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Biomedical subjects

N Levin

Publications and source records attributed to N Levin.

At least 73 records · Page 4Linked to original sources

Gunshot residue particles formed by using ammunitions that have mercury fulminate based primers.

Ammunition having mercury fulminate-based primers are commonly manufactured by Eastern Bloc countries and used extensively in the Middle East. Gunshot residue (GSR) particles formed by firing these types of ammunition were examined. It was observed that much lower percentage of mercury-containing GSR particles were found in samples taken from a shooter as compared to the percentage of such particles in samples from cartridge cases. This fact must therefore be taken into account when interpreting case results. A plausible explanation for the results described is proposed.

Cyanates↗

Regulation of basal ACTH secretion by corticosterone is mediated by both type I (MR) and type II (GR) receptors in rat brain.

The mechanisms involved in the physiology of the secretion of ACTH are reviewed. The secretion is regulated by the biological consequences of the occupancy of high affinity mineralocorticoid (MR) and lower affinity glucocorticoid receptors (GR) for corticosterone at specific sites of the rat brain. The regulation by this mechanism of basal secretion during the circadian rhythm, the effect of adrenalectomy and of corticosterone replacement is discussed. Experiments with RU486, a specific glucocorticoid antagonist, suggest that occupancy of both MR and GR is required for normal control of ACTH at the time of peak activity. The occupancy of the GR for a few hours per day apparently suffices to maintain steady levels of the products of GR-responsive genes throughout the body.

Adrenal Glands↗

Lumbar nerve root compression and interstitial cystitis--response to decompressive surgery.

An identifiable lumbar nerve root compression appears to cause urological dysfunction consistent with interstitial cystitis. Ten patients (9 females, 1 male) were evaluated for chronic pelvic pain. Cystoscopic and histological appearances were consistent with a diagnosis of interstitial cystitis. Magnetic resonance studies of the lower spine consistently demonstrated a lateral compression of the L5 dorsal nerve root. Decompression of the lateral foramina of L5 resulted in immediate relief of pain in 9 patients, who have been followed up for 6 months without a recurrence. Possible mechanisms involving sympathetic dystrophy of the pelvic plexus are reviewed.

Cystitis↗

Kinetics and quality assurance: prescription therapy through kinetic modeling.

With recent startling statistics showing an increase in mortality risk of dialysis patients in the United States compared to other countries, managers and practitioners have been motivated to carefully examine not only the dialysis prescription, but what is actually delivered to the patient. In October 1990, prior to ANNA's Clinical Concerns in Nephrology meetings in Cincinatti and San Antonio, attendants were invited to participate in an education session examining the monitoring and evaluation of prescription therapy for peritoneal and hemodialysis. The title of the session was "The Nurse's Role in Prescription Therapy--What Does it Really Mean?" The sponsor was Fresenius USA, Inc. This educational offering gave the nephrology nurse the opportunity to learn how to manage the delivery of care based on the theory of kinetic modeling for peritoneal and hemodialysis therapy. Quality assurance indicators, data collection tools, and the latest technology were described for the monitoring and evaluation of the adequacy of therapy. The following article is adopted from the original transcripts of the five-member panel of experts who participated in the session. We appreciate the willingness of the speakers to share this timely and important material with the ANNA Journal readers.

Data Collection↗

Pentoxifylline improves pulmonary gas exchange.

Pentoxifylline is a xanthine derivative with hemorrheologic and vascular properties that may improve gas exchange in patients with chronic obstructive pulmonary disease (COPD). We tested this hypothesis in 12 patients with COPD (mean FEV1 = 40 percent predicted; mean DCO, 8.6 ml/min/mm Hg) randomly divided into a treatment and control group and six healthy volunteers. Following establishment of baseline DCO and maximum expiratory flow volume (MEFV) curve values, each subject in the treatment and healthy groups took 400 mg of pentoxifylline three times a day for 12 weeks. Weekly DCO and MEFV curves were measured before treadmill exercise in both COPD groups and before and after exercise in the healthy group. The MEFV curve parameters from the final three weeks of therapy did not differ significantly from baseline values. During this time, however, the treatment COPD group's resting DCO rose by 8.2 +/- 2.4 percent over baseline level (p less than 0.01). Treadmill walk time increased from 17.7 +/- 2.9 minutes to 23.2 +/- 2.9 minutes (p less than 0.02). This was accompanied by improved exercise oxygen saturation measured by oximetry (SoxiO2). Premedication SoxiO2 fell from 92.8 +/- 1.2 percent to 88.6 +/- 2.5 percent during exercise, and from 94.4 +/- 1.1 percent to only 91.8 +/- 1.0 percent after 12 weeks of medication (p less than 0.05). No such improvement was noted in the control COPD group. Although the healthy group's resting SoxiO2 and DCO did not change during treatment, their exercise DCO increased significantly from 36.3 +/- 3.1 ml/min/mm Hg to 41.8 +/- 3.5 ml/min/mm Hg (p less than 0.001). These data demonstrate that pentoxifylline improves gas exchange, possibly by increasing cardiac output, and/or by raising mixed venous PO2, and/or by improving blood flow to underperfused alveoli.

Adult↗

Aortic arch anomaly presenting as exercise-induced asthma.

We present the case of a young woman with a right aortic arch who first became symptomatic when she began a vigorous exercise program. Her symptoms were very suggestive of exercise-induced bronchospasm. Her flow-volume curves, however, showed evidence of variable intrathoracic large airways obstruction. A magnetic resonance imaging scan confirmed the presence of severe tracheal narrowing caused by her right aortic arch.

Adult↗

Pharmacological evidence that the inhibition of diurnal adrenocorticotropin secretion by corticosteroids is mediated via type I corticosterone-preferring receptors.

These studies were performed to determine pharmacologically the corticosteroid receptor type that mediates the effects of corticosterone (B) on ACTH secretion in adrenalectomized rats. We have compared the effects of treating young male rats at the time of adrenalectomy and throughout the next 5 days with B, dexamethasone (DEX), or aldosterone (ALDO) in doses that elevated plasma levels to concentrations in the range between 0.2-30 nM. Plasma ACTH, corticosteroid-binding globulin (CBG), and thymus weight were measured in the morning or evening, and these steroid-sensitive end points were related to the circulating concentrations of B (total B - CBG-bound B), total DEX, and total ALDO. For the inhibition of ACTH the rank order of potency of the three steroids was B greater than DEX greater than or equal to ALDO in the morning (estimated IC50, 0.7 +/- 0.1, 2.3 +/- 0.5, and 4.9 +/- 1.6 nM for B, DEX, and ALDO, respectively). There was a significant shift to the right in steroid efficacy between morning and evening (estimated IC50 in the evening, 3.9 +/- 0.2 and 9.3 +/- 0.8 nM for B and DEX; ALDO at the concentrations achieved was ineffective). The rightward shift in efficacy may result from the circadian increase in drive to ACTH secretion. The rank order of potency for B and DEX on ACTH and the agreement between the steady state IC50 values achieved for these steroids and the Kd values determined for B and DEX with type I receptors in vitro strongly suggest that feedback control of basal diurnal ACTH by corticosteroids is mediated by association with type I, B-preferring receptors. By contrast, DEX was 3 times more potent than B on CBG (estimated IC50, 1.5 and 4.5 nM, respectively) and tended to be more effective on thymus weight, suggesting that the effects of corticosteroids on these peripheral targets are mediated by association of the steroids with type II glucocorticoid receptors. ALDO coinfused with DEX or B did not alter the inhibitory effects of these on ACTH, suggesting that ALDO does not interfere with these type I, B-preferring receptors in vivo. Because there is little if any evidence for type I corticosteroid receptors in the hypothalamus, these results strongly suggest that the majority of corticosteroid feedback inhibition of basal morning and evening ACTH secretion is mediated transynaptically by the activity of extra-hypothalamic neurons.

Adrenalectomy↗

Modulation of basal and corticotropin-releasing factor-stimulated proopiomelanocortin gene expression by vasopressin in rat anterior pituitary.

In several anterior pituitary hormone systems, factors that stimulate hormone release also stimulate hormone biosynthesis. In the corticotropes of the anterior pituitary, CRF stimulates ACTH release as well as cAMP accumulation and transcription of the POMC gene. Arginine vasopressin (AVP) is a well documented coregulator of ACTH release and potentiates CRF-stimulated cAMP accumulation. The present studies were undertaken to determine if AVP also potentiates the early effects of CRF on POMC gene expression in rat anterior pituitary primary cultures. We have measured the levels of the POMC primary transcript, processing intermediate, and mature mRNA in nuclear RNA samples and POMC mRNA in cytoplasmic RNA samples as well as ACTH release after treatment with CRF and/or AVP. After a 30-min treatment with 0.5 nM CRF, POMC primary transcript levels were increased by 200-400%. Thirty-minute or 1-h treatments with AVP alone (10 or 100 nM) did not affect primary transcript levels, but increased the amount of the processing intermediate, while a 2-h incubation with 100 nM AVP significantly decreased POMC primary transcript levels. The effects of CRF on the POMC primary transcript and nuclear processing intermediate were not potentiated by cotreatment with AVP, although a potentiation of CRF-stimulated ACTH release was observed. POMC nuclear and cytoplasmic mRNA levels were not affected by these 2-h or less treatments, while an 18-h incubation with 0.5 nM CRF alone or in combination with 100 nM AVP increased POMC cytoplasmic mRNA levels to about 140% of vehicle-treated control values. When a 1-h AVP treatment (100 nM) preceded presentation of CRF, we observed an attenuation of the stimulation of POMC primary transcript and processing intermediate levels by the 1-h CRF treatment. The effects of CRF on POMC primary transcript and processing intermediate levels in these experiments are consistent with a CRF-induced increase in POMC gene transcription. Our findings that AVP decreased primary transcript levels and attenuated the effects of CRF on this end point suggest that: 1) AVP clearly does not act in a synergistic manner with CRF to stimulate POMC gene expression; and 2) AVP possibly affects RNA stability and/or processing.

Adrenocorticotropic Hormone↗

Management of blood pressure changes during recombinant human erythropoietin therapy.

Onset or exacerbation of hypertension has been observed as a possible complication of recombinant human erythropoietin (r-HuEPO; EPOGEN [epoetin alfa], AMGEN Inc, Thousand Oaks, CA) therapy for the anemia of end-stage renal disease. This effect is attributed to an overly rapid rise in the hematocrit level and the accompanying consequences, which include increased hemoglobin, blood viscosity, and red cell mass, as well as normalization of the cardiac index of anemia. The sluggish response to these changes by compensatory mechanisms, resulting in increased peripheral vascular resistance, may be the means by which BP becomes elevated during therapy. Although more than one third of patients receiving r-HuEPO therapy have developed sustained increases in diastolic pressure of 10 mmHg or more, this potential problem is controllable. Prevention or correction of hypertension is accomplished by initiating therapy with a low-dose regimen that is slowly increased, thereby preventing a rapid rise in the hematocrit level. Drug intervention, together with dialysis prescription modification and restriction of dietary salt and fluid to regulate weight, can effectively control BP. Discontinuation of therapy for severe and uncontrollable hypertension rarely becomes necessary.

Anemia↗

Aerobic training effects of electrically induced lower extremity exercises in spinal cord injured people.

Eleven people with spinal cord injury (SCI) (C4-T6) participated in a program of functional electric stimulation (FES) of their paralyzed leg muscles using the REGYS I system. Individualized protocols consisted of an initial phase of weight lifting, an intermediate phase of ergometer pedalling against 0 Kilopond (kp) alternated with 1/8kp for six two-minute runs separated by two-minute rest periods, and a final phase of 36 sessions of continuous ergometer pedalling against variable resistance. A metabolic analyzer measured exercise stress test parameters before and after each phase while subjects pedalled against incremented resistance. Peak oxygen consumption and total stress test time increased markedly. The respiratory exchange ratio (R=VCO2/VO2) at termination, however, did not differ from unity at any phase, indicating that fatigue (defined as a failure to maintain a pedalling frequency of 35 rpm) occurred when the anaerobic threshold was reached, and that FES exercise can increase the aerobic capacity of persons with SCI. The initial velocity of quadriceps shortening (derived from patellar tendon displacements) also decreased in five of eight subjects tested, suggesting corresponding increases in quadriceps twitch time. Since muscle inactivity converts slow-twitch to fast-twitch fibers, our subjects' increased muscle endurance accompanied by decreased muscle-shortening velocity were compatible with a disproportionate increase in the function of slow-twitch fibers relative to fast-twitch fibers. Although these findings demonstrate that lower extremity FES exercises can safely achieve significant aerobic training effects in patients with SCI, the peak levels of cardiorespiratory performance were similar to those reported for quadriplegic people performing maximal voluntary upper extremity exercises.

Adult↗

Corticosterone acts on the brain to inhibit adrenalectomy-induced adrenocorticotropin secretion.

To determine the site (brain and/or pituitary) at which corticosterone (Cort) acts to inhibit adrenalectomy-induced ACTH secretion, the following experiments were performed in male rats. Rats in which brain and pituitary feedback sites were to be left intact were subjected to sham hypothalamic lesions. Rats in which only pituitary sites were to be left were subjected to either medial basal hypothalamic (MBH) or para-ventricular nuclei (PVN) lesions. Two days later all rats were adrenalectomized and replaced with varying amounts of Cort (by sc pellet). Lesioned rats also received sc pumps that delivered 0-5 micrograms/day rat CRF. All rats were killed 5 days after adrenalectomy. Sham-lesioned groups exhibited the expected dose-related inhibition of plasma and pituitary ACTH concentrations by Cort, with normal values obtained at plasma Cort levels between 4.4 and 7.7 micrograms/dl. By contrast, rats with MBH and PVN lesions exhibited no ACTH responses to adrenalectomy when CRF infusions were between 0 and 1 micrograms/day. In rats with MBH and PVN lesions receiving 5 micrograms/day CRF, plasma ACTH concentrations were elevated and were not inhibited by plasma Cort values up to 6 micrograms/dl. Plasma ACTH was inhibited in rats with MBH lesions infused with 5 micrograms/day CRF when plasma Cort levels were 30.6 micrograms/dl. These rats also exhibited marked thymic atrophy. We conclude from these results that Cort normally acts only on a brain site to inhibit adrenalectomy-induced increases in ACTH secretion. Only when plasma Cort concentrations are markedly elevated can evidence for pituitary feedback be demonstrated in vivo.

Adrenal Glands↗