Biomedical subjects
Publications and source records attributed to J Lawrence.
The managed care backlash has shifted to a new target: HMO medical directors. Federal law shields employer-sponsored health plans from most state oversight and lawsuits, but angry enrollees have begun taking a back route, turning state medical boards on doctors in charge of utilization review. One attorney calls them "the soft underbelly of managed care."
Benchmarking may not be the panacea it once seemed--especially the old model of buying data about competitors. Savvy managers have found new ways to set and beat their goals. Some are benchmarking against their own past performance, some are comparing with top performers instead of just local competition, and others are even looking outside the field for role models. "You need to identify best practices," urges one top benchmarking guru. "Look at the data clusters of those who do it significantly, whatever 'it' is."
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Carnosine is a naturally occurring dipeptide (beta-alanyl-L-histidine) found in brain, innervated tissues, and the lens at concentrations up to 20 mM in humans. In 1994 it was shown that carnosine could delay senescence of cultured human fibroblasts. Evidence will be presented to suggest that carnosine, in addition to antioxidant and oxygen free-radical scavenging activities, also reacts with deleterious aldehydes to protect susceptible macromolecules. Our studies show that, in vitro, carnosine inhibits nonenzymic glycosylation and cross-linking of proteins induced by reactive aldehydes (aldose and ketose sugars, certain triose glycolytic intermediates and malondialdehyde (MDA), a lipid peroxidation product). Additionally we show that carnosine inhibits formation of MDA-induced protein-associated advanced glycosylation end products (AGEs) and formation of DNA-protein cross-links induced by acetaldehyde and formaldehyde. At the cellular level 20 mM carnosine protected cultured human fibroblasts and lymphocytes, CHO cells, and cultured rat brain endothelial cells against the toxic effects of formaldehyde, acetaldehyde and MDA, and AGEs formed by a lysine/deoxyribose mixture. Interestingly, carnosine protected cultured rat brain endothelial cells against amyloid peptide toxicity. We propose that carnosine (which is remarkably nontoxic) or related structures should be explored for possible intervention in pathologies that involve deleterious aldehydes, for example, secondary diabetic complications, inflammatory phenomena, alcoholic liver disease, and possibly Alzheimer's disease.
The upper limit of vulnerability is the strength above which ventricular fibrillation is no longer inducible with a shock delivered during the vulnerable phase of the cardiac cycle. It has been demonstrated that the upper limit of vulnerability correlates with the defibrillation threshold in a paced rhythm. The purpose of this study is to evaluate the correlation of the upper limit of vulnerability determined in normal sinus rhythm with the defibrillation threshold using a simplified protocol in patients undergoing placement of an ICD. We studied 28 patients who underwent ICD implantation. CPI generators and Endotak leads were used in all patients. Device-based testing was used to determined the defibrillation threshold and the upper limit of vulnerability. The upper limit of vulnerability was tested with three shocks delivered at 0, 20, and 40 ms before the peak of the T wave during normal sinus rhythm. The defibrillation threshold was determined by a simple step up-down protocol. The upper limit of vulnerability (9.0 +/- 4.5 J) did not significantly differ from the defibrillation threshold (9.9 +/- 4.0 J), P = NS. A close correlation was present, correlation coefficient = 0.75, P < 0.0001. The upper limit of vulnerability was within 5 J of the defibrillation threshold in 27 (96%) of the 28 patients. The upper limit of vulnerability underestimated the defibrillation threshold by 10 J in one patient who had a defibrillation threshold of 15 J. The upper limit of vulnerability determined in normal sinus rhythm correlates significantly with the defibrillation threshold in patients undergoing ICD implantation. The protocol is simple and easily implemented clinically.
Although rare in childhood, gastric volvulus and wandering spleen share a common etiology: congenital absence of intraperitoneal visceral attachments. We report an unusual case of a patient who presented with three episodes of intractable vomiting and abdominal mass but no abdominal pain. A diagnosis could not be made until the third episode because the gastric volvulus resolved each time on placement of a nasogastric (NG) tube before any further tests could be done. During the third episode, diagnostic imaging was performed before inserting an NG tube, and the diagnosis of a mesenteroaxial gastric volvulus and an abnormally positioned spleen was made. Although both conditions are caused by abnormalities of fixation, the association of gastric volvulus and wandering spleen has been reported only once before.
An understanding of the mechanisms of virologic cross-resistance between human immunodeficiency virus type 1 protease inhibitors is important for the establishment of effective treatment strategies for patients who no longer respond to their initial protease inhibitor. Protease gene sequencing results from patients treated with saquinavir showed significant increases in the frequency of the G48V protease mutation in patients receiving higher doses of the drug. In addition, all six patients who developed the G48V mutation during saquinavir therapy developed the V82A mutation either on continued saquinavir or after a switch to nelfinavir or indinavir. In vitro susceptibility assays showed that all 13 isolates with reduced susceptibilities to two or more protease inhibitors had either the G48V or L90M mutation, along with an average of six other protease mutations. Reduced susceptibility to nelfinavir was found in 14 isolates, but only 1 possessed the D30N mutation. These results suggest that mutations selected in vivo by initial saquinavir therapy may provide more cross-resistance to the other protease inhibitors than has been previously reported.
BACKGROUND AND PURPOSE: To assess the prevalence of depressive symptoms, their clinical correlates, and the effects of depressive symptoms on stroke recovery, a relatively unselected, well-diagnosed cohort of consecutive stroke survivors was followed prospectively. METHODS: Consecutive admissions to a regional stroke center who met World Health Organization and National Institute of Neurological Disorders and Stroke criteria for stroke were eligible. Subarachnoid hemorrhage and brain stem strokes were excluded. Patients underwent CT, single-photon emission CT, and standardized neurological and cognitive examinations at entry. At 3 months and 1 year after stroke, depressive symptoms were assessed with the Montgomery Asberg Depression Rating Scale (MADRS) and the Zung Self-Rating Depression Scale (SDS). Functional outcome was measured with the Functional Independence Measure, and handicap was assessed by the Oxford Handicap Scale. RESULTS: We assessed 436 patients at entry (mean +/- SD age, 74.9 +/- 11.6 years). There were 150 patients available for assessment at 3 months and 136 at 1 year. Marked depressive symptoms were noted in 22% (SDS) to 27% (MADRS) at 3 months and 21% (SDS) to 22% (MADRS) at 1 year. Patents with marked depressive symptoms had more neurological impairment (P<.008), were more likely to be female (P<.05), and were more likely to have previous histories of depression (P<.03). There was no relationship between depressive symptoms and age, lesion volume, or side of lesion. Depressive symptoms were correlated with functional outcome (r = -.31, P<.0001) and handicap (r = .41, P<.0001) at 3 months and 1 year (r= -.28, P<.001; r = .35, P<.0001). CONCLUSIONS: Depressive symptoms and functional outcome are correlated. In view of the prevalence of depressive symptoms in this population, diagnosis and treatment of depression are important in optimizing recovery.
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