tbuckley/cabot-search huggingface dataset:
MULTIPLE PERIPHERAL NEURITIS OCCURRING WITH SULFONAMIDE THERAPY
Authors: M. A. Blankenhorn
Journal: Annals of Internal Medicine (1944)

Article1 March 1944MULTIPLE PERIPHERAL NEURITIS OCCURRING WITH SULFONAMIDE THERAPYM. A. BLANKENHORN, F.A.C.P.M. A. BLANKENHORN, F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-20-3-423 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptMultiple peripheral neuritis occurring with sulfonamide therapy may become an important consideration as such therapy is extended and as the drugs are used prolongedly in infections. The incidence of such neuritis at present is difficult to ascertain. Only isolated cases are reported. It is said that the complication is rare and that it may follow prolonged use and large dosage.1During the treatment of approximately 627 patients on the medical service of the Cincinnati General Hospital in 1942, peripheral neuritis occurred in six instances in which sulfonamides must be considered as a possible cause.Multiple peripheral neuritis is not a...Bibliography1. KEEFER CF: Toxic reactions following sulfonamide treatment, New England Jr. Med., 1942, ccxxvi, 266-271. CrossrefGoogle Scholar2. BLANKENHORN MA: Deficiency diseases—incidence at The Cincinnati General Hospital, Ohio State Med. Jr., 1942, xxxviii, 1005-1010. Google Scholar3. ARING CD: The use of vitamins in clinical neurology, Bull. New York Acad. Med., 1943, xix, 17-33. Google Scholar4. LEWYSPIESARING FHTDCD: The incidence of neuropathy in pellagra, Am. Jr. Med. Sci., 1940, cxcix, 840-849. Google Scholar5. ARINGBEANROSEMANROSENBAUMSPIES CDWBEMTD: The peripheral nerves in cases of nutritional deficiency, Arch. Neurol. and Psychiat., 1941, xlv, 772-787. CrossrefGoogle Scholar6. WILSONHADDEN GSB: Neuritis and multiple neuritis following serum therapy, Jr. Am. Med. Assoc., 1932, xcviii, 123-125. CrossrefGoogle Scholar7. YOUNG F: Peripheral nerve paralyses following the use of various serums, Jr. Am. Med. Assoc., 1932, xcviii, 1139-1143. CrossrefGoogle Scholar8. ARING CD: Diseases of the nerves and spinal cord incident to nutritional deficiency, Med. Clin. N. Am., 1943, xxvii, 419-429. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Cincinnati, Ohio*Read at the regional meeting of the American College of Physicians, Columbus, Ohio, May 14, 1943.From the Department of Internal Medicine, University of Cincinnati College of Medicine and the Cincinnati General Hospital, Cincinnati, Ohio. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byPeripheral Neuropathy and Serous Meningitis Due to Horse Serum 1 March 1944Volume 20, Issue 3Page: 423-430KeywordsDrug therapyHospital medicineMedical servicesSulfonamide ePublished: 1 December 2008 Issue Published: 1 March 1944 PDF downloadLoading ...
Abstract 2709: Identification of Aurintricarboxylic Acid (ATA) as an inhibitor of TWEAK-Fn14 signaling in glioblastoma cells
Authors: Harshil D. Dhruv, Ethan Holiday, Donald Chow, Holly Yin, Michael E. Berens, Nhan L. Tran
Journal: Cancer Research (2014)

Abstract The long-term survival of patients with glioblastoma (GB) is compromised by the proclivity for local invasion into the surrounding normal brain, escaping surgical resection and contributing to therapeutic resistance. Tumor necrosis factor-like weak inducer of apoptosis (TWEAK), a member of the tumor necrosis factor superfamily, can stimulate glioma cell invasion via binding to fibroblast growth factor-inducible 14 (Fn14) and subsequent activation of the transcription factor NF-κB. In order to discover a small molecule inhibitors that disrupt Fn14-TWEAK signaling axis and subsequently glioma cell invasion, we developed a cell-based drug screening assay using HEK293 cells that overexpresses Fn14 and harbors NF-κB driven Firefly luciferase protein expression. In preliminary drug screening assay using LOPAC1280 library of 1280 pharmacologically active compound, Aurintricarboxylic Acid (ATA) showed suppression of NF-κB driven Firefly Luciferase activity downstreatm of TWEAK-Fn14 signaling. Conversely, ATA did not show any suppression in NF-κB driven Firefly Luciferase activity downstream of TNFα-TNFR1 signaling, suggesting that ATA is a specific inhibitor of TWEAK-Fn14-NF-κB signaling. In vitro, we demonstrated that ATA suppresses TWEAK induced chemotactic migration of glioma cells (T98G and A172) and display no general cytotoxicity. In summary, this work reports a new small molecule inhibitor of TWEAK-Fn14 signaling that could be useful in enhancing the therapeutic targeting of this deadly disease. Citation Format: Harshil D. Dhruv, Ethan Holiday, Donald Chow, Holly Yin, Michael E. Berens, Nhan L. Tran. Identification of Aurintricarboxylic Acid (ATA) as an inhibitor of TWEAK-Fn14 signaling in glioblastoma cells. [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 2709. doi:10.1158/1538-7445.AM2014-2709
Black Box Warning for Anemia Drug
Authors: Rita Rubin
Journal: JAMA (2015)

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
Studies of Carbohydrate Metabolism in the Newborn Infant: VII. Tests of Carbohydrate Tolerance in Premature Infants
Authors: M CORNBLATH, S H WYBREGT, G S BAENS
Journal: JAMA (1963)

The rate of disappearance of an exogenous load of glucose (1 gm/kg) administered rapidly intravenously is reduced in premature infants under 3 days of age as compared to infants over 7 days of age, children, and adults. Premature infants are not leucine sensitive and respond to tolbutamide with less of a hypoglycemia under 3 days of age than after 7 days. Galactose (1 gm/kg) is cleared more slowly in the premature infant than the adult, but is rapidly converted to glucose. After intravenous fructose (1 gm/kg), there is a transient drop in blood glucose and an immediate rise in lactic acid in the premature infant. Subsequently, a hyperglucosemia occurs. Glucagon and glucagon plus epinephrine produce a hyperglycemic response in the premature infant; the hyperglycemia being greater after 7 days of age as compared to that between 3 to 7 days. In the premature infant, the metabolic needs of the relatively large brain, which is glucose dependent and is not insulin sensitive, may exceed the capacity of the liver to produce glucose during fasting. This may explain the relatively low levels of glucose in the blood of these infants.
Abstract 19177: Effect of Aging on Human Mesenchymal Stem Cell Therapy in Ischemic Cardiomyopathy Patients
Authors: Samuel Golpanian, Jill El-Khorazaty, Adam Mendizabal, Darcy L Difede, Wayne Balkan, Joshua M Hare
Journal: Circulation (2014)

Background: The role of patient age on the efficacy of mesenchymal stem cell (MSC) therapy in ischemic cardiomyopathy (ICM) is controversial, with some data suggesting a decline in responsiveness with age. We hypothesized that the therapeutic effect of culture expanded MSCs persists even in older subjects. Methods: We divided ICM patients from the TAC-HFT and POSEIDON trials who received MSCs via transendocardial stem cell injection (TESI) into two age groups: <60 yrs vs. ≥ 60 yrs. Functional capacity measures: Six Minute Walking Distance (6MWD) and quality of life measures: Minnesota Living with Heart Failure Questionnaire (MLHFQ) score were compared at baseline, at 6 months and 1 year post-TESI. Cardiac imaging parameters including absolute scar size, ejection fraction (EF), end-diastolic volume (EDV), end-systolic volume (ESV), and sphericity index (SI) were compared at baseline and 1-year post-TESI. Results: Median age of the 49 patients was 63.2 years (range, 32.5-79.0 yrs) with 47% being <60 and 53%...
Mechanism of action studies using a Smac mimetic reveal positive and negative roles of inhibitor of apoptosis proteins (IAPs) in TNFα signaling
Authors: Leigh Zawel, Alex Gaither, Dale Porter, Yao Yao, Christopher Straub, Tim Ramsey, Vadim Iourgenko, Huang Alan, Robert Schlegel, Mark Labow, Stephen Fawell, William Sellers
Journal: Cancer Research (2008)

SY26-04  The Inhibitor of Apoptosis Protein (IAP) XIAP is an attractive therapeutic target for cancer since (a) it is highly expressed in many diverse tumor types, (b) it is a known negative regulator of caspases and thus, programmed cell death (c) extensive structural data is available for BIR3, the Caspase 9 inhibitory domain of XIAP bound to peptide fragments derived from a naturally occurring IAP antagonist Smac/Diablo (d) ablation of XIAP function in experimental systems, either genetically or with Smac mimetics, hypersensitizes tumor cells to cytotoxic chemotherapy and in some contexts is sufficient as a single agent to induce tumor cell apoptosis.  To elucidate the mechanism behind single agent activity of the Smac mimetic LBW242, an siRNA-based lethality rescue screen was performed. Multiple hits clustered in the TNFα signaling pathway and surprisingly, XIAP itself was found to be required for LBW242-mediated cell killing.  Structural and biophysical studies indicate that despite the fact that LBW242 was modeled after the Smac-peptide/XIAP BIR3 interaction, it binds CIAP1 more tightly than XIAP. This binding event induces proteosome-mediated degradation of CIAP1. Loss of CIAP1 in LBW242-sensitive tumor cell lines results in NFKB-mediated TNFα induction and facilitates TNFα-mediated apoptosis. XIAP was found to play a positive signaling role in NFKB transcriptional signaling. Further dissection of the role of IAP proteins in regulating NFKB signaling may shape clinical strategies for the testing of this new class of anti-cancer therapeutic.
Abstract 9432: Febuxostat -A Xanthine Oxidase Inhibitor- May Improve Cardiorenal Interaction: A Randomized Controlled Pilot Study
Authors: Shigemasa Tani, Atsuhiko Takahashi, Ken Nagao, Atsushi Hirayama
Journal: Circulation (2014)

Introduction:  There is growing evidence of an association between high uric acid (UA) levels and cardiovascular disease. However, little data is available about the mechanism by which UA metabolism affects cardiorenal interaction, which leads to cardiovascular disease. Febuxostat, a selective xanthine oxidase inhibitor, was approved in 2012 in Japan not only for the treatment of patients with only gout, but also for those with only hyperuricemia.   Hypothesis:  We hypothesized that febuxostat might modify cardiorenal interactions by suppressing the renin-aldosterone system and improving the renal function in hypertensive hyperuricemic patients.   Methods:  We conducted a 6-month, prospective, randomized, open-label study in which we classified hypertensive hyperuricemic patients to either a febuxostat group (n = 30) or a control group (n = 30). The serum UA level of the patients was monitored, and the dose of febuxostat was adjusted to maintain the serum UA level    Results:  In the febuxostat group, the plasma renin activity (PRA), plasma aldosterone concentration (PAC), and serum UA level significantly decreased by 33% (p    Conclusions:  These results support the hypothesis that febuxostat might not only reduce serum UA level, but also improve cardiorenal interaction. These preliminary findings require confirmation in larger clinical trials.
Abstract P320: Dietary Flavonoid Intake and Ischemic Stroke
Authors: Margarethe Goetz, Viola Vaccarino, Terry Hartman, Bill McClellan, Aaron Anderson, Suzanne Judd
Journal: Circulation (2015)

Introduction: Diets rich in plant-based foods have been associated with lower stroke risk. Plant-based foods contain a variety of potentially cardioprotective compounds, including flavonoids. We assessed the hypothesis that total flavonoid and flavonoid subclass intakes are associated with incident ischemic stroke in a population-based cohort oversampled for non-Hispanic blacks and Stroke Belt residents. Methods: Between 2003 and 2007, REGARDS enrolled black and white Americans age ≥ 45 years. Participants were 20,413 men and women who completed a Block 98 food frequency questionnaire (FFQ) and without stroke at baseline. Total flavonoid and flavonoid subclass (anthocyanidin, flavan-3-ol, flavanone, flavonol, flavone, proanthocyanidin and isoflavone) intakes were estimated using the food consumption reported by the FFQ and the flavonoid contents of each food using USDA databases. Incident strokes were captured by participant report and adjudicated by experts. Quintiles of flavonoid intake were examined as predictors of incident stroke using Cox regression models using the first quintile as the referent. Tests for trend used the quintile medians. Results: Adjusting for age and caloric intake, there was a statistically significant inverse association between total flavonoid intake and ischemic stroke (Q5 v Q1: HR=0.68; 95% CI=0.51, 0.90; p-trend=0.04) however, this association weakened after additional adjustment for demographic, socioeconomic and health behavior factors as well as self-reported CHD at baseline (Q5 v Q1: HR=0.77; 95% CI=0.58, 1.03; p-trend=0.31). A similar pattern was seen for flavanones (age, energy adjusted HR=0.74; 95% CI= 0.57, 0.95; p-trend=0.02; fully adjusted HR= 0.82; 95%CI=0.65, 1.05; p-trend=0.06). Effect estimates for total flavonoids, flavanones, proanthocyanidins, and isoflavones, suggested a protective, though nonlinear association with risk reduction emerging at the second quintile, though these did not achieve statistical significance (total flavonoids, fully adjusted HR (95% CI): Q2= 0.80 (0.61, 1.04); Q3= 0.85 (0.65, 1.11); Q4=0.92 (0.70, 1.19); Q5= 0.77 (0.58, 1.03)). Total flavonoid and flavanone intake were significantly associated with IS in fully adjusted models in women (total: Q5 v Q1 HR=0.62; 95% CI= 0.41, 0.94; p-trend=0.15; flavanones HR=0.65; 95% CI=0.44, 0.95; p-trend=0.03) but not in men (total: Q5 v Q1 HR=0.95; 95% CI= 0.63, 1.42; flavanones HR=0.80; 95% CI=0.58, 1.09; p-interaction=0.67). There was no effect modification by race or region of residence. Conclusion: Total dietary flavonoids and flavanones are associated with a reduction in risk of incident ischemic stroke, particularly in women. The emergence of a protective effect at the second quintile for total flavonoids, flavanones, proanthocyanidins and isoflavones is consistent with previous studies of dietary flavonoid intake and CVD mortality.
Abstract 18420: Myozap-deficiency Inhibits SRF Signaling and Causes Severe Cardiomyopathy in Response to Pathological Biomechanical Stress in vivo
Authors: Ashraf Y Rangrez, Derk Frank, Reza Poyanmehr, Alexander Bernt, Matthias Eden, Christian Kuhn, Norbert Frey
Journal: Circulation (2014)

Background: We recently showed that the intercalated disc (ID) protein Myozap activates Rho-dependent SRF signaling both in vitro, and in vivo. Conversely, knockdown of its ortholog in Zebrafish led to severe contractile dysfunction and cardiomyopathy. Methods and Results: We generated a Myozap null mutant (MZP-ko) by global deletion of Myozap in mice. The absence of Myozap caused neither structural defects nor a baseline cardiac phenotype and led only to mild cardiac hypertrophy upon aging. Of note, induction of SRF target genes and the activation of SRF per se were markedly inhibited in MZP-ko mice. Nevertheless, biomechanical stress induced by transverse aortic constriction (TAC) triggered an excessive increase in cardiac hypertrophy (43% or 36% increased heart wt:body wt or LV wt:body wt ratios, p&lt;0.001), an increased cell surface area, as well as accelerated fibrosis, followed by “super”- induction of the hypertrophic gene program (ANF/BNP). Moreover, MZP-ko mice revealed a severe reduction of fractional shortening (average %FS for MZP-ko 14.5% compared to 33.5% for wild-type littermates, p&lt;0.001) and clinical signs of heart failure (54% increase in lung/body weights, p&lt;0.001) which also caused a profound increase in mortality in response to TAC. Furthermore, expression of other ID proteins like N-Cadherin, Desmoplakin and Connexin 43 was found significantly altered upon pressure overload in MZP-ko mice. Finally, we observed a downregulation of Dysbindin, a novel interaction partner of Myozap and known inducer of ERK1/2 signaling in TAC operated MZP-ko mice. Consistently, activation of ERK1/2 was blunted in MZP-ko mice after TAC. Conclusions: We here show that myozap deficiency in vivo inhibits SRF- and ERK1/2-signaling leading to a maladaptative response to increased biomechanical stress, followed by cardiomyopathy, heart failure and cardiac death. Moreover, myozap deficiency severely altered the expression of its direct ID interaction partners such as Dysbindin and Desmoplakin. In a broader perspective, our data identify signaling at the level of the intercalated disc as a critical component of cardiac remodeling.
SEVERE ACIDOSIS DUE TO PHENOL POISONING: REPORT OF TWO CASES
Authors: I L BENNETT, D F JAMES, A GOLDEN
Journal: Annals of Internal Medicine (1950)

Case Reports1 February 1950SEVERE ACIDOSIS DUE TO PHENOL POISONING: REPORT OF TWO CASESIVAN L. BENNETT JR., M.D., DAVID F. JAMES, M.D., ABNER GOLDEN, M.D.IVAN L. BENNETT JR., M.D., DAVID F. JAMES, M.D., ABNER GOLDEN, M.D.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-32-2-324 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptIn view of the fact that acidosis in phenol poisoning has received little attention in the literature, and because of the therapeutic importance of reversing this condition, report of such cases seems indicated. We have recently observed two patients with phenol poisoning in whom the most prominent systemic manifestation was acidosis and in whom a dramatic response was obtained with intravenous sodium bicarbonate.CASE REPORTSCase 1. A 50 year old morphine addict was admitted to Grady Hospital on February 14, 1947, at 2:00 a.m., approximately 45 minutes after swallowing 2 ounces of liquefied phenol (88 per cent) with suicidal...Bibliography1. ClarkeBrown TWED: The value of alcohol in carbolic acid poisoning, J. A. M. A. 46: 782-790, 1906. CrossrefGoogle Scholar2. Gibbs OS: Treatment of phenol poisoning, British M. J. 1: 581-582, 1931. CrossrefMedlineGoogle Scholar3. Bastedo WA: Materia Medica, Pharmacology and Therapeutics, 1937, W. B. Saunders Co., Philadelphia. Google Scholar4. Røe O: Methanol poisoning, Acta med. Scandinav. 126: Suppl. 182, 1946. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Atlanta, Georgia*Received for publication August 8, 1947.From the Department of Medicine, Emory University School of Medicine, and the Medical Service, Grady Hospital, Atlanta, Ga. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byPhenol and PhenolicsHousehold and Industrial ProductsPhenol and PhenolicsSummary Review of the Health Effects Associated With PhenolPhenol: A review of environmental and health risks 1 February 1950Volume 32, Issue 2Page: 324-327KeywordsAddictsBicarbonatesHospital medicineMedical servicesMorphineSodiumSwallowing ePublished: 1 December 2008 Issue Published: 1 February 1950 PDF downloadLoading ...
Tetraspanins CD9 and CD81 are molecular partners of trimeric FcɛRI on human antigen-presenting cells
Authors: W. M. Peng, C. F. Yu, W. Kolanus, A. Mazzocca, T. Bieber, S. Kraft, N. Novak
Journal: Allergy (2011)

To cite this article: Peng WM, Yu CF, Kolanus W, Mazzocca A, Bieber T, Kraft S, Novak N. Tetraspanins CD9 and CD81 are molecular partners of trimeric FcɛRI on human antigen-presenting cells. Allergy 2011; 66: 605–611. Abstract Background: Most functions of tetraspanins are not related to cell-surface receptor ligand binding, but are mediated by direct interactions with their partner proteins. Functions of trimeric FcɛRI, expressed by antigen-presenting cells (APCs), range from amplification of allergic inflammatory reactions to their active suppression. Cell-type-specific protein–protein interactions might play a role in the regulation of these bidirectional tasks. Therefore, we intended to study the interactions of trimeric FcɛRI with tetraspanins. Methods: The expression levels of tetraspanins CD9, CD37, CD53, CD63, CD81, CD82, and CD151 on skin dendritic cells of atopic dermatitis (AD) patients or healthy individuals were detected by flow cytometry. Tetraspanin expression on FcɛRIpos and FcɛRIneg monocyte subpopulations was evaluated. Flow cytometry, confocal microscopy, immunoprecipitation, and immunoblotting experiments were performed to observe the relationship between tetraspanins CD9 and CD81 and FcɛRI. Furthermore, plate stimulation experiments were performed, and cytokines in the supernatants were detected. Results: We found that human FcɛRIpos APCs expressed high amounts of tetraspanins and that the tetraspanins CD9 and CD81 were associated with FcɛRI. Concomitant activation of FcɛRI and CD9 on human monocytes increased FcɛRI-mediated cytokine release. Conclusion: Taken together, we show for the first time that CD9 and CD81 act as molecular partners of trimeric FcɛRI on human APC, which might be of importance in allergic diseases such as AD.