tbuckley/cabot-search huggingface dataset:
Effects of insulin and dietary myoinositol on impaired peripheral motor nerve conduction velocity in acute streptozotocin diabetes.
Authors: D A Greene, P V De Jesus, A I Winegrad
Journal: Journal of Clinical Investigation (1975)

The factors influencing the development of impaired sciatic motor nerve conduction velocity (MNCV) in acute experimental diabetes were examined. Decreased MNCV developed by the 14th day after streptozotocin administration but only in rats which became hyperglycemic. Insulin treatment, begun on day 3, failed to prevent imparied MNCV in diabetic rats in which improved or normal weight gain and a decreased degree of hyperglycemia was induced. However, insulin treatment prevented the development of impaired MNCV in a group of diabetic rats in which the tail vein plasma glucose concentration was never found to exceed 160 mg/dl during days 6 through 14, andin which the mean plus or minus SEM of the average plasma glucose concentration for each animal during the same period was 75 plus or minus 18 mg/dl. In normal rats fed diets containing 0.011% or 0.069% free myoinositol (a presumably normal range), sciatic nerve free myoinositol concentrations were 90- and 60-fold higher than those in plasma. On these diets the development of impaired MNCV in the diabetics was associated with a decrease in nerve free myoinositol as compared with nerves from normals fed the same diet, despite similar plasma levels in the normals and diabetics. Plasma and nerve free myoinositol increased with increasing dietary myoinositol content in both normals and diabetics, and nerve myoinositol content could be acutely increased by an i.p. myoinositol load. By supplementing the diets with 1.0% myoinositol, the difference in nerve myoinositol in normal and diabetic rats on day 14 was abolished; on this diet the development of impaired MNCV in the diabetics was moderated or totally prevented, despite persistent hyperglycemia and elevated nerve sorbitol and fructose concentrations. Insulin treatment that prevented impaired MNCV prevented a decrease in nerve myoinositol in diabetics. These studies suggest that insulin deficiency, and possibly hyperglycemia, are primary factors in the development of imparied MNCV in acute experimental diabetes. However, the development of impaired MNCV appears to be related in some manner to a derangement in the regulation of nerve free myoinositol content, which appears to be subject to modification by increases in plasma myoinositol concentration over a critical range.
Effect of Budesonide/Formoterol Pressurized Metered-Dose Inhaler (BUD/FM pMDI) in African-American Patients with Moderate to Severe Asthma: Responder Analysis in Patients with Versus without Fixed Airflow Obstruction (FAO)
Authors: Bradley E. Chipps, Donald P. Tashkin, Tom Uryniak, Frank Trudo
Journal: Journal of Allergy and Clinical Immunology (2013)
Cost of dementia care in US to double by 2040
Authors: M. McCarthy
Journal: BMJ (2013)

The cost of dementia care in the United States is currently estimated to be as high as $215bn (£141bn; €166bn) per year and can be expected to double by 2040, according to a study in the current issue of the New England Journal of Medicine .1

The findings suggest that the cost of dementia care in the US is far higher than the cost of care for heart disease or cancer.

The main component of the cost of …
Priorities for the Use of Resources in Medicine
Authors: Hugh H. Hussey
Journal: JAMA (1978)

In November 1976 the Fogarty International Center convened a meeting sponsored jointly with the Royal Society of Medicine and the Royal Society of Medicine Foundation, Inc. Most of the 43 participants were from the United States and Great Britain. During three days, formal presentations and discussion periods directed attention to the need for prudent use of resources. A reader of the compilation now published will discover little that is new among the topics considered— additional constraints (regulations) affecting physicians' decision making, the influence of rapidly expanding technology on medical costs, the continuing education of physicians, the roles of nurses and other allied health personnel in patient care, the reasons for differences in health care in the United States and England, the maldistribution of physicians geographically and by specialty, and the excessive numbers of surgeons and "unnecessary surgery" in the United States. On the last point, as well as others in
Chronic thromboembolic pulmonary hypertension: a tribute to pulmonary endarterectomy
Authors: F. Couturaud, I. Frachon, C. Leroyer
Journal: European Respiratory Journal (2009)

Our understanding of chronic thromboembolic pulmonary hypertension (CTEPH), in terms of both its natural history and pathophysiology, has greatly improved since the landmark descriptions given by Moser and Braunwald 1 more than 40 yrs ago. At that time, small case series were available, depicting the clinical features of patients suffering from “long-standing thromboembolic pulmonary hypertension”, “chronic massive thromboembolic obstruction” or “chronic obstruction of large pulmonary arteries”. These patients shared a history of long-term dyspnoea on exertion with normal spirometry values, evidence of pulmonary hypertension, and right ventricular dysfunction in association with the presence of marked defects at the ventilation/perfusion scan; the occurrence of a single or multiple venous thromboembolism episodes, usually several years previously, was constantly mentioned in the diagnostic work-up 2–5. The success of a surgical procedure, namely pulmonary endarterectomy, has transformed this lethal disorder into a potentially curable form of pulmonary hypertension 1. As a consequence, the referral of cases suitable for surgery has gradually increased with time: at the University of San Diego (San Diego, CA, USA) there were 41 operated cases in 1980, rising to 323 cases in 1992 6, 7. This has enabled us to broaden our knowledge, with the help of further involvement from European centres 8–11].

Forty years ago, the frequency of CTEPH was estimated to be 0.1% of patients who survived an episode of pulmonary embolism 12 …
TRICHINOSIS IN THE UNITED STATES; WITH THE REPORT OF A CASE.
Authors: FREDERICK A. PACKARD
Journal: JAMA (1897)

Feb. 5, 1897, an Italian was admitted to my ward at the Philadelphia Hospital, complaining greatly of pains in the thighs and legs. Owing partly to his natural mental obtuseness, partly to his nationality, the history that could be obtained even with the aid of an interpreter, was by no means satisfactory. On this account many points in his history are vague, while some of the facts in his case could not be determined. He gave his age as 28 years, his occupation that of a farm hand. He could give us but little information in regard to the locality in which he had last worked, but said that it was in New Jersey. After three months of enforced idleness (from lack of work) he started to work on a farm on February 1. The work being too laborious for him he left the farm, although he seems not to
Regulatory T-cell deficiency and immune dysregulation, polyendocrinopathy, enteropathy, X-linked–like disorder caused by loss-of-function mutations in LRBA
Authors: Louis-Marie Charbonnier, Erin Janssen, Janet Chou, Toshiro K Ohsumi, Sevgi Keles, Joyce T Hsu, Michel J Massaad, Maria Garcia-Lloret, Rima Hanna-Wakim, Ghassan Dbaibo, Abdullah A Alangari, Abdulrahman Alsultan, Daifulah Al-Zahrani, Raif S Geha, Talal A Chatila
Journal: Journal of Allergy and Clinical Immunology (2014)
Red-Cell Pseudomosaicism in Congenital Methemoglobinemia
Authors: Alan S. Keitt, Thomas W. Smith, James H. Jandl
Journal: New England Journal of Medicine (1966)

THE several rare familial disorders constituting the "congenital methemoglobinemias" arise from either of two kinds of inborn errors of metabolism. One kind, accounting for the hemoglobin-M group, involves specific inherited structural defects in hemoglobin that impede the normal mechanisms for reducing the ferrohemes of endogenous methemoglobin back to their native ferroheme state.1 A second group comprises defects in the energy-dependent mechanisms for reducing methemoglobin; by far the most common of these defects affects a specific enzymatic step in the reduction of methemoglobin, is inherited through autosomal genes and is clinically manifest only in homozygotes.2 Efforts to characterize this inborn error . . .
Nitritoid Reactions to Gold Treatment for Arthritis
Authors: William R. Austad
Journal: JAMA (1970)

<h3>To the Editor.—</h3> The side effects of gold sodium thiomalate therapy in the treatment of rheumatoid arthritis include dermatitis, stomatitis, nephritis (with or without proteinuria), and bone marrow depression (with or without eosinophilia). A less commonly mentioned side effect is the vasomotor or nitritoid reaction.<sup>1-3</sup> During a one-month period, two patients with rheumatoid arthritis receiving gold therapy developed the nitritoid or vasomotor reaction. Following are their brief summaries. <h3>Report of Cases.—Case 1.—</h3> A 47-year-old white woman with a ten-year history of seronegative, nonnodular rheumatoid arthritis was first seen at the William Beaumont General Hospital Clinic, while she was receiving a maintenance dosage of gold sodium thiomalate, 50 mg every two weeks. Gold injections were given on (1) March 31, 1969, 50 mg, without reaction; (2) April 9, 50 mg, with mild nitritoid reaction; (3) May 7, 35 mg, without reaction; (4) May 23, 35 mg, with a mild
Effects of acidification on the mobility of metals and metalloids: an overview.
Authors: J M Wood
Journal: Environmental Health Perspectives (1985)

The exchange rates for metals and metalloids between sediments, soils, water and aquatic biota are discussed in terms of normal and acidified ecosystems. Where it is possible, the pathways for a number of toxic elements are presented with special emphasis on the impact of acidification on changing chemical speciation, and on the potential toxicity of such acid-generated chemical species. Concerns for the impact of acidification on the stability of ecosystems, the safety of drinking water, bioaccumulation in fish and in plants are addressed.
The prevalence and significance of circulating antibodies to gastric intrinsic factor and parietal cells in gastric carcinoma
Authors: B. Ungar, R. G. Strickland, C. M. Francis
Journal: Gut (1971)

The prevalence of circulating antibodies to gastric intrinsic factor and parietal cells was examined in 60 patients with histologically proven gastric carcinoma and was found not to differ from the prevalence of these antibodies in control subjects of similar age and sex distribution.Amongst the 60 patients with gastric carcinoma seven were thought to have actual or potential pernicious anaemia. The absence of an increased prevalence of antigastric antibodies in gastric carcinoma indicates that gastritis itself, whether autoimmune or not, is the likely common denominator underlying the predisposition to gastric carcinoma in both pernicious anaemia and chronic atrophic gastritis.
Vaccination with Legionella pneumophila membranes induces cell-mediated and protective immunity in a guinea pig model of Legionnaires' disease. Protective immunity independent of the major secretory protein of Legionella pneumophila.
Authors: S J Blander, M A Horwitz
Journal: Journal of Clinical Investigation (1991)

We have examined the capacity of Legionella pneumophila membranes to induce cell-mediated immune responses and protective immunity in a guinea pig model of Legionnaires' disease. Guinea pigs immunized by aerosol with L. pneumophila membranes developed strong cell-mediated immune responses to L. pneumophila membranes as demonstrated by cutaneous delayed-type hypersensitivity and in vitro splenic lymphocyte proliferation. Guinea pigs immunized by aerosol or by subcutaneous inoculation with L. pneumophila membranes developed strong protective immunity against lethal aerosol challenge with L. pneumophila. Overall, in six independent experiments, 39 of 49 (80%) guinea pigs immunized with L. pneumophila membranes survived challenge compared with 2 of 40 (5%) sham-immunized controls (P = 2 x 10(-13). In contrast, guinea pigs immunized by aerosol with formalin-killed L. pneumophila did not develop either a strong cell-mediated immune response to L. pneumophila antigens or protective immunity to lethal aerosol challenge. The capacity of L. pneumophila membranes to induce protective immunity was independent of the major secretory protein of L. pneumophila, which we previously demonstrated is an immunoprotective molecule. Purified L. pneumophila membranes did not contain detectable major secretory protein (MSP) on immunoblots; immunization of guinea pigs with L. pneumophila membranes did not induce anti-MSP antibody; and guinea pigs developed comparable protective immunity after immunization with membranes from either an L. pneumophila strain that secretes the major secretory protein or an isogenic mutant that does not. This study demonstrates that (a) immunization with L. pneumophila membranes but not formalin-killed L. pneumophila induces strong cell-mediated immune responses and protective immunity, (b) L. pneumophila membranes contain immunoprotective molecules distinct from the major secretory protein of L. pneumophila, and (c) L. pneumophila membranes have potential as a vaccine against Legionnaires' disease.
A human population bottleneck can account for the discordance between patterns of mitochondrial versus nuclear DNA variation
Authors: J. C. Fay, C. I. Wu
Journal: Molecular Biology and Evolution (1999)

Whether or not humans have experienced a reduction in population size in the recent past is a controversial issue germane to the origin and colonization of our own species (Stringer and Andrews 1988). A change in population size can result in deviations from the neutral patterns of nucleotide variation expected at equilibrium. Using the frequency distribution of mutations segregating in extant populations, the magnitude of a deviation can be measured by Tajima’s (1989a) D statistic or by a number of alternative measures (Fu and Li 1993; Fu 1996). In a population of constant size, variation at a neutrally evolving locus is expected to have a D value of approximately zero. Following a reduction in population size, rare frequency mutations are lost more readily than are common mutations (Nei, Maruyama, and Chakraborty 1975), and transient positive D values are expected (Tajima 1989b). Following an increase in population size, there is a temporary excess of new mutations segregating at rare frequencies, and negative D values are expected. The sign of Tajima’s D subsequent to a population bottleneck can be positive, negative, or zero depending on the length of time since the bottleneck and the severity of the bottleneck. If a bottleneck is so severe that all variation is eliminated or lasts so long that the population reaches a new equilibrium, Tajima’s D follows the pattern produced by an expansion in population size. However, following an incomplete bottleneck, Tajima’s D is transiently positive before becoming negative and eventually approaching its equilibrium (Tajima 1989b). In humans, mitochondrial variation is characterized by an excess of rare frequency mutations and a negative D value, which has been interpreted as the result of a recent expansion in population size (Merriwether et al. 1991; Rogers and Harpending 1992). In contrast, most nuclear loci are characterized by the opposite pattern, an excess of common mutations and positive D values, which can result from a recent reduction in population size (Hey 1997; Harding et al. 1997; Clark et al. 1998; Zietkiewicz et al. 1998). The conflicting profiles of mitochondrial and nuclear variation have led to the suggestion that these patterns cannot be simultaneously accounted for by human population history, which must be shared by both genomes (Hey 1997).
Nitric oxide synthesis in cardiac myocytes and fibroblasts by inflammatory cytokines
Authors: T. Shindo, U. Ikeda, F. Ohkawa, Y. Kawahara, M. Yokoyama, K. Shimada
Journal: Cardiovascular Research (1995)

Journal Article Nitric oxide synthesis in cardiac myocytes and fibroblasts by inflammatory cytokines Get access Takayuki Shindo, Takayuki Shindo aDepartment of Cardiology Jichi Medical School, Minamikawachi, Tochigi 329-04, Japan Search for other works by this author on: Oxford Academic PubMed Google Scholar Uichi Ikeda, Uichi Ikeda * aDepartment of Cardiology Jichi Medical School, Minamikawachi, Tochigi 329-04, Japan *Correspondence to Dr Ikeda. Search for other works by this author on: Oxford Academic PubMed Google Scholar Fujio Ohkawa, Fujio Ohkawa aDepartment of Cardiology Jichi Medical School, Minamikawachi, Tochigi 329-04, Japan Search for other works by this author on: Oxford Academic PubMed Google Scholar Yasuhiro Kawahara, Yasuhiro Kawahara bDepartment of Internal Medicine, First Division, Kobe University School of Medicine, Kobe, Japan Search for other works by this author on: Oxford Academic PubMed Google Scholar Mitsuhiro Yokoyama, Mitsuhiro Yokoyama bDepartment of Internal Medicine, First Division, Kobe University School of Medicine, Kobe, Japan Search for other works by this author on: Oxford Academic PubMed Google Scholar Kazuyuki Shimada Kazuyuki Shimada aDepartment of Cardiology Jichi Medical School, Minamikawachi, Tochigi 329-04, Japan Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 29, Issue 6, June 1995, Pages 813–819, https://doi.org/10.1016/S0008-6363(96)88617-2 Published: 01 June 1995 Article history Received: 18 July 1994 Accepted: 25 January 1995 Published: 01 June 1995
Health Insurance Coverage
Authors: Robert Kuttner
Journal: New England Journal of Medicine (1999)

The most prominent feature of American health insurance coverage is its slow erosion, even as the government seeks to plug the gaps in coverage through such new programs as Medicare+Choice, the Health Insurance Portability and Accountability Act (HIPAA), expansions of state Medicaid programs, and the $24 billion Children's Health Insurance Program of 1997. Despite these efforts, the proportion of Americans without insurance increased from 14.2 percent in 1995 to 15.3 percent in 1996 and to 16.1 percent in 1997, when 43.4 million people were uninsured. Not as well appreciated is the fact that the number of people who are underinsured, . . .
THE DANGERS OF POTASSIO CHLORATE.
Authors: PAUL BARTHOLOW
Journal: JAMA (1904)

Every obscure subject in medical literature should be reviewed from time to time on principles broader and more general than can usually be employed in text-books or special articles; and particularly when such obscurity is caused by a want of precision of language, by errors in the use of terms—faulty or loose terminology—and, what is more serious, by a failure to distinguish between two objects, which, though alike, are chemically and physiologically speaking, separate agencies. For instance, a frequent and widespread source of error—and consequently of danger—arises from a confusion in the nomenclature. That is to say, potassic chlorate has been confounded, both in medical writings and in prescriptions, with potassic chlorid (KCL). Secondly, by a false analogy, the chlorate has been thought to have properties and effects identical with the chlorid, and not to be any stronger. For the belief that potassic chlorate and potassic chlorid are interchangeable, or
18F-FDG PET/CT Findings in a Patient With Sweet Syndrome Associated With Myelodysplastic Syndrome
Authors: Aisheng Dong, Yang Wang, Lei Gao, Changjing Zuo
Journal: Clinical Nuclear Medicine (2013)

A 73-year-old man was admitted to our hospital because of a 2-year history of repeated painful edematous erythemas on the skin and pancytopenia for the last 8 months. FDG PET/CT demonstrated multiple cutaneous foci with increased tracer accumulation throughout the body, multiple FDG-avid lymph nodes in the mediastinum, bilateral pulmonary hili and abdomen, and diffusively increased FDG uptake of bone marrow. A skin biopsy revealed infiltration by neutrophilic granulocytes consistent with Sweet syndrome. Myelodysplastic syndrome was established on bone marrow aspiration and biopsy.
Deficits in Social Cognition and Response Flexibility in Pediatric Bipolar Disorder
Authors: Erin B. McClure, Julia E. Treland, Joseph Snow, Mariana Schmajuk, Daniel P. Dickstein, Kenneth E. Towbin, Dennis S. Charney, Daniel S. Pine, Ellen Leibenluft
Journal: American Journal of Psychiatry (2005)

OBJECTIVE: Little is known about neuropsychological and social-cognitive function in patients with pediatric bipolar disorder. Identification of specific deficits and strengths that characterize pediatric bipolar disorder would facilitate advances in diagnosis, treatment, and research on pathophysiology. The purpose of this study was to test the hypothesis that youths with bipolar disorder would perform more poorly than matched healthy comparison subjects on measures of social cognition, motor inhibition, and response flexibility. METHOD: Forty outpatients with pediatric bipolar disorder and 22 comparison subjects (no differences in age, gender, and IQ) completed measures of social cognition (the pragmatic judgment subtest of the Comprehensive Assessment of Spoken Language, facial expression recognition subtests of the Diagnostic Analysis of Nonverbal Accuracy Scale, the oral expression subtest of the Test of Language Competence), inhibition and response flexibility (stop and stop-change tasks), and motor inhibition (continuous performance tasks). RESULTS: Pediatric bipolar disorder patients performed more poorly than comparison subjects on social-cognitive measures (pragmatic judgment of language, facial expression recognition) and on a task requiring response flexibility. These deficits were present in euthymic patients. Differences between patients and comparison subjects could not be attributed to comorbid attention deficit hyperactivity disorder. CONCLUSIONS: Findings of impaired social cognition and response flexibility in youths with pediatric bipolar disorder suggest continuity between pediatric bipolar disorder and adult bipolar disorder. These findings provide a foundation for neurocognitive research designed to identify the neural mechanisms underlying these deficits.
Determination of Glutaraldehyde Residues on Flexible Endoscopes after Chemothermal Treatment in an Endoscope Washer-Disinfector
Authors: B. Dietze, H. Neumann, U. Mansmann, H. Martiny
Journal: Endoscopy (2001)

Although there are several cases of glutaraldehyde-induced colitis following colonoscopy there is only one study on residues after disinfecting. Our report describes the determination of water-soluble glutaraldehyde residues after processing endoscopes with a glutaraldehyde-containing disinfectant.A gastroscope and a colonoscope were processed in a washer-disinfector and then immersed in 201 of NaCl solution. Glutaraldehyde was determined by high performance liquid chromatography in 84 samples. Samples were taken after immersing the endoscopes for 5 h and 24 h with and without rinsing the channels.After 5 h and with the channels having been rinsed, the median for colonoscopes was only 0.409 mg/l. The highest level of glutaraldehyde was 0.846 mg/l.After endoscopes have been processed in the washer-disinfector there is no risk of a glutaraldehyde-induced colitis, proctitis or diarrhoea.