tbuckley/cabot-search huggingface dataset:
Cocaine-Related Vasculitis Causing Upper-Limb Peripheral Vascular Disease
Authors: John A. Spittell, Peter C. Spittell
Journal: Annals of Internal Medicine (2001)

Letters6 November 2001Cocaine-Related Vasculitis Causing Upper-Limb Peripheral Vascular DiseaseJohn A. Spittell Jr., MD and Peter C. Spittell, MDJohn A. Spittell Jr., MDMayo Clinic and Mayo Foundation; Rochester, MN 55905 (Spittell, Spittell)Search for more papers by this author and Peter C. Spittell, MDMayo Clinic and Mayo Foundation; Rochester, MN 55905 (Spittell, Spittell)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-135-9-200111060-00023 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:In the patient with upper-limb peripheral vascular disease described by Drs. Kumar and Smith (1), an interesting differential diagnosis is present. The authors found that laboratory studies excluded connective tissue disorders and confirmed their patient's use of cocaine. However, several other causes should have been considered before the occlusive arterial disease in the patient's hands was attributed to “cocaine vasculitis.” First, chronic repetitive blunt trauma to the hands in certain occupations and hobbies can cause palmar and digital occlusive arterial disease; this occurs most often in the dominant hand but can occur in both hands (2). Second, ...References1. Kumar PD, Smith HR. Cocaine-related vasculitis causing upper-limb peripheral vascular disease [Letter]. Ann Intern Med. 2000;133:923-4. [PMID: 11103072] LinkGoogle Scholar2. Spittell PC, Spittell JA. Occlusive arterial disease of the hand due to repetitive blunt trauma: a review with illustrative cases. Int J Cardiol. 1993;38:281-92. [PMID: 8463009] CrossrefMedlineGoogle Scholar3. Creager MA, Beckman JA. Assessment of arterial and venous thrombosis.. In: Loscalzo J, Schafer AI, eds. Thrombosis and Hemorrhage. 2nd ed. Baltimore: Williams & Wilkins; 1998:491-2. Google Scholar4. Spittell JA. Some uncommon types of occlusive peripheral arterial disease. Curr Probl Cardiol. 1983;8:1-35. [PMID: 6357641] CrossrefMedlineGoogle Scholar Author, Article, and Disclosure InformationAuthors: John A. SpittellJr., MD; Peter C. Spittell, MDAffiliations: Mayo Clinic and Mayo Foundation; Rochester, MN 55905 (Spittell, Spittell) PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoCocaine-Related Vasculitis Causing Upper-Limb Peripheral Vascular Disease P. Dileep Kumar and Howard R. Smith Cocaine-Related Vasculitis Causing Upper-Limb Peripheral Vascular Disease P. Dileep Kumar and Howard R. Smith Metrics Cited byCocaineCocaine 6 November 2001Volume 135, Issue 9Page: 843KeywordsArteriesCocaineConnective tissueDeep vein thrombosisPeripheral vascular diseaseProtein C deficiencyProtein S deficiencyResearch laboratoriesVasculitis ePublished: 6 November 2001 Issue Published: 6 November 2001 Copyright & PermissionsCopyright © 2001 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Etanercept for psoriatic arthritis
Authors: D. D Gladman
Journal: BMJ (2010)

Patients who do not respond to standard doses are unlikely to benefit from a higher one

In the linked randomised controlled trial (doi:10.1136/bmj.c147) Sterry and colleagues compared the effectiveness of two different etanercept regimens (50 mg once a week or twice a week) in treating the skin manifestations of psoriasis in people who also had psoriatic arthritis over 12 weeks.1 

Psoriatic arthritis is an inflammatory arthritis that affects about 30% of patients with psoriasis. Over the past few decades it has become clear that the disease is more common and more severe than previously thought. Studies in the 1940s indicated that the frequency of psoriatic arthritis in patients with psoriasis was 7%, but more recent studies suggest a frequency of 30%.2 Psoriatic arthritis may cause joint destruction, disability, and reduced quality of life. Patients with the disease have more disability and a worse quality of life than those with psoriasis alone.3 Although disease modifying antirheumatic drugs have been used to treat psoriatic arthritis, they have not altered the disease course or prevented the progression of joint damage.4

Since the advent …
Primary Care — Will It Survive?
Authors: Thomas Bodenheimer
Journal: New England Journal of Medicine (2006)

The American College of Physicians recently warned that “primary care, the backbone of the nation's health care system, is at grave risk of collapse.”1 And indeed, primary care is facing a confluence of factors that could spell disaster. Patients are increasingly dissatisfied with their care and with the difficulty of gaining timely access to a primary care physician; many primary care physicians, in turn, are unhappy with their jobs, as they face a seemingly insurmountable task; the quality of care is uneven; reimbursement is inadequate; and fewer and fewer U.S. medical students are choosing to enter the field.The great . . .
Arsenic: health effects, mechanisms of actions, and research issues.
Authors: C O Abernathy, Y P Liu, D Longfellow, H V Aposhian, B Beck, B Fowler, R Goyer, R Menzer, T Rossman, C Thompson, M Waalkes
Journal: Environmental Health Perspectives (1999)

A meeting on the health effects of arsenic (As), its modes of action, and areas in need of future research was held in Hunt Valley, Maryland, on 22-24 September 1997. Exposure to As in drinking water has been associated with the development of skin and internal cancers and noncarcinogenic effects such as diabetes, peripheral neuropathy, and cardiovascular diseases. There is little data on specific mechanism(s) of action for As, but a great deal of information on possible modes of action. Although arsenite [As(III)] can inhibit more than 200 enzymes, events underlying the induction of the noncarcinogenic effects of As are not understood. With respect to carcinogenicity, As can affect DNA repair, methylation of DNA, and increase radical formation and activation of the protooncogene c-myc, but none of these potential pathways have widespread acceptance as the principal etiologic event. In addition, there are no accepted models for the study of As-induced carcinogenesis. At the final meeting session we considered research needs. Among the most important areas cited were a) As metabolism and its interaction with cellular constituents; b) possible bioaccumulation of As; c) interactions with other metals; d) effects of As on genetic material; e) development of animal models and cell systems to study effects of As; and f) a better characterization of human exposures as related to health risks. Some of the barriers to the advancement of As research included an apparent lack of interest in the United States on As research; lack of relevant animal models; difficulty with adoption of uniform methodologies; lack of accepted biomarkers; and the need for a central storage repository for stored specimens.
Hyperventilation of exercise to induce asthma?
Authors: P M Tweeddale, D J Godden, I W Grant
Journal: Thorax (1981)

Bronchoconstriction was induced in asthmatic patients by means of isocapnic hyperventilation with dry air. Responses both within a day and between days did not differ significantly and corresponded closely with those observed after exercise. The mean fall in forced expiratory volume in one second (FEV1) observed with both techniques was equivalent to 36%. Isocapnic hyperventilation with dry air, as used in this study, was a potent stimulus and provoked a reproducible response. The method was physically less demanding than exercise and was more acceptable to patients.
Histological studies of Auerbach's plexuses of the oesophagus, stomach, jejunum, and colon in patients with achalasia of the oesophagus: correlation with gastric acid secretion, presence of parietal cells and gastric emptying of solids.
Authors: A Csendes, G Smok, I Braghetto, P Gonzalez, A Henriquez, P Csendes, D Pizurno
Journal: Gut (1992)

Histological changes in the Auerbach9s plexuses of the oesophagus, stomach, jejunum, and colon were analysed in a prospective study in 34 patients with achalasia of the oesophagus. At the distal end of the oesophagus ganglia cells were absent in 91% of cases as well as in the middle third of the stomach (20%). The Auerbach9s plexuses were normal in the jejunum and colon. The results of gastric acid secretion showed that the peak acid output was significantly lower in achalasia patients compared with controls (p less than 0.001). There was no correlation between the mean ganglion neuronal count in the gastric plexuses and the rate of gastric acid output (r = 0.33). Gastric emptying of solids was also evaluated, but there was no correlation between gastric emptying and the mean ganglion neuronal count in the gastric Auerbach9s plexuses. The rate of gastric emptying of solids was similar in controls and patients with achalasia. These studies suggest that denervation of the oesophagus in patients with achalasia, which is a constant finding in several previous reports may extend beyond the oesophagus to the stomach in nearly half the cases.
Abstract LB-369: Sphingosine-1-phosphate (S1P) as a novel target in renal cancer (RCC)
Authors: Rupal S. Bhatt, Liang Zhang, Andrea Bullock, Xiaoen Wang, Kelli Moreno, Sabina Signoretti, Michael B. Atkins, Roger Sabbadini, James W. Mier
Journal: Cancer Research (2010)

Abstract Although treatment of patients (pts) with metastatic RCC with VEGFR2 inhibitors induces disease regression, these responses tend to be short-lived. Mouse models of VEGFR TKI treatment of RCC were used to study the mechanisms of resistance and identify novel targets. Drug-induced growth arrest was associated with enhanced expression of sphingosine kinase (sphk) whose only product is the bioactive signaling lipid, S1P. To explore the role of this pathway in mice bearing 786-O RCC were treated with a neutralizing antibody against S1P. Vehicle treated tumors increased by 2mm after 5.8 ± 4.1 days (n=6) and treatment with 10mg/kg or 50mg/kg anti-S1P led to growth after 15.3 ± 3.5 days (n=7) and 20.5 ± 3.9 days (n=6) respectively (P&amp;lt;0.01 for PBS vs. 10mg/kg or 50mg/kg), demonstrating that anti-S1P exhibits single agent activity in treatment naïve tumors. To assess the activity of S1P ab in the setting of sunitinib resistance, mice whose tumors developed resistance to sunitinib, were switched to either an anti-isotype negative control antibody, or anti-S1P. Treatment with anti-S1P produced relative tumor stabilization: 23.0 ± 16.5 days (n=10) vs. isotype control 6.9 ± 2.1 days for switch to isotype (n=7, P=0.01). In an A498 RCC tumor xenograft model, vehicle and isotype treated tumors increased by 2mm after 5.0 ± 1.17 days (n=7) compared to15.3 ± 5.8 days (n=6) for mice treated with 50mg/kg anti-S1P (P&amp;lt;0.01) and time to reach sacrifice size of 20mm was 30.7 ± 3.8 days (n=7) in vehicle and isotype treated tumors and 45.0 ± 8.6 days (n=6) with 50mg/kg anti-S1P (P=0.01). S1P levels in pts with RCC were found to be significantly higher than control pts (2.7 ± 0.032uM (n=23) vs 0.588 ± 0.057 M (n=20, P&amp;lt;0.0001). Thus, the S1P pathway is a novel target for the treatment of both treatment naïve and VEFGR TKI refractory RCC and anti-S1P therapy is an attractive new option for clinical investigation in RCC patients. The humanized anti-S1P mAb, ASONEPTM, has recently completed Phase I clinical trials in cancer and planning for Phase II efficacy trials is underway. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr LB-369.
ENUCLEATION OF TONSILS AND REMOVAL OF ADENOIDS UNDER GAS ANAESTHESIA
Authors: J. F. O'Malley
Journal: BMJ (1913)

Ianotlher from beneath tlle tip of tlhe chin to meet this at right aingles, the anterior triangle is first cleared of the fascia, fat, and lymphatic glands belonging to the sub- mental, submlaxillarv, inferior parotid, and carotid groups, talking care to prevent tearina of these glands, as other- wise cancer implantation followed by recurrent nodules, or, rore-frequently, widespread and rapid-malignant inlduration of the whole side of the neck, might result.Drainage tubes are inserted before closing this wound, to rellove blood-stained exudation or secretion from any of
Genome-wide association study in Chinese men identifies two new prostate cancer risk loci at 9q31.2 and 19q13.4
Authors: Jianfeng Xu, Zengnan Mo, Dingwei Ye, Meilin Wang, Fang Liu, Guangfu Jin, Chuanliang Xu, Xiang Wang, Qiang Shao, Zhiwen Chen, Zhihua Tao, Jun Qi, Fangjian Zhou, Zhong Wang, Yaowen Fu, Dalin He, Qiang Wei, Jianming Guo, Denglong Wu, Xin Gao, Jianlin Yuan, Gongxian Wang, Yong Xu, Guozeng Wang, Haijun Yao, Pei Dong, Yang Jiao, Mo Shen, Jin Yang, Jun Ou-Yang, Haowen Jiang, Yao Zhu, Shancheng Ren, Zhengdong Zhang, Changjun Yin, Xu Gao, Bo Dai, Zhibin Hu, Yajun Yang, Qijun Wu, Hongyan Chen, Peng Peng, Ying Zheng, Xiaodong Zheng, Yongbing Xiang, Jirong Long, Jian Gong, Rong Na, Xiaoling Lin, Hongjie Yu, Zhong Wang, Sha Tao, Junjie Feng, Jishan Sun, Wennuan Liu, Ann Hsing, Jianyu Rao, Qiang Ding, Fredirik Wiklund, Henrik Gronberg, Xiao-Ou Shu, Wei Zheng, Hongbing Shen, Li Jin, Rong Shi, Daru Lu, Xuejun Zhang, Jielin Sun, S Lilly Zheng, Yinghao Sun
Journal: Nature Genetics (2012)
Chronic Thyroiditis and Mitral Valve Prolapse
Authors: ALLAN D. MARKS
Journal: Annals of Internal Medicine (1985)

Mitral valve prolapse is more prevalent in patients with autoimmune diffuse toxic goiter, suggesting a possible etiologic association. The prevalence of mitral valve prolapse was determined in 75 patients with chronic lymphocytic thyroiditis, another autoimmune thyroid disorder, and in 50 healthy control subjects. Mitral valve prolapse was found in 31 of 75 (41%) patients with chronic lymphocytic thyroiditis and in 4 of 50 (8%) controls (odds ratio, 8.10; 95% confidence interval, 2.64 to 24.83;p < 0.0005). The age-race adjusted odds ratio was 9.26 (95% confidence interval, 2.83 to 30.26; p < 0.0005). No correlation between the prevalence of mitral valve prolapse and the presence of hypothyroidism, serum antithyroid antibodies, or the duration of chronic lymphocytic thyroiditis was found. The prevalence of mitral valve prolapse is substantially increased in patients with the autoimmune thyroid disorders.
Opportunity in health visiting.
Authors: M Hall
Journal: BMJ (1978)

tricyclic and, if that should fail, of an MAO inhibitor.I have been impressed with the good response of about half of these very severely affected patients to such therapy.Elithorn' stated that migraine is "undeniably a hunting-ground for the drug-happy physician."This, of course, is true, but such a statement should not deter efforts to find an effective treatment for this distressing and persistent disorder.
Closing in on Type 1 Diabetes
Authors: H McDevitt
Journal: New England Journal of Medicine (2001)

In this issue of the Journal, Martin et al.1 present a striking report of a boy with X-linked agammaglobulinemia in whom typical type 1 insulin-dependent diabetes mellitus developed at the age of 14 years. This report is of great interest because it shows that type 1 diabetes can develop in the complete absence of B cells and autoantibodies. This is convincing evidence that B cells are not required for the development of this disease and that the principal effector mechanisms are mediated by T cells.Martin et al. showed that the patient's cultured T cells proliferated in response to two . . .
Cyclosporin A in atopic dermatitis
Authors: J.S. ROSS, R.D.R. CAMP
Journal: British Journal of Dermatology (1990)

Over the past 10 years, oral cyclosporin A (CyA) has been used to treat a range of inflammatory and immunologically mediated dermatological conditions, but only psoriasis has been shown to be responsive in double-blind, controlled trials. Thirteen patients with severe atopic dermatitis were treated for up to 31 months. Ten patients had a good response, one patient a moderate response and two a slight response. In two of these patients, CyA was withdrawn after more than 2 years of continuous treatment because of increasing plasma creatinine levels. Cyclosporin A appears to be useful in the treatment of severe, therapy-resistant atopic dermatitis, but careful monitoring of side-effects and dose adjustments are required.
Abstract 4013: Functional analysis of Bcr-Abl-dependent phosphorylation of SOCSs
Authors: Jilong Chen, Guijie Guo
Journal: Cancer Research (2010)

Abstract Previous studies have demonstrated that constitutive activation of JAK/STAT (Janus tyrosine kinase/signal transducers and activators of transcription) signaling is required for efficient transformation by the Abelson murine leukemia virus (A-MuLV), which results from the expression of the v-Abl oncogene. Although the activation of JAK/STAT signaling pathway in cells expressing BCR-ABL still remains controversial, there is increasing evidence that deregulation of the JAK or STAT activity plays an important role in BCR-ABL malignant transformation. The suppressors of cytokine signaling (SOCS) are inhibitors of Jak kinases and as such are critically involved in a negative feedback loop of Jak/STAT signal transduction pathway. The mechanism by which Abl oncogene bypasses SOCS negative regulation remains poorly defined. Here, we found that co-expression of BCR-ABL with some SOCS proteins resulted in phosphorylation of SOCSs. Moreover, we observed that BCR-ABL-dependent phosphorylation of SOCSs altered SOCS function at least at two levels. One involves alteration of direct interaction of SOCSs with JAKs, which maintains JAK kinase activity. The other level involves inhibition of interaction of SOCS box with the Elongin BC complex, which disrupted the formation of E3 ubiquitin ligase complex that mediates proteosomal degradation of JAK kinases. Together, these results suggest that the BCR-ABL may regulate the inhibitory function of SOCSs through mediating phosphorylation of SOCS proteins. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4013.
Tricarboxylic acid cycle activity in postischemic rat hearts.
Authors: R G Weiss, R Kalil-Filho, A Herskowitz, V P Chacko, M Litt, M D Stern, G Gerstenblith
Journal: Circulation (1993)

BACKGROUND Although myocardial oxidative tricarboxylic acid (TCA) cycle activity and contractile function are closely linked in normal cardiac muscle, their relation during postischemic reperfusion, when contractility often is reduced, is not well defined. METHODS AND RESULTS To test the hypothesis that oxidative TCA cycle flux is reduced in reperfused myocardium with persistent contractile dysfunction, TCA cycle flux was measured by analyzing the time course of sequential myocardial glutamate labeling during 13C-labeled substrate infusion with 13C nuclear magnetic resonance spectroscopy in beating isolated rat hearts at 37 degrees C. Total TCA cycle flux, indexed by both empirical and mathematical modeling analyses of the 13C data, was not reduced but rather increased in hearts reperfused after 17-20 minutes of ischemia (left ventricular pressure, 73 +/- 5% of preischemic values) compared with flux in developed pressure-matched controls (e.g., total flux, 2.5 +/- 0.4 versus 1.6 +/- 0.1 mumol.min-1.g wet wt-1, respectively; p &lt; 0.01). No TCA cycle activity was detectable by 13C nuclear magnetic resonance in hearts reperfused after 40-45 minutes of ischemia, which lacked contractile recovery and had ultrastructural evidence of irreversible injury. CONCLUSIONS These results suggest that TCA cycle activity is not persistently decreased in dysfunctional reperfused myocardium after a brief ischemic episode and therefore cannot account for the reduced contractile function at that time.
Abstract B57: Oncostatin M promotes progression of Pten-deficient prostate cancer
Authors: Daniel A. Smith, Yang Zong, Atsushi Kiba, Owen N. Witte
Journal: Cancer Research (2012)

Abstract Chronic inflammation has been proposed to play a crucial role in several cancers including gastric, pancreatic, colon and lung, with recent evidence suggesting involvement in prostate cancer. While both interleukin 6 (IL6) and the related cytokine oncostatin M (OSM) have been implicated in prostate cancer, there have been few studies using in vivo models. To address this issue, we employed a dissociated prostate tissue recombination system using epithelium derived from conditional Pten knockout mice. Loss of Pten is common in prostate cancer and generates an intermediate murine prostatic intraepithelial neoplasia (mPIN) lesion in our system, providing an ideal means to assess functional synergy. We hypothesize that increased expression of these cytokines in the prostate microenvironment will promote malignant progression of intermediate prostate cancer lesions. Paracrine expression of IL6 did not transform naïve prostate epithelium nor did it exhibit functional synergy with Pten null epithelium in our system. Grafts expressing OSM alone did not transform naïve tissue, though in contrast, presented dramatic functional synergy with loss of Pten in prostate epithelium. Loss of Pten combined with OSM exhibited progression to poorly differentiated adenocarcinoma with features of epithelial-to-mesenchymal transition (EMT). Transformed tissues displayed loss of cytokeratin expression with down-regulation and mis-localization of e-cadherin. These tumors exhibit activation of several pathways downstream of OSM signaling including STAT3 and Erk1/2 as seen by immunohistochemical analysis. Further, we interrogated the role of OSM in promoting hormone refractory prostate cancer by castrating host animals following tumor establishment. Loss of Pten alone failed to progress beyond mPIN lesions and eventually regressed at 6 months post castration. In dramatic contrast, grafts expressing the OSM ligand exhibited initial regression with castration resistant growth following a latency period, recapitulating events commonly observed in human disease. Our evidence suggests that in the context of Pten loss, IL6 does not appear to promote prostate malignancy in the murine system. Conversely, we have identified that OSM synergizes with loss of Pten to promote aggressive prostate malignancy. Paracrine expression of OSM results in activation of several pathways, providing a means to interrogate hierarchy within signaling modules in the context of prostate cancer progression. Our study further indicates that OSM could play a role in promoting castration resistance, allowing investigation of potential points for therapeutic intervention. Citation Format: Daniel A. Smith, Yang Zong, Atsushi Kiba, Owen N. Witte. Oncostatin M promotes progression of Pten-deficient prostate cancer [abstract]. In: Proceedings of the AACR Special Conference on Advances in Prostate Cancer Research; 2012 Feb 6-9; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2012;72(4 Suppl):Abstract nr B57.