Biomedical subjects

N G Levinsky

Publications and source records attributed to N G Levinsky.

77 records · Page 5Linked to original sources

PubMedDate not supplied

Enhancing learning during a clinical clerkship: the value of a structured curriculum.

Third-year clerkships, organized around clinical experiences, may provide students with an uneven or narrowly focused fund of clinical knowledge. This paper describes the results of a comparative trial in which a structured curriculum, based on learning objectives, was introduced into an internal medicine clerkship at one of three teaching hospitals of a single medical school; the other two hospitals, providing similar patient care experiences, were used for comparison purposes. Students who did their clerkship at the hospital using the structured curriculum scored significantly higher on the Medicine section of the National Board Part II examination when scores were adjusted for past academic performance. The structured curriculum was very well received and, according to student perceptions, achieved the goal of expanding their basic clinical knowledge beyond that derived from reading only in connection with patient care. These results support the use of curricular guidelines and objectives as a means of enhancing students' cognitive experience during clinical clerkships.

Clinical Clerkship↗

PubMedDate not supplied

Vasopressin stimulates urinary kallikrein excretion in the isolated erythrocyte-perfused rat kidney.

We have found that arginine vasopressin (AVP) (10 pg/ml) stimulates urinary kallikrein in the isolated erythrocyte perfused rat kidney. (In this model, perfusate flow rate approximates blood flow rates in vivo and morphology is normal.) Urinary kallikrein excretion rose from 6.9 +/- 0.8 to 14.9 +/- 2.4 ng/min 20 min after the addition of AVP to the perfusate, and then fell towards baseline levels over the next 30 min. 1-Desamino-8-D-AVP (8 pg/ml) caused a comparable increase in kallikrein excretion. Prostaglandin synthesis inhibition with indomethacin did not alter the stimulatory effect of AVP on kallikrein excretion. Parathyroid hormone 1-34 (144 ng/ml) and calcitonin (102 ng/ml) also increased urinary kallikrein. Kallikrein excretion rose from 9.1 +/- 2.0 to 24 +/- 4.5 ng/min in response to calcitonin and from 8.3 +/- 1.6 to 43.7 +/- 3.4 ng/min following the addition of parathyroid hormone to the perfusate. Kallikrein was found to accumulate in the perfusate in a linear fashion. Based on the slope of the relationship between perfusate kallikrein and time, the rate of release of kallikrein into the perfusate was estimated to be 0.79 ng/min in control kidneys. The rate of release of kallikrein into the perfusate in kidneys treated with AVP was the same (0.74 ng/min). Thus while kallikrein is released into the perfusate, this process is not influenced by AVP. In conclusion, AVP stimulates release of kallikrein into the urine (but not the perfusate) independently of systemic events. The effect of AVP is not mediated by prostaglandins. This effect of AVP is mediated via stimulation of the V2 receptor and also occurs in response to two other hormones (calcitonin and parathyroid hormone) that are known to stimulate adenyl cyclase in the rat distal nephron.

Animals↗

PubMedDate not supplied

Ischemia in the isolated erythrocyte-perfused rat kidney. Protective effect of hypothermia.

We have examined the effects of 25 min of ischemia in the isolated erythrocyte-perfused rat kidney (IEPK). We have previously shown that, in this model, perfusate flow rate is close to blood flow rates in vivo and morphology is normal. The functional and morphological consequences of both warm ischemia (at 37 degrees C) and ischemia induced during mild hypothermia (27 degrees C) were compared. (1) Warm ischemia resulted in a 51% increase in renal vascular resistance (RVR) during the reflow period, while glomerular filtration rate (GFR) was reduced to 24% of control levels. (2) Kidneys subjected to warm ischemia showed marked morphological damage localized to the proximal tubule. There was dilatation of the proximal segments and widespread loss of the proximal brush border due both to shedding into the lumen and interiorization into the cell. In contrast to the proximal tubular damage, the cells of the medullary thick ascending limb segments were intact. However, the lumena of many of these segments were filled with cytoplasmic blebs and necrotic cell debris. There was also pronounced vascular congestion of the capillary plexus in the inner stripe of the outer medulla. (3) Hypothermia to 27 degrees C resulted in almost complete protection against ischemic injury: RVR and GFR were not different from control values. Also, kidneys subjected to cold ischemia showed only isolated areas of mild brush border damage; no evidence of tubular obstruction or vascular congestion was present. (4) Thus, warm ischemia in the IEPK results in functional and morphological effects comparable to those found in vivo. Post-ischemic vasoconstriction as well as medullary congestion occur in the absence of systemic hormones and renal nerves. These consequences of ischemia are prevented by modest hypothermia.

Animals↗

PubMedDate not supplied

Regulation of renal rK1-kallikrein in spontaneously hypertensive rats.

Urinary and renal rK1-kallikrein was studied in spontaneously hypertensive rats (SHR) and their normotensive controls (WKY). It was demonstrated that the antiserum used for kallikrein radioimmunoassay (RIA) reacts with rK1- but not with rK7-protein. The specificity of the kininogenase assay was tested: rK7 had only 8% of the activity of rK1. Urinary kallikrein excretion by RIA was reduced by about two thirds in 5-week-old SHR compared WKY (11.5 versus 37.1 micrograms/24 h). On the contrary, the kidney content of rK1-kallikrein by RIA was increased by 40% in these rats (11.6 versus 8.4 ng/mg protein). The increase in kidney rK1 was confirmed by kininogenase assays. The same pattern of reduced urinary and increased renal rK1-kallikrein was observed in 8-week-old SHR rats. Kidney rK1-kallikrein mRNA tended to be lower (0.10 > p > 0.05) in SHR compared to WKY rats, suggesting that the increased kidney rK1 content is not due to increased rK1 synthesis. We hypothesize that the combination of high kidney content and low urinary excretion may be due to a defective mechanism for secretion of rK1 into the urine by tubular epithelial cells.

Aging↗

PubMedDate not supplied

Reduced ratio of active-to-total urinary kallikrein in essential hypertension.

Urinary kallikrein excretion was studied in 34 patients with mild, normal-renin, essential hypertension without evidence of target organ damage and in 23 normotensive controls, using assays that measure both active (kininogenase activity) and total (active plus inactive) kallikrein. There was no significant difference in either active or total kallikrein excretion between the two groups. However, the ratio of active-to-total enzyme was decreased in the hypertensives (0.83 +/- 0.03 units/micrograms) compared to the normotensives (1.00 +/- 0.05 units/micrograms) (p less than 0.002). The active-to-total ratio was inversely related to sodium excretion in both groups, indicating that the proportion of active to inactive enzyme increased in response to reduced sodium intake. We conclude that, although absolute excretion of active and total kallikrein is not decreased, enzyme activity per microgram of total kallikrein excreted is reduced in mild, normal-renin essential hypertension. This abnormality may be due to a defective enzyme, or to a reduced excretion of active relative to inactive kallikrein. The latter could result from the presence of a urinary kallikrein inhibitor or to reduced activation of a proenzyme.

Adult↗