confluent fourth passage rat costochondral growth zone or resting zone chondrocytes were cultured in Dulbecco's Modified Eagle's Medium containing [3H]25-hydroxyvitamin D3 ([3H]25OHD3), 2% fetal bovine serum, and antibiotics. Metabolism of [3H]25OHD3 was measured by analyzing the lipid extracts of the conditioned medium and the cell layer for [3H]1,25OHD3, [3H]1,25-(OH)2D3, and [3H]24,25-(OH)2D3 using flow-through scintillation spectroscopy of HPLC eluates. Chemically synthesized radioinert vitamin D3 metabolites were used as standards, and their migration was determined by absorbance at 254 nm. To ensure that the radioactive peaks were 1,25-(OH)2D3 and 24,25-(OH)2D3, the fractions were rechromatographed into three other HPLC solvent systems. Biological activity was confirmed; the addition of HPLC-purified 1,25-(OH)2D3 produced by growth zone chondrocytes elicited a dose-dependent stimulation of alkaline phosphatase specific activity in growth zone cell cultures, but had no effect on the resting zone cells. There was a time-dependent increase in both [3H]1,25-(OH)2D3 and [3H]24,25-(OH)2D3 in the conditioned medium of both types of cultures. At 24 h, the percent conversion of [3H]25OHD3 to [3H]1,25-(OH)2D3 was 5.3 +/- 1.2, and the percent conversion to [3H]24,25-(OH)2D3 was 1.8 +/- 0.4 in growth zone chondrocyte cultures. No such effect was found in cultures freeze-thawed five times or without cells. When resting zone cells were cultured with [3H]25OHD3, the percent conversion to 1,25-(OH)2D3 and 24,25-(OH)2D3 was 4.5 +/- 1.0 and 1.7 +/- 0.4, respectively. The addition of dexamethasone significantly increased the percent production of 1,25-(OH)2D3 at 6 and 24 h and at 6 h by resting zone and growth zone cells, respectively, compared to the control values. Recombinant human transforming growth factor-beta 1 increased the percent production of 1,25-(OH)2D3 after 1 h in resting zone cells and, after 24 h, the production of 24,25-(OH)2D3 in growth zone cells. Radiolabeled 1,25-(OH)2D3 and 24,25-(OH)2D3 were not detected in the cell layer.(ABSTRACT TRUNCATED AT 400 WORDS)

24,25-Dihydroxyvitamin D 3↗

PubMed1992

Persistent hypotension associated with hypermedullipinemia: a new syndrome.

A new syndrome is described in a patient with advanced renal insufficiency. This consists of severe and persistent hypotension causing weakness but associated with a clear mental status. Also present is evidence for decreased vascular reactivity. The hypotension was not orthostatic. The hypotension was associated with a circulating vasodepressor substance having the characteristics of medullipin 1. The medullipin appears to have been derived from the remaining right kidney. Hypotension existed despite the presence of major prohypertensive mechanisms, including an endstage kidney, hyperreninemia and hyperaldosteronemia. It is likely that hypotension due to hypermedullipinemia is an entity occurring in the human being.

Adult↗

PubMed1992

Secretion of medullipin I by the kidney requires oxygen.

OBJECTIVE: To test the hypothesis that the secretion of medullipin I by the kidney involves an oxidative step. DESIGN: Medullipin I is secreted by kidney renomedullary interstitial cells and is converted to medullipin II by the liver. Medullipin I can be derived from the kidney in the renal venous effluent by perfusing normal rat kidneys with 95% O2- 5% CO2 at an elevated pressure (180 mmHg). To evaluate whether the secretion of medullipin I involves an oxidative step normal rat kidneys were perfused at an elevated pressure in the presence of O2, in the absence of O2 and after treatment of the kidneys with a powerful antioxidant. METHODS: Normal rat kidneys were perfused with 5% albumin bubbled with O2-CO2 at 180 mmHg. This was the control procedure for each of the three approaches. In approach (1), the kidneys were perfused with 5% albumin bubbled with N2. In approach (2), the kidneys were perfused with 'blood' treated with carbon monoxide. In approach (3), the kidneys were treated with the antioxidant butylated hydroxytoluene then perfused with 5% albumin bubbled with O2-CO2. Each perfusate was tested for medullipin I activity by rapid intravenous injection into the SHR. RESULTS: All three approaches, which exclude the action of molecular O2, prevented the secretion of medullipin I by the kidneys. CONCLUSION: The secretion of medullipin I by the kidneys involves an oxidative step.

Animals↗

PubMed1992

Evidence that interleukin-4 suppression of lymphokine-activated killer cell induction is mediated through monocytes.

Recombinant human interleukin-4 (IL-4) and transforming growth factor-beta (TGF-beta) reduce recombinant interleukin-2 (IL-2) induction of lymphokine-activated killer (LAK) cell activity from human peripheral blood mononuclear cells (PBMC). Monocytes can be removed from PBMC by adherence, leaving a peripheral blood lymphocyte population (PBL) which also responds to IL-2 to generate LAK activity. PBL generation of LAK cytotoxicity is susceptible to inhibition by TGF-beta, but not by IL-4. Readdition of purified monocytes to PBL is accompanied by return of the suppressive action of IL-4 on the generation of LAK activity. Induction of LAK cytolysis from Percoll-isolated T cells (greater than 90% CD3+) is also refractory to the inhibitory effect of IL-4. When PBMC were cultured in IL-2, with and without IL-4, subsequent sorting of CD3+ and CD3- lymphocytes by flow cytometry demonstrated that IL-4 had suppressed LAK induction in both effector populations. This suggests that, although isolated CD3+ cells are not susceptible to IL-4 suppression of IL-2 activation, they are sensitive to inhibition when part of a mixed PBMC population. Evidence is presented for the first time that this suppression is mediated via the action of IL-4 on monocytes.

Cell Adhesion↗

PubMed1991

[Phlegmonous enteritis--a rare cause of acute abdomen].

A 73 year old woman presenting with an acute abdomen was diagnosed as having phlegmonous enteritis after microscopic examination revealed the characteristic finding of a diffuse suppurative inflammation limited to the submucosa in the resected ileal segment. Culture of Klebsiella pneumoniae, and the microscopic demonstration of gram positive cocci and gram negative rods confirmed the bacterial etiology of this disease. There was no evidence of mucosal injury in this patient, but the possible role of ischemia secondary to atherosclerotic vascular disease cannot be assessed. Because of the associated high morbidity and mortality, phlegmonous enteritis should be considered in the differential diagnosis of acute abdomen.

Abdomen, Acute↗

PubMed1991

Secretion of medullipin I by isolated kidneys perfused under elevated pressure.

1. Medullipin I (Med I) is a hormone extracted from renal papillae and its renomedullary interstitial cells (RIC). Med I is stimulated by elevation of the renal artery perfusion pressure. 2. When isolated normal rat kidneys were perfused either with oxygenated blood or with 5% albumin bubbled with O2 at elevated perfusion pressures, Med I appeared to be secreted into the renal venous effluent (RVE). Addition of Tween 20, treatment of the assay rat with SKF 525A, inhibitor of cytochrome P-450 and removal of the liver from the systemic circulation prevented vasodepression of both the RVE and extracted Med I. The lipid in the RVE gave the same dose-response as extracted Med I. 3. Lowering the renal artery perfusion pressure below normal inhibited the secretion of Med I. As the perfusion pressure was elevated Med I secretion appeared to increase. 4. Previous observations and the present study support the view that the renin-angiotensin system and the Medullipin system are double feedback systems involved in blood pressure control.

Angiotensin II↗

PubMed1991

Antihypertensive action of medullipin I given by mouth.

Perfusion of normal rat kidneys with 5% human albumin in a balanced salt solution bubbled with oxygen yielded medullipin I (Med I) in the renal venous effluent. The presence of Med I in the renal venous effluent has been established by thin-layer chromatography, by the type of vasodepressor effect when injected intravenously as a bolus into the hypertensive rat, by inhibition of the vasodepressor effect of the renal venous effluent by Tween 20 and SKF 525A (proadifen, inhibitor of cytochrome P-450), and by removal of the liver from the circulation (a procedure that inhibits extracted Med I). Med I so derived lowered blood pressure of spontaneously hypertensive rats when injected into the stomach by an indwelling tube or when given by mouth. The lowering of blood pressure was attended by no change in cardiac output and no change in heart rate. Med I given by mouth to the spontaneously hypertensive rat is a vasodilator that suppresses sympathetic tone, acting in the same way as Med I extracted from renal papillae and given intravenously. Importantly, the antihypertensive action was demonstrated in the spontaneously hypertensive rat, a model of hypertension considered to mimic idiopathic or essential hypertension of humans. Med I is a promising therapeutic agent for hypertension.

Administration, Oral↗

PubMed1991

Medullipin system. Generation of medullipin II by isolated kidney-liver perfusion.

Perfusion of isolated normal rat kidneys with blood at elevated blood pressure (180-200 mm Hg) followed by perfusion of the renal perfusate through an isolated normal rat liver under venous pressure yielded in the plasma of the hepatic effluent a vasodepressor lipid having the chromatographic and biological characteristics of medullipin II. These findings support the view that medullipin II is the final product of the renohepatic axis of blood pressure control.

Animals↗

PubMed1991

Phase II study of mitoxantrone, leucovorin, and infusional fluorouracil for treatment of metastatic breast cancer.

A new combination of mitoxantrone, folinic acid (leucovorin), and infusional fluorouracil (5-FU) was administered to 57 previously treated patients with metastatic breast cancer to evaluate the response rate, response duration, and toxicity of this regimen. Fifty-three patients who received 313 courses of therapy were assessable for response and toxicity. Median age was 48 years (range, 33 to 80 years), and the patients had received an average of 1.5 chemotherapy regimens before this study. Of 53 assessable patients, 24 (45%, or 42% of all entered patients) experienced partial responses (PRs) with a median duration of 6 months (range, 2 to 13 months). Nine (69%) of 13 assessable patients without prior doxorubicin treatment responded, compared with 15 (38%) of 40 with prior doxorubicin (P less than .05). Toxicity was generally mild with dose reductions necessitated more often by mucositis and/or diarrhea than by myelosuppression. One patient with prior high-dose doxorubicin treatment developed congestive heart failure. The combination of mitoxantrone, leucovorin, and infusional 5-FU is an active and well-tolerated regimen for metastatic breast cancer and deserves further evaluation in patients without prior doxorubicin therapy.

Adult↗

PubMed1990

MR of uncommon congenital and vascular lesions of the intracranial visual pathways.

The MR findings of two patients with rare congenital abnormalities of the optic pathways are reported and illustrated, including one case of unilateral aplasia of the optic chiasm, tract, and visual radiations and another patient with anophthalmos. In three other patients with unusual vascular causes of visual disturbance, MR was important in early establishment of an accurate diagnosis and had consequent implications for decisions regarding further patient management.

Adult↗

PubMed1990

Suppression of lymphokine-activated killer (LAK) cell induction mediated by interleukin-4 and transforming growth factor-beta 1: effect of addition of exogenous tumour necrosis factor-alpha and interferon-gamma, and measurement of their endogenous production.

Recombinant human interleukin-4 (rhIL-4) and transforming growth factor-beta 1 (TGF-beta 1) suppressed the induction of lymphokine-activated killer (LAK) activity induced by recombinant human interleukin-2 (rhIL-2) in peripheral blood lymphocytes. DNA synthesis and the expression of the p55 alpha chain of the IL-2 receptor (Tac antigen) were also inhibited. The inhibitory effect was greatest when these factors were added during the first 48 h of a 4-day culture, with reduced cytolytic activity against both natural killer (NK) resistant and NK-sensitive tumour cell line targets. The suppressive action of both cytokines was accompanied by a reduction in tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) levels in lymphocyte culture supernatants. Recombinant human IFN-gamma (rhIFN-gamma), but not recombinant human TNF-alpha (rhTNF-alpha) was able to overcome the inhibitory effect of recombinant human interleukin-4 (rhIL-4) on LAK induction and DNA synthesis but not Tac antigen expression. However, cytotoxicity induced by rhIFN-gamma alone was also suppressed by rhIL-4 and TGF-beta 1, inferring that rhIFN-gamma-mediated abrogation of rhIL4 suppression was not simply a direct IL-2-independent effect on cytotoxicity. In addition, rhIL-4 did not increase TGF-beta production from rhIL-2-activated peripheral blood mononuclear cells, suggesting that rhIL-4 did not mediate reduction of rhIL-2 responses through the induction of TGF-beta release.

Cell Division↗

PubMed1989

Computed tomography of Grave's ophthalmopathy. Diagnosis, management, and posttherapeutic evaluation.

Computed tomography (CT) is emphasized in the diagnosis and management of Grave's ophthalmopathy. This report illustrates the value of CT in evaluating the extent of disease, choice and timing of treatment, radiation therapy planning, and posttreatment follow-up of nine patients with Grave's ophthalmopathy. Eight patients had bilateral disease, and three patients had evidence of optic nerve compression. Postirradiation follow-up CT was done in three patients. Eight patients treated with radiation obtained good response.

Aged↗