tbuckley/cabot-search huggingface dataset:
High Titer of Autoantibodies to GAD Identifies a Specific Phenotype of Adult-Onset Autoimmune Diabetes
Authors: Tetsuro Kobayashi, Shoichiro Tanaka, Akira Shimada, Taro Maruyama
Journal: Diabetes Care (2007)

Buzzetti et al. (1) reported a presence of two subgroups of adult-onset autoimmune diabetes at the cutoff value of GAD antibodies (GADA) titer of 32 arbitrary units (AU). Our previous report on a prospective-based observation of a Japanese population demonstrated that high GADA titer (>10 AU) is critical for predicting the progression within 5 years …
Shunt Between Right Subclavian Vein and the Left Heart in Superior Vena Cava Obstruction Due to Lung Cancer
Authors: JUNICHI TAKI, HISASHI BUNKO, NORIHISA TONAMI, KINICHI HISADA
Journal: Clinical Nuclear Medicine (1990)

A case in which there was a shunt between systemic veins and the left heart in superior vena cava syndrome due to lung cancer is reported. Superior vena cava syndrome developed one and a half years after right upper lobectomy with combined resection of thoracic wall. Radionuclide venography from the right antecubital vein showed immediate visualization of the left ventricle and aorta, before the right atrium and right ventricle were seen. In the superior vena cava syndrome due to a malignant tumor, this rare pathway as well as usual collaterals should be considered.
Lactic Acid and the Phlogiston Debt
Authors: P. Harris
Journal: Cardiovascular Research (1969)

Journal Article Lactic Acid and the Phlogiston Debt Get access Peter Harris Peter Harris From the Institute of Cardiology, London Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 3, Issue 4, October 1969, Pages 381–390, https://doi.org/10.1093/cvr/3.4.381 Published: 01 October 1969 Article history Received: 28 March 1969 Published: 01 October 1969
Neurogenic Diabetes Insipidus: Management with dDAVP (1-Desamino-8-D Arginine Vasopressin)
Authors: WILLIAM E. COBB
Journal: Annals of Internal Medicine (1978)

We used dDAVP, the 1-desamino-8-D arginine analogue of arginine vasopressin with high antidiuretic and low vasopressor potency, to treat 29 patients with neurogenic diabetes insipidus for up to 22 months. Intranasal dDAVP, 2.5 to 15 microgram twice daily, provided excellent control in most patients. Individual responses were independent of age, weight, and severity of diabetes insipidus. Resistance to dDAVP may be a rare complication of prolonged therapy. Two patients with acute postoperative diabetes insipidus were effectively treated with 5 microgram of dDAVP every 14 to 18 h. Compared to previous therapy, side effects of dDAVP were minimal (headaches in two patients), and control of symptoms and urine volume was as good as with vasopressin tannate in oil or better than chlorpropamide and lysine vasopressin nasal spray. We conclude that intranasal dDAVP, because of efficacy, long duration of action, and infrequent side effects, is the preferred treatment of neurogenic diabetes insipidus in children and adults.
Smoking and Cancer Morphology
Authors: Alvan R. Feinstein
Journal: JAMA (1970)

<h3>To the Editor:—</h3> Having initiated the study of cigarette smoking and histologic morphology in patients with lung cancer that was "reported" inThe Journal(<b>211</b>:2081, 1970), I regret its premature publication in yourMedical Newssection. Your report was based on material presented at the recent meeting of the American Association of Pathologists and Bacteriologists by Dr. Raymond Yesner, who collaborated in this project and recorded many of the histologic findings. The results presented at that meeting were based on a preliminary analysis of the data, and they contain only Dr. Yesner's interpretations of those data. The final report may show differences in the percentages because new statistical tabulations have been necessitated by a recent change in the criteria used for consolidation of histologic categories. Even if the percentages remain unchanged, however, I disagree with the interpretation that heavier smoking "caused" greater degrees of malignancy in lung cancer. The
Case-control study of leukaemia and non-Hodgkin's lymphoma among children aged 0-4 years living in west Berkshire and north Hampshire health districts.
Authors: E Roman, A Watson, V Beral, S Buckle, D Bull, K Baker, H Ryder, C Barton
Journal: BMJ (1993)

OBJECTIVE--To investigate the relation between parental employment in the nuclear industry and childhood leukaemia and non-Hodgkin9s lymphoma. DESIGN--Case-control study. SETTING-West Berkshire and Basingstoke and North Hampshire District Health Authorities. SUBJECTS--54 children aged 0-4 years who had leukaemia or non-Hodgkin9s lymphoma diagnosed during 1972-89, who were born in the study area and were resident there when cancer was diagnosed. Six controls were selected for each case: four from hospital delivery registers and two from livebirth registers maintained by the NHS central register. Controls were matched for sex, date of birth (within six months), and area of residence at birth and time of diagnosis. MAIN OUTCOME MEASURES--Parents9 employment by the nuclear industry and exposure to ionising radiation at work. RESULTS--Five (9%) of the 54 cases and 14 (4%) of the 324 controls had fathers or mothers, or both, who had been employed by the nuclear industry (relative risk 2.2, 95% confidence interval 0.6 to 6.9). Nuclear industry employees who work in areas where exposure to radiation is possible are given film badges to monitor their exposure to external penetrating ionising radiation. Three fathers of cases and two fathers of controls (and no mothers of either) had been monitored in this way before their child was conceived (relative risk 9.0, 95% confidence interval 1.0 to 107.8). No father (of a case or control) had accumulated a recorded dose of more than 5 mSv before his child was conceived, and no father had been monitored at any time in the four years before his child was conceived. A dose-response relation was not evident among fathers who had been monitored. CONCLUSIONS--These results suggest that the children of fathers who had been monitored for exposure to external penetrating ionising radiation in the nuclear industry may be at increased risk of developing leukaemia before their fifth birthday. The finding is based on small numbers and could be due to chance. If the relationship is real the mechanisms are far from clear, except that the effect is unlikely to be due to external radiation; the possibility that it could be due to internal contamination by radioactive substances or some other exposure at work should be pursued. The above average rates of leukaemia in the study area cannot be accounted for by these findings.
Coronary spasm, variant angina, and recurrent myocardial infarctions.
Authors: A D Johnson, J H Detwiler
Journal: Circulation (1977)

A 24-year-old male student had three myocardial infarctions, one prior to and two following the angiographic documentation of normal coronary arteries. A spontaneous episode of variant angina prompted repeat coronary angiography, during which intravenous ergonovine caused spasm of the left anterior descending coronary artery, transient ST-segment elevation, and ischemic chest pain; the previously normal right coronary artery was found to be occluded proximally. This constellation of clinical and angiographic findings suggests that coronary spasm can cause acute myocardial infarction as well as variant angina.
Increased Expression of Catalase and Superoxide Dismutase 2 Reduces Cone Cell Death in Retinitis Pigmentosa
Authors: Shinichi Usui, Keiichi Komeima, Sun Young Lee, Young-Joon Jo, Shinji Ueno, Brian S Rogers, Zhihao Wu, Jikui Shen, Lili Lu, Brian C Oveson, Peter S Rabinovitch, Peter A Campochiaro
Journal: Molecular Therapy (2009)

Oxidative and nitrosative damage are major contributors to cone cell death in retinitis pigmentosa (RP). In this study, we explored the effects of augmenting components of the endogenous antioxidant defense system in models of RP, rd1, and rd10 mice. Unexpectedly, overexpression of superoxide dismutase 1 (SOD1) in rd1 mice increased oxidative damage and accelerated cone cell death. With an elaborate mating scheme, genetically engineered rd10 mice with either inducible expression of SOD2, Catalase, or both in photoreceptor mitochondria were generated. Littermates with the same genetic background that did not have increased expression of SOD2 nor Catalase provided ideal controls. Coexpression of SOD2 and Catalase, but not either alone, significantly reduced oxidative damage in the retinas of postnatal day (P) 50 rd10 mice as measured by protein carbonyl content. Cone density was significantly greater in P50 rd10 mice with coexpression of SOD2 and Catalase together than rd10 mice that expressed SOD2 or Catalase alone, or expressed neither. Coexpression of SOD2 and Catalase in rd10 mice did not slow rod cell death. These data support the concept of bolstering the endogenous antioxidant defense system as a gene-based treatment strategy for RP, and also indicate that coexpression of multiple components may be needed. Oxidative and nitrosative damage are major contributors to cone cell death in retinitis pigmentosa (RP). In this study, we explored the effects of augmenting components of the endogenous antioxidant defense system in models of RP, rd1, and rd10 mice. Unexpectedly, overexpression of superoxide dismutase 1 (SOD1) in rd1 mice increased oxidative damage and accelerated cone cell death. With an elaborate mating scheme, genetically engineered rd10 mice with either inducible expression of SOD2, Catalase, or both in photoreceptor mitochondria were generated. Littermates with the same genetic background that did not have increased expression of SOD2 nor Catalase provided ideal controls. Coexpression of SOD2 and Catalase, but not either alone, significantly reduced oxidative damage in the retinas of postnatal day (P) 50 rd10 mice as measured by protein carbonyl content. Cone density was significantly greater in P50 rd10 mice with coexpression of SOD2 and Catalase together than rd10 mice that expressed SOD2 or Catalase alone, or expressed neither. Coexpression of SOD2 and Catalase in rd10 mice did not slow rod cell death. These data support the concept of bolstering the endogenous antioxidant defense system as a gene-based treatment strategy for RP, and also indicate that coexpression of multiple components may be needed.
Adverse Prognosis of Patients With Hypertrophic Cardiomyopathy Who Have Epicardial Coronary Artery Disease
Authors: Paul Sorajja, Steve R. Ommen, Rick A. Nishimura, Bernard J. Gersh, Peter B. Berger, A. Jamil Tajik
Journal: Circulation (2003)

Adult patients with hypertrophic cardiomyopathy (HCM) may develop concomitant atherosclerotic coronary artery disease (CAD). There is a paucity of data on the clinical outcomes of HCM patients who have CAD.We examined the outcome of 433 adult patients with HCM according to the presence and severity of CAD. All patients were aged > or =21 years, had a left ventricular ejection fraction of > or =50%, and were without a history of prior surgical revascularization (mean age, 63 years; 212 men). Compared with HCM patients with mild-to-moderate or no CAD, those with severe CAD demonstrated markedly reduced survival. Ten-year overall survival was 46.1%, 70.5%, and 77.1% for patients with severe, mild-to-moderate, and no CAD, respectively (unadjusted P=0.0001; adjusted P=0.0006). For the end point of cardiac death, this survival was 62.3%, 81.0%, and 80.9% (unadjusted P=0.009; adjusted P=0.004). For the end point of sudden cardiac death, this survival was 77.4%, 93.2%, and 90.3% (unadjusted P=0.01; adjusted P=0.01). The presence of severe CAD also was highly predictive of these events (risk ratio for respective event: 2.31, 2.15, and 2.77) in multivariate models that additionally identified age, prior stroke, hyperlipidemia, and atrial fibrillation as significant covariates.Among adult patients with HCM who undergo coronary angiography, those who have concomitant severe CAD are at increased risk of death. This risk far exceeds historical death rates of CAD patients with normal left ventricular function.
AFRICAN-AMERICANS WITH HYPERTROPHIC CARDIOMYOPATHY PRESENT MORE PRONOUNCED ECG ABNORMALITIES THAN CAUCASIANS
Authors: Lars Lindholm Sorensen, Aurelio Pinheiro, Veronica Dimaano, Iraklis Pozios, Hongchang Luo, Xioping Lin, Thomas Fritz-Hansen, Peter Sogaard, Niels Thue Olsen, Maria Abraham, Theodore Abraham
Journal: Journal of the American College of Cardiology (2014)
Leishmaniasis Vaccination
Authors: Steven G. Reed
Journal: The Journal of Experimental Medicine (2001)

In the history of vaccine development, key observations have gradually led to our ability to take rational approaches toward the induction of protective immunity to microbial pathogens. The earliest efforts consisted of inoculating lesion material into healthy individuals resulting in the then inexplicable prevention of the development of similar disease. Centuries later, after researchers found that microscopic forms were responsible for the major human diseases such as tuberculosis and smallpox, vaccines consisting of inoculating weakened or attenuated organisms were developed. The discovery of the cell populations that mediate antibody and cellular immune responses, followed by the identification of the cytokine mediators of cellular immunity and the ability to identify, isolate, purify, and produce antigenic molecules of various pathogens has permitted a rational approach toward vaccine development. Perhaps no disease model has been more widely used to understand the roles of cell populations and cytokines in mediating disease susceptibility and resistance than the infection of inbred mice with the Leishmania parasite 1. For example, BALB/c mice infected subcutaneously with Leishmania major develop nonhealing, disseminated, fatal infections, whereas C57BL mice similarly infected are more resistant, and heal their infections. In addition to susceptibility factors determined by host genetics, it has recently been appreciated that the insect that transmits leishmania to humans may play a key role in the establishment of infection. The study by Valenzuela et al. in this issue 2 exploits this information in what may prove to be a unique approach to vaccination.
Genetic risk factors for chronic obstructive pulmonary disease
Authors: AJ Sandford, TD Weir, PD Pare
Journal: European Respiratory Journal (1997)

Cigarette smoking is the major risk factor for chronic obstructive pulmonary disease (COPD). However, only a minority of cigarette smokers develop symptomatic disease. Studies of families and twins suggest that genetic factors also contribute to the development of COPD. We present a detailed literature review of the genes which have been investigated as potential risk factors for this disease. The only established genetic risk factor for COPD is homozygosity for the Z allele of the alpha1-antitrypsin gene. Heterozygotes for the Z allele may also be at increased risk. Other mutations affecting the structure of alpha1-antitrypsin or the regulation of gene expression have been identified as risk factors. Genes, including those for alpha1-antichymotrypsin, alpha2-macroglobulin, vitamin D-binding protein and blood group antigens, have also been associated with the development of COPD. Variants of the cystic fibrosis transmembrane regulator gene have been identified as risk factors for disseminated bronchiectasis. The genetic basis to chronic obstructive pulmonary disease has begun to be elucidated and it is likely that several genes will be implicated in the pathogenesis of this disease. The knowledge gained from such studies may also prove relevant to other inflammatory diseases.
Cyst-Gastrostomy via the Cyst: An Unusual Laparoscopic Approach
Authors: W. G. Ainslie, M. Larvin, M. J. McMahon
Journal: Endoscopy (2002)

A 55-year-old woman with chronic pancreatitis was admitted to hospital with abdominal pain. Ultrasound identified a large cyst in the upper abdomen. A computed tomography (CT) scan confirmed a pancreatic pseudocyst, which extended over the lesser curve and lay predominantly anterior to the stomach. It also involved the splenic hilum and showed evidence of a recent bleed (Figure [1]). Angiography showed patent splenic vessels and no evidence of active bleeding. The patient was initially treated conservatively, but magnetic resonance imaging (MRI) showed that the cyst was enlarging. Laparoscopic exploration was undertaken.
CTS1: a p53-derived chimeric tumor suppressor gene with enhanced in vitro apoptotic properties.
Authors: E Conseiller, L Debussche, D Landais, C Venot, M Maratrat, V Sierra, B Tocque, L Bracco
Journal: Journal of Clinical Investigation (1998)

The clinical potential of the p53 tumor suppressor gene is being evaluated currently for gene therapy of cancer. We have built a variant of wild-type p53, chimeric tumor suppressor 1 (CTS1), in which we have replaced the domains that mediate its inactivation. CTS1 presents some very interesting properties: (a) enhanced transcriptional activity; (b) resistance to the inactivation by oncogenic forms of p53; (c) resistance to the inactivation by MDM2; (d) lower sensitivity to E6-induced degradation; (e) ability to suppress cell growth; and (f ) faster induction of apoptosis. Thus, CTS1 is an improved tumor suppressor and an alternative for the treatment of wild-type p53-resistant human tumors by gene therapy.
Acute Influence of Internal Mammary Artery Implantation on Ventricular Function
Authors: J. JUDSON MCNAMARA, HAROLD C. URSCHEL
Journal: Circulation (1969)

Ventricular function was studied acutely before and after internal mammary artery implantation in dogs with the following findings: (1) A single ventricular function study alone did not significantly alter the ventricular function curve obtained 45 minutes later. (2) Single IMA implant and two tunnels without implants appeared to depress ventricular function, although the depression was not significant in degree or frequency when compared with control values. (3) Double internal mammary artery implants depressed ventricular function more than 10% in eight of ten animals studied which was significantly more frequent than in control group I ( P &lt; 0.05). In addition, the magnitude of the depression (average 18.3%) was significant when compared with pre-implant control values ( P &lt;0.05).
RAPID RESPONSES FROM BMJ.COM
Authors: Samuel Y Wong
Journal: BMJ (2004)

Following are two of the Rapid Responses generated by this commentary, all of which can be read in their entirety at http://bmj.bmjjournals.com/cgi/eletters/329/7466/602. 

—Editor 

I read with interest the article by Dietrich et al. It is indeed encouraging if telephone care management programs are effective for improving patient health outcomes and satisfaction in the treatment of depression. However, before we conclude the effectiveness of telephone management programs in the treatment of depression, we should see if other confounding variables besides telephone management could have accounted for the observed results.

One factor is the potential beneficial effects of increased physician visits for depression observed in …
DIAGNOSIS OF MACULAR LEPROSY
Authors: Walter C. Alvarez
Journal: JAMA (1952)

To the Editor:—  In regard to the article on the diagnosis of leprosy by Dr. Robert K. Maddock, inThe Journalfor Jan. 5, 1952 (page 44), I would like to say that for a few years following 1895 my father, Dr. Luis F. Alvarez, was in charge of research in leprosy in Hawaii. After studying at Johns Hopkins, he returned to Honolulu and built up a board of health research laboratory at Kalihi. There he worked for several years trying to find a remedy for leprosy.  He soon devised a method that was highly successful in the diagnosis of the macular form of the disease. With a fine mouse-tooth forceps he would raise a tiny bit of the skin in a suspicious patch and snip it off with sharp scissors. He would drop this into a small mortar with a few drops of water, and, as a boy, it
Alterations of INK4A and INK4B Genes in Adult Soft Tissue Sarcomas: Effect on Survival
Authors: I. Orlow, M. Drobnjak, Z.-F. Zhang, J. Lewis, J. M. Woodruff, M. F. Brennan, C. Cordon-Cardo
Journal: JNCI Journal of the National Cancer Institute (1999)

The INK4A and INK4B genes map to chromosome 9p21, with the INK4A gene encoding two protein products, p16 and pl9ARF. Alterations of the INK4A and INK4B genes occur frequently in certain primary malignant neoplasms. This study was undertaken to evaluate the frequency of INK4A and INK4B gene alterations in a cohort of adult soft tissue sarcomas.The status of the INK4A and INK4B genes was determined in 46 soft tissue sarcomas by use of the following methods: Southern blotting, polymerase chain reaction (PCR), single-strand conformation polymorphism analysis, comparative multiplex PCR, and a methylation assay focusing on the p16 promoter. Associations between alterations of the INK4A and INK4B genes and clinicopathologic variables, as well as with p53 and pRB (retinoblastoma protein) status, were evaluated by use of the two-tailed Fisher's exact test. Disease-specific survival was evaluated by use of the Kaplan-Meier method and the logrank test. Proportional hazards analysis was used to obtain estimates of relative risks. All P values are two-sided.Homozygous and hemizygous deletions, but no point mutations, were observed in these two genes. The overall frequency of gene alteration (deletion or rearrangement) was approximately 15% for the INK4A and INK4B genes, with changes restricted to high-grade sarcomas. Statistically significant associations were observed between INK4A/INK4B deletions (P = .036) or alterations (P = .005) and poor survival. Alteration of the INK4A and INK4B genes was the only statistically significant predictor for poor survival when controlling for tumor grade and size (P = .03).Coincident homozygous deletion of the INK4A and INK4B genes occurs frequently in adult soft tissue sarcomas. Loss of p16 and pl9ARF function in primary tumors, although not equivalent to alterations in p53 and pRB function, appears to be associated with cancers that have an aggressive biologic behavior.
Hereditary Hearing Loss
Authors: Kathleen Shaver Arnos
Journal: New England Journal of Medicine (1994)

In the past few years, new genetic techniques have been used successfully to locate and characterize genes for several types of hereditary hearing loss. The effects of this new knowledge on clinical practice and the lives of people with hearing loss will be far-reaching and controversial. Hearing loss affects an estimated 28 million people in the United States. Hereditary factors account for a considerable proportion of all cases of hearing loss. There are over 200 types of hereditary hearing loss,1 approximately one third of which are associated with other medical, physical, or developmental abnormalities (known as syndromic hearing loss). For . . .
Bites by the Saw-scaled or Carpet Viper (Echis carinatus): Trial of Two Specific Antivenoms
Authors: D. A. Warrell, N. M. Davidson, L. D. Omerod, H. M. Pope, B. J. Watkins, B. M. Greenwood, H. A. Ried
Journal: BMJ (1974)

Echis carinatus is the most important cause of morbidity and mortality from snake bite in Nigeria and in many other parts of the world. Forty-six patients with systemic poisoning by this snake were given echis antivenom made either by the South African Institute for Medical Research (S.A.I.M.R.) or by Behringwerke (North and West African polyvalent antivenom). A simple test of blood coagulability was used to assess whether an adequate neutralizing dose of antivenom had been given. An average of 15·2 ml S.A.I.M.R. antivenom restored normal coagulability permanently in all 23 patients in one group, but in the other group receiving an average dose of 37·9 ml Behringwerke antivenom normal clotting resulted in only 18 out of 23 patients. Local tissue swelling was similar in both groups, but local necrosis occurred in three patients treated with Behringwerke antivenom and in none given S.A.I.M.R. antivenom.