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Biomedical subjects

R L Sherman

Publications and source records attributed to R L Sherman.

At least 19 recordsLinked to original sources
PubMed1990

Recovery of function following unilateral denervation, but not unilateral decentralization, of the pineal gland as indicated by measurements of pineal melatonin content and urinary melatonin metabolites.

The rat pineal gland is an attractive system for studies on the capacity of neural systems to recover following partial injury, allowing both for the creation of precise subtotal lesions and for the measurement of recovery of function at the cellular level. The pineal gland receives overlapping sympathetic innervation from the right and left internal carotid nerves from neurons whose cell bodies are located in the two superior cervical ganglia. This innervation regulates several aspects of pineal metabolism in a circadian fashion, with the most dramatic being a marked increase in the night-time activity of N-acetyltransferase, a key enzyme regulating the rate of melatonin synthesis. We have previously shown that a highly divergent pattern takes place in the night-time activity of this enzyme following two different unilateral lesions of the sympathetic innervation to the gland. Thus, following a unilateral lesion of the internal carotid nerve (unilateral denervation), there is an initial decline in N-acetyltransferase activity; however, normal activity is again seen during the second and subsequent nights. In contrast, a unilateral lesion of the cervical sympathetic trunk, the nerve that innervates the superior cervical ganglion (unilateral decentralization), results in "permanent" impairment of N-acetyltransferase activity. In the present study, we report that the functional capacity of the entire pathway for melatonin synthesis is similarly affected following these lesions, as reflected by the levels of melatonin and of its precursor N-acetylserotonin in the pineal gland, as well as the levels of the main melatonin metabolite 6-hydroxy-melatonin in the urine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Major cerebral vessels injury caused by a seatbelt shoulder strap: case report.

Major cerebral arterial injury may result from penetrating or blunt trauma. In blunt trauma, clinical suspicion of such injury may not be raised, especially if the cranial CT scan is negative. We report a case of a seatbelt shoulder strap to the neck resulting in injury to three major cerebral vessels as demonstrated by cerebral angiography. Although the initial cranial CT scans were negative, a cerebral infarction ultimately developed. The patient was managed conservatively and recovered most of her functions. The importance of clinical suspicion and cerebral angiography is stressed.

Adult↗
PubMed1987

Inadequacy of predicted creatinine clearance as guide to chemotherapy.

Many chemotherapeutic agents are nephrotoxic and/or excreted via the kidney. Thus, careful evaluation of renal function is important since drug dosages are often lowered in patients with impaired renal function. When the creatinine clearance as calculated by the method of Cockcroft and Gault from the patient's age, weight, and serum creatinine was compared to the measured creatinine clearance in the same patients, the correlation coefficient was low (r = 0.40) and the average difference between the predicted and measured creatinine clearance values was 25.3%. Thus, in our patient population, creatinine clearance calculated by the method of Cockcroft and Gault did not correlate well with measured creatinine clearance and thus was not useful as a clinical tool.

Adult↗
PubMed1979

Apparent acute renal failure associated with therapeutic aspirin and ibuprofen administration.

Aspirin and ibuprofen may cause a decrease in renal function which, although statistically significant, is usually small. We report a patient with active systemic lupus erythematosus and apparent acute renal failure associated with the administration of these drugs. Renal biopsy revealed no light microscopic evidence of drug nephrotoxicity although patchy nonspecific ultrastructural changes in the tubular epithelium were seen. The renal failure reversed rapidly when the drugs were withdrawn.

Acute Kidney Injury↗
PubMed1978

Cellular reactivity to altered glomerular basement membrane in glomerulonephritis.

Glomerular basement membrane may be altered during glomerulonephritis, exposing antigens that are recognized as foreign. Immunochemical studies suggest that removal of peripheral glycopeptides from the basement membrane with glycosidase mimics this pathogenetic event. To examine these hypotheses, we studied 24 patients with biopsy-proved glomerulonephritis by means of the lymphocyte-blast-transformation assay. Three preparations of normal glomerular basement membrane were used: two mimicked the native state for the peripheral glycopeptides, and one was altered by glycosidases. Results showed minimal differences in responses to native glomerular basement-membrane preparations among patients with glomerulonephritis and control groups. However, patients with glomerulonephritis had a significant blastogenic response to the glycosidase-treated glomerular basement membrane as compared to patients with nonglomerular renal disease and normal controls (P less than 0.0005). These studies suggest that cellular reactivity to altered glomerular basement-membrane antigens can be detected in certain forms of progressive glomerulonephritis.

Antigens↗
PubMed1977

Focal glomerular sclerosis.

There seems to be little doubt that FGS is a nonspecific lesion that represents one way in which the renal glomerulus responds to a variety of injuries. This is illustrated by the large number of diverse conditions with which the lesion is associated including various forms of glomerulonephritis, pyelonephritis, hereditary nephritis, and heroin usage. Nevertheless, there remains a relatively large isiopathic group which, though possibly heterogeneous, displays a number of characteristic clinical and pathologic features including the following: 1. Steroid-resistant nephrotic syndrome; 2. Hematuria and hypertension; 3. Normal serum complement; 4. Progressive renal insufficiency; 5. Typical pathologic lesion most common in or restricted to juxtamedullary cortex; 6. Absence of clearly defined evidence of immune complex deposition by immunofluorescent or electron microscopic studies; 7. Recurrence of the lesion following renal transplantation. The pathogenesis of these changes is unclear, the evidence for an immune complex mechanism meager, and the suggestion that the disease is mediated by a humoral mechanism remains to be explored. The potential recurrence of this lesion in the transplanted kidney affords a unique opportunity to study the disease early in its course by a variety of techniques that may help to clarify this still poorly understood entity.

Basement Membrane↗
PubMed1974

Electron microscopic studies in hereditary nephritis.

A characteristic electron microscopic lesion-longitudinal splitting of the glomerular basement membranes with accumulation of dark particles-was found in some cases of hereditary nephritis, especially in Alport syndrome. A somewhat similar but less specific alteration was present in the tubular basement membranes and in the Bowman capsule. The lesions tended to exhibit a familial segregation. The possible pathogenesis of the lesions and their relation to physiologic abnormalities are briefly discussed.

Basement Membrane↗
PubMedDate not supplied

Fibrinogen catabolism in systemic lupus erythematosus.

Because there is mounting evidence that localized intravascular coagulation may contribute to tissue injury following a variety of immunologic events, including immune complex diseases, fibrinogen catabolism was studied in patients with systemic lupus erythematosus to determine factors correlating with accelerated coagulation. 125I-fibrinogen half-life in controls was 90.1+/- 11 hours and the mean SLE half-life was 60.5 +/- 12. SLE patients in complete clinical remission had normal half-lives, but patients with symptomatic clinical disease, including renal disease, had significantly reduced fibrinogen survival. Accelerated fibrinogen consumption also correlated with positive tests for anti-DNA antibodies, but not with hypocomplementemia. These observations support the hypothesis that the coagulation system is activated in patients with immune complex diseases. Further studies are required to define the role, if any, that coagulation may play in causing tissue injury.

Adult↗