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Biomedical subjects

M S Bronze

Publications and source records attributed to M S Bronze.

At least 19 recordsLinked to original sources
PubMed2005

Systemic bone loss and induction of coronary vessel disease in a rat model of chronic inflammation.

Clinically, osteopenia or low bone mass has been observed in a variety of chronic inflammatory diseases, and elevated proinflammatory mediators have implicated this process. The purpose of this study was to develop an in vivo model of bone loss induced by chronic systemic inflammation. Time-release pellets designed to deliver one of three doses of LPS: Low (3.3 microg/day), High (33.3 microg/day), or Placebo over 90 days, were implanted subcutaneously in 3-month-old male Sprague-Dawley rats (n = 8/group). Neutrophil counts, indicative of ongoing inflammation, were elevated (P < 0.05) in both LPS groups at 30 days post-implant and remained significantly elevated in the High dose throughout the 90-day study period. At the end of the study, bone loss occurred in the femur as indicated by decreased bone mineral density (BMD) in both LPS-treated groups, but vertebral BMD was reduced in the High dose animals only. Microcomputed tomography revealed that trabecular bone volume (BV/TV) of the proximal tibial metaphysis tended to be reduced in the High dose LPS group. Deleterious effects on trabecular number (TbN) and trabecular separation (TbSp) were observed in both LPS-treated groups, but only the High dose group reached statistical significance. These alterations in trabecular microarchitecture resulted in compromised biomechanical properties. No changes in cortical thickness, porosity, or area of the tibia midshaft were evident at either dose of LPS. Up-regulation of the proinflammatory mediators, cyclooxygenase (COX)-2, interleukin (IL)-1, and tumor necrosis factor (TNF)-alpha was demonstrated in the metaphyseal region where the deleterious effects of LPS were observed. In addition to these alterations in bone, trichrome staining indicated changes in the coronary arterioles, consistent with vascular disease. Utilization of a LPS time-release pellet appears to provide an in vivo model of chronic inflammation-induced bone loss and a potentially novel system to study concurrent development of osteopenia and vascular disease.

Absorptiometry, Photon↗
PubMed2000

Osteonecrosis complicating highly active antiretroviral therapy in patients infected with human immunodeficiency virus.

Few patients with osteonecrosis that complicates human immunodeficiency virus (HIV) infection have been reported. We describe 5 patients whose symptoms of osteonecrosis developed with viral suppression and improvement in CD4 lymphocyte counts as a result of antiretroviral therapy. In addition, we review previously reported cases. The mean patient age was 35 years, and HIV was the sole risk factor in only 33%. Eighteen patients (55%) were receiving antiretroviral treatment when osteonecrosis was diagnosed. For 16 patients whose CD4 lymphocyte counts were reported, the mean CD4 count was 350 cells/mm(3). In 10 of these patients, the occurrence or worsening of symptoms of osteonecrosis appeared to be related to successful antiretroviral therapy. We conclude that osteonecrosis is an emerging manifestation of HIV infection and that it may be either a consequence of immunologic and virologic improvement resulting from antiretroviral therapy or a complication caused by the drugs themselves.

Adult↗
PubMed2000

Enhanced extracellular growth of Staphylococcus aureus in the presence of selected linear peptide fragments of human interleukin (IL)-1beta and IL-1 receptor antagonist.

Replication of Staphylococcus aureus is significantly enhanced in the presence of recombinant interleukin (IL)-1beta. In this study, specific binding of IL-1beta to the surface of S. aureus significantly increased growth of S. aureus in the presence of IL-1beta and IL-1ra in a concentration-dependent manner. Although IL-1ra enhanced the growth of S. aureus, there was a significant reduction in IL-1beta-mediated growth enhancement of S. aureus when 25-fold excess amounts of IL-1ra (in comparison with the IL-1beta concentration) were present in the culture medium. Thus, IL-1beta may influence the growth of S. aureus through a receptor-mediated event. By using 5 linear peptides spanning limited regions of IL-1beta, the growth-promoting regions were localized to amino acid residues 118-147 and 208-240. These results build on the newly evolved concept of direct interactions between the soluble mediators of inflammation and infectious agents.

Culture Media↗
PubMed2000

Sternal osteomyelitis caused by mycobacterium tuberculosis: case report and review of the literature.

Sternal osteomyelitis caused by Mycobacterium tuberculosis is rare; since the advent of modern antituberculous therapy, a limited number of detailed cases have been reported. Most patients were relatively young, free of underlying disease, and lived in a country in which tuberculosis is endemic. The disease presented indolently with sternal pain and swelling. Extrasternal disease is detectable in less than half. Diagnosis was based on histologic examination of infected tissues and mycobacterial cultures. Most patients recovered after surgical debridement and combination drug therapy. Tuberculous sternal osteomyelitis should be considered in patients with sternal pain and swelling.

Adult↗
PubMed1999

Isoniazid drug and food interactions.

Isoniazid inhibits the metabolism of several drugs, resulting in clinically significant interactions in some patients. Clinical trials and case reports have documented that isoniazid can cause increased phenytoin and carbamazepine serum concentrations and toxicity. In relatively high doses, isoniazid can also cause increased effect of theophylline and warfarin. Isoniazid inhibits metabolism of selected benzodiazepines and vitamin D. Inhibition of monoamine oxidase and histaminase by isoniazid can cause significant drug-food interactions. Food greatly decreases isoniazid bioavailability. Although probably best recognized as an inhibitor of drug metabolism, isoniazid has a biphasic effect of inhibition-induction on one cytochrome P450 isozyme, CYP2E1, which partially explains the interaction with acetaminophen and increased risk of hepatotoxicity. Continued investigations will likely result in discovery of new isoniazid interactions.

Antitubercular Agents↗
PubMed1999

Effects of cytokines and endotoxin on the intracellular growth of bacteria.

Patients with unresolving acute respiratory distress syndrome (ARDS) have persistently elevated levels of proinflammatory cytokines in the lungs and circulation and increased rates of bacterial infections. Phagocytic cells hyperactivated with lipopolysaccharide (LPS), which induces high levels of proinflammatory cytokines in monocytic cells, are inefficient in killing ingested bacteria despite having intact phagocytic activity. On the other hand, phagocytic cells that are activated with an analogue of LPS that does not induce the expression of proinflammatory cytokines effectively ingest and kill bacteria. We hypothesized that in the presence of high concentrations of proinflammatory cytokines, bacteria may adapt and utilize cytokines to their growth advantage. To test our hypothesis, we primed a human monocytic cell line (U937) with escalating concentrations of the proinflammatory cytokines tumor necrosis factor alpha, interleukin-1beta (IL-1beta), and IL-6 and with LPS. These cells were then exposed to fresh isolates of three common nosocomial pathogens: Staphylococcus aureus, Pseudomonas aeruginosa, and an Acinetobacter sp. In human monocytes primed with lower concentrations of proinflammatory cytokines (10 to 250 pg) or LPS (1 and 10 ng), intracellular bacterial growth decreased. However, when human monocytes were primed with higher concentrations of proinflammatory cytokines (1 to 10 ng) or LPS (1 to 10 micrograms), intracellular growth of the tested bacteria increased significantly (P <0.0001). These results were reproduced with peripheral blood monocytes obtained from normal healthy volunteers. The specificity of the cytokine activity was demonstrated by neutralizing the cytokines with specific antibodies. Our findings provide a possible mechanism to explain the frequent development of bacterial infections in patients with an intense and protracted inflammatory response.

Acinetobacter↗
PubMed1998

Impending paradoxical embolism.

The advent of echocardiography has led to the more frequent discovery of impending paradoxical embolism. Paradoxical embolism should be considered whenever there is an arterial embolism from an unidentified source in the presence of a concomitant venous thromboembolic phenomenon. Patients with paradoxical embolism present with neurological abnormalities or features suggesting arterial embolism. Annually, paradoxical embolism may account for up to 47,000 strokes in the United States, and a patent foramen ovale has been reported in up to 35% of the normal population. Events that give rise to pulmonary hypertension may result in a right-to-left shunt through a patent foramen ovale allowing a venous thromboembolism access to the arterial circulation. Herein we report a case of impending paradoxical embolism and review the pertinent literature.

Diagnosis, Differential↗
PubMed1998

Citrobacter freundii empyema in a patient with occult pulmonary histoplasmosis.

The genus Citrobacter includes three species of organisms that are uncommonly associated with human infection. When they are pathogenic, there are usually one or more associated respiratory, urinary, skin-soft tissue, and central nervous system infections and neonatal sepsis. These infections occur in the wake of significant systemic illness or complicate antibiotic usage. Rarely, infection has been associated with active tuberculosis. The authors report a case of Citrobacter freundii empyema in a patient with occult pulmonary histoplasmosis.

Aged↗
PubMed1997

Group G streptococcal arthritis: case report and review of the literature.

Nongonococcal septic arthritis in adults is usually caused by infections with staphylococcal or streptococcal species. In patients with underlying diseases, especially those with chronic joint disease or malignancy, bacterial isolates from infected joint spaces may include group G streptococci. Occasionally, group G streptococcal arthritis may occur in otherwise healthy individuals. We report a case of pyogenic sacroiliitis in a healthy young adult and review the pertinent literature concerning group G streptococcal arthritis.

Adolescent↗
PubMed1996

The reemergence of serious group A streptococcal infections and acute rheumatic fever.

Acute rheumatic fever and life-threatening group A streptococcal infections have reemerged during the past 15 years to once again become a serious health threat in the developed countries of the world. Reports of outbreaks of acute rheumatic fever in many parts of this country and others have shattered the complacency that the health-care community had acquired related to this devastating sequela of streptococcal pharyngitis. Invasive streptococcal infections, often associated with loss of limbs of life despite optimal antibiotic therapy, have underscored the potential virulence of these organisms. A new clinical entity, streptococcal toxic shock syndrome, has emerged as a consequence of the new invasive strains of group A streptococci. In this article, the authors summarize the recent changes in the epidemiology of group A streptococcal infections and rheumatic fever and review the potential reasons for the increased virulence of these organisms. In addition, they discuss prospects for a streptococcal M protein vaccine designed to control these infections and their sequelae.

Anti-Bacterial Agents↗
PubMed1996

Case report: Candida zeylanoides infective endocarditis complicating infection with the human immunodeficiency virus.

Despite the frequent occurrence of mucosal candidiasis in patients infected with HIV, systemic candidiasis is uncommon and usually associated with intravenous catheters, parenteral nutrition, or antibiotics and neutropenia. Most of the fungal isolates are usually Candida albicans, Candida tropicalis or Candida parapsilosis. The authors report a case of infective endocarditis due to Candida zeylanoides that occurred in a patient infected with HIV in the absence of the usual risk factors for systemic candidiasis.

Adult↗
PubMed1996

Adherence of Streptococcus uberis to bovine mammary epithelial cells and to extracellular matrix proteins.

Adherence of an encapsulated (UT 101) and a non-encapsulated (UT 102) strain of Streptococcus uberis to a bovine mammary epithelial cell line (MAC-T) and to extracellular matrix proteins (ECMP) including fibronectin, collagen and laminin was investigated. S. uberis was co-cultured at 4 degrees C with MAC-T cell monolayers. Both strains of S. uberis adhered to MAC-T cells. However, the non-encapsulated strain of S. uberis adhered better to MAC-T cells than the encapsulated strain. Preincubation of MAC-T cells with lipoteichoic acid (LTA) and/or treatment of S. uberis with antibodies directed against the carboxyl-terminal half of type 24 M protein reduced adherence of both strains of S. uberis to MAC-T cells. Adherence to ECMP was measured by incubating bis-carboxyethyl-carboxyfluorescein acetomethyl ester (BCECF-AM) labelled S. uberis in 96-well plates coated with fibronectin, collagen or laminin. Both strains adhered to ECMP, however, the encapsulated strain adhered better to ECMP than the non-encapsulated strain. Results of this investigation demonstrated that both strains of S. uberis evaluated were capable of adhering to bovine mammary epithelial cells and to ECMP. Adherence of S. uberis to mammary epithelium may be an extremely important mechanism in the establishment and progression of bovine intramammary infections.

Animals↗
PubMed1994

Critical role of the group A streptococcal capsule in pharyngeal colonization and infection in mice.

To study the role of the group A streptococcal capsule in pharyngeal colonization, we used two acapsular mutants derived from a type 24 strain of group A Streptococcus by transposon mutagenesis. One mutant had a stable acapsular phenotype due to a transposon-associated chromosomal deletion of essential capsule synthetic genes, while the second mutant could revert to the encapsulated phenotype at a low frequency (< 10(-4)) upon spontaneous excision of the transposon from the capsule-synthesis region of the chromosome. Both acapsular mutants were sensitive to phagocytic killing in vitro and had reduced virulence in mice after intraperitoneal challenge. Mice inoculated intranasally with the stable acapsular mutant rapidly cleared the organisms from the pharynx, and no mice died. In contrast, throat cultures of animals challenged with the revertible mutant yielded many encapsulated revertants, and mortality was similar to that of animals challenged with the parent strain. The rapid emergence of a population of encapsulated revertants in the pharynx implies that the capsule conferred a powerful selective advantage in this environmental niche. Together with the complete avirulence of the stable acapsular mutant, these observations indicate that the hyaluronic acid capsule plays a critical role in colonization and infection of the pharynx by group A streptococci.

Animals↗