tbuckley/cabot-search huggingface dataset:
Malignant Cells in Serous Effusions Complicating Bronchial Carcinoma
Authors: A. I. Spriggs
Journal: Thorax (1954)

Phosphoinositides and their metabolizing enzymes are involved in Aβ<sub>42</sub> metabolism and Alzheimer9s disease pathogenesis. In yeast and mammals, Eighty-five requiring 3 (EFR3), whose <i>Drosophila</i> homolog is Rolling Blackout (RBO), forms a plasma membrane-localized protein complex with phosphatidylinositol-4-kinase Type IIIα (PI4KIIIα) and a scaffold protein to tightly control the level of plasmalemmal phosphatidylinositol-4-phosphate (PI<sub>4</sub>P). Here, we report that RBO binds to <i>Drosophila</i> PI4KIIIα, and that in an Aβ<sub>42</sub>-expressing <i>Drosophila</i> model, separate genetic reduction of PI4KIIIα and RBO, or pharmacological inhibition of PI4KIIIα ameliorated synaptic transmission deficit, climbing ability decline, premature death, and reduced neuronal accumulation of Aβ<sub>42</sub>. Moreover, we found that RBO-PI4KIIIa downregulation increased neuronal Aβ<sub>42</sub> release and that PI4P facilitated the assembly or oligomerization of Aβ<sub>42</sub> in/on liposomes. These results indicate that RBO-PI4KIIIa downregulation facilitates neuronal Aβ<sub>42</sub> release and consequently reduces neuronal Aβ<sub>42</sub> accumulation likely via decreasing Aβ<sub>42</sub> assembly in/on plasma membrane. This study suggests the RBO-PI4KIIIα complex as a potential therapeutic target and PI4KIIIα inhibitors as drug candidates for Alzheimer9s disease treatment. <b>SIGNIFICANCE STATEMENT</b> Phosphoinositides and their metabolizing enzymes are involved in Aβ<sub>42</sub> metabolism and Alzheimer9s disease pathogenesis. Here, in an Aβ<sub>42</sub>-expressing <i>Drosophila</i> model, we discovered and studied the beneficial role of downregulating RBO or its interacting protein PI4KIIIα—a protein that tightly controls the plasmalemmal level of PI<sub>4</sub>P—against the defects caused by Aβ<sub>42</sub> expression. Mechanistically, RBO-PI4KIIIα downregulation reduced neuronal Aβ<sub>42</sub> accumulation, and interestingly increased neuronal Aβ<sub>42</sub> release. This study suggests the RBO-PI4KIIIα complex as a novel therapeutic target, and PI4KIIIα inhibitors as new drug candidates.
Follicular dendritic cell-induced microRNA-mediated upregulation of PRDM1 and downregulation of BCL-6 in non-Hodgkin's B-cell lymphomas
Authors: J Lin, T Lwin, J-J Zhao, W Tam, Y S Choi, L C Moscinski, W S Dalton, E M Sotomayor, K L Wright, J Tao
Journal: Leukemia (2010)
Monument in Geneva Of Michael Servetus
Authors: Risteard Mulcahy
Journal: JAMA (1966)

<h3>To the Editor:—</h3> You write about the life and death of Michael Servetus in your issue of Dec 13, 1965. Servetus was burnt at the stake at Champel near Geneva on Oct 27, 1553, more than 400 years ago. The citizens of Geneva afterwards acknowledged their error in taking the life of this great Reformation figure, and his memory is preserved by them by an old stone monument which still stands in their city. During a recent visit, I saw the monument, and I was saddened to see that it was rather neglected— with a profuse growth of ramblers and rough saplings obscuring one side of the stone. Still, it is worthwhile to pay a visit to his memorial in Geneva.
High-Resolution Computed Tomographic Evaluation of Airway Distensibility and the Effects of Lung Inflation on Airway Caliber in Healthy Subjects and Individuals with Asthma
Authors: ROBERT H. BROWN, NICOLA SCICHILONE, BEATRICE MUDGE, FIONA B. DIEMER, SOLBERT PERMUTT, ALKIS TOGIAS
Journal: American Journal of Respiratory and Critical Care Medicine (2001)

The effects of a deep inspiration (DI) in individuals with asthma differ from those observed in healthy subjects. It has been postulated that the beneficial effect of lung inflation is mediated by airway stretch. One hypothesis to explain the defects in the function of lung inflation in asthma is that a DI may be unable to stretch the airways. This may result from attenuation of the tethering forces between the airways and the surrounding parenchyma. In the current study, we used high-resolution computed tomography (HRCT) to examine the ability of a DI to distend the airways of subjects with asthma (n = 10) compared with healthy subjects (n = 9) at baseline and after increasing airway tone with methacholine (MCh). We found that both at baseline and after the induction of smooth muscle tone with MCh, a DI distended the airways of healthy and asthmatic subjects to a similar extent, indicating that abnormal interdependence between the lung parenchyma and the airways is unlikely to play a major role in the loss or attenuation of the beneficial effect of lung inflation that characterizes asthma. Furthermore, we observed that after constriction had already been induced by MCh, following a DI, bronchodilation occurred in the healthy subjects but further bronchoconstriction occurred in the subjects with asthma. Our findings suggest that an abnormal excitation contraction mechanism in the airway smooth muscle of subjects with mild asthma counteracts the bronchodilatory effect of a DI. Therefore, the mechanism for reduced bronchodilation after DIs in subjects with mild asthma could be intrinsic to the airway smooth muscle.
Tumour suppressor protein p53 released by nuclease digestion increases at the onset of rat liver regeneration
Authors: Francesc Miró, Jean-Claude Lelong, Floria Pancetti, Nerea Roher, Arlette Duthu, Maria Plana, Jean Christophe Bourdon, Oriol Bachs, Evelyne May, Emilio Itarte
Journal: Journal of Hepatology (1999)
Ellipsoidal shell subtraction model of right ventricular volume. Comparison with regional free wall dimensions as indexes of right ventricular function.
Authors: M P Feneley, J R Elbeery, J W Gaynor, S A Gall, J W Davis, J S Rankin
Journal: Circulation Research (1990)

Pulse-transit sonomicrometry was used to measure the base-apex (a), anteroposterior (b), and septal-free wall (c) diameters of the left ventricle and the septal-free wall diameter of the right ventricle (d) in eight excised and three isolated, pump-perfused canine heart preparations, as well as in nine conscious dogs. In the three perfused hearts and in four of the excised hearts, right ventricular free wall regional segment lengths and segment area also were assessed. Biventricular volumes were measured directly with intracavitary balloons in all isolated hearts. When left ventricular balloon volume was held constant, relations between right ventricular free wall dimensions and right ventricular balloon volume were highly linear. With increments in left ventricular volume, however, these relations remained linear but shifted progressively upward, indicating an independent relation between right ventricular free wall dimensions and left ventricular cavitary volume. An ellipsoidal shell subtraction model (pi/6.abd minus right ventricular free wall volume) was developed to estimate right ventricular cavitary volume from cardiac dimensions. With this method, a highly linear relation was observed between calculated right ventricular volume and right ventricular balloon volume (mean r = 0.99 +/- 0.01). Moreover, this relation appeared to be independent of changes in left ventricular balloon volume. With the shell subtraction model, dynamic right ventricular volume was computed in nine conscious dogs, and in four, stroke volume derived from dimensions was compared with right ventricular stroke volume measured with ultrasonic flow probes. A highly linear relation was observed, suggesting the accuracy of the shell subtraction method in vivo. Right ventricular end-systolic pressure-volume and stroke work/end-diastolic volume relations then were evaluated, and both proved to be highly linear in the right ventricle (both mean r = 0.99 +/- 0.01). Thus, the shell subtraction model allows a simple estimate of dynamic right ventricular volume in the intact heart and facilitates assessment of right ventricular performance in vivo.
Technetium-99m RBC Scintigraphy in the Evaluation of Small Bowel Leiomyoma
Authors: KATHLEEN L. McDONALD
Journal: Clinical Nuclear Medicine (1987)

Hypervascularity and persistent uptake were demonstrated in a small bowel leiomyoma not actively bleeding at the time of Tc-99m RBC scintigraphy. The potential value of Tc-99m RBC scanning in the evaluation of benign small bowel tumors is discussed.
Early assessment of reperfusion therapy using cardiac troponin T
Authors: Satoshi Abe, Shinichi Arima, Tsuminori Yamashita, Masaaki Miyata, Hideki Okino, Hitoshi Toda, Kunihiro Nomoto, Makoto Ueno, Minoru Tahara, Kazuaki Kiyonaga, Shoichiro Nakao, Hiromitsu Tanaka
Journal: Journal of the American College of Cardiology (1994)
Ethnicity and other risk factors for acute lower limb cellulitis: a U.K.-based prospective case–control study
Authors: J. Halpern, R. Holder, N.J. Langford
Journal: British Journal of Dermatology (2008)

Background Acute lower limb cellulitis is a common yet potentially serious condition. Previous studies have identified risk factors in the non‐U.K. population. Ethnicity has been postulated as a possible risk factor but has not previously been investigated. Objectives To identify risk factors for acute lower limb cellulitis in the U.K. population. Methods One hundred and fifty consecutive patients with cellulitis requiring hospital admission and 300 controls were recruited to this prospective case–control study. Controls were matched for age and sex. Results Strongly predictive risk factors for acute lower limb cellulitis in the U.K. include being of white ethnicity and preceding episodes of injury to the affected leg. No systemic illnesses were identified as increasing an individual's risk of presenting with cellulitis. Conclusions This study has identified that patients of white ethnicity are at higher risk of developing acute lower limb cellulitis compared with other ethnic groups. The importance of local risk factors has also been shown in the U.K. population.
A "Free Clinic" Patient Population and Drug Use Patterns
Authors: LEWIS L. JUDD, ARNOLD J. MANDELL
Journal: American Journal of Psychiatry (1972)

The free clinic is a relatively new medical institution and few data exist on the kinds of populations it serves. The authors studied a group of patients who appeared at a free clinic in San Diego. They found that most of the patients were white and middle class in origin; that drug abuse was high but was not a common presenting problem; that the group was suspicious of the validity of information published in "Establishment" news media; and that hallucinogens would he more widely used if they were more available.
Effect of Carbonated Water on Gastric Acid Secretion
Authors: Leon A. Greenberg, John McC. Turner
Journal: New England Journal of Medicine (1955)

THE effect of carbonated water on gastric functions has been a subject of numerous investigations. However, almost all of them have dealt with the effects of ingested carbon dioxide on the rate of gastric emptying1 2 3 4 5 6 7; very few have concerned gastric secretion.8 Thus, although most of the data reported in the literature indicate that carbon dioxide generally causes a more rapid gastric evacuation, there is little and incomplete evidence about whether it causes an increased, decreased or unchanged secretion of gastric acid in response to a test meal.The events of gastric activity after the ingestion of a meal are . . .
TRAUMATIC INFECTED INTERSTITIAL MYOSITIS AS A CAUSE OF PARANEPHRIC ABSCESS
Authors: Alfred Brown
Journal: JAMA (1934)

In December 1927<sup>1</sup>I called attention to the occurrence of an abscess of the lumbar region which was situated outside the perirenal fat in a space bounded in front by the posterior parietal peritoneum and perirenal capsule, behind and laterally by the deep muscles of the back, above by the diaphragm and below by the lower boundary of the false pelvis. This type of abscess I considered to be due to trauma in the form of a muscle strain or contusion which caused a tear either of the muscle fibers themselves or of the capsule of the muscle, from which a localized area of hemorrhage or exudate resulted. Subsequent infection of this area caused the abscess. Two cases were cited which appeared to bear out this hypothesis, which at the time was offered as a hypothesis without definite proof. In the paper I wrote: "If this assumption of hemorrhage
Diagnosing Wilson Disease
Authors: Joseph C. Yarze, Santiago J. Munoz, Lawrence S. Friedman
Journal: Annals of Internal Medicine (1992)

Letters1 July 1992Diagnosing Wilson DiseaseJoseph C. Yarze, MD, Santiago J. Munoz, MD, Lawrence S. Friedman, MDJoseph C. Yarze, MDSearch for more papers by this author, Santiago J. Munoz, MDSearch for more papers by this author, Lawrence S. Friedman, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-117-1-91_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editors:In their review of Wilson disease, Stremmel and colleagues (1) suggest that normal ceruloplasmin levels may be found only in acute or fulminant liver involvement because ceruloplasmin is an acute-phase reactant. Elevation of the ceruloplasmin level into the normal range in Wilson disease, however, is most likely in patients with chronic active hepatitis or with a superimposed inflammatory or neoplastic disorder (2). Additionally, the ceruloplasmin level is elevated during pregnancy or estrogen use. In contrast, fulminant hepatic failure in any disease, including Wilson disease, may be associated with hypoceruloplasminemia caused by diminished hepatic synthetic capacity (3). Hypoceruloplasminemia...References1. StremmelMeyerroseNiederauHefterKreuzpaintnerStrohmeyer WKCHGG. Wilson disease: Clinical presentation, treatment and survival. Ann Intern Med. 1991;115:720-6. LinkGoogle Scholar2. ScottGollanSamourianSherlock JJSS. Wilson's disease presenting as chronic active hepatitis. Gastroenterology. 1978;74:645-51. CrossrefMedlineGoogle Scholar3. McCulloughFlemingThistleBaldusLudwigMcCall ACJWJJ. Diagnosis of Wilson's disease presenting as fulminant hepatic failure. Gastroenterology. 1983;84:161-7. CrossrefMedlineGoogle Scholar4. SternliebScheinberg II. The role of radiocopper in the diagnosis of Wilson disease. Gastroenterology. 1979;77:138-42. CrossrefMedlineGoogle Scholar1. StremmelMeyerroseNiederauHefterKreuzpaintnerStrohmeyer WKCHGG. Wilson disease: clinical presentation, treatment, and survival. Ann Intern Med. 1991;115:720-6. LinkGoogle Scholar1. Skeen M. Wilson disease—penicillamine therapy and late presentation [Letter]. Ann Intern Med. 1992;116:424. 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 byIdentification and characterization of a novel splice-site mutation in the Wilson disease geneMutation analysis of Taiwanese Wilson disease patientsHigh‐affinity copper block of GABA A receptor‐mediated currents in acutely isolated cerebellar Purkinje cells of the rat 1 July 1992Volume 117, Issue 1Page: 91-91KeywordsAcute liver failureAcute phase proteinsChronic hepatitisEstrogensHepatitis ALiverLiver diseasesPregnancy Issue Published: 1 July 1992 PDF downloadLoading ...
Platelet GPIIb/IIIa antagonist, XV459, in heparin‐induced thrombocytopenia
Authors: Shaker A. Mousa, Sarfraz Ahmad
Journal: American Journal of Hematology (2006)

Heparin-induced thrombocytopenia (HIT) is a serious, immune-related complication of heparin therapy. One of the most severe manifestations of HIT is the development of thromboembolic events, which is based on platelet activation and aggregation caused by HIT-associated antibodies. Therapeutic options for patients with HIT are limited despite advancement toward the development of alternative (nonheparin) anticoagulants, such as direct thrombin inhibitors and indirect anti-factor Xa agents. Platelet GPIIb/IIIa receptor antagonists have been shown to be the final common pathway for platelet aggregation regardless of the use of activator or anticoagulant. In this study, the ability of a novel platelet GPIIb/IIIa antagonist, a free acid form of roxifiban (XV459), to block platelet activation/aggregation in response to highly characterized heparin-PF4 antibody-positive plasma/heparin was examined using light transmittance aggregometry, serotonin release, and (125)I-fibrinogen binding assays to human platelets. XV459 at 20 nM maximally inhibited (P < 0.001) the platelet-activation/aggregation responses as mediated by the HIT antibody-positive plasma (in the presence of therapeutic heparin concentrations). Compared with controls, both HIT antibodies/heparin and TEAC (a mixture of thrombin [0.1 IU/ml], epinephrine [1 microg/ml], arachidonate [0.1 mM], and collagen [10 microml]) resulted in significantly higher levels of fibrinogen binding to human platelets (5-7-fold increase; P < 0.001). Concentration-dependent profiles of XV459 on the mean percent inhibition of (125)I-fibrinogen binding in the presence of HIT antibodies and TEAC were achieved ( approximately 50% inhibition at 10 nM XV459). The platelet GPIIb/IIIa receptor antagonist (XV459) might be of potential benefit in the management of thrombotic thrombocytopenia produced by heparin and/or related glycosaminoglycans.
Meta-analysis of Clear Cell Renal Cell Carcinoma Gene Expression Defines a Variant Subgroup and Identifies Gender Influences on Tumor Biology
Authors: A. Rose Brannon, Scott M. Haake, Kathryn E. Hacker, Raj S. Pruthi, Eric M. Wallen, Matthew E. Nielsen, W. Kimryn Rathmell
Journal: European Urology (2011)
Understanding the Anatomic Basis for Obstructive Sleep Apnea Syndrome in Adolescents
Authors: Richard J. Schwab, Christopher Kim, Sheila Bagchi, Brendan T. Keenan, François-Louis Comyn, Stephen Wang, Ignacio E. Tapia, Shirley Huang, Joel Traylor, Drew A. Torigian, Ruth M. Bradford, Carole L. Marcus
Journal: American Journal of Respiratory and Critical Care Medicine (2015)

Structural risk factors for obstructive sleep apnea syndrome (OSAS) in adolescents have not been well characterized. Because many adolescents with OSAS are obese, we hypothesized that the anatomic OSAS risk factors would be more similar to those in adults than those in children.To investigate the anatomic risk factors in adolescents with OSAS compared with obese and lean control subjects using magnetic resonance imaging (MRI).Three groups of adolescents (age range: 12-16 yr) underwent MRI: obese individuals with OSAS (n = 49), obese control subjects (n = 38), and lean control subjects (n = 50).We studied 137 subjects and found that (1) obese adolescents with OSAS had increased adenotonsillar tissue compared with obese and lean control subjects; (2) obese OSAS adolescents had a smaller nasopharyngeal airway than control subjects; (3) the size of other upper airway soft tissue structures (volume of the tongue, parapharyngeal fat pads, lateral walls, and soft palate) was similar between subjects with OSAS and obese control subjects; (4) although there were no major craniofacial abnormalities in most of the adolescents with OSAS, the ratio of soft tissue to craniofacial space surrounding the airway was increased; and (5) there were sex differences in the pattern of lymphoid proliferation.Increased size of the pharyngeal lymphoid tissue, rather than enlargement of the upper airway soft tissue structures, is the primary anatomic risk factor for OSAS in obese adolescents. These results are important for clinical decision making and suggest that adenotonsillectomy should be considered as the initial treatment for OSAS in obese adolescents, a group that has poor continuous positive airway pressure adherence and difficulty in achieving weight loss.
Predictors of Response to Steroid Therapy for Eosinophilic Esophagitis and Treatment of Steroid-Refractory Patients
Authors: W. Asher Wolf, Cary C. Cotton, Daniel J. Green, Julia T. Hughes, John T. Woosley, Nicholas J. Shaheen, Evan S. Dellon
Journal: Clinical Gastroenterology and Hepatology (2014)
TRANSPLACENTAL TRANSMISSION OF HOMOTRANSPLANTATION ANTIBODIES
Authors: Nicholas A. Halasz, Marshall J. Orloff
Journal: The Journal of Experimental Medicine (1963)

Pregnant rabbits were sensitized to unrelated does by skin transplantation. The offspring of these sensitized animals rejected skin from the same donor in a markedly accelerated fashion. The transplacental passage of agents responsible for homograft rejection is therefore suggested. Since accelerated rejection rather than enhancement occurred, more than the usual humoral antibodies must have been thus transmitted. The presence of another antibody-like substance is postulated. This appears to be sessile in nature, usually fixed to lymphocytes, but transmissible without these cells under special circumstances, such as occur in micropore chambers or hemochorial placentae. These allow the prolonged dose contact of sensitized and non-sensitized lymphocytes, and thus may permit the transfer of this, usually sessile, but apparently non-fixed antibody.
Dysfunctional Voltage-Gated K <sup>+</sup> Channels in Pulmonary Artery Smooth Muscle Cells of Patients With Primary Pulmonary Hypertension
Authors: Jason Xiao-Jian Yuan, Ann M. Aldinger, Magdalena Juhaszova, Jian Wang, John V. Conte, Sean P. Gaine, Jonathan B. Orens, Lewis J. Rubin
Journal: Circulation (1998)

Background —Primary pulmonary hypertension (PPH) is a rare disease of unknown cause. Although PPH and secondary pulmonary hypertension (SPH) share many clinical and pathological characteristics, their origins may be disparate. In pulmonary artery smooth muscle cells (PASMCs), the activity of voltage-gated K + (K V ) channels governs membrane potential (E m ) and regulates cytosolic free Ca 2+ concentration ([Ca 2+ ] cyt ). A rise in [Ca 2+ ] cyt is a trigger of vasoconstriction and a stimulus of smooth muscle proliferation. Methods and Results —Fluorescence microscopy and patch clamp techniques were used to measure [Ca 2+ ] cyt , E m , and K V currents in PASMCs. Mean pulmonary arterial pressures were comparable (46±4 and 53±4 mm Hg; P =0.30) in SPH and PPH patients. However, PPH-PASMCs had a higher resting [Ca 2+ ] cyt than cells from patients with SPH and nonpulmonary hypertension disease. Consistently, PPH-PASMCs had a more depolarized E m than SPH-PASMCs. Furthermore, K V currents were significantly diminished in PPH-PASMCs. Because of the dysfunctional K V channels, the response of [Ca 2+ ] cyt to the K V channel blocker 4-aminopyridine was significantly attenuated in PPH-PASMCs, whereas the response to 60 mmol/L K + was comparable to that in SPH-PASMCs. Conclusions —These results indicate that K V channel function in PPH-PASMCs is inhibited compared with SPH-PASMCs. The resulting membrane depolarization and increase in [Ca 2+ ] cyt lead to pulmonary vasoconstriction and PASMC proliferation. Our data suggest that defects in PASMC K V channels in PPH patients may be a unique mechanism involved in initiating and maintaining pulmonary vasoconstriction and appear to play a role in the pathogenesis of PPH.