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Biomedical subjects

B Levy

Publications and source records attributed to B Levy.

At least 91 records · Page 5Linked to original sources
PubMed1994

Aging free from negative stereotypes: successful memory in China and among the American deaf.

This study explores whether negative stereotypes about aging contribute to memory loss in old age. The research participants consisted of old and young Chinese hearing, American Deaf, and American hearing individuals. Members of the mainland Chinese and the American Deaf cultures were recruited on the basis of the belief that they would be less likely than hearing Americans to be exposed to and accept negative stereotypes about aging. The expected results were (a) an interaction in which the 3 groups of younger Ss would perform similarly on the memory tasks, whereas the older Deaf and older Chinese participants would outperform the older American hearing group and (b) a positive correlation between view toward aging and memory performance among the old Ss. The data supported both hypotheses. The results suggest that cultural beliefs about aging play a role in determining the degree of memory loss people experience in old age.

Adolescent↗
PubMed1994

Recurrent syncope and quadriplegia.

A 72-year-old man had posturally induced syncopal episodes, followed by quadriparesis, coma, and death. Neuroimaging studies supported the clinical diagnosis confirmed by neuropathological findings.

Aged↗
PubMed1994

Clinical impact of rapid in vitro susceptibility testing and bacterial identification.

During the past decade, a variety of instrument-assisted bacterial identification and antimicrobial susceptibility test systems have been developed which permit provision of test results in a matter of hours rather than days, as has been the case with traditional overnight procedures. These newer rapid techniques are much more expensive than older methods. It has been presumed but not proven that the clinical benefits of rapid testing to patients with infection offset the added cost. The intent of this study was to objectively define the clinical impact of rapid bacterial identification and antimicrobial susceptibility testing. A 1-year study was performed in which infected, hospitalized patients in a tertiary-care, teaching, medical center were randomly assigned to one of two groups: patients for whom identification and susceptibility testing was performed by using a semi-automated, rapid, same-day procedure and those for whom testing was accomplished by using traditional overnight techniques. The two groups were compared with respect to numerous demographic descriptors, and then patients were monitored prospectively through the end of their hospitalization with the aim of determining whether there existed objectively defineable differences in management and outcome between the two groups. The mean lengths of time to provision of susceptibility and identification test results in the rapid test group were 11.3 and 9.6 h, respectively. In the overnight test group, these values were 19.6 and 25.9 h, respectively (P < 0.0005). There were 273 evaluable patients in the first group and 300 in the second group. Other than the length of time required to provide susceptibility and identification test results, no significant differences were noted between the two groups with respect to > 100 demographic descriptors. With regard to measures of outcome, the mean lengths of hospitalization were also the same in both groups. Mortality rates were however, lower in the rapid test group (i.e., 8.8% versus 15.3%). Similarly, statistically significantly fewer laboratory studies, imaging procedures, days of intubation, and days in an intensive or intermediate-care area were observed with patients in the rapid test group. Rapid testing was also associated with significantly shortened lengths of elapsed time prior to alterations in antimicrobial therapy. Lastly, patient costs for hospitalization were significantly lower in the rapid test group. The results of this study indicate the rapid same-day bacterial identification and susceptibility testing in the microbiology laboratory can have a major impact on the care and outcome of hospitalized patients with infection.

Adolescent↗
PubMed1994

Vascular Ca overload produced by vitamin D3 plus nicotine diminishes arterial distensibility in rats.

In humans, aging produces many structural changes in blood vessels, one of the most pronounced being arterial calcium overload. Simultaneously arteries become increasingly rigid. The slow evolution of the two processes renders it difficult to evaluate the importance of vascular calcium overload in the development of decreased compliance. To gain insight into this relationship, rapid vascular calcium overload was produced by treating young rats with vitamin D3 and nicotine. When rats were allowed 16 days or longer to recover from such treatment, analysis of plasma parameters revealed no overt toxicity, and growth rate was similar to that of controls. Pronounced calcium overload was seen primarily in compliance arteries. Changes in systemic arterial compliance, characteristic impedance, pulse-wave velocity, and carotid compliance all reflected a substantial increase in arterial rigidity. Linear regression analysis revealed significant correlations between the various indicators of arterial distensibility and arterial calcium content. In conclusion, treatment of young rats with vitamin D3 and nicotine may provide a suitable model with which to investigate how calcium overload is involved in the induration of compliance arteries.

Aging↗
PubMed1994

Differential regulation of angiotensin II and losartan binding sites in glomeruli and mesangial cells.

The aim of the present report was to examine the effect of several agents on angiotensin II (ANG II) and losartan receptors using 125I-[Sar1,Ala8]ANG II and [3H]losartan as radiolabeled ligand, respectively. ANG II receptors were downregulated in glomeruli from rats infused with ANG II during 3 wk or rats receiving losartan orally during 1 wk. The number of sites (Bmax) was reduced, but the dissociation constant (Kd) value was unchanged. Losartan receptors were downregulated in glomeruli from rats receiving losartan, but remained unchanged in glomeruli from rats infused with ANG II. Since in vivo administration of losartan results in increase of plasma ANG II and formation of metabolites, in vitro studies using human mesangial cells were performed to better analyze the present findings. Treatment of mesangial cells during 4 days by ANG II, losartan, or its metabolite, EXP-3174, also produced downregulation of 125I-[Sar1,Ala8]ANG II binding sites with a decreased Bmax and unchanged Kd value. Only treatment of mesangial cells by ANG II or EXP-3174 produced downregulation of [3H]losartan binding sites. In contrast, exposure of these cells to losartan resulted in upregulation of [3H]losartan binding sites. Under all conditions, only Bmax was modified. Whereas internalization of [3H]losartan in mesangial cells was negligible under all experimental conditions, there was an increase of the percentage of internalized 125I-[Sar1,Ala8]ANG II after exposure of the cells to ANG II or AT1 antagonists. No change was observed in mesangial cell AT1 receptor mRNA levels. This study demonstrates that 1) AT1 mRNA is expressed in human mesangial cells; 2) the characteristics of 125I-[Sar1,Ala8]ANG II and [3H]losartan binding sites in rat glomeruli and human mesangial cells are different, with Kd and Bmax values greater in both preparations when [3H]losartan was utilized; 3) both types of binding sites obey different regulations, and the effects of losartan in vivo are due in part to the associated increase in plasma ANG II levels and the transformation of the drug into its metabolite, EXP-3174; 4) downregulation of AT1 receptors does not depend on changes in mRNA expression but is associated with increased relative internalization.

Administration, Oral↗
PubMed1994

Enzyme replacement therapy for murine mucopolysaccharidosis type VII.

Recombinant mouse beta-glucuronidase administered intravenously to newborn mice with mucopolysaccharidosis type VII (MPS VII) is rapidly cleared from the circulation and localized in many tissues. Here we determine the tissue distribution of injected enzyme and describe its effects on the histopathology in 6-wk-old MPS VII mice that received either one injection of 28,000 U recombinant beta-glucuronidase at 5 wk of age or received six injections of 28,000 U given at weekly intervals beginning at birth. These mice were compared with untreated 6-wk-old MPS VII mice. The single injection decreased lysosomal distention in the fixed tissue macrophage system. MPS VII mice that received multiple injections had 27.8, 3.5, and 3.3% of normal levels of beta-glucuronidase in liver, spleen, and kidney, respectively. Brain had detectable beta-glucuronidase, ranging from 2.0-12.1% of normal. Secondary elevations of alpha-galactosidase and beta-hexosaminidase in brain, spleen, liver, and kidney were decreased compared with untreated MPS VII mice. Although no improvement was observed in chondrocytes, glia, and some neurons, the skeleton had less clinical and pathological evidence of disease and the brain had reduced lysosomal storage in meninges and selected neuronal groups. These data show that recombinant beta-glucuronidase treatment begun in newborn MPS VII mice provides enzyme to most tissues and significantly reduces or prevents the accumulation of lysosomal storage during the first 6 wk of life. Whether therapy begun later in life can achieve this level of correction remains to be established.

Animals↗
PubMed1994

Mucopolysaccharidosis VII: postmortem biochemical and pathological findings in a young adult with beta-glucuronidase deficiency.

The postmortem biochemical and pathological findings in the first patient reported with mucopolysaccharidosis VII are described. Clinical, radiographic, and biochemical features of this 19-yr-old black man were initially reported in 1973 when, at age 2 1/2 yr his enzymatic defect, deficiency of beta-glucuronidase, was identified. The autopsy findings are now described with biochemical data further characterizing the enzyme deficiency and resultant glycosaminoglycan accumulation. He had dysostosis multiplex and extensive cardiovascular lesions including arterial stenosis, and marked fibrous thickening of the atrioventricular and aortic valves. Microscopic evidence of lysosomal storage was found in bone, cartilage, arteries and cardiac valves, liver, spleen, lymph nodes, eyes, adrenal, pituitary, and the central nervous system. In the brain, storage was localized to specific regions, primarily intraneuronal, and appeared ultrastructurally as delicate whorled filamentous accumulations in lysosomes. Similar filamentous storage also occurred in medial cells of the aorta. Multiple postmortem tissues contained only trace amounts of beta-glucuronidase and elevated glycosaminoglycans, predominantly chondroitin 4- and 6-sulfate.

Adult↗
PubMed1993

Clinical study of bendazac lysine for in vivo contact lens cleaning.

Bendazac Lysine (BZL), a nonsteroidal anti-inflammatory drug (NSAID), prevents denaturation of proteins secondary to chemical and physical activity. The major protein deposited on soft contact lenses is lysozyme, derived from the preocular tear film. We evaluated the effectiveness of eye drops formulated with BZL for in vivo prevention of proteinaceous deposits on contact lenses and found them to be useful in inhibiting protein deposition during a 6-month clinical trial.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1993

Enzyme replacement with recombinant beta-glucuronidase in the newborn mucopolysaccharidosis type VII mouse.

beta-Glucuronidase injected i.v. into newborn mucopolysaccharidosis VII mice was cleared from the circulation in less than 1 h and taken up by tissues in a distribution corresponding to the location of the mannose 6-phosphate receptor. One h after a 3.5-mg/kg beta-glucuronidase injection, beta-glucuronidase levels were equal to or greater than normal in every organ examined with the exception of the brain, where 31% normal activity was present. Enzyme was detectable histochemically in the major sites of pathology for mucopolysaccharidosis VII including bone, brain, heart, and fixed tissue macrophages. The half-life of recombinant beta-glucuronidase activity in various organs of injected mucopolysaccharidosis VII mice was 1.5 to 4.5 d. These studies show that recombinant beta-glucuronidase administered to newborn mice reaches the sites of clinically important storage in murine mucopolysaccharidosis VII.

Animals↗
PubMed1993

Treatment of murine mucopolysaccharidosis type VII by syngeneic bone marrow transplantation in neonates.

BACKGROUND: Bone marrow transplantation (BMT) proved an effective therapy for murine mucopolysaccharidosis type VII (MPS VII) in adult gusmps/gusmps mice with well developed clinical and pathologic characteristics of the disease. MPS VII mice transplanted as adults had a marked decrease in lysosomal storage material in many organs, although not in the skeleton and brain (1). Since untreated newborn MPS VII mice appear normal and have minimal lysosomal storage material detectable microscopically, we postulated that BMT in newborn mice might prevent the subsequent accumulation of storage material. EXPERIMENTAL DESIGN: One-day-old mutant and phenotypically normal mice were exposed to 2, 4, 6 and 8 Gray and then injected intravenously with syngeneic bone marrow cells from homozygous normal females. Transplanted mice were examined biochemically and microscopically at 10 weeks and 10 months of age. RESULTS: Newborn mice receiving BMT lived longer than untreated mutants, had less severe facial dysmorphism, and better mobility. beta-Glucuronidase activity in liver, spleen, kidney and brain increased with increasing radiation dose. The secondary elevations of alpha-galactosidase and beta-hexosaminidase observed in MPS VII, were significantly reduced in liver and spleen in all radiation groups. Treated mutants had less histologic evidence of lysosomal storage disease in bones, joints and periarticular tissue as compared with untreated mutants. Neonatal BMT also reduced storage in the leptomeninges, ependyma and retinal pigment epithelium and caused a slight decrease in neuronal storage at high radiation dose. Radiation dose dependent cerebellar and retinal dysplasia and long bone growth retardation was observed when the therapy was initiated in newborn mice but not when the animals were transplanted as adults. CONCLUSIONS: BMT is a more effective therapy for MPS VII when it is performed at birth rather than in adults. Alternate means of ablating host hematopoietic stem cells should be employed as a pretreatment for BMT due to the severe side effects of radiation on newborns.

Animals↗
PubMed1992

Neurophysiological basis of cognitive deficits in long-term survivors of childhood cancer.

Thirty-three survivors of childhood cancer were tested with event-related potentials (P300), motor reaction time tests, and neuropsychological tests to assess the underlying physiological basis of treatment-related cognitive sequelae. Thirteen patients had received intrathecal chemotherapy, 11 had received intrathecal chemotherapy plus cranial radiotherapy, and nine had been treated without any form of central nervous system therapy. Neuropsychological performance of the groups treated without cranial radiotherapy was normal, but the group given cranial radiotherapy was significantly impaired. Mean reaction time and P300 latency were somewhat slower in the group given intrathecal chemotherapy relative to the group given no central nervous system treatment, but were significantly delayed in the group given cranial radiotherapy. Correlations of reaction time and P300 latency with neuropsychological test scores were also obtained. Results suggest that slowing of cortical activity secondary to white-matter damage may underlie cognitive decline in children treated with intensive central nervous system therapies, especially cranial radiotherapy.

Adolescent↗
PubMed1992

Acceptor requirements for GDP-fucose:xyloglucan 1,2-alpha-L-fucosyltransferase activity solubilized from pea epicotyl membranes.

GDP-fucose:xyloglucan (XG) fucosyltransferase from growing Pisum epicotyl tissue was solubilized in detergent and used to examine the capacity of intact XG from Tamarindus seeds, and its partial hydrolysis products, to act as fucose acceptors with GDP-[14C]fucose as donor. Native seed XG (Mr greater than 10(6) Da) was partially depolymerized by incubation with Trichoderma cellulase for various periods of time. Cellulase was inactivated and reaction mixtures were incubated with GDP-[14C]fucose plus solubilized pea fucosyltransferase and then fractionated on columns of Sepharose CL-6B or Bio-Gel P4. Specific activities (Bq/microgram carbohydrate) of fragments with Mr ranging from 10(6) to 10(4) Da were constant throughout the size ranges, indicating that all stretches of the XG chains were available for fucosylation. More complete cellulase hydrolysis yielded subunit oligosaccharides that chromatographed in a cluster of hepta-, octa-, and nonasaccharides, none of which acted as fucosyl acceptors when incubated with pea fucosyltransferase. However, a substantial amount (up to half of hydrolysate) of larger transient oligosaccharides was also formed with a size equivalent to three of the oligosaccharide subunits. Octasaccharide subunits in this trimer were readily fucosylated. This fucosyltransfer was inhibited by uncombined (free) subunit oligosaccharides, which implies that the latter could bind to the transferase and displace at least part of the trimer, even though they could not themselves be fucosylated. Reduction of the trimer oligosaccharide with NaB3H4, followed by further hydrolysis with cellulase, resulted in tritiated nonasaccharide and unlabeled octasaccharide in a concentration ratio of 1:2. The tamarind XG trimer which accepts fucose is therefore composed mainly of the subunit sequence: octa-octa-nonasaccharide (reducing). One of the terminal oligosaccharide subunits in this trimer, probably the nonasaccharide, appears to be required as a recognition (binding) site in fucosyltransferase in order for adjacent octasaccharide(s) to be fucosylated by the active (catalytic) enzyme site.

Cell Membrane↗
PubMed1992

Hypotony and corneal edema secondary to patching in normal eyes.

Over the past decade investigators have used patching when studying corneal response to eye lid closure. In these studies, corneal edema was thought to be secondary to hypoxia, and the results were used to predict corneal response to contact lens wear. None of these studies have measured or controlled the intraocular pressure (IOP) during eye patching. Reports in the literature indicate that hypotonous and hypertensive events may induce corneal edema. In order to evaluate the IOP and corresponding corneal changes, measurements were made on subjects with patched eyes. Thirty subjects were unilaterally patched and randomized into tight and light patch groups to maintain complete lid closure for 4 h. Measurements of IOP and corneal thickness (CT) were made at baseline and at hourly intervals. The contralateral eye served as the control for each subject. Our results indicate a significant decrease in IOP and a corresponding increase in CT in the tight patched group as compared to the light patch group, and baseline controls. These results suggest that the corneal edema which results from patching of the eye may be due to hypotony, or a combination of factors affecting corneal function, rather than hypoxia.

Bandages↗
PubMed1992

Acute ptosis secondary to contact lens wear.

Ocular ptosis secondary to the wearing of rigid contact lenses has been reported. Generally this ptosis is not of the classical variety, and appears to be an edematous or inflammatory response of the lid to the presence of the lens. We report a case of acute ptosis secondary to rigid lens wear in a patient who had undergone cataract surgery. The patient had been a contact lens wearer before surgery, and developed the relative ptosis postsurgically in the nonoperated eye. The ptosis resolved without any form of intervention other than ceasing to wear the contact lens. We feel that in cases where rigid lens wear is discontinued unilaterally for any reason, and a relative ptosis is noted, it should be given time to resolve before any therapeutic regimen is considered.

Acute Disease↗
PubMed1992

Microbial changes in the ocular environment with contact lens wear.

A group of 30 subjects, each fit with a single disposable or non-disposable soft contact lens, was further randomized to a daily wear or extended wear schedule to determine the effect of lens wear on the normal conjunctival flora. Cultures of the subjects' inferior cul-de-sacs were taken at baseline before any lens wear and after one week of lens wear. Additionally, each subjects' lens was removed in a sterile manner and cultured at the end of the one week wear period. In all subjects, the fellow eye was used as a control. There were no statistically significant differences with respect to bacterial culture results between experimental and control eyes. Also, there were no significant differences between the pre- and post-lens wear groups. And no significant differences were found when the larger groups were broken down into different wear schedules and lens types and compared. The results of this study suggest that the ocular flora is not markedly changed after one week of contact lens wear. Also raised is the question of whether an altered ocular flora is an etiologic factor in the development of infectious keratitis in contact lens wearers.

Bacteria↗
PubMed1991

Increased life span and correction of metabolic defects in murine mucopolysaccharidosis type VII after syngeneic bone marrow transplantation.

The gusmps/gusmps mouse has no beta-glucuronidase activity and develops murine mucopolysaccharidosis type VII (MPS VII). The clinical and pathologic abnormalities are similar to those found in humans with severe MPS VII. Mutant mice are dysmorphic, dwarfed, and have a shortened life span. Pathologic findings include widespread lysosomal storage. To determine whether bone marrow transplantation (BMT) corrects these abnormalities, genetically identical mutant animals were given syngeneic bone marrow transplants using cells from +/+ mice. Initial experiments showed that levels of beta-glucuronidase activity in recipient tissues correlated with the amount of radiation administered before BMT. Two groups of mice given BMT therapy were observed for periods of 1 and 2 years, respectively. These mice were evaluated using a combination of clinical, biochemical, histochemical, and pathologic analyses. Spleen, liver, cornea, and glomerular mesangial cells showed essentially complete correction at all radiation doses. Storage was partially corrected in meninges and perivascular cells in brain, and in renal tubular epithelial cells at the higher radiation doses. Life span in BMT-treated animals was increased approximately three-fold, approaching that seen in normal mice after BMT. These results support the position that BMT has a place in the therapeutic regimen for MPS VII.

Animals↗