tbuckley/cabot-search huggingface dataset:
Leukocyte antimicrobial function in patients with leprosy.
Authors: D J Drutz, M J Cline, L Levy
Journal: Journal of Clinical Investigation (1974)

Patients with lepromatous leprosy are unresponsive to lepromin skin-test material and possess defective lymphocyte function in vitro, including impaired mitogenesis in response to antigens of Mycobacterium leprae. It has been claimed that their macrophages cannot digest M. leprae in vitro; such a defect could explain both lepromin nonreactivity and impaired lymphocyte function on the basis of failure of the afferent limb of the immune response (i.e., defective macrophage "processing" of M. leprae). The present studies indicate that macrophages from patients with lepromatous and tuberculoid leprosy and from normal donors do not differ in their ability to digest heat-killed M. leprae in vitro, or in their ability to sustain the viability of M. leprae in tissue culture; that monocytes, macrophages, and polymorphonuclear leukocytes of leprosy patients and controls possess equivalent microbicidal activity against Listeria monocytogenes, Escherichia coli, Proteus vulgaris, Staphylococcus aureus, and Candida albicans; and that polymorphonuclear leukocytes from patients with lepromatous leprosy iodinate ingested bacteria normally. Whether the basic immune defect leading to the development of lepromatous leprosy resides in the lymphocyte or in the macrophage remains to be determined. However, the present study shows that phagocytic cells from patients with either principal form of leprosy function normally in a variety of sophisticated tests of antimicrobial function.
Ga-67 Lung Uptake in Patients with Adult Respiratory Distress Syndrome
Authors: RUTH HARDOFF, SYLVIANNE BURSZTEIN-DE MYTTERAERE
Journal: Clinical Nuclear Medicine (1992)

Nine patients with adult respiratory distress syndrome (ARDS) were studied with Ga-67 imaging in search for a site of infection. Different degrees and two patterns of Ga-67 lung uptake scoring in comparison with liver uptake were demonstrated. All patients had diffuse lung uptake, whereas five of them also showed additional focal lung activity. In only one patient was an abdominal focal uptake detected. Chest radiographs of all patients revealed diffuse and focal lung infiltrates that correlated with the Ga-67 uptake patterns. Therefore, Ga-67 imaging was unhelpful in differentiating patients with ARDS with lung infection from patients without lung infection. The intensity of Ga-67 uptake, as expressed by Ga-67 scoring, correlated with the course and outcome of ARDS. Patients exhibiting a high Ga-67 score had long periods of hospitalization and eventually died (four patients), whereas those who had low Ga-67 scores had a short disease course and survived (five patients). It is concluded that Ga-67 imaging in ARDS patients is unable to detect lung infection; however, it may be useful in the assessment of patients' prognosis.
Doctors have moral imperative to call for end to embargo on Cuba
Authors: D. Parnham-Cope
Journal: BMJ (1997)

Progress in reducing inpatient mortality from acute myocardial infarction is slowEditor-Brown et al report a substantial increase in the use of beneficial interventions for patients admitted to hospital with acute myocardial infarction in Nottingham from 1982 to 1992. 1 However, they found no change in inpatient mortality adjusted for age and sex.This contrasts with findings in Ontario, Canada, where hospital discharge abstracts show that inpatient mortality fell from 1981 to 1991 2 and has since fallen further (data on request).Brown et al suggest that the disparate results may reflect coding errors in the Ontario administrative data.Our group has assessed the classification of deaths from acute myocardial infarction in inpatients in the Ontario discharge abstracts.Matching Ontario administrative data to data from the GUSTO-I and LATE trials, we found the specificity of the administrative data to be 100% (1403/1403 alive), with overall sensitivity of 94% (104/111 deaths detected). 3he classification of acute myocardial infarction itself is more problematic.The sensitivity of the primary diagnosis of acute myocardial infarction is high, but specificity varies. 4 5There are two common reasons for false positive coding.Firstly, patients may be admitted to a coronary care unit with possible acute myocardial infarction but this diagnosis is ruled out and they are sent home quickly.Alternatively, patients recently admitted to hospital with acute myocardial infarction are readmitted for coronary angiography or with complications other than overt reinfarction, and the code for acute myocardial infarction is wrongly used again.Thus the analysis of outcomes in Ontario excluded both patients with a primary diagnosis of acute myocardial infarction who were discharged in under four days and patients who had been admitted to hospital for acute myocardial infarction in the preceding three months. 2t is therefore doubtful that imprecise coding explains the improving outcomes of acute myocardial infarction in Ontario.Indeed, only systematic coding errors could explain the observed trends in inpatient mortality, and we have found neither evidence nor a rationale for this.Ontario's administrative data do mirror the findings of Brown et al in two respects 2 : admissions for acute myocardial infarction, particularly among elderly patients, increased over the period studied, and inpatient mortality ranged from 16% to 21%, which is much higher than in the large randomised trials of thrombolytic treatment.Thus while the trends in Ontario are more positive than those in Nottingham, we agree with Brown et al that the cardiovascular megatrials have been enrolling skewed patient populations 3 and that progress in the battle to reduce inpatient mortality from acute myocardial infarction remains slow.
New words for old: lower urinary tract symptoms for "prostatism"
Authors: P Abrams
Journal: BMJ (1994)

New words for old: lower urinary tract symptoms for "prostatism" Avoids spurious suggestion ofdiagnostic accuracy Extraordinary interest currently exists in the treatment of men over 45 who are referred with the label "prostatism."This has been generated partly by commercial interest and patients' increased awareness and expectations and partly by the advent of new treatments.Several new drugs to relieve bladder outflow obstruction, including ao adrenergic blockers and 5-a reductase inhibitors, have been or are about to be licensed.Drug companies have expended huge efforts in increasing patients' and doctors' awareness of prostatic disease.New techniques to destroy part or all of the prostate have been developed, including thermotherapy, thermal ablation, high intensity focused ultrasonography, transurethral needle ablation, and laser prostatectomy.Added to this are the techniques of intraurethral prostatic stenting and balloon dilatation ofthe prostate.'Surveys have shown that urinary symptoms are very common in older men, with prevalences varying from 11% for straining up to 78% for nocturia.'Interestingly, British and
Abstract 2609: Nelfinavir induces liposarcoma apoptosis through inhibition of regulated intramembrane proteolysis of sterol regulatory element binding protein-1 and activating transcription factor 6
Authors: Min Guan, Chunling Jiang, Kristen N. Fousek, Song Guo, Warren Chow
Journal: Cancer Research (2010)

Abstract We previously reported that nelfinavir induces a G1 cell cycle block and apoptosis selectively in liposarcoma cell lines as a consequence of up-regulation of SREBP-1 expression. We demonstrate now that nelfinavir-induced up-regulation of SREBP-1 and ATF6 is a direct result of inhibition of site-2 protease, which together with site-1 protease mediates regulated intramembrane proteolysis from their precursor state to their transcriptionally-active forms. The resulting endoplasmic reticulum stress and concurrent inhibition of the unfolded protein response induces caspase activation. Time-lapse, confocal microscopy studies demonstrate that nelfinavir inhibits the normal translocation of transfected SREBP-1-EGFP and ATF6-EGFP fusion proteins from the cytoplasm to the nucleus. siRNA-mediated knockdown of site-1 and/or site-2 protease leads to inhibition of SREBP-1 intracellular trafficking to the nucleus and reduces liposarcoma cell proliferation. Treatment of LiSa-2 liposarcoma cells with 4-(2-aminoethyl)benzenesulfonyl fluoride, a serine protease inhibitor of S1P did not affect SREBP-1 processing. In contrast, 1, 10-phenanthroline, an S2P-specific inhibitor, reproduces the molecular and biological phenotype observed in nelfinavir-treated cells, which confirms S2P is a target of nelfinavir. In vivo evaluation of nelfinavir in a murine liposarcoma xenograft model shows inhibition of tumor growth in the absence of significant toxicity. These results provide new insight into the mechanism of nelfinavir-mediated induction of ER stress and cell death in liposarcomas and are the first report to therapeutically target S2P against cancer. 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 2609.
New Horizons for Intravenous Feeding
Authors: Stanley J. Dudrick
Journal: JAMA (1971)

Dr. Rhoads: We are deeply honored to receive the Joseph Goldberger Award, memorializing as it does a man whose contributions in helping to elucidate the metabolic significance of the vitamin B complex, initiated a wave of important discoveries in the field of nutrition. The award has been enhanced by the reputations and contributions of the several scientists who have been recipients in the past. Dr. Dudrick and I wish to acknowledge frankly our great indebtedness to our associates, past and present, in studies of surgical nutrition. These include Dr. I. S. Ravdin, who was one of the first surgeons to recognize the relevance of nutritional studies to the progress of surgical science, and who stayed with the field almost exclusively through the 1930s and early 1940s; to Dr. Harry M. Vars, who joined the Harrison Department of Surgical Research in 1936 as a biochemist and who has devoted his entire
The Tradition of the College
Authors: WESLEY W. SPINK
Journal: Annals of Internal Medicine (1964)

Convocation Oration1 July 1964The Tradition of the CollegeWESLEY W. SPINK, M.D., F.A.C.P.WESLEY W. SPINK, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-61-1-147 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTonight I wish to direct my remarks to those individuals who have just joined the ranks of the American College of Physicians as Fellows. In taking the College Oath of Fellowship you have participated in a tradition that extends over several centuries.We are living in a revolutionary age—politically, scientifically, and socially. There is little time for reflection upon the past. It is the present and future that engage our interest. However, great leaders have benefited from a survey of the past. A broad perspective of history gave wisdom to the leadership of Churchill.Much of our College tradition has... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Minneapolis, MinnesotaConvocation Address, Forty-fifth Annual Session of the American College of Physicians, April 9, 1964. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byTThe Royal College of Physicians of LondonJ. R. E., E. J. H.Fiftieth BirthdayJ. R. E. 1 July 1964Volume 61, Issue 1Page: 147-152KeywordsFellowshipsForecasting ePublished: 1 December 2008 Issue Published: 1 July 1964 PDF downloadLoading ...
Dermatologic disease accounts for a large number of hospital admissions annually
Authors: Robert S. Kirsner, Doris G. Yang, Francisco A. Kerdel
Journal: Journal of the American Academy of Dermatology (1999)

Severe skin disease uncommonly requires hospitalization. The number of patients hospitalized for skin disease annually in the United States has never been reported.We evaluated the number of patients admitted for skin disorders.Using data from 2 national databases, the Healthcare Cost and Utilization Project-3 Nationwide Inpatient Sample (HCUP-3 NIS) 1992-1994 and Medicare Provider Analysis and Review (MEDPAR) 1990-1996 file, we evaluated the total discharges, total charges, and reimbursement of the dermatology-specific (272, 273, 283, and 284) and -related (263, 264, 265, 266, 271, 277, 278, and 279) diagnosis-related groups (DRGs).In 1994, the HCUP-3 NIS data showed that a total of 468,014 discharges were classified under Dermatology DRGs, whereas in 1996 MEDPAR data gave a figure of 183,310 discharges with a total Medicare reimbursement of $892 million. In both data sets, dermatology-specific DRGs show a decrease over time, although dermatology-related DRGs generally showed an opposite increasing pattern. The top 10 states reimbursed by Medicare in 1996 for the discharges grouped under the DRGs mentioned above were New York, California, Pennsylvania, Florida, Texas, Ohio, Illinois, Michigan, New Jersey, and Massachusetts.Many patients are admitted annually for skin disease. The minority are admitted by dermatologists.
Effects of pemphigus antibody on the organization of microtubules and keratin-intermediate filaments in cultured human keratinocytes
Authors: Y. KITAJIMA, S. INOUE, H. YAOITA
Journal: British Journal of Dermatology (1986)

It has been suggested that pemphigus antibodies (PA) react with the surface molecules on keratinocytes, and induce the production and release of proteases resulting in acantholysis. If this is the case, the immunoreactions on the cell surface may send signals to the interior of the cell across the membrane. The present study was carried out to determine whether or not cytoskeletons [microtubules (MT) and keratin‐intermediate filaments (KIF)] respond to PA‐immunoreactions in cultured human keratinocytes, by indirect immunofiuorescence micros‐copy using anti‐keratin and anti‐x‐tubulin antibodies. During incubation for 30 min to 72 h in a PA‐containing medium with a normal concentration of Ca2 + (1.2 mM), no changes in MT or KIF organization were detected. Alterations in the organization of these filaments were observed 96 h after addition of PA. When cells grown in a normal medium for 5–7 days were transferred to a medium containing PA and a low level of Ca2+ (0.07–0.14 mM) the reorganization of KIFs and MTs occurred after 1 h incubation. However, no reorganization of the cytoskeletons was detected in the absence of cell detachment. These observations suggest that the pemphigus antibody‐induced reorganization of MTs and KIFs does not precede acantholysis and is probably secondary to it, but is not a direct transmembrane response. The present study also showed that immunofluorescence microscopy of KIFs may be one of the most sensitive methods for detecting early cell‐to‐cell dissociation in cultured keratinocytes.
Controlled prospective evaluation of the diagnostic yield of a laryngopharyngeal screening examination during upper gastrointestinal endoscopy
Authors: B Mullhaupt
Journal: Gut (2004)

Examination of the laryngopharyngeal area is not always performed during routine upper gastrointestinal (UGI) endoscopies although older studies reported pathological findings in 0.9-3.5% of cases. The aim of our study was to prospectively evaluate the positive and negative predictive value of screening the laryngopharyngeal area during routine UGI endoscopy.
Abstract 3758: Global expression profiling of highly degraded RNA by DASL assay from formalin-fixed paraffin-embedded lung tissue
Authors: Li Su
Journal: Cancer Research (2010)

Abstract Microarray-based genome-wide gene expression analysis on fresh frozen tissue is widely used in cancer studies. Compared to fresh frozen tissues, formalin-fixed paraffin-embedded (FFPE) tissues are more accessible in clinical setting for genomic analysis, but its use has been hampered by technical difficulty. Recently, cDNA-medi¬ated annealing, selection, extension, and ligation (DASL) assay was developed by Illumina (San Diego, CA) to investigate the global gene expression profiling of highly degraded RNA from FFPE samples. In this study, we tested the potential of the Whole-Genome DASL Assay for Expression Profiling in FFPE Samples (covering up to 24,000 annotated probes) in biomarker discovery for lung disease research. We obtained biopsy tissue from two lung cancer patients and six acute respiratory distress syndrome (ARDS) patients. Five 5 μm-thick slides from each specimen were evaluated by a pathologist for tumor cellularity (lung cancer) or diffuse alveolar damage (ARDS), and RNA was extracted using commercially available (Roche High Pure RNA Paraffin) kits. The DASL expression profiles on 2 ARDS FFPE-extracted RNA samples had poor quality as determined by low detection rate (&amp;lt;25%) and low array-wide average signals. The other 6 (75%) of the RNA samples had a median detection of 8,442 genes with a range between 7,306 and 10,616 genes. These array data also had strong array-wide average signals and low noise. Our study demonstrated that DASL expression profiling technology, genome-wide expression profiles can be successfully generated from FFPE lung tissues. 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 3758.
A Dissociation of Positive Staircase (Bowditch) from Ouabain-Induced Positive Inotropism
Authors: JOHN L. McCANS, GEORGE E. LINDENMAYER, RONALD G. MUNSON, RANDOLPH W. EVANS, ARNOLD SCHWARTZ
Journal: Circulation Research (1974)

The effects of verapamil on myocardial contractility were examined in perfused rabbit ventricular preparations. Verapamil (0.2 µ M ) decreased the time derivative of developed force (dF/dt) of the preparations paced at 90 beats/min to 39 ± 3% ( SE ) of the control value. Partial reversal to 76 ± 5% of the control value was achieved by subsequent perfusion with drug-free Krebs solution. Verapamil hastened the decline and delayed the return of contractility in response to a cycle of calcium washout and reperfusion. It converted the response to increased heart rate from positive (Bowditch effect) to negative inotropism. Moreover, the sensitivity to the drug was frequency related; the drug concentration required to induce a 50% decrease in dF/dt was an inverse function of heart rate, suggesting that the drug altered contractility by interfering with a phenomenon associated with systole. Verapamil did not decrease the magnitude of the positive inotropic response to 0.5 µ M ouabain, although a significant delay in the development of the response was observed. After 8 minutes of ouabain perfusion dF/dt had increased 35 ± 2% in the absence of verapamil but only 13 ± 1% in the presence of 1.0, µ M verapamil. The maximum response to ouabain was a 39 ± 4% increase at 9 minutes in the absence of verapamil and a 34 ± 2% increase at 23 minutes in the presence of verapamil. These results suggest that the responses to increased frequency and to cardiac glycosides are not explained by a common mechanism such as sodium-calcium exchange occurring during diastole or any other diastole-related mechanism for calcium influx. However, the possibility that both events are mediated by some common mechanism occurring during systole has not been eliminated.
Association of human APOBEC3 cytidine deaminases with the generation of hepatitis virus B x antigen mutants and hepatocellular carcinoma
Authors: Rongzhen Xu, Xuzhao Zhang, Wei Zhang, Yongmin Fang, Shu Zheng, Xiao-Fang Yu
Journal: Hepatology (2007)

Human APOBEC3 (apolipoprotein B mRNA editing enzyme, catalytic polypeptide 3) cytidine deaminases have been shown to be potent inhibitors of diverse retroviruses including Vif-deficient human immunodeficiency virus 1 (HIV-1), hepatitis virus B (HBV), adeno-associated virus, and endogenous retroelements. Despite the fact that these enzymes are known to be potential DNA mutators and to target retroviral DNA for cytidine deamination, the pathological effects of their deregulated expression in human diseases are not yet clear. Mutants of the viral HBx protein have been implicated in the carcinogenesis of hepatocellular carcinoma (HCC); however, little is known about how or why such mutants are generated in the human liver. Here, we report that a number of APOBEC3 deaminases preferentially edit the HBx region of HBV DNA and generate C-terminally truncated HBx mutants. Our functional studies indicated that APOBEC3-mediated HBx mutants, especially the C-terminally truncated mutants, cause a gain of function that enhances the colony-forming ability and proliferative capacity of neoplastic cells. Furthermore, we detected G-to-A hypermutation-mediated HBx mutants in preneoplastic liver tissues of selected patients with active chronic HBV infections. We also observed that the APOBEC3B (A3B) cytidine deaminase was widely up-regulated in HCC tumor tissues; it also promoted the growth of neoplastic human HepG2 liver cells and up-regulated heat shock transcription factor1 (HSF1) expression.These findings suggest that some of the APOBEC3 deaminases play a role in the carcinogenesis of HCC through the generation of HBx mutants, providing preneoplastic and neoplastic hepatocytes with a selective clonal growth advantage. Deregulated expression of A3B in liver tissues may also have the potential to promote genetic instability and tumorigenesis.
Effect of Distension of the Gallbladder on Plasma Renin Activity in Anesthetized Pigs
Authors: Claudio Molinari, Elena Grossini, David A. S. G. Mary, Giovanni Vacca
Journal: Circulation (2000)

Gallbladder pathology has been associated with cardiovascular disease. Recently, we showed that gallbladder distension in anesthetized pigs reflexly increased heart rate, arterial pressure, and coronary and renal vascular resistance through efferent sympathetic mechanisms. Renin release is affected by sympathetic output, and angiotensin liberation may result in vasoconstriction. This study was undertaken to determine whether gallbladder distension primarily causes a reflex change in plasma renin activity (PRA) and to assess its influence on observed pressor and coronary responses as well as on regional vascular resistance.In 34 alpha-chloralose-anesthetized pigs, balloons positioned within the gallbladder were distended for 30 minutes with volumes of Ringer's solution equal to those of withdrawn bile. In 19 pigs, gallbladder distension at constant heart rate, arterial pressure, and renal flow increased PRA in the absence of changes in urinary sodium excretion. This increase was abolished by cervical vagotomy, section of renal nerves, or blockade of beta-adrenergic receptors. In another 15 pigs, blockade of angiotensin II receptors significantly attenuated the pressor and coronary, mesenteric, and iliac vasoconstriction responses to gallbladder distension.The present study showed that innocuous gallbladder distension primarily caused a reflex increase in PRA. This increase, which involved afferent vagal pathways and efferent sympathetic mechanisms related to beta-adrenergic receptors, contributed significantly to the pressor and coronary, mesenteric, and iliac vasoconstriction responses to gallbladder distension.