tbuckley/cabot-search huggingface dataset:
DISEASES OF THE NERVOUS SYSTEM PRODUCING DYSFUNCTION OF OTHER ORGANS AND DYSFUNCTION OF OTHER ORGANS PRODUCING OR SIMULATING DISEASES OF THE NERVOUS SYSTEM
Authors: Lewis J. Pollock
Journal: Annals of Internal Medicine (1935)

Article1 January 1935DISEASES OF THE NERVOUS SYSTEM PRODUCING DYSFUNCTION OF OTHER ORGANS AND DYSFUNCTION OF OTHER ORGANS PRODUCING OR SIMULATING DISEASES OF THE NERVOUS SYSTEMLEWIS J. POLLOCK, M.D.LEWIS J. POLLOCK, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-8-7-805 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptDysfunction of respiration, circulation, secretion, excretion, digestion, growth, metabolism and reproduction occurs alike in diseases of the nervous system and of other organs. The signs and symptoms of such dysfunction necessitate the differentiation of such diseases.The disturbances of function following encephalitis lethargica illustrate how diversified the dysfunction of the body may become as the result of a disease of the nervous system. To note a few of these disturbances, mention may be made of the disorders of sleep, of somnolence, insomnia and reversal of time of sleeping, of the disturbance in temperature regulation, of hypothermia, associated with general lowering... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Chicago, Illinois*Read at the Chicago meeting of the American College of Physicians, April 20, 1934. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 January 1935Volume 8, Issue 7Page: 805-813KeywordsDigestionEncephalitisExcretionHypothermiaInsomniaNervous systemRespirationSigns and symptomsSleepTemperature ePublished: 1 December 2008 Issue Published: 1 January 1935 PDF downloadLoading ...
Local and Regional Anesthesia, with Chapters on Spinal, Epidural, PARAVERTEBRAL, AND Parasacral Analgesia, AND on OTHER Applications of Local and Regional Anesthesia to the Surgery of the Eye, Ear, Nose and Throat, and to Dental Practice.
Authors: Carroll Woolsey Allen, Rudolph Matas
Journal: JAMA (1918)

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Estrogen Plus Progestin and Risk of Venous Thrombosis
Authors: Richard E Blackwell
Journal: JAMA (2005)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Women facing prophylactic mastectomy need more advice.
Authors: Roger Dobson
Journal: BMJ (2003)

More counselling, increased support, and better information are needed by women making decisions about prophylactic mastectomy.

Women who go ahead with surgery are not prepared for the level of postoperative incapacity, and after surgery most women experience pain or discomfort for between 10 days and six months, say the authors of a new study (Breast 2003;12:1-9).

The study, designed to explore the attitudes and beliefs of women at high risk of developing breast cancer, was based on interviews with 60 women who opted for prophylactic mastectomy and 20 women who declined.

The study, carried out by Professor M Bebbington Hatcher and Professor Lesley Fallowfield, from Cancer Research UK's Psychosocial Oncology Group at the University of Sussex, found substantial differences between the women who opted for surgery and those who declined. Women opting for surgery were more anxious than those who declined.

The decision to undergo surgery appeared not to be related to the results of genetic testing. “For many, the test was not possible because they had no living affected family member with the disease,” says the report.
A memorable patient: When guidelines fail
Authors: J. Godfrey
Journal: BMJ (2001)

She was a 78 year old widow who lived in sheltered accommodation and, despite being partially sighted because of advancing glaucoma, was still able to get about with her white cane. She rarely visited our surgery, and when she did it was for a flu jab or regarding moderate generalised osteoarthritis. This morning, however, she limped into my consulting room apologetically and said, “The heel of my right foot is hurting, doctor. I'm finding it difficult to walk to the shops. My eyesight doesn't help either.”

I set out to examine her foot. There was nothing grossly abnormal. It was well perfused, no swellings, and no evidence of any trauma. Deep palpation over the calcaneum produced tenderness. “Bingo,” I thought, “plantar fasciitis, with or without calcaneal spur.” I reached for an x ray form when I suddenly remembered the fate of the previous x …
Emerging Infections on Center Stage at First Major International Meeting
Authors: J Stephenson
Journal: JAMA (1998)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Abstract 9629: Combination Therapy of Cilostazol and Bepridil Suppresses Recurrent Ventricular Fibrillation Related to J-Wave Syndromes
Authors: Tetsuji Shinohara, Mikiko Nakagawa, Naohiko Takahashi
Journal: Circulation (2014)

Introduction: Brugada syndrome (BrS) and idiopathic ventricular fibrillation (VF) associated with infero-lateral early repolarization patterns (early repolarization syndrome (ERS)) are termed “J-wave syndromes”. In such patients, an implantable cardioverter-defibrillator (ICD) is first-line therapy for prevention of sudden cardiac death. However, frequent ICD shocks due to recurrent VF remain serious problems. We investigated if combination therapy using cilostazol and bepridil could suppress recurrent VF. Methods: Our cohort comprised 22 consecutive patients (BrS, 16; ERS, 3; unknown, 3) with J-wave syndromes in whom ICDs were implanted for spontaneous episodes of VF. We enrolled 7 patients with J-wave syndromes who experienced ICD shocks due to recurrent VF after ICD implantation. At first, cilostazol was instituted. In all subjects, palpitations due to sinus tachycardia caused by cilostazol were symptomatic. Addition of bepridil attenuated cilostazol-induced palpitations (87±12 to 66±7 bpm, P&lt;0.01) and maintained the suppressive effect of cilostazol against VF. Results: Prior to the onset of the cilostazol/bepridil combination therapy, all 7 patients had a total of 20 shocks over an accumulated period of 79 months. In contrast, after the onset of therapy, they accumulated a combined follow-up period of 375 months, and during that significantly longer period only one of them received 2 shocks. Three patients underwent replacement of the ICD generator 4-5 years after ICD implantation. Cilostazol was discontinued 2 days before replacement because of its anti-platelet effects. In all 3 patients, temporary discontinuation of cilostazol led to the reappearance of J waves, culminating in VF and an appropriate ICD shock in one of them. J waves disappeared upon re-institution of cilostazol. Conclusions: These data suggest that combination therapy of cilostazol and bepridil may be effective and safe in suppressing VF recurrence in some cases of J-wave syndromes.
671. Overexpression of Manganese Superoxide Dismutase (MnSOD) Prevents Photodynamic Therapy (PDT)-Induced Porcine Esophageal Stricture
Authors: Anurag Agarwal, Michael W. Epperly, Yaron Perry, James D. Luketich, Joel S. Greenberger
Journal: Molecular Therapy (2004)

Photodynamic therapy (PDT) is used in treatment of esophageal cancer and for ablation of Barrett's esophagus. A complication of this procedure is esophageal stricture. We sought to determine whether overexpression of MnSOD prevented formation of PDT-induced esophageal stricture in a pig model. Pigs were injected intravenously with Photofrin (2 mg/kg) and MnSOD-PL complex (10 mg plasmid DNA) by an endoscope placed either at the site of PDT treatment (10 cm from gastroesophageal (GE) junction) or at the top of the esophagus, which allowed the pig to swallow the plasmid/liposome complex thereby coating the entire esophagus. An endoscope was placed 10 cm from the GE junction after injection of Photofrin and MnSOD-PL, a laser was inserted through the endoscope, then 400 Joules of light was delivered to the esophagus. PDT treatment was repeated 48 hours later. Control pigs were treated as above with no injection of MnSOD-PL. Pigs were followed for the development of esophageal stricture by weekly endoscopic exam and were weighed every two days. Esophageal biopsies were collected at various times following PDT. RNA was extracted and quantitative real time PCR was performed to determine gene expression for inflammatory cytokines including TNF-a and TGF-β. At 14 days after PDT treatment, control pigs lost significant weight and esophageal stricture was detected by endoscopic exam. By 20 days after PDT treatment, control pigs had severe esophageal stricture determined by endoscopy, weight loss, and barium swallow. Esophageal stricture in control PDT-treated pigs was documented by histopathology. In contrast, pigs intraesophageally treated with MnSOD-PL 24 hours before PDT had no weight loss, showed continual weight gain through 150 days after PDT and no esophageal stricture was detected by endoscopic exam. At 150 days after treatment, all MnSOD-PL-treated pigs were sacrificed, esophagus examined, and no stricture was detected. Thus, increased expression of MnSOD-PL may protect normal esophagus from PDT-induced stricture.
Mitomycin C Treatment for Conjunctival—Corneal Intraepithelial Neoplasia
Authors: Joseph Frucht-Pery, Joel Sugar, Jules Baum, John E. Sutphin, Jacob Pe’er, Hana Savir, Edward J. Holland, David M. Meisler, Jill A. Foster, Robert Folberg, Yaacob Rozenman
Journal: Ophthalmology (1997)
155. Non-Viral Gene Therapy for Type 1 Diabetes by Electrotransfer of Insulin and Glucokinase Genes to Skeletal Muscle
Authors: Kirk J. Wangensteen, Zongyu J. Chen, Clifford J. Steer, Stephen C. Ekker
Journal: Molecular Therapy (2004)

Alpha1-antitrypsin (α1-AT) deficiency is caused by mutations in the α1-AT gene, a protease inhibitor, and can result in emphysema and/or liver disease. The lung disease is caused by a decrease in secreted α1-AT enzyme, a loss-of-function which results in tissue damage from unchecked leukocyte proteases. In contrast, the liver disease occurs by a gain-of-function, whereby mutant protein polymers are retained in the endoplasmic reticulum of hepatocytes. In persuit of an alternative to the only current treatment for the liver disease, to transplant the organ, we are investigating a genetic therapy that would combine the technologies of RNA interference (RNAi) with the Sleeping Beauty transposon system. The RNAi pathway consists of endogenous enzymes that destroy mRNAs selectively in response to small RNAs that are complimentary in sequence. Small inhibitory RNAs (siRNAs), which can be transcribed from plasmid constructs introduced into cells, have been shown to mediate RNAi in vitro and in vivo. Moreover, siRNAs can mediate long-term repression of a target gene if they are constitutively expressed from the genome. The Sleeping Beauty (SB) transposon system can integrate DNA transgenes into the genome for long-term expression in vitro and in vivo, and is being developed as a novel, non-viral gene therapy tool. A SB transposon vector was constructed to express siRNAs that target human α1-AT mRNA. The results demonstrate that siRNA transposons can be used to reduce wildtype and mutant α1-AT expression in cultured cells, whereas the house-keeping gene GAPDH was not affected. Next, we plan to test these siRNA transposons in vivo, in the transgenic mouse model of α1-AT liver disease. This gene therapy model combines two technologies, RNAi and the SB transposon, for a potential new therapeutic for the liver disease associated with mutant α1-AT.
Abstract 13943: Hypertrophic Cardiomyopathy with Left Ventricular Apical Aneurysm Represents a High-Risk Subgroup Necessitating Aggressive Preventive Therapy: A Long-term Follow-Up Study
Authors: Ethan J Rowin, Barry J Maron, Tammy S Haas, John R Lesser, Mark S Link, Martin S Maron
Journal: Circulation (2014)

Background: Increasing penetration of high spatial resolution cardiovascular magnetic resonance (CMR) imaging into routine cardiovascular practice has resulted in more frequent identification of a subset of hypertrophic cardiomyopathy (HCM) patients with thin-walled, scarred left ventricular (LV) apical aneurysms. Prior experience involved relatively small numbers of patients with short follow-up and therefore the risk associated with this subgroup remains incompletely defined. Therefore, we assembled a large HCM cohort with LV apical aneurysms and long-term follow-up in order to clarify clinical course and prognosis. Methods and Results: Of 2,400 HCM patients, 60 (2.5%) were identified by CMR with LV apical aneurysm, 24 to 86 years of age, including 19 (32%) &lt;45 years old; 70% male, and followed for 5.6 ± 3.5 years. Over the follow-up period, 24 patients experienced 31 adverse disease-related complications including: appropriate implantable cardioverter-defibrillator discharge for VT/VF (n=11), received or listed for heart transplant (n=6), heart failure death (n=5), nonfatal thromboembolic events (n=4), resuscitated out-of-hospital cardiac arrest (n=3), and sudden death (n=2). In addition, an intracavitary thrombus was identified in the apical aneurysm in 9 patients without a thromboembolic history. Combined HCM-related death and aborted life threatening event rate was 8.6% per year, nearly 6-fold greater than the 1.5% annual mortality rate reported in the general HCM population. Conclusions: Patients with LV apical aneurysms represent a high-risk subgroup within the diverse HCM spectrum, associated with substantial increased risk for disease-related morbidity and mortality, including advanced heart failure, thromboembolic stroke and sudden death. Identification of this unique HCM phenotype should prompt consideration for primary prevention ICD, and anticoagulation for stroke prophylaxis.
Erratum: Corrigendum: Mcl-1 is essential for the survival of plasma cells
Authors: Victor Peperzak, Ingela Vikström, Jennifer Walker, Stefan P Glaser, Melanie LePage, Christine M Coquery, Loren D Erickson, Kirsten Fairfax, Fabienne Mackay, Andreas Strasser, Stephen L Nutt, David M Tarlinton
Journal: Nature Immunology (2013)
Abstract 4195: Peroxisome proliferator-activated receptor α is regulated by E2F1-induced miR-19a in a feedback loop in glioma progression
Authors: Junxia Zhang, Yan Shi, Yingyi Wang, Wenkang Luan, Yongping You
Journal: Cancer Research (2014)

Abstract The peroxisome proliferator-activated receptor α (PPARα) is a nuclear receptor, which belongs to the super-family of steroid hormone receptor. To date, the biologic function of PPARα in human cancers is still controversial and needs further investigation. In our study, we explored the clinical feature, biological function and potential mechanism of PPARα in glioma. PPARα expression was significant lower in high grade tissues than low grade tissues in whole genome gene profiling of 158 glioma tissues. PPARα activation using fenofibrate inhibited glioma cells proliferation, invasion and aerobic glycolysis. Further, PPARα was a direct target of miR-19a and miR-19a was modulated by E2F1 at transcriptional level. Moreover, PPARα activation repressed E2F1 activation by modulating transcriptional complexes formed with E2F1 and pRB proteins. Finally, we confirmed PPARα/E2F1/ miR-19a feedback loop in vivo using nude mouse glioma xenograft and human glioma tissues. To our knowledge, it is first time to demonstrate that PPARα regulates glioma development by E2F1-induced miR-19a in a feedback loop and provide important clues for understanding the key roles of PPARα functional network in glioma. Note: This abstract was not presented at the meeting. Citation Format: Junxia Zhang, Yan Shi, Yingyi Wang, Wenkang Luan, Yongping You. Peroxisome proliferator-activated receptor α is regulated by E2F1-induced miR-19a in a feedback loop in glioma progression. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4195. doi:10.1158/1538-7445.AM2014-4195
Development of a panel of biomarkers for the diagnosis of prostate cancer
Authors: Rachel A. Fallon, Colin Wheeler, Jens Koopmann, Nick Workman, Mike B. McAndrew
Journal: Clinical Cancer Research (2010)

Abstract The issues surrounding the use of PSA in the diagnosis of prostate cancer (PC) are well documented. In community practice the PSA cut-off point of 4 ng/mL is considered sensitive but relatively non-specific (sensitivity of 86% and specificity of 33%)1 and there is a need for a diagnostic test with greater discriminatory power. The development of autoantibodies associated with prostate cancer has been described2. In general, the appearance of such antibodies can precede disease symptoms by many years, making them attractive as potential biomarkers for early diagnosis. We have developed a unique “functional protein” array platform which utilises 925 correctly folded proteins chosen for their roles in disease and used this to detect autoantibodies in PC serum samples. We have taken advantage of the multiplex nature of array assays and applied complex data analysis strategies to identify panels of biomarkers which may have clinical utility in the diagnosis of prostate cancer. Serum samples (case; n = 73 and control; n = 60) were analysed using protein arrays. Data analysis was performed using a multi-scaling and outlier removal step for quadruplicate signals from all 133 protein arrays. Data were arbitrarily split into test and training sets and the data from the training set was then used with both support vector machines and genetic programming to identify classifiers which would successfully distinguish case from control samples. Classifiers were assessed for performance by referring to the combined sensitivity and specificity (S+S score) using the test set. Data were repeatedly split into test and training sets and analysis cycles repeated until a stable set of classifiers was identified. A set of biomarkers was identified which can distinguish PC from control samples with both sensitivity and specificity above 90%. Further development and validation of this panel is on-going with a larger cohort. 1. Hoffman et al. Prostate-specific antigen testing accuracy in community practice. BMC Family Practice (2002) 3:19. 2. Wang et al. Autoantibody signatures in prostate cancer. N Engl J Med. (2005) 353:1224.
Neutrophils co-cultured with human breast cancer cells express endogenous Oncostatin M (OSM)
Authors: Marisa M. Queen, Lee Rooney, Randy Ryan, Cheryl Jorcyk
Journal: Cancer Research (2005)

Proc Amer Assoc Cancer Res, Volume 46, 2005

4705 

Oncostatin M (OSM) is a pleiotropic cytokine belonging to the interleukin-6 family and is expressed by several cell types including, activated human T-lymphocytes and macrophages. Recent evidence suggests that OSM may promote tumor progression by enhancing angiogenesis and metastasis. Tumor-associated and tumor-infiltrating neutrophils (TANs) and macrophages (TAMs) can account for as much as 50% of the total tumor mass in invasive breast carcinomas. It is thought that tumors secrete factors that elicit a wound-repair response from TAMs and TANs, and that this response inadvertently stimulates tumor progression. Our preliminary findings have shown that human neutrophils express OSM when co-cultured with human MDA-MB-231 breast cancer cells. Neutrophils were isolated from whole blood and then plated with breast cancer cells at different ratios. Neutrophils and breast cancer cells alone expressed low levels of OSM by immunohistochemisty but when co-cultured together at a ratio of 10:1 neutrophils expressed high levels of OSM. In addition, ELISA data demonstrated increased levels of OSM by neutrophils co-cultured with human breast cancer cells. In summary, our findings could provide a rational for the development of cancer therapies designed to inhibit OSM release from leukocytes. Funded through NIH grant P20RR16454.