Biomedical subjects

Carol M Mason

Publications and source records attributed to Carol M Mason.

7 recordsLinked to original sources

PubMed2005

Pulmonary host defenses and factors predisposing to lung infection.

Hospital-acquired pneumonia remains a leading cause of nosocomial infections and is associated with significant rates of morbidity and mortality. Multiple host-, pathogen-, and intervention-related factors contribute to the development of pneumonia in this setting. Potentially deleterious impacts of illness or therapeutic modalities impair the host's ability to resist the development of pneumonia while in the hospital and predispose to a spectrum of pathogens of greater virulence than found in the community. Recognition of factors contributing to pneumonia in the hospital setting may offer the opportunity to intervene, minimizing, to the extent possible, the serious consequences of this nosocomial complication.

Cross Infection↗

PubMed2005

The nurse practitioner's role in helping patients achieve lipid goals with statin therapy.

PURPOSE: To discuss the merits of statins in achieving lipid goals and the role of nurse practitioners (NPs) in improving adherence to medical regimens with the goals of improving patient outcomes, reducing cardiovascular disease (CVD) risk within the population at large, and enhancing patients' ability to reach their individual goals. DATA SOURCES: Original research articles, journal articles, professional association practice guidelines. CONCLUSIONS: Despite extensive research clearly documenting the relation between lowering low-density lipoprotein cholesterol (LDL-C) and decreasing rates of cardiovascular events and deaths, lipid-lowering therapy is not being aggressively managed to achieve optimal lipid levels and CVDs remain the leading cause of death among adults in the United States. Contributing factors include lack of patient adherence with prescribed therapy, absence of dose titration when needed, and suboptimal follow-up. Two pathways to improving compliance are the following: first, use of a starting dose of a more efficacious statin to allow more patients to reach their LDL-C goal and, second, more effective primary care programs with NPs as team leaders who can assess and diagnose patients, then develop individual treatment plans and follow-up with patients to ensure that their lipid goals are met. IMPLICATIONS FOR PRACTICE: NPs are well suited to manage patients with hypercholesterolemia. The NP can bridge all aspects of care for the patient by overseeing assessment and treatment of cardiovascular risk factors, including elevated levels of LDL-C, initiating pharmacotherapy when needed, and establishing for each patient an individualized program that features education, support, and follow-up.

Anticholesteremic Agents↗

PubMed2005

Pulmonary interleukin-23 gene delivery increases local T-cell immunity and controls growth of Mycobacterium tuberculosis in the lungs.

Interleukin-23 (IL-23) is a heterodimeric cytokine that shares IL-12 p40 but contains a unique p19 subunit similar to IL-12 p35. Previous studies indicate a greater importance for intact IL-12/23 p40 expression than IL-12 p35 for immunity against Mycobacterium tuberculosis, suggesting a role for IL-23 in host defense. The effects of IL-23 on the outcome of pulmonary infection with M. tuberculosis have not been described. Here, we show that local delivery of replication-defective adenovirus vectors encoding IL-23 (AdIL-23) greatly stimulated expression of both gamma interferon (IFN-gamma) and IL-17 in lung tissues of otherwise normal mice. When given 72 h prior to infection with M. tuberculosis, AdIL-23 significantly reduced the bacterial burden at 14, 21, and 28 days. Markedly lower levels of lung inflammation were observed at 28 days than in control mice pretreated with control adenovirus (AdNull) or vehicle controls. AdIL-23 pretreatment resulted in increased numbers of CD4(+) CD25(+) activated T cells in lungs and draining lymph nodes compared to control groups and more CD4(+) T cells bearing surface memory markers in lung lymph nodes. IL-23 gene delivery also significantly enhanced host anti-mycobacterial T-cell responses, as shown by elevated levels of IFN-gamma and IL-17 secreted in vitro following restimulation with M. tuberculosis purified protein derivative. Overall, our data show that transient IL-23 gene delivery in the lung is well tolerated, and they provide the initial demonstration that this factor controls mycobacterial growth while augmenting early pulmonary T-cell immunity.

Adenoviridae↗

PubMed2004

Immunity against mycobacteria.

Mycobacterium tuberculosis is the most prevalent infectious pathogen in the world, largely due to its unique interactions with the human immune system. Even in a normal host, a frequent outcome of infection with M. tuberculosis is failure to completely eradicate the organisms, despite the development of cell-mediated immunity. Viable organisms persist in a state in which they do not progressively replicate, leading to latent infection, which carries a risk of breakdown into active (reactivation) tuberculosis at some point later in life. Key features of the immune response against mycobacteria are reviewed here, and potential mechanisms by which the organisms may subvert these host defenses are discussed. Despite the multicellular nature of the host response to infecting mycobacteria, the organisms cannot be eradicated and contribute to the ongoing worldwide epidemic with tuberculosis.

Journal Article↗

PubMed2004

Alcohol exacerbates murine pulmonary tuberculosis.

Alcohol consumption has been described as a risk factor for infection with Mycobacterium tuberculosis, but its contribution to tuberculosis has been difficult to isolate from other adverse socioeconomic factors. Our objective was to evaluate the impact of alcohol consumption on pulmonary infection with M. tuberculosis in a murine model. BALB/c mice were maintained on the Lieber-DeCarli liquid ethanol diet or a liquid control diet and infected intratracheally with low-dose M. tuberculosis H37Rv. Lung organism burdens, lung and lung-associated lymph node CD4(+)- and CD8(+)- lymphocyte numbers and rates of proliferation, and CD4(+)-lymphocyte cytokine production levels were compared between the groups. The alcohol-consuming mice had significantly higher lung organism burdens than the control mice, and the CD4(+)- and CD8(+)-lymphocyte responses to pulmonary infection with M. tuberculosis were blunted in the alcohol group. Lymphocyte proliferation and production of gamma interferon were decreased in the CD4(+) lymphocytes from the alcohol-consuming mice. Additionally, lung granulomas were significantly smaller in the alcohol-consuming mice. In conclusion, murine alcohol consumption is associated with decreased control of pulmonary infection with M. tuberculosis, which is accompanied by alterations in the region-specific CD4(+)- and CD8(+)-lymphocyte responses and defective lung granuloma formation.

Alcoholism↗

PubMed2003

Managing the spectrum of dyslipidemia in primary care.

Dyslipidemia, especially elevated low-density lipoprotein cholesterol (LDL-C), increases the risk of coronary heart disease and subsequent morbidity or mortality. For more than a decade, the National Cholesterol Education Program (NCEP) has endeavored to raise awareness of the dangers of dyslipidemia and to encourage the implementation of recommended treatment strategies. However, despite this initiative, previously published NCEP targets were not met. The recently released NCEP-Adult Treatment Panel III guidelines recommend more aggressive LDL-C reduction, elevation of categorical low high-density lipoprotein binding protein, and increased monitoring of moderate triglyceride elevations. Although the 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitors (statins) are the most powerful medications available to reduce LDL-C, studies have shown that more than half of patients treated with these drugs do not achieve therapeutic targets and the resultant decrease in coronary heart disease events. There are a number of possible reasons for this, including potency of the statins and a lack of compliance on the part of patients and providers. Another concern with the available statins is the issue of drug-drug interactions. Some of these concerns may be addressed by newer agents in this drug class that are in development. They appear to have the potential to induce even greater reductions in LDL-C and to positively affect other lipoproteins. They also have the potential for less risk of drug-drug interactions. Nurse practitioners can play a pivotal role in improving the management of dyslipidemia by ensuring the proper implementation of current guidelines, helping patients adhere to treatment protocols, and remaining abreast of developments that may pave the way toward even more effective intervention in the future.

Anticholesteremic Agents↗

PubMed2003

Ventilation-induced lung injury is associated with an increase in gut permeability.

Mechanical ventilation is associated with several harmful effects mainly related to high tidal volumes (Vt). Ventilator-induced lung injury can be responsible for an increased production of inflammatory mediators. We evaluated remote consequences on the gut of lung triggered inflammatory response, neutralizing anti-tumor necrosis factor (TNF) antibody was administered to assess the role of TNF in lung and gut permeability changes. Rats were anesthetized and ventilated for 2 h. A control group (Con: Vt = 10 mL/kg) was compared with a high Vt group (HV: Vt = 30 ml/kg). One microCi of I125-labeled human serum albumin was injected to measure extravascular albumin space. Gut permeability was evaluated by plasma-to-lumen ratio leakage of I125 human serum albumin. Extravascular albumin space increased in the HV group from 446 +/- 50 microL to 2783 +/- 887 microL. Gut index of permeability increased from 5.1 +/- 1.2 to 14.2 +/- 4.9. Anti-TNF antibody prevented both lung and gut increase in permeability. High tidal volume ventilation resulted in an increase in lung edema and gut permeability, antagonism of TNF with neutralizing antibodies abrogated the increase in gut permeability as well as lung edema.

Animals↗