Publications by authors named "Romain P"

The routine work of any molecular biology laboratory includes the daily use of microorganisms, including strains of E. coli, transformed with a variety of plasmids expressing at least one antibiotic resistance gene (ARG). Therefore, to avoid the accidental release of ARGs into environmental water, methods for disinfection of liquid laboratory waste must be effective in destroying nucleic acids.

View Article and Find Full Text PDF

In this article, we provide a comprehensive analysis and a normative assessment of rationing through inconvenience as a form of rationing. By "rationing through inconvenience" in the health sphere, we refer to a nonfinancial burden (the inconvenience) that is either intended to cause or has the effect of causing patients or clinicians to choose an option for health-related consumption that is preferred by the health system for its fairness, efficiency, or other distributive desiderata beyond assisting the immediate patient. We argue that under certain conditions, rationing through inconvenience may turn out to serve as a legitimate and, compared to direct rationing, even a preferable tool for rationing; we propose a research agenda to identify more precisely when that might be the case and when, alternatively, rationing through inconvenience remains ethically undesirable.

View Article and Find Full Text PDF

Background: The relationship between body mass index (BMI) and cardiopulmonary adverse events (CAEs) for ambulatory colonoscopy is unclear.

Aim: To assess the association of BMI and CAEs associated with ambulatory colonoscopy.

Methods: This is a retrospective cohort analysis of 418 patients who underwent outpatient colonoscopy at the Durham Veterans Affairs Medical Center categorized as normal/overweight (BMI < 30), obese (BMI 30-34), or morbidly obese (BMI ≥ 35).

View Article and Find Full Text PDF

Conflicts of interest represent circumstances in which professional judgments or actions regarding a primary interest, such as the responsibilities of a medical researcher, may be at risk of being unduly influenced by a secondary interest, such as financial gain or career advancement. The secondary interest may be financial or non-financial, and the resultant bias may be conscious or unconscious. The presence of conflicts of interest poses a problem for professional, patient, and public trust in research and the research enterprise.

View Article and Find Full Text PDF

Background: Transcriptome sequencing is a powerful tool for measuring gene expression, but as well as some other technologies, various artifacts and biases affect the quantification. In order to correct some of them, several normalization approaches have emerged, differing both in the statistical strategy employed and in the type of corrected biases. However, there is no clear standard normalization method.

View Article and Find Full Text PDF

This paper presents a method to develop objective discomfort evaluation indicators for a task oriented motion using the concept of less constrained movement. The basic idea is to compare imposed and less constrained movements in order to identify relevant biomechanical parameters for defining objective discomfort indicators. The task of automotive pedal clutching was chosen for illustrating the proposed method.

View Article and Find Full Text PDF

Minimizing the potential adverse effects of clinical investigators' financial conflicts of interest involves, in part, determining how much of an investigator's "business" should be disclosed to participants in research studies. What should be disclosed and why? How will we know if disclosure matters?

View Article and Find Full Text PDF

The anticardiolipin or antiphospholipid antibody syndrome is characterized by an increased incidence of venous and arterial thromboses. This syndrome may occur in association with systemic lupus erythematosus or independently. Gastroenterological manifestations have included Budd-Chiari syndrome, hepatic infarction, esophageal necrosis with perforation, intestinal ischemia and infarction, pancreatitis, and colonic ulceration.

View Article and Find Full Text PDF

Mixed cryoglobulinemia is a systemic vasculitis with clinical manifestations ranging from the characteristic benign-appearing syndrome of palpable purpura, arthrologies, and fatigue to severe vasculitis involving vital organs. A strong association of the disease with hepatitis C virus infection and the demonstration of the specific concentration of the virus in the cryoglobulins have implicated hepatitis C virus in the etiopathogenesis of the disease. The increase in illicit intravenous drug use in the past 30 years seems to have raised the occurrence in the United States of this once uncommon disease and changed the demographics: there seem to be more male intravenous drug users in their forties with the disease than women without risk factors for hepatitis C virus infection in their fifties and sixties.

View Article and Find Full Text PDF

We examined the hypothesis that both misoprostol (miso), a prostaglandin E(1) (PGE(1)) analog, and nonsteroidal anti-inflammatory drugs (NSAIDs) have significant and largely inhibitory effects on T-cell activation and, consequently, influence T-cell function. Studies were done using a macrophage-independent system for T-cell activation by mitogenic combinations of immobilized anti-T-cell monoclonal antibodies (mabs), including combinations of anti-CD3 with anti-CD4 or anti-CD6. The results indicate that misoprostol, like other prostaglandins, can inhibit T-cell proliferation and the expression of mRNAs for cytokines critical in T-cell growth and immunoregulation.

View Article and Find Full Text PDF

We present 10 cases of mixed cryoglobulinemia in patients infected with hepatitis C, including pertinent clinical, serologic, and pathological data. The findings attributable to MC appear to be similar in patients who are HCV-infected as in those with unknown HCV status. The prevalence of MC in HCV-infected patients appears to be lower in our region (13%) than in southern Europe (50-90%) although some of this difference is due to our requirement that patients included in our study have a cryocrit of at least 5%.

View Article and Find Full Text PDF

The CD6 glycoprotein is expressed primarily on lymphocytes and conveys co-activating signals to T cells, but its exact function and ligand(s) are unknown. A novel mAb, termed UMCD6, was demonstrated to recognize CD6 by immunoprecipitation, Western blotting, and reactivity with COS cells transfected with CD6 cDNA. UMCD6 was mitogenic for T cells and was strongly synergistic with phorbol ester in inducing T cell activation.

View Article and Find Full Text PDF

A variant human H2B histone gene (GL105), previously shown to encode a 2300 nt replication independent mRNA, has been cloned. We demonstrate this gene expresses alternative mRNAs regulated differentially during the HeLa S3 cell cycle. The H2B-Gl105 gene encodes both a 500 nt cell cycle dependent mRNA and a 2300 nt constitutively expressed mRNA.

View Article and Find Full Text PDF

Leukocytes express a family of high m.w. glycoproteins called leukocyte common Ag (CD45), which are involved in phosphotyrosine signal transduction.

View Article and Find Full Text PDF

We analyzed the cell surface phenotype of CD8+ cells in both peripheral blood and synovial fluid (SF) of patients with rheumatoid arthritis (RA) and osteoarthritis (OA). Utilizing the monoclonal antibodies anti-CD45RA, anti-CD29 and anti-S6F1-, one can define both suppressor effector (CD45RA+CD29-S6F1-) and killer effector (CD45RA-CD29+S6F1+) cells within the CD8 population. In patients with OA, normal proportions of CD8+CD45RA+, CD8+CD29+ and CD8+S6F1+ cells were found in both peripheral blood and SF.

View Article and Find Full Text PDF

CD6 (T12) is a 130-kDa glycoprotein present on the surface of human T cells. Previously, we demonstrated that the anti-T12 and anti-2H1 monoclonal antibodies recognized different epitopes on CD6, and both were capable of transducing activation signals to T cells. Anti-T12 augmented suboptimal signaling via the TCR/CD3 complex and directly activated separated CD4+ but not CD8+ cells.

View Article and Find Full Text PDF