False-positive HIV test: implications for the patient.
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Biomedical subjects
Publications and source records attributed to J F Sullivan.
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To examine the adequacy of hypertension control, we monitored the blood pressure (BP) of 53 hemodialysis patients who received treatment for hypertension. BP measurement using an ambulatory BP monitor began 1 hour before dialysis and continued every 30 to 60 minutes for 48 hours until the next dialysis. Diet, medications including antihypertensive drugs, and hemodialysis prescription were not changed during this study. Each patient had a mean of 68 BP measurements during the monitoring period. Mean (+/- SD) systolic and diastolic BP levels of all patients over 48 hours were 158.6 +/- 22.7 mm Hg and 88.7 +/- 16.6 mm Hg, respectively, without diurnal variations. In these, BP loads (the percentage of systolic BP exceeding 150 mm Hg and diastolic BP exceeding 90 mm Hg) were 58.4% and 39.4%, respectively, suggesting that hypertension was inadequately controlled for more than half of the study period. Eight patients (15%) maintained BP within normal ranges at all times. All patients lost weight (2.9 +/- 0.9 kg) at the end of dialysis by ultrafiltration. However, only 27 patients (51%) had a greater than 5% decrease in mean arterial BP post-dialysis, which returned to predialysis levels within 12 to 24 hours. Reduction of BP postdialysis was significantly more common among black patients (72%) than white patients (30%) (P less than 0.01). However, there was no difference in age, cause of kidney disease, amount of ultrafiltration, and BP loads between those whose BP decreased and those whose did not. BP monitoring was repeated in eight patients, 2 to 3 months after adjustment of their antihypertensive regimens.(ABSTRACT TRUNCATED AT 250 WORDS)
The synovial fluid aspirated from patients with symptomatic arthritis was analyzed for the presence of tumor necrosis factor (TNF), interleukin 6 (IL-6) and interleukin 8 (IL-8). All three cytokines were found in both inflammatory and non-inflammatory arthritides: IL-8 levels ranged from less than 20 to 38,990 pg/ml, IL-6 from less than 10 to 72,300 pg/ml and TNF from less than 4 to 61 pg/ml. No inhibitors of cytokine activity were found. IL-8 and IL-6 were present in significantly higher levels in patients with inflammatory arthritis compared to patients with osteoarthritis, and there was significant correlation between the IL-6 and IL-8 levels. These findings document the presence of multiple cytokines in the synovial fluid specimens of patients with arthritis, and demonstrate that higher cytokine levels accompany inflammatory arthritis.
Examination of the differences in caries patterns in 5-year-old children between adjacent English South Coast districts prompted a more specific study using larger samples in more discrete localities. Although the overall caries levels varied significantly between the two districts, no significant differences were found between two defined areas of social deprivation. The children in one area were predominantly of Indian or Pakistani background and in the other mainly white Caucasian and it is suggested that differences in caries experience are related to indicators of social deprivation, rather than ethnicity. Even in relatively affluent districts, where caries levels are no longer a general problem, the dental needs of vulnerable groups of children may remain unidentified within a more favourable overall picture, and thus unmet, unless specific areas are monitored closely taking into account indicators of social deprivation.
We studied the clinical course of 59 lupus patients with end-stage renal disease (ESRD) to determine their long-term prognosis and delineate the evolution of their lupus activity. The study population was predominantly female (86%) and young (mean age, 27.4 years), and they were observed for a mean of 6.5 years from the inception of dialysis. At the time dialysis was initiated, only 21 patients (35.6%) had clinically active systemic lupus erythematosus (SLE). The remaining patients progressed to ESRD despite the absence of clinical lupus activity. Lupus activity was clinically apparent in 55.4% of patients in the first year, 6.5% in the fifth, and none in the tenth year. In 45% of patients, lupus activity was clinically inactive at entry to ESRD and remained inactive throughout the observation period. Serological activity declined proportionally, but to a lesser extent than clinical activity. Cumulative patient survival was 81.1% and 74.6% at the fifth and tenth year, respectively, from the inception of dialysis treatment; similarly it was 78% at the fifth and tenth year after the transplantation. Graft survival was 60.4% at the fifth and 45.5% at the tenth year. No one had recurrence of clinical lupus nephritis in the graft for up to 16 years of follow-up. Fourteen patients died from either infectious or cardiovascular complications, but none from SLE per se. This long-term study with a large number of lupus patients confirms our previous findings that the progression of renal disease to ESRD may be mediated by nonimmunologic mechanisms, as well as immunologic insults.(ABSTRACT TRUNCATED AT 250 WORDS)
Variants designed using PROTEUS have been produced in an attempt to engineer stabilizing salt bridges into subtilisin BPN'. All the mutants constructed by site-directed mutagenesis were secreted by Bacillus subtilis, except L75K. Q19E, expressed as a single variant and also in a double variant, Q19E/Q271E, appears to form a stabilizing salt bridge based on X-ray crystal structure determination and differential scanning calorimeter measurements. Although the double mutant was found to be less thermodynamically stable than the wild-type, it did exhibit an autolytic stability about two-fold greater under hydrophobic conditions. Four variants, A98K, S89E, V26R and L235R, were found to be nearly identical to wild-type in thermal stability, indicative of stable structures without evidence of salt bridge formation. Variants Q271E, V51K and T164R led to structures that resulted in varying degrees of thermodynamic and autolytic instability. A computer-modeling analysis of the PROTEUS predictions reveals that the low percentage of salt bridge formation is probably due to an overly simplistic electrostatic model, which does not account for the geometry of the pairwise interactions.
The National Animal Disease Center's experience with personnel exposure or infection with pathogenic agents is summarized. A total of 128 laboratory-associated exposures to infectious disease agents were reported. Of these exposures, 103 resulted from known accidents. The other 25 were identified only after the development of clinical or serological manifestations of infection. Thirty-four cases of laboratory-acquired infections were reviewed. Class 3 organisms--Chlamydia sp., Brucella sp. and Mycobacterium sp.--were responsible for 76% of the infections encountered, with Brucella sp. incriminated most frequently. The most commonly reported cause of exposure was associated with hypodermic syringe use. Unknown routes of exposure, presumed to be aerosol related, were the overwhelming explanation involved in the laboratory-associated infections.
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In spite of demonstrated validity, Halstead's Category Test has been criticized as overly time consuming. In order to evaluate this assumption, groups of severely head-injured and general neurological cases were administered the Category Test as part of routine evaluation, and the time to completion of the test was recorded. The results indicated that 93% of the patients completed the test in less than 1 h and that 50% completed it in less than 40 min. In 81% of the cases, the test lasted from 20-50 min.
The clinical courses of 36 patients with systemic lupus erythematosus (SLE) in whom chronic renal failure developed and who required dialysis for more than three months were studied. At the time dialysis was initiated, 14 of 36 patients (38.9 percent) had clinically active SLE, but only three of 24 (12.5 percent) had activity in subsequent years while receiving dialysis therapy. In the majority of patients, however, renal disease progressed to end-stage despite clinical quiescence of SLE. During the follow-up period (mean +/- SD, 36 +/- 39.8 months), eight patients died--six from infections and two from cardiac disease. Actuarial survival rates at one, two, and five years after dialysis treatment were 91.1, 78.8, and 68.9 percent, respectively. This study suggests that the progression of renal disease to end-stage in patients with SLE may be mediated by nonimmunologic mechanisms as well as SLE-related immunologic insults. In most of these patients undergoing long-term dialysis, SLE remains clinically inactive despite persistent serologic abnormalities. Survival of the patients undergoing dialysis is comparable with that of the general dialysis population.
As previously reported, the circulating half-life of carboxyterminal PTH is greatly prolonged in renal failure (mean t1/2 33.20 +/- 10.18 hrs), while intact PTH is much less affected (t1/2 less than one hour). Preoperative intact PTH levels were strongly predictive of clinical response to subtotal parathyroidectomy, and may help to differentiate the nature of metabolic bone disease in symptomatic dialysis patients. Intact PTH levels showed strong correlation with postoperative calcium metabolism, allowing prediction of extent of postoperative hypocalcemia. Carboxyterminal PTH levels, influenced by renal function as well as by functional parathyroid state, were poorly predictive of response to parathyroidectomy and not correlated with postoperative calcium metabolism.
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Captopril, an orally active inhibitor of angiotensin-I-converting enzyme, was administered in a single dose to five anephric patients who had extremely low plasma renin activities. The drug did not lower blood pressure or significantly alter plasma renin activity in any patient but increased mean arterial pressure slightly in three. These results suggest that the blood-pressure lowering effect of captopril depends on an active renal renin-angiotensin system. Though additional mechanisms, such as accumulation of vasodilator kinins resulting from kininase II inhibition, may also contribute to captopril's action, these mechanisms apparently require the presence of the kidney to have a clinically detectable effect.
The clinical association of decreased serum and hepatic zinc in patients with cirrhosis of the liver presumably arising from excess ethanol ingestion prompted a study of the activities of zinc and alcohol in experimental animals. The purpose of this study was to determine the effect of zinc deficiency upon lipid peroxidation in the liver. The effect of ethanol and zinc deficiency on lipid peroxidation was also evaluated. Rats were used in the experimental design, one group received a control diet, and one was maintained on a zinc-deficient diet. One-half of each group also received 3.85 g ethanol per kilogram body weight daily. Lipid peroxidation in vivo was determined by estimation of diene conjugation of microsomal lipids. The in vitro lipid peroxidation potential was measured by the generation of malonic dialdehyde by enzymatic as well as nonenzymatic reactions. Analysis of this data indicated that increased hepatic microsomal lipid peroxidation was associated with zinc deficiency whether using in vivo or in vitro indices of measurement. Review of the data from individual animals indicated that the lowest levels of serum zinc were associated with increased hepatic content of phospholipids. The degree of lipid peroxidation in the zinc deficient animals was not increased by ingestion of alcohol.
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Serum selenium as well as serum zinc, copper, magnesium, calcium and manganese were investigated in a control group of adult males and in 11 groups of patients in various disease states. Not only the change of each trace element but also the possible association between elements was studied in the various groups. All patients were fasting when sampled and studied only after the acute phase of the disease was corrected. Trace metal determinations were performed by atomic absorption spectrophometry (Mg, Ca, Cu, Zn) and by neutron activation analysis (Se, Mn). All patients showed low serum zinc when compared to controls. Cirrhotic patients had a low serum selenium level as well as low calcium, magnesium and zinc. Emphysemia and cancer patients had an elevated serum copper concentration while copper and manganese levels were elevated in congestive heart failure, infection and pschoses. To our knowledge this is the first time low serum selenium values have been demonstrated to be associated with the low serum zinc, calcium and magnesium levels found in cirrhotic patients.
Zinc metabolism in cirrhotic patients was studied, indicating some improvement that did not alter the abnormalities of zinc metabolism significantly and showed no evidence of correlation of abnormalities with the clinical improvement or lack thereof in the patients studied.