Biomedical subjects
Publications and source records attributed to R J Friedman.
Pseudomembranous colitis has been reported as a complication of therapy with a number of different antibiotics. We present here a case of pseudomembranous colitis following therapy with oxacillin, in which the causative organism and the toxin it produces were isolated from the patient's stool. We believe this is the first documented case of oxacillin-induced pseudomembranous colitis.
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In previous experiments, injury-induced atherosclerosis has been shown to be associated with the development of fatty streaks. The findings suggested that fatty streaks might represent a stage in healing of intimal injury evolving to fibrous plaques, free of lipid. The present experiment was designed to study the incidence and evolution of these lesions during a 2-week period of lesion retrogression following removal of a catheter placed in the aorta for 1 week. The findings indicate that as fat-containing lesions, either of the thromboatherosclerotic or fatty streak varieties, decreased, the amount of nonlipid-containing fibrous lesions increased.
This study was designed to investigate the mechanisms involved in fibromusculoelastic lesion formation produced by selective de-endothelialization by the intra-arterial balloon catheter technique in thrombocytopenic rabbits. Thrombocytopenia was induced and maintained for up to 30 days by daily injections fo highly specific sheep anti-rabbit platelet sera (APS). Evidence for re-endothelialization was obtained by i.v. Evans blue dye 30 min before sacrifice. Rabbits received daily injections of APS, which reduced the mean platelet count to 5,600/cm3; control animals received identically treated normal sheep sera on the same schedule, and had mean daily platelet counts of 363,000/cm3. Evaluation of intimal thickness was assessed by counting cell layers in semithin sections. Intimal thickening in aortae from rabbits treated with APS was strikingly suppressed, in contrast to those from normal sheep sera-treated animals which showed a mean intimal thickness of 18 cell layers within 28 days often after de-endothelialization. Re-endothelialization was not affected by APS treatment. These results indicate that the proliferation of smooth muscle cells is dramatically inhibited by reduction of platelets.
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We have previously shown that repeated or continuous intimal injury caused by an indwelling aortic catheter causes a variety of lesions in rabbits maintained on a diet unsupplemented by lipid. These include fatty streaks, lipid-free fibrous plaques and lipid-rich raised thromboatherosclerotic plaques. Whether lipid-rich raised lesions are a result of injury or co-existing thrombosis or both is not clear. The present experiment was designed to answer this question. Anti-platelet serum (APS) to washed sonicated rabbit platelets was raised in sheep. PE 60 polyethylene catheters were placed in the aortas of 35 rabbits by way of a femoral artery. The animals were randomly divided into 2 groups. The experimental group (17 rabbits) received an intravascular injection of 1.0 ml of APS followed 8 hours later by a subcutaneous injection of 0.5 ml. Thereafter, 0.5 ml APS was given subcutaneously each day for 13 additional days. The control group (18 rabbits) received no APS. Platelet counts were done prior to surgery, at 5 minutes following surgery, at 4 days, 8 days and just prior to killing. Extent of lesions was estimated by photographing the opened aortas, projecting the photographs on cardboard, cutting out the areas occupied by the different lesions and weighing the cardboard. The mean weight of raised lesions in the control group was 6 to 7 times greater than in the experimental groups. Statistical analysis of this difference based on Welsh's "t" test for unequal variances was highly significant (P less than 0.001). Platelet counts in the experimental groups varied from 0 to 20,000 at 14 days. In animals with platelet counts less than or equal to 1,000 mm3 raised lesions were completely prevented. In a second experiment the effect of APS was compared with normal sheep serum (NSS). A similarly significant inhibition of raised lesions occurred in the APS group. The extent of lesions in the NSS control was similar to that in the No-APS group of the first experiment. These findings indicate that thrombosis is more important than injury in the development of lipid-rich raised lesions.
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For four consecutive weeks, 61 rabbits received weekly injections of lymphocytotoxic-positive human serum into the left carotid artery and of autologous serum into the right carotid artery as a control. Serum cholesterol and serum triglyceride levels were measured before the study, in the second and fourth weeks of the study, and weekly thereafter. The results show that repeated intimal injury caused raised, lipid-containing thromboatherosclerotic lesions and that there was a consistent regression to lipid-free fibromusculoelastic plaques from the first week after completion of the injection regimen to the fourth week. Apparently, regeneration of an intact covering cell layer resulted in the elimination of lipid deposits from raised lesions, resulting in lipid-free fibromusculoelastic plaques. In addition, fatty streaks were observed to occur during regression. A statistically significant rise in serum cholesterol level during the phase of progression of lesions and a subsequent fall during regression were observed.
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Since Duguid suggested that atherosclerosis represents essentially the organization of mural thrombi, there have been many attempts to produce the disease experimentally by damaging the arterial wall. A single injury to the inner lining of an artery causes lipid-free lesions, composed of smooth muscle cells and collagen, covered by endothelium. Previously, we reported the development of atherosclerotic lesions in normolipemic rabbits as a result of repeated or continuous intimal injury by an indwelling aortic polyethylene catheter. However, it was difficult to control the location or duration of the intimal injury. The present investigation was designed to produce repeated endothelial injury in a defined segment of rabbit carotid artery. Sixty-two rabbits received injections of either lymphocytotoxic-positive (LP) or lymphocytotoxic-negative (LN) human serum into a segment of left carotid artery. Autologous rabbit serum was injected into the right carotid artery as a control. Eight rabbits received a single injection of LP and were killed 4 weeks latermforty-two rabbits received injections of human serum at weekly intervals, for a maximum of four injections, and were killed 1 week after the last injectionmthirty-two of 42 rabbits received repeated injections of LP; 10 received repeated injections of LN. Raised, lipid-containing lesions were present in 21 of 26 rabbits receiving four repeated injections of LP. No, or very minimal (fewer than three cells thick), intimal thickening was found in the 10 LN rabbits and in all control right carotid arteries. In eight rabbits receiving one injection of LP, fibrous intimal thickening without lipid accumulation, fatty streaks, and edematous plaques were found. Electron microscopy of arteries from 12 rabbits sampled at 1,5, and 60 minutes after exposure to LP indicated that the initial damage was loss of endotheliummthe results consistently showed lipid in raised, thrombus-covered (non-reendothelialized) lesions. Nonraised, endothelialized lesions did not show lipid. These findings support the belief that atherosclerosis occurs in response to repeated endothelial injury.
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Five healthy young men were studied during 24-30 wk of continuous bed rest. During the first 12 wk of bed rest, untreated subjects increased calcium excretion in the urine by 109 mg/day and in the feces by 147 mg/day. The rate of total body calcium loss was 0.5-0.7% per month. Losses of central calcaneus mineral, assessed by gamma ray transmission scanning, occurred at a tenfold higher rate, whereas the mineral content of the radius did not change. Changes in phosphorus balance resembled the calcium pattern, and increased excretion of nitrogen and hydroxyproline also occurred during bed rest. Upon reambulation, the subjects' calcium balance became positive in 1 month and recovery of their calcaneus mineral was complete within 10-20 wk. Treatment with potassium phosphate supplements (1327 mg P/day) entirely prevented the hypercalciuria of bed rest, but fecal calcium tended to increase. During the first 12 wk, calcium balance was slightly less negative (mean - 193 mg/day) than during bed rest without added phosphate (mean - 267 mg/day). This effect was not seen during the second 12 wk of bed rest. The patterns of magnesium excretion were similar to those of calcium. Fecal and urinary phosphorus excretions were doubled, and phosphorus balance became positive (+ 113 mg/day). Mineral loss from the central calcaneus was similar to that of untreated subjects. It is concluded that this form of phosphate supplementation reduces urinary calcium excretion but does not prevent bone loss during bed rest.
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A compartment syndrome is a neurovascular compromise resulting from an increased local tissue pressure. Compartment syndromes can have many etiologies and may arise in any area of the body that has little or no capacity for tissue expansion. The sequelae are severe in the absence of immediate diagnosis and treatment. The diagnosis is usually a clinical one but compartment pressure measurements are often helpful. Many methods of treatment have been investigated, but definitive treatment consists of immediate removal of the constricting force, most often accomplished with surgical fasciotomy.
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Ninety-three cadaveric proximal humeri and matching scapulae with no evidence of shoulder disease were obtained. High-resolution roentgenograms were made. They were the digitized, and a custom computer program was used to obtain periosteal and endosteal dimensions (humeral canal width, shaft width, tuberosity offset, head offset, radius of curvature, head diameter, canal flare index, glenoid height and depth, arc of enclosure, radius of curvature, and depth of cancellous bone, among others). Statistical analyses included correlations among pairs of dimensions, regression analysis, and confidence intervals to estimate each geometric parameter. To represent the degree of conformity and constraint between the humeral head and glenoid, a conformity index (radius of head/radius glenoid) and constraint index (arc of enclosure/360) were calculated for each shoulder. Most of the parameters measured approximated a Gaussian distribution. Pairwise correlations of the geometric parameters showed that many were significantly associated at the 5% level (p < 0.05) with a high correlation coefficient (r > 0.4), meaning that the variations between the parameters were not purely random but rather they were related and that this relationship was useful in a predictive sense. With these key parameters identified, one can design components with an optimum fit or match an existing design to a patient's anatomy with a high degree of accuracy. No correlation was found between the radii of curvature for the humeral head and glenoid in either the coronal or sagittal plane or between the humeral head diameter and arc of enclosure. The mean conformity index was 0.72 in the coronal and 0.63 in the sagittal plane. Only 16% of the specimens had a conformity index greater than 0.9, indicating the radii of curvature matched. The vast majority had a more curved humeral head and flatter glenoid. Also, there was more constraint to the glenoid in the coronal versus sagittal plane (constraint index = 0.18 vs 0.13). These anatomic features help prevent superior-inferior translation of the humeral head but allow translation in the sagittal plane. This database of basic anatomic geometry defines the anatomic relationships of the proximal humerus and glenoid cavity that allow for a precise bone-implant fit and assesses the match between the shape of existing components and the patient's anatomy.