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Biomedical subjects

J E Hall

Publications and source records attributed to J E Hall.

At least 163 records · Page 9Linked to original sources
PubMed1997

Protrusio acetabuli and bilateral basicervical femoral neck fractures in a patient with Marfan syndrome.

A 22-year-old man with Marfan syndrome and bilateral protrusio acetabuli presented with bilateral femoral neck stress fractures after vigorous stretching exercises for hip "stiffness." Fifteen years later, his fractures, which were treated with internal fixation, have healed, his acetabular protrusion has not worsened, and his perceived hip "stiffness" persists. This case demonstrates a rare manifestation of Marfan syndrome, protrusio acetabuli, and a possible side effect of vigorous stretching in the face of abnormal joint mechanics.

Acetabulum↗
PubMed1996

Targeting the minor groove of DNA: crystal structures of two complexes between furan derivatives of berenil and the DNA dodecamer d(CGCGAATTCGCG)2.

Crystal structures are reported of complexes of two novel furan derivatives of berenil with alkyl benzamidine groups bound to the DNA sequence d(CGCGAATTCGCG)2. They have both been determined to 2.2 A resolution and refined to R factors of 16.9% and 18.6%. In both structures the alkyl substituents, cyclopropyl and isopropyl, are found to be orientated away from the floor of the minor groove. The drugs are located in the minor groove by two strong amidinium hydrogen bonds, to the O2 of the thymines situated at the 5' and 3' ends of the AT-rich region. The isopropyl-substituted derivative has a tight hydrogen-bonded water network in the minor groove at one amidine site, which alters the orientation of the isopropyl substituent. This compound has superior DNA-binding properties and activity against Pneumocystis carinii and Cryptosporidium parvum infections in vivo compared to the cyclopropyl derivative, which in turn is superior to the parent furan compound. We suggest that the nature and extent of the interactions of these compounds in the DNA minor groove play an important role in these activities, possibly in conjunction with a DNA-binding protein. The overall effect of these alkyl benzamidine substitutions is to increase the binding of the drugs to the minor groove.

Crystallography, X-Ray↗
PubMed1996

Junctional permeability measurements in the embryonic chick lens.

The purpose of this paper is two-fold: to measure junctional permeability of different types of dissociated lens cells and to compare the junctional permeability of dissociated lens cells to that of cells in the intact lens. Dissociated embryonic chick lens cells and intact embryonic chick lenses were loaded with the fluorescent dye 5,6 carboxyfluorescein diacetate. The return of fluorescence after bleaching an individual cell was used to estimate cell-to-cell permeability. Use of the confocal microscope facilitated quantitation of the return of fluorescence as well as optical sectioning needed to measure cell-to-cell permeability in an intact lens. Two types of dissociated cells were studied: spherical and short elongated cells. The average rate constant for 5,6 carboxyfluorescein transfer between these cells was 7.9 x 10(-3) sec-1 and 8.1 x 10(-3) sec-1, respectively. The junctional permeability for both types of cells was reduced by lowering internal pH to 6.0 by bathing the cells in a sodium acetate solution. Permeability measurements of the central epithelial cells of an isolated whole lens gave an average rate constant of 2.6 x 10(-3) sec-1, comparable to the rates measured in the dissociated cells. These results establish that the photobleach method can be used in intact lens to quantitatively assess junctional permeability and that dissociated epithelial cells have very nearly the same junctional permeabilities as cells in the intact lens.

Animals↗
PubMed1996

Chronic adrenergic receptor blockade does not prevent hyperinsulinemia-induced hypertension in rats.

Increased adrenergic activity has been suggested to mediate the hypertension associated with hyperinsulinemia. This study tested whether combined alpha1- and beta-adrenergic receptor blockade would prevent insulin-induced hypertension when euglycemia was maintained by continuous intravenous glucose infusion. Sprague-Dawley rats (n = 16) were instrumented with artery and vein catheters and placed in metabolic cages. Propranolol and prazosin (10 mg/kg/day each) were infused continuously intravenously in 9 rats and 7 other rats received vehicle. Mean arterial pressure (MAP) and heart rate (HR) were measured 24 h per day using computerized methods. After a control period, a 7-day intravenous infusion of insulin (1.5 microU/kg/min) was begun and glucose was coadministered intravenously at 23 mg/kg/min to prevent hypoglycemia. The MAP averaged 93 +/- 1 mm Hg in the blockade rats during the control period, which was significantly lower than the 98 +/- 1 mm Hg in the normal rats. During insulin infusion, MAP increased similarly in both groups, with a 10 +/- 2 mm Hg and 11 +/- 1 mm Hg increase in normal and blockade rats, respectively, by day 7. The HR also increased in both groups: from 417 +/- 8 beats/ min to 426 +/- 13 beats/min (P = NS) in normal rats and from 379 +/- 10 beats/min to 419 +/- 10 beats/min (P < .05) in blockade rats. Control sodium excretion averaged 2.5 +/- 0.1 mEq/day in both groups and no significant change in sodium balance was measured in either group. All variables returned toward control after stopping insulin. These results suggest that increased adrenergic activity is not required for chronic hyperinsulinemia to raise blood pressure in rats.

Adrenergic alpha-Antagonists↗
PubMed1996

Evaluation of photoscreener instruments in a childhood population. 1. Otago photoscreener and Dortmans videophotorefractor.

OBJECTIVE: To evaluate two photoscreeners in a childhood population. STUDY DESIGN: Double-masked study. SUBJECTS AND METHOD: One hundred and thirteen children aged between 11 and 44 months with either normal vision or known visual disorders were photoscreened without cycloplegia by the Otago and Dortmans (prototype) photoscreeners. Each child had a full ophthalmological examination either on the day of screening or in the proceeding six months. Photoscreen images were reviewed by an independent observer for indicators of amblyopiogenic risk factors, and compared to the full ophthalmological examination to determine sensitivity and specificity for each instrument. RESULTS: The Otago photoscreener returned a sensitivity of 70% and specificity of 82% for the detection of amblyopiogenic risk factors. The Dortmans photoscreener returned a sensitivity of 70% and specificity of 90%. Both photoscreeners were portable and easily operated. CONCLUSION: Children can be screened successfully for amblyopiogenic risk factors with these photoscreening systems. Further evaluation is required to determine specificity in a normal population. This would also provide information on the potential usefulness of photoscreeners in a cost effective childhood vision screening program.

Amblyopia↗
PubMed1996

Graphic analysis for the study of metabolic states.

Graphic analyses have been used in the study of physiology as a means to better understand dynamic processes and to visualize the mechanisms of their interactions. A graphic analysis of glucose homeostasis was constructed by considering the main factors that influence glucose dynamics. The analysis is achieved by equating curves representing both the inflow and outflow of glucose from the circulation as dependent upon the serum insulin concentration. The point where these two curves intersect is the steady-state balance for blood glucose exchange and is termed the equilibrium point. With the use of this graphic depiction of glucose homeostasis, it is now possible to study the influence of multiple factors on glucose dynamics. A variety of metabolic states can also be analyzed by reconstructing the effects of the pathophysiology on the form and shape of the curves. Some of the metabolic states that have been analyzed by this technique include starvation, exercise, obesity, type I and type II diabetes mellitus, stress, hypopituitarism, hyperpituitarism, and hyperthyroidism. Although the analyses do not reflect all of the controversial nuances of the field, they do provide a means for a general approach to the study of glucose homeostasis and serve as a methodology that can be extrapolated to many areas of physiological study.

Audiovisual Aids↗
PubMed1996

Cardiac output and renal function during insulin hypertension in Sprague-Dawley rats.

Hyperinsulinemia has been reported to cause hypertension in rats; however, the renal and hemodynamic mechanisms are not known. In this study, changes in renal function, cardiac output (CO), and total peripheral resistance (TPR) were measured during chronic insulin infusion in eight rats (approximately 350 g). After a 4-day control period, a 7-day insulin infusion was begun (1.5 mU.kg-1.min-1 iv), together with glucose (22 mg.kg-1.min-1 iv) to prevent hypoglycemia. Mean arterial pressure (MAP), CO, TPR, and heart rate were measured 24 h/day. MAP increased from 92 +/- 1 to 100 +/- 2 mmHg on day 1 and was 108 +/- 4 mmHg by day 7 of insulin. CO tended to decrease during insulin infusion, although not significantly, averaging 94 +/- 4% of the control value of 121 +/- 7 ml/min. Heart rate did not change significantly from the control value of 384 +/- 8 beats/min. TPR increased significantly to 122 +/- 11% of control by day 7. In five rats, glomerular filtration rate and effective renal plasma flow decreased to 73 +/- 4 and 66 +/- 5% of control, respectively, during insulin. Urinary sodium excretion averaged 2.6 +/- 0.1 and 2.7 +/- 0.1 meq/day during the control and insulin-infusion periods, respectively. These results indicate that insulin hypertension in rats is initiated by an increase in TPR rather than by increased CO. Also, the fact that sodium balance was maintained at elevated arterial pressure suggests that the ability of the kidneys to excrete sodium was impaired chronically during insulin infusion.

Animals↗
PubMed1996

Hypertension in obese Zucker rats. Role of angiotensin II and adrenergic activity.

We designed our studies to determine whether blood pressure is elevated in obese Zucker rats compared with lean control rats and to test the importance of the renin-angiotensin and adrenergic nervous systems in long-term blood pressure control in this genetic model of obesity. We monitored mean arterial pressure 24 hours per day using computerized methods in 13- to 14-week-old lean and obese Zucker rats maintained on a fixed, normal sodium intake (3.3 mmol/d). Mean arterial pressure (average of 5 days) was higher in obese (100 +/- 1 mm Hg) than in lean (86 +/- 1) rats. Although control plasma renin activity was lower in obese than in lean rats (3.66 +/- 0.15 versus 5.48 +/- 0.11 ng angiotensin I/mL per hour), blood pressure sensitivity to exogenous angiotensin II was greater in obese than in lean rats. Blockade of endogenous angiotensin II receptors with losartan (10 mg/kg per day) for 7 days also caused a greater decrease in blood pressure in obese (36 +/- 2 mm Hg, n = 6) than in lean (25 +/- 1, n = 5) rats. However, combined alpha- and beta-adrenergic blockade with terazosin (10 mg/kg per day) and propranolol (10 mg/kg per day), respectively, for 8 days caused only modest decreases in blood pressure in obese (9 +/- 3 mm Hg, n = 8) and lean (4 +/- 2, n = 6) rats, despite effective alpha- and beta-adrenergic blockade. These results suggest that increased arterial pressure in obese Zucker rats depends in part on angiotensin II. However, additional mechanisms may also contribute to increased blood pressure in obese Zucker rats.

Adrenergic alpha-Antagonists↗
PubMed1996

Ovarian 17-hydroxyprogesterone hyperresponsiveness to gonadotropin-releasing hormone (GnRH) agonist challenge in women with polycystic ovary syndrome is not mediated by luteinizing hormone hypersecretion: evidence from GnRH agonist and human chorionic gonadotropin stimulation testing.

Women with polycystic ovary syndrome (PCOS: hyperandrogenism and oligomenorrhea) have been shown to have exaggerated ovarian 17-hydroxyprogesterone (17-OHP) responses after GnRH agonist stimulation, suggestive of disordered ovarian cytochrome P450c17 alpha activity. However, most hyperandrogenic women also have an exaggerated LH response to both native GnRH and GnRH agonists. To assess whether the known LH hyperresponsiveness in PCOS patients mediates their exaggerated 17-OHP response to GnRH agonist challenge or whether the 17-OHP response can be duplicated by direct stimulation of the ovary with a fixed amount of hCG, 25 PCOS women [age, 20.6 +/- 1.1 yr; body mass index (BMI), 24.9 +/- 1.3 kg/m2] and 5 controls (age, 29.4 +/- 2.3 yr; BMI, 29.2 +/- 3.0) underwent both GnRH agonist (leuprolide acetate) and hCG testing. In addition, 23 normal women (age, 26.5 +/- 1.5 yr; BMI, 27.2 +/- 1.7 kg/m2) underwent hCG testing, and 21 other normal women (age, 19.3 +/- 0.5 yr; BMI, 23.0 +/- 0.8 kg/m2) underwent leuprolide acetate challenge. Blood was sampled before and 24 h after (the previously determined time of the peak response) leuprolide acetate (500 micrograms, sc) and hCG (5000 IU, im) stimulation tests. The tests were administered during the early follicular phase in women who were ovulatory and in randomized order in the subjects receiving both stimuli. Peak serum 17-OHP levels did not differ between leuprolide acetate or hCG stimulation in PCOS patients or controls when measured at 24 h (324.9 +/- 41.9 vs. 360.4 +/- 54.0 in PCOS; 183.2 +/- 19.6 vs. 141.2 +/- 11 ng/dL in controls). Peak 17-OHP levels after hCG challenge and GnRH agonist stimulation were highly correlated (r = 0.82; P < 0.001) in the subjects receiving both stimuli. Although leuprolide acetate elicited a higher estradiol (E2) response than hCG in all subjects, serum E2 levels increased significantly after hCG treatment in both patients and controls (P < 0.001 and P < 0.0001). The small, but significant, increase in serum E2 after hCG stimulation suggests that a rigid two-cell model of ovarian steroidogenesis may be an oversimplification of in vivo physiology. Our results suggest that exaggerated 17-OHP responses to GnRH agonist stimulation in hyperandrogenic women are not mediated by the known hyperresponsiveness of LH in these patients, but are due to increased ovarian androgen sensitivity to LH stimulation.

17-alpha-Hydroxyprogesterone↗
PubMed1996

Homologous in vitro bioassay for follicle-stimulating hormone (FSH) reveals increased FSH biological signal during the mid- to late luteal phase of the human menstrual cycle.

Monitoring of the secretory dynamics of FSH during the human menstrual cycle has demonstrated conflicting results between the amounts of FSH measured by dimer-specific immunoassays and previous heterologous in vitro bioassays. These differences suggest somewhat different models of the steroidal and nonsteroidal regulation of FSH secretion and its control of folliculogenesis in the human. We have developed a homologous in vitro bioassay, using the recombinant human FSH receptor cotransfected into Chinese hamster ovary cells with a cAMP-responsive luciferase reporter gene, that overcomes many of the theoretic shortfalls of previous assays and allows reevaluation of the changes in bioactive FSH across the menstrual cycle. Bioactive FSH levels measured across 12 menstrual cycles in 11 normal women ranged from 4-40 IU/L. FSH bioactivity was constant during the menstrual cycle, with elevations noted only during the mid- to late luteal phase. Bioactive FSH levels were similar to immunoactive FSH levels across the cycle as indicated by a ratio of bioactive to immunoreactive FSH (FSH B/I) of 1.10 +/- 0.04 across the follicular and early luteal phases. However, during the mid- to late luteal phase, the mean FSH B/I rose to 1.65 +/- 0.07, which significantly exceeded that during the rest of the cycle (P < 0.001). This change in FSH B/I occurs at a critical time during folliculogenesis when the next cohort of follicles is being recruited and appears to be secondary to a decrease in immunoreactive FSH unaccompanied by a similar decrease in in vitro bioactivity. There was good agreement between immunoassay and bioassay results on the day of the midcycle gonadotropin surge (FSH B/I = 1.07 +/- 0.14), which was not different from that in the follicular phase (days -17 to -2; FSH B/I = 1.06 +/- 0.05) or the FSH B/I measured in postmenopausal women (0.93 +/- 0.2). These observations using a novel homologous human FSH in vitro bioassay indicate that bioactive FSH levels are not declining during the time of active corpus luteum formation and secretory activity. Thus, there is a previously undetected increased biologic signal during the mid- to late luteal phase, suggesting that the influence of elevated FSH on the cohort of developing follicles (including the subsequent dominant follicle) begins earlier during the luteal-follicular transition than previously predicted by FSH immunoreactivity.

Adult↗
PubMed1996

Chronic Monteggia lesions in children. Complications and results of reconstruction.

We retrospectively reviewed the results of operative treatment of chronic Monteggia lesions (Bado type I or the equivalent) with anterior radiocapitellar dislocation in seven patients. The mean age at the time of the reconstruction was six years and nine months (range, eleven months to twelve years), and the mean time from the injury to the operation was twelve months (range, five weeks to thirty-nine months). The mean duration of follow-up was four years and six months (range, two years to eleven years and three months). There were fourteen complications, including malunion of the ulnar shaft in one patient; residual radiocapitellar subluxation in two patients (one anterior and one posterolateral); radiocapitellar dislocation (dynamic anterior subluxation of the radial head in supination) in one patient; transient ulnar-nerve palsy in three patients (with residual weakness in two); partial laceration of the radial nerve in one patient; loss of the fixation in two patients; and non-union of the ulnar osteotomy site, compartment syndrome, conversion reaction, and possible fibrous synostosis of the forearm in one patient each. The patients lost a mean of 36 degrees of pronation and a mean of 27 degrees of supination of the forearm compared with the contralateral, uninjured extremity. Two patients demonstrated a loss of flexion of the elbow of 8 and 13 degrees and three had a loss of extension (mean, 15 degrees) compared with the contralateral side. There were three good, two fair, and two poor results.

Age Factors↗
PubMed1996

Pressure-volume regulation in hypertension.

In all forms of hypertension, including human essential hypertension, pressure natriuresis is abnormal because sodium excretion is the same as in normotension despite increased arterial pressure. Considerable evidence indicates that this resetting of pressure natriuresis plays a key role in causing hypertension, rather than merely occurring as an adaptation to increased blood pressure. Because human essential hypertension is a heterogeneous disease, it is likely that multiple neurohumoral and intrarenal defects contribute to abnormal pressure natriuresis and increased blood pressure. Physiological studies have shown that renal abnormalities that cause increased distal and collecting tubule reabsorption, decreased glomerular filtration coefficient or loss of nephrons also cause decreased slope of pressure natriuresis (salt-sensitive hypertension), whereas increased preglomerular resistance causes a parallel shift of pressure natriuresis (salt-insensitive hypertension). Comparison of the characteristics of pressure natriuresis (such as salt-sensitivity of blood pressure) in hypertensive subjects with those forms of experimental hypertension of known origin can provide insight into the etiology of human hypertension. With long-standing hypertension, pathological changes in the glomeruli and renal arterioles may further shift pressure natriuresis and exacerbate hypertension.

Animals↗
PubMed1996

Central role of the kidney and abnormal fluid volume control in hypertension.

In human essential hypertension, and in all forms of experimental hypertension studied thus far, volume regulation and the relationship between blood pressure (BP) and sodium excretion (pressure natriuresis) are abnormal. Considerable evidence indicates that resetting of pressure natriuresis plays a key role in causing hypertension, rather than merely occurring as a consequence of increased BP. In patients with essential hypertension, resetting of pressure natriuresis is characterized either by a parallel shift to higher BPs and salt-insensitive hypertension, or by a decreased slope of pressure natriuresis and salt-sensitive hypertension. This clearly indicates that essential hypertension cannot be ascribed to a single abnormality of kidney function. Multiple physiological studies have shown that salt-sensitive hypertension can be elicited by renal abnormalities that cause either loss of functional kidney mass or an inability to modulate the renin-angiotensin-aldosterone (RAA) system appropriately; these abnormalities include loss of functional nephrons, decreased glomerular capillary filtration coefficient, patchy renal ischemia, and increased distal and collecting tubular reabsorption. Renal abnormalities that cause salt-insensitive hypertension are characterized by normal functional kidney mass, and the ability to appropriately modulate the renin-angiotensin system during changes in sodium intake; important causes of salt-insensitive hypertension include widespread increases in preglomerular resistance and increased reabsorption in the proximal tubules and loops of Henle. By comparing the characteristics of pressure natriuresis in essential hypertensive subjects with those found in experimental hypertension of known origin, we can gain considerable insight into the etiology of human hypertension.

Blood Pressure↗
PubMed1995

Spatial organization of cardiac gap junctions can affect access resistance.

In the heart, gap junctions electrically couple myocytes together. Electron- and light-microscope-based analyses have revealed that cardiac gap junctions show a variety of organizational patterns. At the level of gap-junctional channel aggregates, freeze fracture has demonstrated diverse channel packing arrangements in the membranes of different myocardial tissues. Ultrastructural and immunohistochemical studies have shown variation and specialization in the 3-dimensional spatial distribution of gap junctional contacts between different types of myocardial cells. Here, we estimate the access resistance of various configurations of gap junctions using physical principles and explore how certain of these specializations in gap-junctional organization may influence access resistance, a potentially important determinant of electrical conductance between coupled myocardial cells.

Animals↗