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Biomedical subjects

M Levin

Publications and source records attributed to M Levin.

At least 127 records · Page 7Linked to original sources
PubMed1997

A volumetric approach to virtual simulation of functional endoscopic sinus surgery.

Advanced display technologies have made the virtual exploration of relatively complex models feasible in many applications. Unfortunately, only a few human interfaces allow natural interaction with the environment. Moreover, in surgical applications, such realistic interaction requires real-time rendering of volumetric data-placing an overwhelming performance burden on the system. We report on a collaboration of an interdisciplinary group developing a virtual reality system that provides intuitive interaction with volume data by employing real-time volume rendering and force feedback (haptic) sensations. We describe our rendering methods and the haptic devices and explain its utility of this system in the real-world application of Endoscopic Sinus Surgery (ESS) simulation.

Computer Simulation↗
PubMed1997

ENT endoscopic surgical training simulator.

This paper describes work in progress on the design and development of a prototype simulator for minimally invasive otolaryngology surgical training. The anatomy of the paranasal sinuses is geometrically complex and dangerously close to the brain and orbits, making this procedure challenging to practice and difficult to learn. We discuss the potential role of computer simulation to enhance and accelerate acquisition of surgical skills. The design goals of the prototype include high-fidelity simulation of the endoscopic imagery and haptic cues of surgical palpation. The prototype enables endoscopic navigation and limited interactive tissue manipulation and dissection tasks on a virtual patient using realistic replicas of surgical tools. We present an overview of the system architecture with a discussion of the technological challenges, design issues and current status of the efforts.

Computer Simulation↗
PubMed1997

Immunopathogenesis of HTLV-I associated neurologic disease: massive latent HTLV-I infection in bone marrow of HAM/TSP patients.

The localization of mammalian retroviruses to specified immune organs has significant implications on the pathophysiology of retroviral associated diseases. Human T-cell Lymphotropic Virus Type I (HTLV-I) is considered a CD4+ lymphotropic virus although the virus has been shown to infect a large variety of cells in vitro. Similarly, the human immunodeficiency virus (HIV), once thought to be harbored only in CD4+ peripheral blood lymphocytes (PBL) has been shown to be present in latent form in lymph nodes of HIV infected patients. HTLV-I Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP) is a chronic progressive neurologic disorder of the central nervous system and is believed to result from infection of HTLV-I in association with an immunopathogenic or autoimmune mechanism. Here we describe experiments which utilize the in situ hybridization/polymerase chain reaction technology to demonstrate extensive HTLV-I infection of bone marrow in HAM/TSP patients. We discuss these results in the context of HTLV-I associated neurologic disease and extend these observations to other disorders of potential retroviral etiology and autoimmune involvement.

Bone Marrow↗
PubMed1996

A mutation in the interferon-gamma-receptor gene and susceptibility to mycobacterial infection.

BACKGROUND: Genetic differences in immune responses may affect susceptibility to mycobacterial infection, but no specific genes have been implicated in humans. We studied four children who had an unexplained genetic susceptibility to mycobacterial infection and who appeared to have inherited the same recessive mutation from a common ancestor. METHODS: We used microsatellite analysis, immunofluorescence studies, and sequence analysis to study the affected patients, unaffected family members, and normal controls. RESULTS: A genome search using microsatellite markers identified a region on chromosome 6q in which the affected children were all homozygous for eight markers. The gene for interferon-gamma receptor 1 maps to this region. Immunofluorescence studies showed that the receptor was absent on leukocytes from the affected children. Sequence analysis of complementary DNA for the gene for interferon-gamma receptor 1 revealed a point mutation at nucleotide 395 that introduces a stop codon and results in a truncated protein that lacks the transmembrane and cytoplasmic domains. CONCLUSIONS: Four children with severe mycobacterial infections had a mutation in the gene for interferon-gamma receptor 1 that leads to the absence of receptors on cell surfaces and a functional defect in the up-regulation of tumor necrosis factor alpha by macrophages in response to interferon-gamma. The interferon-gamma pathway is important in the response to intracellular pathogens such as mycobacteria.

Antigens, CD↗
PubMed1996

Assessment of the effect of candidate anti-inflammatory treatments on the interaction between meningococci and inflammatory cells in vitro in a whole blood model.

A wide range of immunomodulating agents are now available which may be of benefit in reducing inflammatory cell activation in meningococcal sepsis. In order to facilitate selection of candidate anti-inflammatory agents for clinical trials, we have used an in vitro whole blood model to evaluate the effects on meningococcal induced neutrophil and monocyte activation, of dexamethasone, prostacyclin, pentoxifylline and a human IgM anti-lipid A monoclonal antibody (HA-1A). Known concentrations of heat and penicillin killed meningococci were added to whole blood and the time course of cellular activation was determined. Using elastase alpha 1-antitrypsin (elastase-alpha 1-AT) and TNF alpha production as markers of neutrophil and monocyte activation respectively, plasma levels of elastase-alpha 1-AT and TNF alpha were found to increase in a dose-dependent manner. Elastase-alpha 1-AT was detected early, with most release occurring between 15-30 min whereas TNF alpha was detected later, between 120-180 min. Dexamethasone, prostacyclin and pentoxifylline caused a dose-dependent inhibition of TNF alpha release but had no effect on elastase release. HA-1A had no effect on either TNF alpha or elastase release. This model may be useful in determining the sequence of inflammatory cell activation and in selecting candidate anti-inflammatory agents for evaluation in clinical trials.

Anti-Inflammatory Agents↗
PubMed1996

Translocation (3;3) in a patient with thrombocytopenia and erythroid dysplasia.

We describe a case with a translocation between the two chromosomes 3 with breakpoints q21 and q26, associated with a unique constellation of hematologic abnormalities. Megakaryocytic dysplasia and peripheral thrombocytosis are the most common abnormalities associated with this chromosome abnormality. Our patient had acute myeloid leukemia (AML), thrombocytopenia, dyserythropoiesis, and an increased myeloid/erythroid ration but no mekakaryocytic dysplasia. Although multilineage involvement has been reported, erythrocyte dysplasia associated with thrombocytopenia and without megakaryocyte dysplasia appears to be extremely rare. Our case supports the speculation that #3 abnormalities with breakpoints q21 and q26 affect a pluripotent stem cell and suggests that megakaryocytic involvement may not be pathognomonic in hematologic abnormalities with t(3;3)(q21;26).

Chromosomes, Human, Pair 3↗
PubMed1996

Defective antigen processing associated with familial disseminated mycobacteriosis.

To gain insights into a possible immune defect predisposing to disseminated mycobacteria infection, we studied three of six surviving children with disseminated Mycobacterium avium complex infection, who had no recognized form of immunodeficiency. We used mycobacteria isolated from the patients and diphtheria, tetanus and pertussis vaccine (DTP) to study antigen-specific T lymphocyte responses. We observed that interferon-gamma (IFN-gamma) production by T cells in response to antigens (both mycobacteria and DTP) in these patients with disseminated infection was greatly impaired. This defect did not seem to be the result of T cell unresponsiveness, as phytohaemagglutinin (PHA) stimulation was able to induce high levels of IFN-gamma comparable to those seen in control patients with localized infection. Further experiments showed that peripheral blood mononuclear cells (PBMC) from patients with disseminated infection were able to present influenza haemagglutinin (HA) peptides to specific T cell clones. However, this ability was lost when the whole HA protein was used as source of antigen. Taken together, these observations support the notion that the primary immune defect in these patients with disseminated mycobacterial infection rests in the antigen-processing functions of their antigen-presenting cells (APC). These findings may provide clues to the wider problem of susceptibility to mycobacteria and other intracellular pathogens and have implications in designing therapy for these patients.

Antigen Presentation↗
PubMed1996

Demographic characteristics of the population of Greater Soweto, 1993.

"This research note provides information and findings on some aspects of urbanisation in Greater Soweto. It outlines the demographic characteristics of the population, namely the characteristics of households; household preferences for services; perceptions on accommodation; age and gender profiles; education levels; the origin of the inhabitants and mobility in and migration to Greater Soweto. Some findings are particularly important for future planning of services and low-income or subsidised housing."

Africa↗
PubMed1996

The influence of capsulation and lipooligosaccharide structure on neutrophil adhesion molecule expression and endothelial injury by Neisseria meningitidis.

Host inflammatory response to meningococcal infection is believed to be a major determinant of disease severity. Isogenic mutants of Neisseria meningitidis serogroup B1940, which differ in expression of capsular polysaccharide and lipooligosaccharide (LOS), were used to examine host responses in a whole blood model of bacteremia and a model of endothelial injury. The parent organism caused significantly less neutrophil shedding of the adhesion molecule, L-selectin, than the three mutant organisms (P < .01) and was most resistant to the bactericidal activity of whole blood. Despite marked differences in bacterial adhesion to endothelial cells (P < .05), no damage was induced by organisms alone. Endothelial injury was observed when neutrophils were incubated with adherent, capsule-deficient organisms (P < .05). The degree of endothelial damage was related to the number of neutrophils adherent to the endothelium. Thus, bacterial capsulation and LOS structure can influence neutrophil activation and endothelial injury and, as such, may be important in the pathogenesis of meningococcal sepsis.

Antigens, Bacterial↗
PubMed1996

Variation in the tumor necrosis factor-alpha gene promoter region may be associated with death from meningococcal disease.

Tumor necrosis factor-alpha (TNF-alpha) plays a central role in the pathophysiology of sepsis. Levels of TNF-alpha are directly correlated with severity in meningococcal disease (MD). A polymorphism in the promoter region of the TNF-alpha gene is associated with differences in the secretion of TNF-alpha. The TNF2 allele is associated with higher constitutive and inducible levels of TNF-alpha secretion than is the TNF1 allele. To investigate whether possession of the TNF2 allele is associated with severity in MD, the frequency of TNF1 and TNF2 alleles in 98 children with MD was compared. There were more deaths among children who had the TNF2 allele (P = .03; relative risk [RR], 2.5; 95% confidence interval [CI], 1.1-5.7) than in those who did not. There was also an increased risk of severe disease in children with the TNF2 allele (P = .02; RR, 1.6; 95% CI, 1.1-2.3). Possession of the TNF2 allele predisposes to a worse outcome in children with meningococcal infection.

Alleles↗