tbuckley/cabot-search huggingface dataset:
Oxidative DNA Damage and Repair in Experimental Atherosclerosis Are Reversed by Dietary Lipid Lowering
Authors: Wim Martinet, Michiel W. M. Knaapen, Guido R. Y. De Meyer, Arnold G. Herman, Mark M. Kockx
Journal: Circulation Research (2001)

Increased oxidative stress is a major characteristic of hypercholesterolemia-induced atherosclerosis. The oxidative environment is mainly created by the production of reactive oxygen species, which are assumed to mediate vascular tissue injury. Oxidative DNA damage resulting from free radical attack remains, however, a poorly examined field in atherosclerosis. Male New Zealand White rabbits were fed a cholesterol-rich diet (0.3%) for 24 weeks. The induced atherosclerotic plaques showed elevated levels of the DNA damage marker 7,8-dihydro-8-oxoguanine (8-oxoG) as demonstrated by immunohistochemistry. 8-oxoG immunoreactivity was found predominantly in the superficial layer of the plaque containing numerous macrophage-derived foam cells but not in the media or in arteries of age-matched control animals. Alkaline single-cell gel electrophoresis revealed that the number of DNA strand breaks was significantly higher in the plaque as compared with control samples of normolipemic animals. These changes were associated with the upregulation of DNA repair enzymes (poly[ADP-ribose] polymerase-1, p53, phospho-p53 [phosphorylated at Ser392], and XRCC1 [x-ray repair cross-complementing 1]). DNA strand breaks normalized after 4 weeks of dietary lipid lowering. However, a significant reduction of 8-oxoG immunoreactivity was only observed after a prolonged period of lipid lowering (12 to 24 weeks). Repair pathways started to decline progressively when cholesterol-fed animals were placed on a normal diet. In conclusion, oxidative DNA damage and increased levels of DNA repair, both associated with diet-induced hypercholesterolemia, are strongly reduced during dietary lipid lowering. These findings may provide a better insight into the benefits of lipid-lowering therapy on plaque stabilization.
Collapsible Airway for Mouth-to-Mouth Resuscitation
Authors: Julius E. Stolfi
Journal: JAMA (1971)

<h3>To the Editor.—</h3> Mouth-to-mouth resuscitation has become the prime method used by those attempting to revive patients near death from drowning, electrocution, asphyxiation, or cardiac arrest. Although simple and effective, this method is objectionable in some aspects. Rescuers hesitate to use it because of the all-too-frequent presence of unpleasant secretions on the lips of victims. They also fear contact with disease-causing organisms. Failures of the method can often be attributed to the inability to depress the patient's tongue and thereby create a clear passageway for the flow of expired air in and out of the patient's lungs. Various types of airways have been used to overcome the objections and shortcomings listed above, but most are available only in hospitals and rarely in the physician's bag. Their size precludes widespread use by firemen, policemen, boy scouts, lifeguards, soldiers, utility employees, ambulance attendants, nurses, and physicians. Lives have been lost that might
Keith Alexander Adair Campbell
Authors: Victor Twyman
Journal: BMJ (2005)

Medical microbiologist who became a pioneer of hospital infection controlRobert Blowers had a lifelong interest in Staphylococcus aureus and hospital infection.From the mid-1950s onwards he produced a succession of publications on the prevention of hospital infections, particularly those following surgery.These ranged across the design of operating theatres, isolation rooms, and surgical clothing, and the prevention of the airborne spread of infection and clinical protocols for wound management.He co-produced the seminal textbook Hospital Infection: Causes and Prevention, which became the "bible" on infection control for nearly 20 years.In 1959 he was a key member of the Ministry of Health working group that produced a report on staphylococcal infections in hospitals.At a Department of Health workshop in December 2004, just a week before Robert's death, his major contribution was recalled by the department's inspector of microbiology and infection control, who had that week sent him a Christmas card with the message "you will be pleased to know that we are at last trying to implement your 1959 recommendations!"
Feature creation as a byproduct of attentional processing
Authors: Pierre Perruchet, Annie Vinter
Journal: Behavioral and Brain Sciences (1998)

Attributing the creation of new features to categorization requirements implies that the exemplars displayed are correctly assigned to their category. This constraint limits the scope of Schyns et al.'s proposal to supervised learning. We present data suggesting that this constraint is unwarranted and we argue that feature creation is better thought of as a byproduct of the attentional, on-line processing of incoming information.
Haemophilus influenzae type-b and non-b-type invasive diseases in urban children (&lt;5years) of Bangladesh: Implications for therapy and vaccination
Authors: Mahbubur Rahman, Shahadat Hossain, Abdullah Hel Baqui, Shereen Shoma, Harunur Rashid, Nazmun Nahar, Mohammed Khalequ Zaman, Farida Khatun
Journal: Journal of Infection (2008)
Religious leaders call for an end to discrimination against people living with AIDS
Authors: T. Sheldon
Journal: BMJ (2010)

In the first summit of its kind, about 40 religious and spiritual leaders from every continent and many faiths pledged this week to work to eliminate stigma and discrimination against people living with HIV/AIDS. They stressed that “AIDS was an illness, and not a sin,” and spoke of “remorse” for the harm people with HIV have suffered in the name of religion.

The summit, held in the Netherlands, was organised by the Geneva based Christian network, the Ecumenical Advocacy Alliance. Leaders who were Buddhist, Christian (Protestant and Roman Catholic), Hindu, Jewish, Muslim, Baha’i, and Sikh met with executive directors of the Joint United Nations Programme …
Mutation of the Cyba gene encoding p22phox causes vestibular and immune defects in mice
Authors: Yoko Nakano, Chantal M. Longo-Guess, David E. Bergstrom, William M. Nauseef, Sherri M. Jones, Botond Bánfi
Journal: Journal of Clinical Investigation (2008)

In humans, hereditary inactivation of either p22phox or gp91phox leads to chronic granulomatous disease (CGD), a severe immune disorder characterized by the inability of phagocytes to produce bacteria-destroying ROS. Heterodimers of p22phox and gp91phox proteins constitute the superoxide-producing cytochrome core of the phagocyte NADPH oxidase. In this study, we identified the nmf333 mouse strain as what we believe to be the first animal model of p22phox deficiency. Characterization of nmf333 mice revealed that deletion of p22phox inactivated not only the phagocyte NADPH oxidase, but also a second cytochrome in the inner ear epithelium. As a consequence, mice of the nmf333 strain exhibit a compound phenotype consisting of both a CGD-like immune defect and a balance disorder caused by the aberrant development of gravity-sensing organs. Thus, in addition to identifying a model of p22phox-dependent immune deficiency, our study indicates that a clinically identifiable patient population with an otherwise cryptic loss of gravity-sensor function may exist. Thus, p22phox represents a shared and essential component of at least 2 superoxide-producing cytochromes with entirely different biological functions. The site of p22phox expression in the inner ear leads us to propose what we believe to be a novel mechanism for the control of vestibular organogenesis.
Treatment of HIV-associated Kaposi's sarcoma with paclitaxel
Authors: M.W. Saville, J. Lietzau, J.M. Pluda, W.H. Wilson, R.W. Humphrey, E. Feigel, S.M. Steinberg, S. Broder, R. Yarchoan, J. Odom, I. Feuerstein
Journal: The Lancet (1995)
The Health Care Proxy and the Living Will
Authors: G J Annas
Journal: New England Journal of Medicine (1991)

American medicine is awash in forms: insurance forms, disability forms, informed-consent forms, and forms for various examinations, to name just a few. Forms can help make the practice of medicine more efficient, but they can also make it more routinized, impersonal, and bureaucratic. Congress and the President have decreed that beginning December 1, 1991, all hospitals, nursing facilities, hospice programs, and health maintenance organizations that serve Medicare or Medicaid patients must provide all their new adult patients with written information describing the patient's rights under state law to make decisions about medical care, including their right to execute a living . . .
A protein kinase A–dependent molecular switch in synapsins regulates neurite outgrowth
Authors: Hung-Teh Kao, Hong-jun Song, Barbara Porton, Guo-li Ming, Josephine Hoh, Michael Abraham, Andrew J. Czernik, Vincent A. Pieribone, Mu-ming Poo, Paul Greengard
Journal: Nature Neuroscience (2002)
Kinetic evidence for compartmentalization of myo-inositol in hepatocytes
Authors: Samuel Harold Sigal, John R. Yandrasitz, Gerard T. Berry
Journal: Metabolism (1993)

myo-Inositol uptake and conversion to phosphatidylinositol (PI) was studied in isolated rat hepatocytes. Uptake of myo-[2-3H]-inositol into the trichloroacetic acid (TCA)-soluble fraction showed no evidence of saturation, while incorporation into lipid had an apparent Km of 0.28 mmol/L for external myo-inositol. With 50 mumol/L myo-[2-3H]-inositol, approximately half of the radiolabel was found in lipid at 30 minutes. Glucose and galactose were weak inhibitors, while phlorizin at 1 mmol/L reduced uptake by 50%. Metabolic inhibitors reduced incorporation of myo-[2-3H]-inositol into lipid, but had no effect on uptake. Hepatocytes maintained myo-inositol levels of 0.4 mmol/L for 60 minutes when incubated with 50 mumol/L myo-inositol, but levels increased when incubated with 1 mmol/L myo-inositol. Efflux of label was studied in hepatocytes prelabeled for 20 minutes with myo-[2-3H]-inositol. Loss of label was initially rapid, but had slowed by 20 minutes, with much of the label remaining in the cells. Phlorizin inhibited the loss of myo-[2-3H]-inositol, while increasing myo-inositol concentration in the medium enhanced efflux. The effects of these agents on the rate of efflux was found in lipid rather than in the TCA-soluble myo-inositol fraction. These findings suggest that myo-inositol is compartmentalized within hepatocytes, with a bulk metabolically inert pool and a smaller active pool that equilibrates with extracellular myo-inositol via an energy-independent carrier-mediated mechanism, and is preferentially available for efflux or for synthesis of phosphoinositides.
Association of Parity With Risk of Type 2 Diabetes and Related Metabolic Disorders
Authors: Anthony J.G. Hanley, Gail McKeown-Eyssen, Stewart B. Harris, Robert A. Hegele, Thomas M.S. Wolever, Jeremy Kwan, Bernard Zinman
Journal: Diabetes Care (2002)

OBJECTIVE—The relationship between parity and risk of diabetes is controversial, and little information is available regarding associations between parity and measures of insulin resistance and β-cell function. The objective of this study was to investigate the association between parity and risk of glucose intolerance and related metabolic disorders using data from a population-based study in a Native Canadian community. RESEARCH DESIGN AND METHODS—Female participants (n = 383, aged 12–79 years) provided fasting blood samples for the determination of glucose, insulin, C-peptide, and proinsulin concentrations. A 75-g oral glucose tolerance test was administered, and diabetes and impaired glucose tolerance were diagnosed according to World Health Organization criteria. Waist circumference and percent body fat were determined. Information regarding occurrence of live births and previously diagnosed diabetes was obtained from interviewer-administered questionnaires. RESULTS—Parity was associated with a significantly reduced risk of diabetes (nulliparous vs. ≥1 birth, odds ratio 0.43, 95% CI 0.19– 0.94, P &amp;lt; 0.05) after adjustment for age and waist circumference. In addition, nondiabetic nulliparous women had significantly elevated concentrations of fasting insulin and proinsulin relative to nondiabetic parous women (all P &amp;lt; 0.05) in analyses adjusted for age and waist circumference. CONCLUSIONS—Our results are consistent with those from other populations experiencing high rates of diabetes and suggest the presence of a diabetes-prone phenotype within the nulliparous subcohort of this population, which may contribute to infertility.
Nitric Oxide Prevents Tumor Necrosis Factor α–Induced Rat Hepatocyte Apoptosis by the Interruption of Mitochondrial Apoptotic Signaling Through S-Nitrosylation of Caspase-8
Authors: Young-Myeong Kim, Tae-Hyoung Kim, Hun-Taeg Chung, Robert V. Talanian, Xiao-Ming Yin, Timothy R. Billiar
Journal: Hepatology (2000)

Mitochondrial cytochrome c release plays a critical role in apoptotic signal cascade after the activation of cell surface death receptors. We investigated the role played by nitric oxide (NO) in mitochondrial apoptotic signaling in tumor necrosis factor α (TNF-α) plus actinomycin D (TNF-α/ActD)-induced apoptosis. NO produced either by S-nitroso-N-acetyl-DL-penicillamine (SNAP) or inducible NO synthase (iNOS) prevented TNF-α/ActD-induced apoptosis in hepatocytes and also inhibited both caspase-8-like (IETDase) and caspase-3-like protease (DEVDase) activity as well as mitochondrial cytochrome c release. Recombinant human (rh) caspase-8 induced the cleavage of the cytochrome c-effluxing factor Bid and cytochrome c release from purified mitochondria in the reconstitution system with Bid +/+ cytosol, but not with Bid −/− cytosol. The addition of SNAP and the caspase-8 inhibitor Ac-IETD-fmk inhibited caspase-8-dependent Bid cleavage and cytochrome c release. The inhibitory effect of NO on caspase-8 was reversed by dithiothreitol (DTT). Furthermore, rh-caspase-8 was found to be modified by S-nitrosylation with 1.7 moles of NO bound per mole of enzyme. Treatment of hepatocytes with interleukin 1β (IL-1β) plus interferon gamma (IFN-γ), which induced iNOS expression and NO production, suppressed TNF-α/ActD-induced Bid cleavage and mitochondrial cytochrome c release. The NOS inhibitor N G -monomethyl-L-arginine (NMA) inhibited the protective effects of IL-1β and IFN-γ. The liver-specific NO donor V-PYRRO/NO also inhibited in vivo elevation of IETDase activity, Bid cleavage, and mitochondrial cytochrome c release in the livers of rats injected with TNF-α plus D-galactosamine. Our results indicate that one mechanism by which NO protects hepatocytes from TNF-α/ActD-induced apoptosis is via the interruption of mitochondrial apoptotic signaling through S-nitrosylation of caspase-8.
3D Echocardiographic Location of Implantable Device Leads and Mechanism of Associated Tricuspid Regurgitation
Authors: Anuj Mediratta, Karima Addetia, Megan Yamat, Joshua D. Moss, Hemal M. Nayak, Martin C. Burke, Lynn Weinert, Francesco Maffessanti, Valluvan Jeevanandam, Victor Mor-Avi, Roberto M. Lang
Journal: JACC. Cardiovascular imaging (2014)
Evidence for Disease Control with Erlotinib after Gefitinib Failure in Typical Gefitinib-Sensitive Asian Patients with Non-small Cell Lung Cancer
Authors: Alvin S. Wong, Richie Soong, Serena Bee-Kee Seah, Siew-Woon Lim, Khoon-Leong Chuah, Min-En Nga, Tan-Min Chin, Ross A. Soo
Journal: Journal of Thoracic Oncology (2008)
Dynamic Flow Study in Warthin??s Tumor of Parotid Gland
Authors: VIDYA V. SAGAR, JOSEPHINE M. PICCONE, ROBERT L. MECKELNBURG
Journal: Clinical Nuclear Medicine (1977)

It is known that Warthin's tumor of the parotid gland shows increased uptake of 99mTc-pertechnetate. The role played by vascularity of the tumor in the increased uptake is not clear. Two cases of histologically proven Warthin's tumor with increased vascularity and increased uptake are reported.
Synthesis and release of proinsulin and insulin by isolated rat islets of Langerhans
Authors: Tomio Tanese, Norman R. Lazarus, Sevim Devrim, Lillian Recant
Journal: Journal of Clinical Investigation (1970)

Isolated rat islets of Langerhans were incubated for 60, 120, and 180 min and the incorporation of leucine-3H into proinsulin and insulin moieties was followed. Synthesis and release of these hormones could be followed by separate extractions of islets and incubation media.
Comparative Evaluation of Left and Right Ventricular Endomyocardial Biopsy
Authors: Ali Yilmaz, Ingrid Kindermann, Michael Kindermann, Felix Mahfoud, Christian Ukena, Anastasios Athanasiadis, Stephan Hill, Heiko Mahrholdt, Matthias Voehringer, Michael Schieber, Karin Klingel, Reinhard Kandolf, Michael Böhm, Udo Sechtem
Journal: Circulation (2010)

Background— Endomyocardial biopsy (EMB) represents the gold standard for diagnosing myocarditis and nonischemic cardiomyopathies. This study focuses on the risk of complications and the respective diagnostic performance of left ventricular (LV), right ventricular (RV), or biventricular EMB in patients with suspected myocarditis and/or cardiomyopathy of unknown origin. Methods and Results— In this 2-center study, 755 patients with clinically suspected myocarditis (n=481) and/or cardiomyopathy of nonischemic origin including those with infiltrative or connective tissue disease (n=274) underwent either selective LV-EMB (n=265; 35.1%), selective RV-EMB (n=133; 17.6%), or biventricular EMB (n=357; 47.3%) after coronary angiography and exclusion of significant coronary artery disease. Cardiovascular magnetic resonance, including late gadolinium enhancement, imaging was performed in 540 patients (71.5%). The major complication rate for LV-EMB was 0.64% and for RV-EMB, 0.82%. Considering postprocedural pericardial effusion that occurred after biventricular EMB, the minor complication rate for LV-EMB varied between 0.64% to 2.89% and for RV-EMB, between 2.24% and 5.10%. Diagnostic EMB results were achieved significantly more often in those patients who underwent biventricular EMBs (79.3%) compared to those who underwent either selective LV-EMB or selective RV-EMB (67.3%; P &lt;0.001). In patients with biventricular EMB, myocarditis was diagnosed in LV-EMB samples in 18.7% and in RV-EMB samples in 7.9% ( P =0.002) , and it was diagnosed in both ventricles in 73.4%. There were no differences in the number of positive LV-EMB, RV-EMB, or LV- and RV-EMB findings when related to the site of cardiovascular magnetic resonance–based late gadolinium enhancement. Conclusions— Both LV-EMB and RV-EMB are safe procedures if performed by experienced interventionalists. The diagnostic yield of EMB may be optimized when samples from both ventricles are available. Preferential biopsy in regions showing late gadolinium enhancement on cardiovascular magnetic resonance does not increase the number of positive diagnoses of myocarditis.
Abstract 3994: Loss of STAT2 enhances the establishment of B16 melanoma tumors
Authors: Chanyu Yue, Ana M. Gamero
Journal: Cancer Research (2012)

Abstract STAT2 is a key component of type I interferon (IFN-I) induced activation of the JAK/STAT signaling pathway. Several studies including ours have shown that STAT2 is a critical signaling mediator in the apoptotic and cell growth inhibitory effects of IFN-I. These findings suggest that STAT2 has tumor suppressive function. To investigate this further, the B16-F1 mouse melanoma cell line was used in a tumor transplantation model to interrogate the role of STAT2 in tumorigenesis. We found that STAT2 null mice injected subcutaneously with B16-F1 melanoma tumor cells showed accelerated tumor growth rate and grew larger tumors compared to those formed in wild type mice. We next compared the antitumor effects of IFN-I in wild type and STAT2 null mice administered intraperitoneally 3 days after tumor injection and given three times weekly until day 21 of the study. IFN-[[Unsupported Character - Symbol Font &amp;#61538;]] therapy of STAT2 null mice was ineffective as tumors continued to grow at the same rate as in saline treated STAT2 null mice. In contrast, wild type mice that received IFN-[[Unsupported Character - Symbol Font &amp;#61538;]] developed smaller tumors compared to saline treated control mice. Evaluation of B16 tumors established in wild type mice by Western blot analysis showed a marked reduction in the levels of STAT2 and STAT1 proteins. Similarly, B16 tumors established in STAT2 null mice also showed low levels of STAT1 protein. To determine whether tumor derived soluble factors were involved in decreasing STAT2 protein; supernatants collected from B16-F1 tumors incubated overnight with serum free medium were used to treat B16-F1 tumor cells grown in vitro. A decrease in STAT2 protein was evident when tumor supernatants derived from tumors established in wild type and STAT2 null mice were used. Taken together our findings reveal that host STAT2 restricts the establishment of melanoma tumors and soluble factors secreted by melanoma tumors reduce STAT2 protein levels thereby diminishing the antitumor effects of IFN. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3994. doi:1538-7445.AM2012-3994
Hereditary Benign Telangiectasia: Punctate Telangiectasia Surrounded by Anemic Halo
Authors: Nini Yesenia Arévalo, Juliana Martínez del Sel, Lucila Donatti, Myriam Dahbar, Hugo Cabrera, Miguel Allevato
Journal: JAMA Dermatology (2013)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Dermatology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Dermatology journal
Consumer hazards of plastics.
Authors: G S Wiberg
Journal: Environmental Health Perspectives (1976)

The modern consumer is exposed to a wide variety of plastic and rubber products in his day to day life: at home, work, school, shopping, recreation and play, and transport. A large variety of toxic sequellae have resulted from untoward exposures by many different routes: oral, dermal, inhalation, and parenteral. Toxic change may result from the plastic itself, migration of unbound components and additives, chemical decomposition or toxic pyrolysis products. The type of damage may involve acute poisoning, chronic organ damage, reproductive disorders, and carcinogenic, mutagenic and teratogenic episodes. Typical examples for all routes are cited along with the activites of Canadian regulatory agencies to reduce both the incidence and severity of plastic-induced disease.