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Biomedical subjects

J E Hall

Publications and source records attributed to J E Hall.

At least 199 records · Page 11Linked to original sources
PubMed1994

Spinal deformity associated with neurenteric cysts in children.

STUDY DESIGN: Neurenteric cysts are uncommon lesions originating from the primitive foregut that may involve adjacent vertebrae and spinal cord. Little is known regarding the natural history of these cysts and associated spinal deformity in children. Five patients with these cysts managed at the authors' institution from 1955 to 1993 were reviewed. OBJECTIVES: The goal of this retrospective review was to determine the natural history of these cysts in children, and to assess the surgical management in each of the five patients. METHODS: Medical charts and radiographic records were reviewed and, when possible, the patients were re-evaluated clinically. RESULTS: All patients had significant anterior vertebral defects, and four had severe kyphosis at presentation. Major complications occurred in three of the four patients treated surgically. CONCLUSIONS: Iatrogenic complications of surgical management of these cysts can be limited by combined anterior and posterior approaches, providing the most complete exposure and maximal stabilization of the associated deformity.

Child↗
PubMed1994

High-fructose diet does not raise 24-hour mean arterial pressure in rats.

High intakes of the simple sugars--glucose, sucrose, and fructose--have been reported to raise significantly systolic pressure in rats. It is not clear, however, if under those conditions the acute measurement of blood pressure, especially with the tail-cuff technique, represents accurately the effect of the diet on mean arterial pressure throughout the day. In this study, 15 Sprague-Dawley rats (approximately 325 g) were chronically instrumented with arterial and venous catheters and placed on a diet containing 61% vegetable starch and 5% dextrose; seven rats remained on this diet throughout the study. After 4 days of control measurements, eight rats were switched to a diet that substituted 66% fructose for the vegetable starch and dextrose. Mean arterial pressure (MAP) was measured 20 h/day by computerized methods. MAP during the 4 control days averaged 100 +/- 3 and 105 +/- 3 mm Hg in low-fructose (LF) and high-fructose (HF) diet rats, respectively. Switching to the HF diet caused no change in MAP, and after 11 days MAP averaged 104 +/- 2 and 108 +/- 3 mm Hg in the LF and HF rats, respectively. In addition, the variability of MAP over the 20-h period each day was not altered by the HF diet, and raising sodium intake fourfold caused a similar rise in MAP in both groups. There also were no significant changes in plasma glucose or insulin concentrations. Thus, a change in dietary simple sugar content from 5% dextrose to 66% fructose did not change MAP or alter blood pressure variability or sodium sensitivity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Exaggerated pressor and chronotropic response to chronic hyperinsulinemia in SH versus WKY rats.

Insulin resistance and the sympathetic nervous system have been suggested to be important factors in the blood pressure response to hyperinsulinemia. This study was designed to investigate whether the response to chronic hyperinsulinemia in 14-week-old SH rats (n = 6), which are reported to be insulin resistant and to have a hyperresponsive sympathetic nervous system, would differ from that in WKY rats (n = 5). Mean arterial pressure (MAP) and heart rate (HR) were monitored 19 h/day by computer. After a 4-day control period, insulin (1.5 mU/kg/min) and glucose (19.3 [WKY] or 13.5 [SH] mg/kg/min) were infused intravenously for 7 days. Plasma insulin increased from 43 +/- 7 and 68 +/- 7 mU/mL to 75 +/- 4 and 91 +/- 11 mU/mL in WKY and SH rats, respectively, with no decrease in plasma glucose in either group. MAP during control averaged 99 +/- 2 and 130 +/- 4 in WKY and SH rats, respectively, and increased 2 +/- 2 mm Hg above control in WKY rats and 18 +/- 4 mm Hg in SH rats on day 1 of insulin. However, after day 2 the change from control was no longer significantly different between the groups and averaged 11 +/- 2 and 15 +/- 6 mm Hg above control on day 7 in the WKY and SH rats, respectively. The change in heart rate from control was 5 +/- 5 and 21 +/- 9 beats per minute in the WKY and SH rats on day 1 of insulin, and this difference also diminished with time.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Resistance to metabolic actions of insulin and its role in hypertension.

Insulin resistance and hyperinsulinemia have been postulated to be important in raising blood pressure in obese as well as lean hypertensive individuals. However, cause-and-effect relationships among these variables have not been clearly established. The three most widely used methods to assess insulin resistance in vivo (fasting plasma insulin, glucose disposal after a glucose load, or glucose disposal during a hyperinsulinemic euglycemic clamp) may provide different estimates of insulin resistance under various physiological and pathophysiological conditions. Fasting hyperinsulinemia may reflect mainly hepatic insulin resistance, whereas impairment of glucose disposal indicates resistance to the metabolic effects of insulin in skeletal muscle. The importance of these different sites of insulin resistance in the etiology of cardiovascular diseases, however, is still unclear. Although hyperinsulinemia and insulin resistance have been speculated to cause hypertension, most of the evidence supporting this hypothesis has come either from correlation studies or from short-term studies of the cardiovascular, renal, and sympathetic effects of insulin. The few long-term studies that have been conducted in dogs and in humans do not support the insulin concept of hypertension. In fact, these studies suggest that the vasodilator actions of insulin tend to reduce, rather than elevate, blood pressure. Correlations between insulin resistance, hyperinsulinemia, and hypertension do not appear to be explainable by the concept that insulin resistance occurs secondary to hypertension. Obesity may be a key factor in explaining these relationships; weight gain appears to cause insulin resistance, compensatory hyperinsulinemia, and hypertension through parallel, but not necessarily linked, mechanisms. However, insulin resistance and compensatory hyperinsulinemia may contribute to increased risk of other cardiovascular diseases associated with hypertension, such as coronary artery disease.

Animals↗
PubMed1994

Louis K. Dahl Memorial Lecture. Renal and cardiovascular mechanisms of hypertension in obesity.

In all forms of hypertension, including human essential hypertension, pressure natriuresis is reset to higher blood pressures. Because human essential hypertension is a heterogeneous disease, it is likely that there are multiple neurohumoral and intrarenal causes of abnormal pressure natriuresis and increased blood pressure. Weight gain is recognized to be an important contributor to essential hypertension, although the mechanisms that link obesity with altered renal function and high blood pressure have not been fully elucidated. In obese dogs and humans, the shift of pressure natriuresis to higher blood pressures appears to be due mainly to increased tubular reabsorption, as glomerular filtration rate and renal plasma flow are increased compared with normal. Multiple causes of increased tubular reabsorption and hypertension in obesity have been postulated, including insulin resistance and hyperinsulinemia, activation of the sympathetic nervous and renin-angiotensin systems, and physical changes within the kidney itself. Support for the insulin resistance-hyperinsulinemia link between obesity and hypertension has been inferred mainly from acute and epidemiologic studies showing a correlation between insulin and blood pressure. Recent studies suggest that chronic hyperinsulinemia, comparable to that found in obesity, cannot account for obesity hypertension in dogs or humans. Activation of the sympathetic nervous system may play a role in obesity-induced hypertension, and there is evidence for a role of altered intrarenal physical forces caused by histological changes within the renal medulla. The quantitative importance of each of these abnormalities in altering renal function and raising blood pressure in obesity remains to be determined but is an important area of research for understanding human essential hypertension.

Animals↗
PubMed1994

Relatively low levels of dimeric inhibin circulate in men and women with polycystic ovarian syndrome using a specific two-site enzyme-linked immunosorbent assay.

The endocrine feedback role of dimeric inhibin on FSH secretion from the pituitary has been well established in many species; however, evidence that inhibin is an important endocrine regulator of FSH in the human is more tenuous. One potential explanation for the equivocal data may be that the inhibin immunoassay used most widely in the human is a heterologous assay with an antiserum that exclusively recognizes the inhibin alpha-subunit in both its monomeric form and in inhibin dimers. The aim of the present study was to quantify serum inhibin levels in a variety of fertile and infertile men and women using a new ultrasensitive enzyme-linked immunosorbent assay that is specific for the dimeric form (alpha/beta) only. The specificity of the present assay was demonstrated by the absence of significant cross-reactivity with Mullerian inhibiting substance, transforming growth factor-beta, activin, FSH, LH, hCG, TSH, and hCG alpha and with the alpha-subunit of inhibin. The assay was sensitive to 1 pg/mL, and serial dilutions of human male and female serum samples paralleled the recombinant 32-kilodalton (kDa) dimeric inhibin standard curve. Complete recovery of exogenous recombinant 32-kDa inhibin added to serum was obtained. Mean serum inhibin levels ranged from a low of 5.7 +/- 0.6 pg/mL in the early follicular phase to 49.0 +/- 11.2 pg/mL in the midluteal phase of the normal menstral cycle and were elevated during ovulation induction (1250 pg/mL) and pregnancy (500 pg/mL). Interestingly, mean levels of dimeric inhibin in women with polycystic ovarian syndrome (PCOS) were indistinguishable from normal follicular phase. The most striking observation was the extremely low mean inhibin levels (< 2 pg/mL) found in normal men, GnRH-deficient men before any pulsatile GnRH treatment, and men with Klinefelter's syndrome, all of which were indistinguishable from levels observed in postmenopausal women. These observations in the male raise the possibly that 1) some forms of circulating and bioactive inhibin in the human are not detected by this assay due to either their conformation or the presence of a unique binding protein for endogenous inhibin that does not bind to recombinant 32-kDa inhibin; or 2) dimeric inhibin is not a major endocrine regulator of FSH in the human male. In addition, the relatively high dimeric inhibin levels at midcycle and in the luteal phase of the normal menstrual cycle, after gonadotropin stimulation, and during pregnancy suggest that dimeric inhibin is predominantly produced by dominant follicles, corpora lutea, and placental tissues.

Adult↗
PubMed1994

The midcycle gonadotropin surge in normal women occurs in the face of an unchanging gonadotropin-releasing hormone pulse frequency.

The midcycle gonadotropin surge is a critical event in normal reproductive cycles and requires functional integration of the hypothalamus, pituitary, and ovary. To determine whether a change in GnRH frequency occurs coincident with the onset or termination of the surge in normal women, 20 studies were performed at a sampling interval of every 5 min for up to 36 h. The frequency of pulsatile GnRH secretion was assessed by the use of two surrogate markers of its secretion, LH and free alpha-subunit (FAS). The timing of the studies was prospectively determined by serial ultrasound and previous cycle history, whereas measurements of LH, FSH, estradiol, and progesterone in daily blood samples were used retrospectively to locate the frequent sampling study in relation to the day of ovulation in each individual. The frequent sampling studies were divided into late follicular phase (LFP; days -4 to -2) and early, mid-, and late portions of the midcycle surge (days -1 to 1) in relation to the 95% confidence limits of the LH peak derived from daily samples in 69 normal ovulatory women. The patterns of LH and FAS secretion were pulsatile at all times during the midcycle surge. The amplitude of LH pulsations increased from the LFP and early surge to the midportion of the midcycle surge (5.9 +/- 6 and 15.1 +/- 5 vs. 39.0 +/- 3 IU/L; P < 0.0001) and decreased from the mid- to the late portion of the surge (13.4 +/- 5 IU/L; P < 0.0001). Likewise, the amplitude of FAS pulse increased from the LFP and early surge to the midportion of the surge (82.4 +/- 59 and 153.1 +/- 50 vs. 421.4 +/- 35 ng/L; P < 0.0001) and decreased from the mid- to the late portion of the surge (190.8 +/- 49 ng/L; P < 0.0002). Although there was excellent concordance of pulsatile secretion of LH and FAS, significantly more pulses of FAS were detected than of LH (P < 0.0001). There was no change in frequency (expressed as interpulse interval) between the LFP and the early and midportions of the surge for LH (70.0 +/- 8, 67.5 +/- 7, and 65 +/- 5 min, respectively) or FAS (55.1 +/- 7, 54.6 +/- 6, and 60.0 +/- 4 min). However, there was an increase in LH interpulse interval (decrease in pulse frequency) in the late portion of the surge (87.0 +/- 6 min) compared to the early and midportions of the surge (P < 0.02 and P < 0.0005, respectively).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1994

Potential for fertility with replacement of hypothalamic gonadotropin-releasing hormone in long term female survivors of cranial tumors.

Dysfunction of the hypothalamic-pituitary axis presenting as hypogonadotropic amenorrhea is a common sequelae of treatment for cranial tumors with surgery and/or radiation. We hypothesized that the site of the defect in this condition is hypothalamic, rather than pituitary, in the majority of patients. Nine women with acquired hypogonadotropic hypogonadism after treatment with transphenoidal pituitary surgery (n = 3), transphenoidal surgery plus conventional radiotherapy (XRT; n = 1), hypothalamic surgery plus XRT (n = 2), or XRT with or without noncentral nervous system surgery (n = 3) underwent assessment of endogenous pulsatile LH secretion and a standard GnRH test followed by iv administration of a physiological replacement regimen of exogenous GnRH. A total of 25 cycles were completed at doses of 75 or 100 ng/kg.bolus. Ovulation occurred in 78% of patients, with all ovulatory patients who desired fertility becoming pregnant. The hormonal responses in these cycles did not differ from the patterns of sex steroids and gonadotropins in normal women. The response to pulsatile GnRH was not influenced by GH deficiency or PRL abnormalities. Of the two patients who failed to ovulate, there was no evidence of folliculogenesis in one, whereas the second consistently developed follicles, but proved incapable of mounting a LH surge despite adequate preovulatory estradiol levels. Both patients had a history of pituitary radiation and surgery. There was no consistent relationship between the results of GnRH testing and the pattern of pulsatile LH secretion. However, the only patient who failed to achieve folliculogenesis was the only patient without a FSH response to GnRH testing and an apulsatile baseline study. Hypothalamic GnRH deficiency is the etiology of hypogonadism in the majority of patients after treatment with hypothalamic or pituitary surgery or cranial irradiation. Therefore, exogenous pulsatile GnRH represents a physiological replacement therapy that completely restores normal gonadotropin dynamics, resulting in ovulation and fertility.

Adolescent↗
PubMed1993

The accumulation of pentamidine and the toxic effects of the drug, its selected analogues and metabolites on isolated alveolar cells.

Radiolabelled [3H]pentamidine is accumulated into 48-h and 7-day cultures of alveolar epithelial type 2 cells and alveolar macrophages in a linear, time and dose-dependent manner, with the rate of uptake being 15.3, 13.4 and 17.9 pmol/micrograms protein per 30 min, respectively. Uptake was not affected by metabolic inhibitors. The differential toxicity of the parent drug pentamidine, five analogues and six metabolites was assessed on freshly isolated and type 2 cells maintained in culture over 24 h. Toxicity, determined by the attachment ability of alkaline phosphatase positive cells containing lamellar bodies was greater in freshly isolated cells. Overall, three/four of the analogues proved less damaging to type 2 cells than the pentamidine with one derivative [1,3-bis(4-amidino-2-methoxy)propane], a compound particularly efficacious against pneumocystis in rats, showing minimal toxicity. Five metabolites (chain hydroxylated derivatives) were less toxic than the parent drug. However, one metabolite (N,N-dihydroxy derivative) was much more toxic than pentamidine to both type 2 cells and alveolar macrophages. It is concluded that as the type 2 cell can accumulate the drug, it represents a target cell which is particularly sensitive to pentamidine and/or some of its metabolites.

Alkaline Phosphatase↗
PubMed1993

A statistical comparison between natural history of idiopathic scoliosis and brace treatment in skeletally immature adolescent girls.

Thirty-two adolescent girls braced for late onset idiopathic scoliosis at Children's Hospital, Boston were compared with thirty-two untreated girls from Our Lady's Hospital for Sick Children, Dublin, Ireland paired on the basis of curve size and site and age at diagnosis. All were Risser 0 at diagnosis. Study period for the braced group was from brace initiation to part-time brace wearing and, for the controls, from diagnosis to last review. There was no statistically significant difference between the groups on any parameter of curve progression. This study raises questions about the efficacy of spinal orthoses in modifying the natural history of late-onset idiopathic scoliosis and removes the ethical problems inherent in a prospective trial in which the only treatment permitted to the control group is surgery.

Adolescent↗
PubMed1993

An overview of the diagnostic considerations in polycystic ovarian syndrome.

The past ten years have been particularly exciting with regard to the elucidation of the pathophysiology of PCOS. It appears that PCOS is about to yield some of its mysteries and to have some of its discrete subsets defined, as Cushing syndrome did 50 years ago. However, future studies of PCOS will require a complex interplay of clinical investigation, molecular and genetic probes, increasingly refined anatomic observations, and fundamental neuroendocrine studies. Each observer has a bias, which must be acknowledged in his/her studies. However, a true synthesis of the abnormalities characteristic of PCOS must continually be sought, for only through a comprehensive view of this syndrome will we come to understand its true pathophysiology; and only then can rational therapies be designed.

Androgens↗
PubMed1993

Activity of cationically substituted bis-benzimidazoles against experimental Pneumocystis carinii pneumonia.

On the basis of a previously observed correlation between the antimicrobial activity and DNA binding strength of dicationic molecules, a series of 10 dicationically substituted bis-benzimidazoles were tested for activity in the rat model of Pneumocystis carinii pneumonia. One of the compounds, 1,4-bis[5-(2-imidazolinyl)-2-benzimidazolyl]butane, was found to be more potent and less toxic than pentamidine.

Animals↗
PubMed1993

A unique, predominant hepatitis C virus variant found in an infant born to a mother with multiple variants.

To demonstrate vertical transmission of hepatitis C virus (HCV) from an HCV-infected, non-human immunodeficiency virus type 1-infected mother to her infant and to assess the distribution of viral species in the mother and infant, the hypervariable region of the gene encoding the putative envelope glycoprotein E2 (E2HV) was sequenced in three mothers and one mother-infant pair. The data indicate that (i) quasi-species distributions of HCV E2HV variants were found in all four mothers, (ii) a single predominant HCV E2HV variant was found in the infant of a mother shown to have nine predominant E2HV variants, and (iii) the infant's E2HV variant was highly related to, but not identical with, the nine variants identified in the mother at the time of birth. These findings indicate that HCV is transmitted from mother to infant and raise the possibility that the transmission occurs in utero.

Amino Acid Sequence↗
PubMed1993

Chronic angiotensin-converting-enzyme inhibition improves cardiac output and fluid balance during heart failure.

The purpose of this study was to examine the sequential changes in renal and cardiovascular function produced by chronic Benazepril administration at different stages of heart failure in dogs. Heart failure was produced by rapid ventricular pacing in five dogs with a normally functioning renin-angiotensin system (angiotensin normal, AN) and six dogs chronically administered the angiotensin-converting-enzyme inhibitor (ACEI) Benazepril. After 7 days of pacing, cardiac output was significantly higher and total peripheral resistance (TPR) lower in the ACEI compared with the AN dogs. Cumulative sodium and water balance increased significantly in both groups, but after 7 days of pacing there were no significant differences between groups. However, the rate of increase in sodium and water balance was significantly less in the ACEI group. Effective renal plasma flow decreased in the AN and ACEI groups during pacing, but there were no between-group differences, and no significant changes in glomerular filtration rate (GFR) occurred in either group. In the AN dogs, pacing was continued for 7-21 days until the onset of decompensated heart failure. Urinary sodium excretion increased on the first day of ACEI infusion during this stage but returned to pre-ACEI levels during the next 2-3 days. No significant improvement in cardiac output was measured during ACEI in decompensated heart failure. These data suggest that chronic ACEI administration can improve renal and cardiac function in early heart failure without impairing GFR but is less chronic ACEI administration can improve renal and cardiac function in early heart failure without impairing GFR but is less effective in later, decompensated stages.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Role of pressure natriuresis in long-term control of renal electrolyte excretion.

If pressure natriuresis is to play an important role in arterial pressure control, renal perfusion pressure must have a long-term effect on urinary sodium excretion. The aim of this study was to quantitate the importance of renal perfusion pressure per se in controlling renal hemodynamics and electrolyte excretion chronically. Female mongrel dogs (n = 6) were instrumented with bilateral renal artery catheters for measurement of renal perfusion pressure and occluders on both renal arteries for servo-control of renal perfusion pressure at different levels; the urinary bladder was split for determination of renal clearances and electrolyte excretion from each kidney separately. Because both kidneys were exposed to the same neurohumoral influences, any changes in renal function could be attributed to differences in renal perfusion pressure between the two kidneys. After 5 days of control, renal perfusion pressure to one kidney was reduced from 86.7 +/- 0.2 to 74.2 +/- 0.6 mm Hg for 12 days, and pressure in the contralateral kidney increased to 91.5 +/- 0.4 mm Hg. Sodium excretion decreased from 41 +/- 2 to 25 +/- 1 mmol/d in the servo-controlled kidney and increased from 41 +/- 1 to 55 +/- 1 mmol/d in the contralateral kidney during 12 days of servo-control. Urine volume, chloride excretion, and potassium excretion exhibited similar patterns during servo-control. In addition, autoregulation of effective renal plasma flow and glomerular filtration rate was relatively well maintained; however, in the low-pressure kidney, glomerular filtration rate was slightly but significantly lower (approximately 8%) than in the contralateral kidney.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗