tbuckley/cabot-search huggingface dataset:
Oral Antihyperglycemic Medication Nonadherence and Subsequent Hospitalization Among Individuals With Type 2 Diabetes
Authors: Denys T. Lau, David P. Nau
Journal: Diabetes Care (2004)

OBJECTIVE—This study examines the association between oral antihyperglycemic medication nonadherence and subsequent hospitalization among individuals with type 2 diabetes. RESEARCH DESIGN AND METHODS—Using administrative claims data (2000–2001) from a managed care organization in the Midwestern U.S., this study analyzed 900 enrollees, aged 18 years and over, with type 2 diabetes who were taking oral antihyperglycemic agents both years but who did not use insulin. Nonadherence was defined as a medication possession ratio (MPR) &amp;lt;80%. Multivariate logistic regression analyses were performed where hospitalization in 2001 was regressed on nonadherence to the oral antihyperglycemic drug regimen in 2000, while controlling for nonadherence to drugs for hypertension and dyslipidemia and for hospitalization in 2000, age, sex, intensity of the diabetes drug regimen, and comorbidities. RESULTS—The proportion of enrollees who were nonadherent to the antihyperglycemic drug regimen in 2001 was 28.9%, whereas 18.8 and 26.9% were nonadherent to antihypertensive and lipid-modifying drugs, respectively. The increase in the hospitalization rate for 2001 was most apparent where the antihyperglycemic MPR for 2000 dropped to &amp;lt;80%. Enrollees who were nonadherent to oral diabetes medications in 2000 were at higher risk of hospitalization in 2001 (odds ratio 2.53; 95% CI 1.38–4.64), whereas nonadherence to drugs for hypertension and dyslipidemia were not significantly associated with hospitalization. CONCLUSIONS—Patients with type 2 diabetes who do not obtain at least 80% of their oral antihyperglycemic medications across 1 year are at a higher risk of hospitalization in the following year.
Angiogenesis? the answer is NO·
Authors: S Babaei
Journal: Cardiovascular Research (2002)

We thank Drs Dulak and Jozkowicz for their interest in appended figure is an attempt to illustrate how different our paper [1].They raise the question of whether induction angiogenic pathways converge on NO as a downstream of VEGF expression by NO in cultured smooth muscle mediator (Fig. 1).cells (SMCs) may have contributed to the angiogenic effects of eNOS in our co-culture model.Although, we agree that this is a potential mechanism whereby NO might R eferences induce angiogenesis, we would like to point out that NO does not always increase angiogenic factor expression, and [1] Babaei S, Stewart DJ.Overexpression of endothelial NO synthase induces angiogenesis in a co-culture model.Cardiovasc Res may even attenuate hypoxia-induced upregulation of 2002;55:190-200.VEGF by inhibition of HIF-1a in aortic SMCs and [2] Tsurumi Y, Murohara T, Krasinski K, Chen D, Witzenbichler B, pulmonary artery EC or AP-1 in aortic SMCs [2,3].Kearney M, Couffinhal T, Isner JM.Reciprocal relation between In order to address this issue in our model, we have VEGF and NO in the regulation of endothelial integrity.Nature Med since measured VEGF production in response to eNOS 1997;3:879-886.
Rare variants in single-minded 1 (SIM1) are associated with severe obesity
Authors: Shwetha Ramachandrappa, Anne Raimondo, Anna M.G. Cali, Julia M. Keogh, Elana Henning, Sadia Saeed, Amanda Thompson, Sumedha Garg, Elena G. Bochukova, Soren Brage, Victoria Trowse, Eleanor Wheeler, Adrienne E. Sullivan, Mehul Dattani, Peter E. Clayton, Vippan Datta, John B. Bruning, Nick J. Wareham, Stephen O’Rahilly, Daniel J. Peet, Ines Barroso, Murray L. Whitelaw, I. Sadaf Farooqi
Journal: Journal of Clinical Investigation (2013)

Single-minded 1 (SIM1) is a basic helix-loop-helix transcription factor involved in the development and function of the paraventricular nucleus of the hypothalamus. Obesity has been reported in Sim1 haploinsufficient mice and in a patient with a balanced translocation disrupting SIM1. We sequenced the coding region of SIM1 in 2,100 patients with severe, early onset obesity and in 1,680 controls. Thirteen different heterozygous variants in SIM1 were identified in 28 unrelated severely obese patients. Nine of the 13 variants significantly reduced the ability of SIM1 to activate a SIM1-responsive reporter gene when studied in stably transfected cells coexpressing the heterodimeric partners of SIM1 (ARNT or ARNT2). SIM1 variants with reduced activity cosegregated with obesity in extended family studies with variable penetrance. We studied the phenotype of patients carrying variants that exhibited reduced activity in vitro. Variant carriers exhibited increased ad libitum food intake at a test meal, normal basal metabolic rate, and evidence of autonomic dysfunction. Eleven of the 13 probands had evidence of a neurobehavioral phenotype. The phenotypic similarities between patients with SIM1 deficiency and melanocortin 4 receptor (MC4R) deficiency suggest that some of the effects of SIM1 deficiency on energy homeostasis are mediated by altered melanocortin signaling.
Integrity in Health Care Institutions: Humane Environments for Teaching, Inquiry, and Healing
Authors: Michael A. Grodin
Journal: JAMA (1991)

Rarely have I so enjoyed an edited collection of essays. Perhaps this is because I am an academic physician working within a large health care institution who is called upon to "teach, inquire, and heal." Or perhaps it is true that when you assemble nationally recognized and experienced physicians, administrators, scholars, teachers, and humanitarians and ask them to address a complex, vitally important, and inadequately explored subject, the results will be insightful and provocative. The modern academic health care institution is the cornerstone of medical and public health teaching, research, patient care, and community service. Yet, what do academic health centers profess? What are their goals? What are their values, and what should be their mission? While there has been a great deal of focus on the roles, responsibility, and individual ethics of providers, there has been a paucity of scholarly analysis of the context and conflicts of institutional ethical,
James Graham Mann
Authors: Dora J Mann
Journal: BMJ (2008)

James Graham Mann’s medical training was interrupted after a year for service in the Royal Air Force, where he was a flight lieutenant in the signals branch; he returned to university in 1946 and did his pre-registration jobs in Ayrshire and his trainee assistantship in Darvel and New Milns.

In 1953 he moved to Shropshire as an …
Oestrogen‐dependent hereditary angio‐oedema with normal C1 inhibitor: description of six new cases and review of pathogenic mechanisms and treatment
Authors: C. Serrano, M. Guilarte, R. Tella, G. Dalmau, J. Bartra, P. Gaig, M. Cerdà, V. Cardona, A. Valero
Journal: Allergy (2008)

Background: Hereditary angio‐oedema (HAE) is a rare condition in which there is a deficiency in the quantity or activity of C1 inhibitor (C1INH). Recently, an additional type of HAE with no alterations in the levels or the function of C1INH has been reported. It is defined as HAE with normal C1INH, and named type III HAE or oestrogen‐dependent HAE. The aim of this study is to describe the clinical and laboratory findings of six new cases of type III HAE and to review the literature about this disease. Methods: A short description of six women with recurrent angio‐oedema is provided. The characteristics of the patients are compared with the previously reported case series in a literature‐based review. Results: The mean age of the patients at onset was 22 years (range 16–30). All of them had angio‐oedema attacks during oestrogen‐based contraceptive treatment and four reported episodes during pregnancy. Four patients reported a positive past family history. Two of them had experienced episodes of laryngeal oedema. None of the patients responded to corticoids or antihistamines during the attacks. Levels and functional activity of C1INH were within the normal range in all cases. Conclusions: Clinical and laboratory findings mirror the observations of previous reports of oestrogen‐dependent angio‐oedema with normal C1INH. This is the first published series of type III HAE in Spain.
Bio-bling: making jewellery from human tissue
Authors: Colin Martin
Journal: BMJ (2006)

A lthough it is not possible to commission a ring for your partner for St Valentine's Day next month incorporating bone grown from cells harvested from your body, such tokens of affection and commitment could well be available in the near future.

Biojewellery is a collaborative project between designer Tobie Kerridge and jeweller Nikki Stott, working at the Royal College of Art, and Dr Ian Thompson, a bioengineer at King's College London (see www.biojewellery.com). Funded primarily by a £60 …
Circulatory Changes in Acute Myocardial Infarction
Authors: ROBERT P. GILBERT, MELVIN GOLDBERG, JOSEPH GRIFFIN
Journal: Circulation (1954)

Using the dye dilution technic of Hamilton the cardiac output was measured in 20 patients with acute myocardial infarction. The blood pressure, circulation time, venous pressure, plasma volume, and hematocrit were also determined. Those patients who developed congestive heart failure had a low cardiac output and a prolonged circulation time. These changes were more pronounced in seven patients with sustained shock. One patient who had just recovered from circulatory collapse was found to have a cardiac output of 9.3 liters per minute.
Inability of Enzyme Immunoassays to Discriminate between Infections with Herpes Simplex Virus Types 1 and 2
Authors: Rhoda Ashley, Anne Cent, Vanna Maggs, Andre Nahmias, Lawrence Corey
Journal: Annals of Internal Medicine (1991)

Objective: To determine the accuracy of three commercial enzyme immunoassays in detecting and subtyping antibodies to herpes simplex virus type 1 or 2. Design: Cross-sectional. Setting: Referral medical center. Patients: Ninety patients with culture-positive lesions caused by infection with herpes simplex virus type 1 or 2. The results of Western blot and glycoprotein G immunodot enzyme assays showed that an additional 53 patients had subclinical herpes simplex virus type 2 infection, that another 20 patients had subclinical herpes simplex virus type 1 infection, and that 23 patients were seronegative. Measurements: Three commercial enzyme immunoassays were used to determine herpes simplex virus antibody subtypes. Main Results: All three commercial assays performed poorly in all patient groups (except in patients who were seronegative for herpes simplex virus). Among the 40 patients with a first episode of genital herpes, seroconversion to the appropriate viral type was shown by the three assays in only 33%, 55%, and 75% of cases. Among patients with recurrent genital herpes, the three commercial assays identified more than 90% of patients with only herpes simplex virus type 2 antibodies but failed to identify herpes simplex virus type 2 infections in 58% to 76% of patients with antibodies to both virus subtypes. The three assays correctly identified only 55%, 75%, and 85% of the 53 "silent carriers" of herpes simplex virus type 2. Overall, the three enzyme immunoassays detected herpes simplex virus type 2 antibodies in 60%, 62%, and 93% of patients with subtype 2 infections and falsely detected type 2 antibodies in 8%, 27%, and 49% of patients with type 1 infections. Conclusion: Currently licensed enzyme immunoassays give inaccurate or misleading results about the correct herpes simplex virus infecting subtype.
Halothane hepatitis: A double defect?
Authors: Leo Ranek
Journal: Hepatology (1986)

We studied susceptibility to halothane hepatitis with an in vitro test that detects cell damage from electrophilic drug intermediates. Metabolites of phenytoin were generated by incubation of phenytoin with rat hepatic microsomes in the presence of the epoxide hydrolase inhibitor 1,1,1-trichloropropene oxide (TCPO), which prevents the further metabolism of phenytoin to an inert metabolite. In lymphocytes exposed to this system, cytotoxicity was measured by trypan blue dye exclusion and was expressed as the percentage increase in trypan blue-positive cells after the addition of TCPO. In the presence of TCPO, lymphocytes from 11 patients with halothane hepatitis exhibited an increase in cytotoxicity at 0.06 mM phenytoin that was eight times greater than the increase in healthy controls (54 ± 10 per cent [mean ± S.E.M.] vs. 7.1 ± 2.2 per cent, p&lt;0.001). Patients with other liver diseases and persons recently exposed to halothane without adverse effects did not differ from healthy controls. In three patients with halothane hepatitis who were studied serially, the lymphocyte abnormality was still present after 13 months. Family studies revealed abnormal results on 10 cytotoxicity tests among 19 members of four families. We propose that there is a familial, constitutional susceptibility factor that predisposes persons to halothane hepatitis.
Deciding About Death-Reply
Authors: Carl M. Kjellstrand
Journal: JAMA (1992)

<h3>In Reply.</h3> —Although this was not the essence of my Editorial, Dr Boyce raises an important point about the mutual interaction of patients' and physicians' morality. Physicians must never be passive agents in dealings with patients. Requests from both patients and others that are in conflict with the physician's basic ethics should be rejected. If a physician feels that stopping life support is murder, he or she must not do so. However, such disagreement cuts both ways, so the respect for basic ethics must be mutual. The physician must respect the patient's ethics just as the patient must respect the physician's. If the physician feels that his or her ethical foundation makes it impossible to comply with a patient's request, the patient must be told so and, if he or she so wishes, be transferred to another physician whose ethics are more similar. Physicians must not violate their patients' wish,
HEMANGIOMA OF THE PHARYNX AND LARYNX
Authors: D. B. Hayden
Journal: JAMA (1925)

This case is reported because of the rarity of the condition. R. L., a man, aged 24, presented himself to the clinic for diagnosis and treatment of a throat condition. The father stated that when the patient was 6 months of age he was subject to a severe spell of dyspnea. A physician advised tracheotomy because of obstruction in the throat. This procedure was refused by the parents, and the patient recovered spontaneously from the attack. Since that time the father had known that there was some growth in the patient's throat, and was convinced that he was born with it. During his boyhood days there had been practically no symptoms, except at times during sleep, when breathing seemed to stop momentarily, because of an apparent obstruction at the larynx. Some hoarseness had also been noticed during the last few years. There had been no hemorrhage from the throat at
Esophageal echocardiographic left ventricular anterolateral wall motion in normal subjects and patients with coronary artery disease.
Authors: M Matsuzaki, Y Matsuda, Y Ikee, Y Takahashi, T Sasaki, Y Toma, K Ishida, T Yorozu, T Kumada, R Kusukawa
Journal: Circulation (1981)

Esophageal echocardiography was developed for recording left ventricular anterolateral wall (LVAW) echocardiograms and was applied clinically to 14 normal subjects and 21 patients with coronary artery disease. LVAW echocardiograms were obtained satisfactorily in 11 of 14 normal subjects (75%) and 20 of 21 patients (95%) with coronary artery disease. LVAW echocardiograms were obtained by conventional anterior echocardiography in eight of 21 patients (38%) with coronary artery disease. In 11 normal subjects, mm/sec (mean 34.3 +/- 5.2 mm/sec); and diastolic wall thickness ranged from 9-12.5 mm (mean 11.2 +/- 0.7 mm). In 20 patients with coronary artery disease, LVAW motion obtained by esophageal echocardiography was classified into five groups according to the excursion, and the findings were in good agreement (80%) with those obtained by left ventriculography. Classification of LVAW motion by conventional echocardiography agreed with that of left ventriculography in only three of eight patients, although all eight patients had abnormal LVAW motion by the conventional method. In all patients except one, whose LVAW echocardiograms were obtained by conventional echocardiography, excursion was much less than that obtained by esophageal echocardiography. We conclude that the projection of an ultrasonic beam from the intraesophageal transducer is a better approach for accurate measurement of LVAW motion.
THE IMPACT OF FITNESS ON ALL-CAUSE MORTALITY IN INDIVIDUALS WITH LEFT VENTRICULAR HYPERTROPHY
Authors: Andreas Pittaras, Michael Doumas, Charles Faselis, Athanasios Manolis, JP Kokkinos, A. Tsimploulis, Vasilios Papademetriou, Ross Fletcher, Peter Kokkinos
Journal: Journal of the American College of Cardiology (2014)
Identification of a Novel Synthetic Thiazolidin Compound Capable of Inducing c-Jun NH2-Terminal Kinase–Dependent Apoptosis in Human Colon Cancer Cells
Authors: Fuminori Teraishi, Shuhong Wu, Lidong Zhang, Wei Guo, John J. Davis, Fengqin Dong, Bingliang Fang
Journal: Cancer Research (2005)

Abstract Development of new therapeutic agents for colon cancer is highly desirable. To this end, we screened a chemical library for new anticancer agents and identified a synthetic compound, 5-(2,4-dihydroxybenzylidene)-2-(phenylimino)-1,3-thiazolidin (DBPT), which kills cancer cells more effectively than it kills normal human fibroblasts. The molecular mechanism of the antitumor action of DBPT was further analyzed in three human colorectal cancer cell lines. DBPT effectively inhibited the growth of colorectal cancer cells, independent of p53 and P-glycoprotein status, whereas normal fibroblasts were unaffected at the same IC50. Over time, DLD-1 cancer cells treated with DBPT underwent apoptosis. The general caspase inhibitor benzyloxycarbonyl-valine-alanine-aspartate-fluoromethylketone partially blocked DBPT-induced apoptosis in a dose-dependent manner. DBPT-induced apoptosis, including cytochrome c release and caspase activation, was abrogated when c-Jun NH2-terminal kinase (JNK) activation was blocked with either a specific JNK inhibitor or a dominant-negative JNK1 gene. However, constitutive JNK activation alone did not replicate the effects of DBPT in DLD-1 cells, and excessive JNK activation by adenovirus encoding MKK7 had little influence on DBPT-induced apoptosis. Our results suggested that DBPT induces apoptosis in colorectal cancer cell lines through caspase-dependent and caspase-independent pathways and that JNK activation was crucial for DBPT-induced apoptosis. DBPT and its analogues might be useful as anticancer agents.
Infant-scalp-vein Needles
Authors: A. D. Holliday-Rhodes
Journal: BMJ (1967)

JBOURff recognized sense.The criteria of Tow and Cheng for hysterectomy, applied to our series, twould result in fewer hysterectomies being performed.Hysterectomy should be reserved, as they themselves assert, for selected cases and not used in childless women who do not need it or in patients with advanced disease ,who die as a consequence of it.Far more important than a contrived argument about hysterectomy is the problem ,of ensuring the effective follow-up of all mole cases, so that patients who need treatment receive it before the chance of recovery is lost.Patients still die because the follow- -up methods available are inadequate or not even used.A reliable centralized follow-up system could now be devised with the technology available in the United King- 4om.There is a case for making hydatidiform mole a notifiable disease.-Iam, etc., ,
Relation between income inequality and mortality in Canada and in the United States: cross sectional assessment using census data and vital statistics
Authors: N. A Ross
Journal: BMJ (2000)

<h3>Abstract</h3> <b>Objective:</b> To compare the relation between mortality and income inequality in Canada with that in the United States. <b>Design:</b> The degree of income inequality, defined as the percentage of total household income received by the less well off 50% of households, was calculated and these measures were examined in relation to all cause mortality, grouped by and adjusted for age. <b>Setting:</b> The 10 Canadian provinces, the 50 US states, and 53 Canadian and 282 US metropolitan areas. <b>Results:</b> Canadian provinces and metropolitan areas generally had both lower income inequality and lower mortality than US states and metropolitan areas. In age grouped regression models that combined Canadian and US metropolitan areas, income inequality was a significant explanatory variable for all age groupings except for elderly people. The effect was largest for working age populations, in which a hypothetical 1% increase in the share of income to the poorer half of households would reduce mortality by 21 deaths per 100 000. Within Canada, however, income inequality was not significantly associated with mortality. <b>Conclusions:</b> Canada seems to counter the increasingly noted association at the societal level between income inequality and mortality. The lack of a significant association between income inequality and mortality in Canada may indicate that the effects of income inequality on health are not automatic and may be blunted by the different ways in which social and economic resources are distributed in Canada and in the United States.
Abstract 4338: The effect of opposing roles of NF-kB on TRAIL-R2 expression in TRAIL cytotoxicity in neuroblastoma cells
Authors: Hye Lim Jung, Myoung Woo Lee, Hye Ryung Kim, Dae Sung Kim, Hye Jin Kim, Soo Hyun Lee, Hee Won Chueh, Keon Hee Yoo, Ki Woong Sung, Hong Hoe Koo
Journal: Cancer Research (2011)

Abstract TNF-related apoptosis-inducing ligand (TRAIL) is a potent inducer of apoptosis in most, but not all, cancer cells. The molecular factors regulating the sensitivity to TRAIL are still incompletely understood. The transcription factor nuclear factor-kappa B (NF-kB) has been implicated, but its exact role is controversial. In this study, we have investigated the role of NF-kB on enhancement of TRAIL cytotoxicity in neuroblastoma cells. IkB kinase (IKK) inhibitor decreased basal NF-kB activity and marginally induced cell death in neuroblastoma cell line SK-NMC. Pretreatment with IKK inhibitor synergistically increased TRAIL-mediated apoptosis via up-regulation of TRAIL- receptor2 (TRAIL-R2) expression in response to the decrease in basal NF-kB activity, indicating that basal NF-kB activity blocks TRAIL-R2 expression in SK-NMC cells. In addition, pretreatment with Cisplatin, a platinum analog and an alkylating agent widely used in neuroblstomas, showed increase in NF-kB activity and induction of apoptotic cell death in SK-NMC cells. Pretreatment with Cisplatin significantly increased TRAIL-mediated apoptosis via up-regulation of TRAIL-R2 expression through induction of NF-kB, suggesting that induced NF-kB is involved in TRAIL-R2 expression up-regulated by Cisplatin. IKK inhibitor or Cisplatin followed by TRAIL treatment increased caspase-8, -9, and -3 activation. Mcl-1 cleavage and Bid truncation. Our results implicate that basal NF-kB activity is involved in TRAIL resistance but induced NF-kB plays a role in TRAIL sensitivity, and suggest that the enhanced sensitivity of SK-NMC cells to TRAIL is associated with an increase in TRAIL-R2 expression. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4338. doi:10.1158/1538-7445.AM2011-4338