tbuckley/cabot-search huggingface dataset:
Correction: Bromergocryptine and Birth Defects
Authors: A.E. Boyd, Seymour Reichlin
Journal: Annals of Internal Medicine (1978)

Letters and Corrections1 April 1978Correction: Bromergocryptine and Birth DefectsA.E. BOYD III, M.D., Seymour Reichlin, M.D., PH.D.A.E. BOYD III, M.D.Search for more papers by this author, Seymour Reichlin, M.D., PH.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-88-4-581_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: In our article on diagnosis and therapy of galactorrhea and amenorrhea syndromes (1) we pointed out the clinical experience with bromergocryptine therapy in pregnancy. We reported that five birth defects, two major and three minor, were observed in 78 infants born to women who had been treated at some period during early pregnancy in Europe. The denominator should have read 108 rather than 78. Recent information provided to us by the manufacturer (Sandoz Laboratories) summarized information on 448 pregnancies that resulted in 369 live births. Among this larger population 11 malformations were cited, of which two (the...Reference1. BOYDREICHLINTURKSOY ASR: Galacorrhea-amenorrhea syndrome: diagnosis and therapy. Ann Intern Med 87:165-175, 1977. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByDrugs affecting autonomic functions or the extrapyramidal system 1 April 1978Volume 88, Issue 4Page: 581-581KeywordsBirthCongenital disordersInfantsPregnancy Issue Published: 1 April 1978 PDF DownloadLoading ...
Bone Mineral Density, Type 1 Diabetes, and Celiac Disease
Authors: Helen Lunt, Christopher M. Florkowski, H. Bramwell Cook, Martin R. Whitehead
Journal: Diabetes Care (2001)

Correspondence in Diabetes Care has highlighted the importance of two secondary causes of reduced bone mineral density (BMD) in type 1 diabetes, namely thyrotoxicosis and primary hyperparathyroidism (1,2). We describe another secondary cause of reduced BMD. Celiac disease is associated with reduced BMD and reversible secondary osteoporosis in the general population (3,4). Celiac disease is not uncommon in type 1 diabetes, with a prevalence of 1–7.8% (5). The association between celiac disease, type 1 diabetes, and osteopenia has been discussed in Diabetes Care (6), but the impact of celiac disease on BMD in type 1 diabetes has not been quantified. …
THE IMPACT OF EXERCISE TRAINING ON LEFT VENTRICULAR TORSION IS SPORT-SPECIFIC: A NEW TWIST ON THE MORGANROTH HYPOTHESIS
Authors: Rory B. Weiner, Adolph Hutter, Gregory Lewis, Francis Wang, Brant Berkstresser, Thomas Wang, Michael Picard, Aaron Baggish
Journal: Journal of the American College of Cardiology (2012)
Treatment of Mushroom Poisoning
Authors: F. Clara
Journal: JAMA (1984)

<h3>To the Editor.—</h3> In their review of the treatment of mushroom poisoning, Hanrahan and Gordon recommend high doses of pyridoxine hydrochloride (25 mg/kg, up to a total daily dosage of 15 to 20 g) for neurological symptoms. Before one follows this recommendation, which is to be found in several standard books also, one should remember that pyridoxine can produce untoward neurological effects, particularly in high doses. In protective doses, pyridoxine activates not only the decarboxylation of glutamic acid, with a formation of γ-aminobutyric acid (GABA) and an increase of the GABA content of the brain (this effect is anticonvulsant in the presence of excess isoniazid or its hydrazones) but also, and to a greater extent, the transamination between GABA and α-ketoglutaric acid, leading to the disappearance of GABA and thus to a decrease in the GABA content of the brain.<sup>1</sup>High doses of pyridoxine as those recommended by Hanrahan
Arthrography and arthrotomy of the knee in sports injuries.
Authors: T Kulthanan, P Noiklang
Journal: British Journal of Sports Medicine (1993)

A total of 266 patients with injuries to the knee sustained during sports activities were managed by arthroscopy and/or arthrotomy. All of them received systemic examination and a standard battery of knee stability tests. Fifty-three were examined by arthrography and all underwent arthrotomy for surgical correction of the lesion diagnosed by both clinical examination and arthrography. Our study showed that clinical examination could give an accurate clinical diagnosis in 88.35% of cases and arthrography in 76.89%. No complication from arthrography was found. Injury occurred most commonly between 21 and 30 years of age and was more common to the right knee than the left. The sport in which most injuries occurred was football.
Physical conditioning decreases norepinephrine-induced vasoconstriction in rabbits. Possible roles of norepinephrine-evoked endothelium-derived relaxing factor.
Authors: H I Chen, H T Li, C C Chen
Journal: Circulation (1994)

BACKGROUND Physical activity can reduce sympathetic tone and may be beneficial to human health. Whether the vascular responses to norepinephrine (NE), an adrenergic vasoconstrictor, could be altered by chronic exercise was unclear. We therefore conducted this study to investigate the effects of endurance exercise training on NE-induced vasoconstrictive response in healthy rabbits. Possible mechanisms were also studied. METHODS AND RESULTS Twenty-four male New Zealand White rabbits were used for this study. They were divided into two groups: control and training. The training group was trained on a treadmill with running speed of 0.88 km/h at a 0 degree grade for 10 to 60 minutes per day, for 5 days a week for a total of 8 weeks. At the end of the experiments, thoracic aortae (3 mm long) were isolated. The vascular tension was measured with a force transducer. The dose-response relation of NE-induced vasoconstriction was determined and compared for control (n = 5) and trained (n = 6) groups. To verify the possible involvement of endothelium-derived relaxing factor (EDRF) in the alteration of NE-induced vasoconstriction after exercise training, we compared the vascular responses to NE in endothelium-intact, N omega-nitro-L-arginine (L-NNA, 10(-4) mol/L)-pretreated, or denuded vessel segments (n = 4 for each experiment of each group). EDRF release in the presence or absence of NE was also evaluated by the increased tension induced by hemoglobin (10(-5) mol/L), an EDRF scavenger (n = 6 for the control group and n = 8 for the trained group). In addition, vascular responses to some specific adrenergic agonists (ie, phenylephrine, an alpha 1-agonist, and clonidine, an alpha 2-agonist) were also studied to see if a specific adrenergic receptor was involved (n = 4 for each experiment of each group). Our results indicated that (1) [NE]ED50 of the thoracic aorta was elevated by exercise training; (2) in the presence of NE, EDRF release from the thoracic aorta, assessed by addition of hemoglobin or L-NNA, was higher in the trained group than in the control group; (3) both phenylephrine (10(-8) mol/L) and clonidine (10(-6) mol/L) could evoke vasorelaxation that would be inhibited by L-NNA; and (4) in addition to causing vasoconstriction, NE could stimulate EDRF release, possibly via alpha 1- and alpha 2-receptors of endothelial cells. CONCLUSIONS Our data suggest that exercise training may decrease NE-induced vasoconstrictive response and may increase NE-stimulated EDRF release.
Services for liver disease in the United Kingdom
Authors: Roger Williams
Journal: BMJ (2005)

Need improving urgently as hepatic morbidity and mortality rise 

M ortality from liver disease is increasing in the United Kingdom. In 2000 liver disease killed more men than Parkinson's disease and more women than cancer of the cervix. The average mortality among patients admitted to hospital with a diagnosis of liver disease was 18.2% in 2004 with a large range, which suggests (once clinical factors have been accounted for) that the standard of care may vary widely from place to place.1

Liver disease has many causes, almost all of them increasing in prevalence. Mortality from alcoholic liver disease has doubled in the past 10 years and, as the chief medical officer pointed out in 2001,2 these deaths occur mainly among men aged 40-60. Fewer than 10% of an estimated 300 000 cases of infection with hepatitis C virus have been diagnosed and the prevalence of the related chronic liver disease is expected to treble by 2020. Moreover 6000 people who are hepatitis B positive are coming into the United Kingdom …
Abstract 2511: Glycogen synthase kinase 3 beta inhibitors protect hippocampal neurons from radiation-induced apoptosis by regulating MDM2/p53 pathway
Authors: Dinesh Kumar Thotala, Dennis E. Hallahan, Eugenia M. Yazlovitskaya
Journal: Cancer Research (2011)

Abstract Exposure of the brain to ionizing radiation can cause neurocognitive deficiencies. The pathophysiology of these neurological changes is complex and includes radiation-induced apoptosis in the subgranular zone of the hippocampus. We have recently found that inhibition of glycogen synthase kinase 3β (GSK-3β) resulted in significant protection from radiation-induced apoptosis in hippocampal neurons. The Molecular mechanisms of this cytoprotection include abrogation of radiation-induced accumulation of p53. Here we show that pretreatment of irradiated HT-22 neurons with small molecule inhibitors of GSK-3β SB216763 or SB415286, or with GSK-3β-specific shRNA resulted in accumulation of the p53-specific E3 ubiquitin ligase MDM2. Knockdown of MDM2 using specific shRNA or chemical inhibition of MDM2 prevented the protective changes triggered by GSK-3β inhibition in irradiated HT-22 and restored radiation cytotoxicity. We found that this could be due to regulation of apoptosis by subcellular localization and interaction of GSK-3β, p53 and MDM2. These data suggest that the mechanisms of radioprotection by GSK-3β inhibitors in hippocampal neurons involve regulation of MDM2-dependent p53 accumulation and interactions between GSK-3β, MDM2 and p53. 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 2511. doi:10.1158/1538-7445.AM2011-2511
Screening for Cervical and Breast Cancer: Is Obesity an Unrecognized Barrier to Preventive Care?
Authors: Christina C. Wee, Ellen P. McCarthy, Roger B. Davis, Russell S. Phillips
Journal: Annals of Internal Medicine (2000)

Background: Compared with thinner women, obese women have higher mortality rates for breast and cervical cancer. In addition, obesity leads to adverse social and psychological consequences. Whether obesity limits access to screening for breast and cervical cancer is unclear. Objective: To examine the relation between obesity and screening with Papanicolaou (Pap) smears and mammography. Design: Population-based survey. Setting: United States. Participants: 11 435 women who responded to the “Year 2000 Supplement” of the 1994 National Health Interview Survey. Measurements: Screening with Pap smears and mammography was assessed by questionnaire. Results: In women 18 to 75 years of age who had not previously undergone hysterectomy (n = 8394), fewer overweight women (78%) and obese women (78%) than normal-weight women (84%) had had Pap smears in the previous 3 years (P < 0.001). After adjustment for sociodemographic information, insurance and access to care, illness burden, and provider specialty, rate differences for screening with Pap smears were still seen among overweight (−3.5% [95% CI, −5.9% to −1.1%]) and obese women (−5.3% [CI, −8.0% to −2.6%]). In women 50 to 75 years of age (n = 3502), fewer overweight women (64%) and obese women (62%) than normal-weight women (68%) had had mammography in the previous 2 years (P < 0.002). After adjustment, rate differences were −2.8% (CI, −6.7% to 0.9%) for overweight women and −5.4% (CI, −10.8% to −0.1%) for obese women. Conclusions: Overweight and obese women were less likely to be screened for cervical and breast cancer with Pap smears and mammography, even after adjustment for other known barriers to care. Because overweight and obese women have higher mortality rates for cervical and breast cancer, they should be targeted for increased screening.
An evaluation demonstrating continued efficacy and improved safety and tolerability in 17 patients switched to PEGASYS® after discontinuation from REBETRON™ for the treatment of chronic hepatitis C
Authors: R.P. Perrillo, K.D. Rothstein, I. Alam, P.J. Thuluvath, M. Palmer, P.J. Pockros, S.C. Pappas, B.S. Doerschuk, S. Cantwell
Journal: Journal of Hepatology (2001)
Erratum to “Topical and intravitreous administration of cationic nanoemulsions to deliver antisense oligonucleotides directed towards VEGF KDR receptors to the eye” [J. Control. Release 145 (3) (2010 Aug 3) 297–305]
Authors: Tal Hagigit, Muhammad Abdulrazik, Faik Orucov, Faty Valamanesh, Martin Lambert, Gregory Lambert, Francine Behar-Cohen, Simon Benita
Journal: Journal of Controlled Release (2011)
Histamine‐induced inhibition of neutrophil chemotaxis and T‐lymphocyte proliferation in man
Authors: T. B. Bury, J. L Corhay, M. F. Radermecker
Journal: Allergy (1992)

Histamine inhibits in vitro human neutrophil chemotaxis and T‐lymphocyte proliferation via H 2 receptors. The aim of this study was to verify these inhibitory effects of histamine in man in vivo. Healthy volunteers were challenged with histamine by intravenous (1 mg), subcutaneous (1 mg) and inhalatory (2.4 mg) routes. Venous blood was taken before and at different times after challenge. Neutrophil chemotaxis was studied by the Boyden assay and T‐lymphocyte proliferation by counting H 3 ‐thymidine incorporation in cultured mononuclear cells. Plasma histamine was measured by radioimmunoassay. Histamine infusion caused transient systemic symptoms as well as a significant decrease of neutrophil chemotaxis (x̄−26%± 6) and of PHA‐pulsed T‐lymphocyte proliferation (x̄−16%± 6) 4 h after histamine challenge. Subcutaneous injection of histamine caused only a significant decrease of neutrophil chemotaxis (x̄−24%± 15) 4 h after injection. Histamine inhalation was well tolerated and caused a significant depression of neutrophil chemotaxis (x̄−40%± 15) and of T‐lymphocyte proliferation (x̄−27%± 6) 2 and 4 h after the challenge. Histamine challenges were always accompanied by a rapid and transient rise in plasma histamine. Inhalation of an H 3 agonist (impromidine) but not of an H 2 agonist (betahistine) caused a decrease of neutrophil chemotaxis and of T‐lymphocyte proliferation. Oral pretreatment with an H 1 antagonist (cimetidine) before histamine inhalation prevented histamine‐induced decrease of neutrophil chemotaxis and T‐lymphocyte proliferation, whereas astemizole, an H 3 antagonist, had no effect. In conclusion, during the few hours following administration, exogenous histamine in man causes a depression of neutrophil chemotaxis and T‐lymphocyte proliferation via H 2 receptors. These observations are consistent with the concept that endogenous histamine may exert some modulatory effects on inflammatory and immune cells in man.
Cell Volume Regulation Modulates NLRP3 Inflammasome Activation
Authors: Vincent Compan, Alberto Baroja-Mazo, Gloria López-Castejón, Ana I. Gomez, Carlos M. Martínez, Diego Angosto, María T. Montero, Antonio S. Herranz, Eulalia Bazán, Diana Reimers, Victoriano Mulero, Pablo Pelegrín
Journal: Immunity (2012)
Why the Hippocratic ideals are dead
Authors: I. Loefler
Journal: BMJ (2002)

Medical ethics in Western medicine have traditionally concerned six major principles, all of which are in the Hippocratic oath: reverence for our teachers and consideration towards our colleagues; the command “first, do no harm”; absolute regard for life; restriction to field of expertise; abuse of privilege; and respect for privacy. In addition Hippocratic medicine is pious, serene, and centres solely on the individual.

Modern medicine lacks piety and serenity 

Contemporary medicine places much less emphasis on reverence for the teachers, if for no other reason than because a doctor has limited exposure to his or her teachers: there are too many of them. Obligations towards the family of the deceased teacher, if they exist at all outside the sphere of emotion, are rarely financial.

Consideration towards colleagues is still an important part of medical ethics, although the practice of treating colleagues and their families for free has decreased greatly. The bad mouthing of colleagues, …
Abstract C24: High systemic cholesterol increases blood vessel endothelial permeability and favors metastasis: Are these events related?
Authors: Ana Magalhaes, Catarina R. Santos, Germana Domingues, Tãnia Carvalho, Sergio Dias
Journal: Cancer Research (2013)

Abstract Here we hypothesize that systemic cholesterol favors metastasis by increasing blood vessel endothelial permeability. The majority of metastatic dissemination occurs through the hematogenous route and factors that alter blood vessel properties can affect the entry of cancer cells in circulation. It is generally accepted that high levels of systemic cholesterol, in particular low density lipoprotein (LDL), have a negative impact in endothelial function. This has been demonstrated mainly in large arteries but less is known about how LDL affects the microvasculature of different organs. High cholesterol has also been associated with poor prognosis in several cancers. In our lab, using orthotopic mouse models of breast cancer, we were able to show that mice in which increased LDL in circulation is induced by a high cholesterol diet, have more metastasis. Here we also show in an “in vitro” system, that LDL increases endothelial permeability and that this can be reverted by blocking the interaction of LDL with the LDL-receptor. Additionally we observe that this higher endothelial permeability is due to cholesterol enrichment of endothelial cells, as nystatin, a cholesterol sequestering agent is also able to revert the phenotype. Back to “in vivo”, using the same orthotopic breast cancer model, we are able to show that high systemic cholesterol increases the number of circulating cancer cells in the blood. We are now testing the hypothesis of whether this is due to increased permeability of tumor blood vessels or of the vessels surrounding the tumor. Citation Format: Ana Magalhaes, Catarina R. Santos, Germana Domingues, Tãnia Carvalho, Sergio Dias. High systemic cholesterol increases blood vessel endothelial permeability and favors metastasis: Are these events related? [abstract]. In: Proceedings of the Third AACR International Conference on Frontiers in Basic Cancer Research; Sep 18-22, 2013; National Harbor, MD. Philadelphia (PA): AACR; Cancer Res 2013;73(19 Suppl):Abstract nr C24.
Manufacturer recalls commonly used painkiller amid fears of possible sabotage
Authors: S. Ginn
Journal: BMJ (2011)

The drug company Reckitt Benckiser has recalled all packs of the painkiller Nurofen Plus (ibuprofen and codeine) after the discovery of rogue medication in some of its blister packs sold over the counter.

A statement issued on 26 August by the company said, “Consumers are being asked to return packs of Nurofen Plus to their nearest pharmacy following five reported cases of other manufacturers’ medicine being found in boxes of Nurofen Plus.” It added, “Distribution of Nurofen Plus has been halted at …
Symptom and Quality of Life Improvement in LUX-Lung 6: An Open-Label Phase III Study of Afatinib Versus Cisplatin/Gemcitabine in Asian Patients With EGFR Mutation-Positive Advanced Non–small-cell Lung Cancer
Authors: Sarayut L Geater, Chong-Rui Xu, Caicun Zhou, Cheng-Ping Hu, Jifeng Feng, Shun Lu, Yunchao Huang, Wei Li, Mei Hou, Jian Hua Shi, Kye Young Lee, Michael Palmer, Yang Shi, Juliane Lungershausen, Yi-Long Wu
Journal: Journal of Thoracic Oncology (2015)

IntroductionIn the phase III, LUX-Lung 6 trial, afatinib prolonged progression-free survival (PFS) versus cisplatin/gemcitabine in Asian patients with epidermal growth factor receptor (EGFR) mutation-positive non–small-cell lung cancer (NSCLC). This article provides detailed assessments of patient-reported outcomes (PROs), a LUX-Lung 6 secondary end point, and explores the relationship between PFS and health-related quality of life (QoL) in these patients.MethodsPatients (n = 364) were randomized (2:1) to oral afatinib (40 mg/day) or up to six cycles of cisplatin/gemcitabine (21-day cycle; cisplatin 75 mg/m2 [d1]; gemcitabine 1000 mg/m2 [d1,8]). QoL was assessed using the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire and its lung cancer-specific module. The relationship between PFS (investigator assessment and independent review) and QoL was evaluated using analysis of covariance and a longitudinal model.ResultsMore patients treated with afatinib versus cisplatin/gemcitabine showed improvements in global health status/QoL (p < 0.0001) and physical (p < 0.0001), role (p = 0.013), and social (p < 0.001) functioning scales. Delayed symptom deterioration and better QoL over time was also observed with afatinib. QoL measured before tumor assessment was considerably poorer for patients with progression than those without progression, with significant differences in mean scores at multiple assessment time points. Results from the longitudinal analysis consistently demonstrated a significant negative impact of progression on QoL (p < 0.0001).ConclusionAfatinib improved PFS and PROs versus chemotherapy in EGFR mutation-positive NSCLC patients. Progression was associated with statistically significant worsening in QoL measured before tumor assessment, underscoring the value of PFS as a clinically relevant end point.