tbuckley/cabot-search huggingface dataset:
Erythroid Aplasia Following Thymomectomy
Authors: George L. River
Journal: JAMA (1966)

THYMIC TUMORS have been reported<sup>(1-5)</sup>in association with a number of interesting and exotic diseases (Table). The patient to be presented had increased red blood cell (RBC) production before removal of a large, benign thymoma. Five months later, when a diagnosis of erythroid aplasia was established, the plasma level of erythropoietin was increased. <h3>Report of a Case</h3> A 53-year-old housewife was referred for evaluation of her condition after a chest tumor was seen on a mobile unit roentgenogram of the chest in July 1963. She had no complaints. A month earlier, slight anemia had been noted when she saw her physician for a "cold." Mild aching of the hands and wrists had occurred intermittently for the previous six years. She had been jaundiced for six weeks in 1930. No history of exposure to known toxic substances could be elicited. Her mother died of "Bright's disease" at age 28. Findings
Monosaccharide-induced lipogenesis regulates the human hepatic sex hormone–binding globulin gene
Authors: David M. Selva, Kevin N. Hogeveen, Sheila M. Innis, Geoffrey L. Hammond
Journal: Journal of Clinical Investigation (2007)

The liver produces plasma sex hormone-binding globulin (SHBG), which transports sex steroids and regulates their access to tissues. In overweight children and adults, low plasma SHBG levels are a biomarker of the metabolic syndrome and its associated pathologies. Here, we showed in transgenic mice and HepG2 hepatoblastoma cells that monosaccharides (glucose and fructose) reduce human SHBG production by hepatocytes. This occurred via a downregulation of hepatocyte nuclear factor-4alpha (HNF-4alpha) and replacement of HNF-4alpha by the chicken OVA upstream promoter-transcription factor 1 at a cis-element within the human SHBG promoter, coincident with repression of its transcriptional activity. The dose-dependent reduction of HNF-4alpha levels in HepG2 cells after treatment with glucose or fructose occurred in concert with parallel increases in cellular palmitate levels and could be mimicked by treatment with palmitoyl-CoA. Moreover, inhibition of lipogenesis prevented monosaccharide-induced downregulation of HNF-4alpha and reduced SHBG expression in HepG2 cells. Thus, monosaccharide-induced lipogenesis reduced hepatic HNF-4alpha levels, which in turn attenuated SHBG expression. This provides a biological explanation for why SHBG is a sensitive biomarker of the metabolic syndrome and the metabolic disturbances associated with increased fructose consumption.
Association of Cigarette Smoking With Chronotropic Incompetence and Prognosis in the Framingham Heart Study
Authors: Michael S. Lauer, Fredric J. Pashkow, Martin G. Larson, Daniel Levy
Journal: Circulation (1997)

In this study, we sought to determine whether cigarette smoking is associated with chronotropic incompetence and to explore prognostic implications of this association.Members of the Framingham Offspring Study (1468 men and 1642 women) underwent graded exercise. Chronotropic incompetence was assessed in two ways: (1) failure to achieve an age-predicted target heart rate and (2) a low chronotropic index, a heart rate response measure that accounts for effects of age, resting heart rate, and physical fitness. Smokers were more likely to fail to reach target heart rate than were nonsmokers (men, 25% versus 15%, odds ratio [OR], 1.97; 95% confidence interval [CI], 1.51 to 2.56; women, 32% versus 18%; OR, 2.10; 95% CI, 1.63 to 2.61) and were more likely to have a low chronotropic index (men, 17% versus 12%; OR, 1.50; 95% CI, 1.12 to 2.03; women, 17% versus 8%; OR, 2.28; 95% CI, 1.68 to 3.09). These associations persisted after adjustment for age, cardiovascular risk factors, pulmonary function, and ST-segment response to graded exercise. During 8 years of follow-up, there were 48 deaths and 90 incident coronary heart disease events among the men. After adjustment for the same confounders, men who were smokers and failed to achieve target heart rate were at particularly high risk for death (adjusted relative risk [RR], 2.45; 95% CI, 1.14 to 5.24) and for coronary heart disease (adjusted RR, 4.92; 95% CI, 2.84 to 8.53). There were too few end points in women for analysis.In this population-based cohort, cigarette smoking was predictive of chronotropic incompetence. Male smokers who manifested chronotropic incompetence were at particularly high risk for death and coronary heart disease events.
Adipose tissues from RA and OA patients differ in cytokine and adipokine production
Authors: M. Plebanczyk, I. Janicka, U. Musialowicz, T. Burakowski, W. Maslinski, P. Maldyk, E. Kontny
Journal: Annals of the Rheumatic Diseases (2011)

<h3>Objectives</h3> Cytokines and adipokines play fundamental role in synovial inflammation and articular destruction. Articular and subcutaneous adipose tissues have been suggested to play a role in inflammatory joint diseases. The aim of present work was to investigate whether adipose tissues from rheumatoid arthritis (RA) and osteoarthritis (OA) patients differ in adipokine and cytokine production. <h3>Materials and methods</h3> Articular (AA) and subcutaneous (ScA) adipose tissue explants, obtained from RA and OA patients who were undergoing knee joint replacement surgery, were cultured (100 mg/ml) for 18 h in medium (DMEM) alone or in the presence of lipopolysaccharide (LPS) (1 μg/ml) or cytokines: tumour necrosis factor (TNF)-α interferon (IFN)-γ and IL-1, IL-15, IL-17 or IL-23 (10 and 40 ng/ml). Concentrations of TNF-α, IL-6, IL-8, IL-1, IL-1Ra, adiponectin and leptin were measured in culture supernatants by ELISA. <h3>Results</h3> Spontaneous secretion of adiponectin was higher in OA than in RA adipose tissues, while production of other cytokines was similar. LPS raised cytokine (TNF-α, IL-1/IL-1Ra, IL-6, IL-8) secretion resulting in higher response in OA than in RA tissues. Upon some (TNF-α, IFN-γ, IL-1) but not other (IL-15, IL-17, IL-23) cytokines treatment secretion of tested cytokines raised significantly. Interestingly, TNF-α triggered higher IL-6 secretion in AA than in ScA (both in RA and OA), while IL-1 was more potent inducer of IL-6 and IL-8 release from OA than RA adipose tissues. Importantly, upon TNF-α (ScA) and IFN-γ (AA) treatment IL-1/IL-1Ra ratio was higher in RA than in OA tissues. Adiponectin levels were unaffected by cytokines, while leptin secretion was raised (by IL-1 and IFN-γ) more potently in OA than RA tissues. <h3>Conclusion</h3> The authors reported that (i) upon proinflammatory cytokines (TNF-α and IFN-γ) stimulation IL-1/IL-1Ra ratio (promoting joint destruction) was higher in RA tissues; (ii) adipose tissues obtained from OA patients secreted more adiponectin (anti-inflammatory adipokine); (iii) upon IL-1 stimulation OA tissues produced more proinflammatory cytokines (IL-6 and IL-8). The authors9 results give direct evidence that adipose tissues from RA and OA patients differ in cytokine and adipokine production associated with proinflammatory and destructive capability.
Circulating immune complexes containing secretory IgA in jejunoileal bypass disease.
Authors: D O Clegg, J J Zone, C O Samuelson, J R Ward
Journal: Annals of the Rheumatic Diseases (1985)

Thirteen patients were studied after jejunoileal bypass (JIB) surgery. Seven developed arthritis and six did not. Circulating immune complexes containing IgG and IgA were detected in the sera of patients with and without arthritis. IgA complexes were shown to contain secretory component, a protein predominantly associated with intraluminal IgA, in significantly higher levels in patients with arthritis. Analytical ultracentrifugation showed complexes of approximately 10 X 8S, consistent with the size of secretory IgA. Arthritis after JIB appears to be associated with circulating immune complexes containing secretory IgA.
Accuracy of Multislice Computed Tomography in the Preoperative Assessment of Coronary Disease in Patients With Aortic Valve Stenosis
Authors: Martine Gilard, Jean-Christophe Cornily, Pierre-Yves Pennec, Cedric Joret, Grégoire Le Gal, Jacques Mansourati, Jean-Jacques Blanc, Jacques Boschat
Journal: Journal of the American College of Cardiology (2006)
Effects of Atrazine on Estrogen Receptor <b>α</b> – and G Protein–Coupled Receptor 30–Mediated Signaling and Proliferation in Cancer Cells and Cancer-Associated Fibroblasts
Authors: Lidia Albanito, Rosamaria Lappano, Antonio Madeo, Adele Chimento, Eric R. Prossnitz, Anna Rita Cappello, Vincenza Dolce, Sergio Abonante, Vincenzo Pezzi, Marcello Maggiolini
Journal: Environmental Health Perspectives (2015)

The pesticide atrazine does not bind to or activate the classical estrogen receptor (ER), but it up-regulates the aromatase activity in estrogen-sensitive tumor cells. The G protein estrogen receptor (GPR30/GPER) has been reported to be involved in certain biological responses to endogenous estrogens and environmental compounds exerting estrogen-like activity.
A Matter of the Heart
Authors: Joshua Liao
Journal: Annals of Internal Medicine (2011)

On Being a Doctor15 November 2011A Matter of the HeartJoshua Liao, BA, BSJoshua Liao, BA, BSFrom Baylor College of Medicine, Houston, TX 77030.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-155-10-201111150-00013 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail I followed my attending physician down the hall. Our shoes clicked sharply against the white tile. The space ahead opened into a crosswalk bridging the hospital towers over the street below. Light streamed in through the large glass panels, painting the ground yellow. White coats littered the corridor, and I glanced beyond them at the cars passing underneath. They felt distant and small.Inside the room, Mr. Lucas sat on the bed folding his brother's clothes. Several suitcases lay open in the corner. Behind him, the curtains glowed red, pulled tight to keep out the fading sun. Pink balloons floated ... Author, Article, and Disclosure InformationAffiliations: From Baylor College of Medicine, Houston, TX 77030.Corresponding Author: Joshua Liao, BA, BS; e-mail, [email protected]edu. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byThe impact of death and dying on the personhood of medical students: a systematic scoping reviewCloak of compassion, or evidence of elitism? An empirical analysis of white coat ceremonies 15 November 2011Volume 155, Issue 10Page: 716KeywordsFallsFearHeartPatientsSafetyShouldersSurgeryThoraxVisionWalking ePublished: 15 November 2011 Issue Published: 15 November 2011 Copyright & PermissionsCopyright © 2011 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Poor sulphoxidation ability in patients with food sensitivity.
Authors: G. K. Scadding, R. Ayesh, J. Brostoff, S. C. Mitchell, R. H. Waring, R. L. Smith
Journal: BMJ (1988)

Patients with well defined reactions to foods were examined for their ability to carry out both sulphur and carbon oxidation reactions by using carbocisteine and debrisoquine as probe compounds. The proportion of poor sulphoxidisers (58 of 74) was significantly greater than that of a previously determined normal control population (67 of 200; p less than 0.005). The proportion of poor carbon oxidisers was not significantly different from the controls. Metabolic defects may play a part in the pathogenesis of adverse reactions to foods.
Statins for all over 50? No
Authors: F. Godlee
Journal: BMJ (2013)

A Mexican mestizo family is reported in which two opposite sexed sibs, born to consanguineous parents, had a skeletal dysplasia. The salient features were a bell shaped thorax owing to short ribs, short limbed dwarfism, pelvic hypoplasia, dislocatable radial heads, elongated distal fibulae, and improvement with age. It is concluded that the present observation probably represents a distinct autosomal recessive thoraco-limb dysplasia identifiable at birth.
THE COFFEY-HUMBER TREATMENT
Authors: W. B. Coffey
Journal: JAMA (1930)

[Note.—The following telegram was received in response to a request for information as to the present status of the work:] <h3>To the Editor:</h3> —We have repeatedly made the following statement: We do not claim to treat or cure cancer. We are carrying out an experimental effort to prove our contention that we have a potent extract from the cortex of the suprarenal. The incidents arising out of this experimental work even at this date do not justify any one to claim we are offering our extract as treatment or cure for cancer. We are placing all available specimens in the hands of the pathologist. We stand or fall on the decision of our recognized authorities. We likewise have stated on the report of your quoted remarks that we approve of your discussion of this important subject.
Gut and mind
Authors: N M Neary
Journal: Gut (2003)

Obesity is a growing epidemic, causally associated with a number of serious medical conditions, including diabetes mellitus, coronary heart disease, and several cancers. The gut hormones ghrelin and peptide YY are secreted from the gut in response to changes to nutritional status. While food intake is stimulated by ghrelin, it is inhibited by peptide YY. The discovery, anatomy, and physiology of ghrelin and peptide YY are discussed, focusing on the adaptive changes in diseases such as obesity and anorexia nervosa. Ghrelin and PYY are important therapeutic targets in the quest to find an effective antiobesity treatment.
Liver progenitor cell markers correlate with liver damage and predict short-term mortality in patients with alcoholic hepatitis
Authors: Pau Sancho-Bru, José Altamirano, Daniel Rodrigo-Torres, Mar Coll, Cristina Millán, Juan José Lozano, Rosa Miquel, Vicente Arroyo, Juan Caballería, Pere Ginès, Ramon Bataller
Journal: Hepatology (2012)

Alcoholic hepatitis (AH) is a severe condition developed in patients with underlying alcoholic liver disease. Ductular reaction has been associated with chronic alcohol consumption but there is no information regarding the extent of liver progenitor cell (LPC) proliferation in AH. The aim of this study was to investigate LPC markers in AH and its correlation with disease severity. Fifty-nine patients with clinical and histological diagnosis of AH were included in the study. LPC markers were assessed by real-time polymerase chain reaction (PCR) and immunohistochemistry. Standard logistic regression analysis and classification and regression trees (CART) analysis were used for statistical analysis. A microarray analysis showed an up-regulation of LPC markers in patients with AH. Real-time PCR demonstrated that epithelial cell adhesion molecule (EpCAM), Prominin-1, and Keratin7 were significantly increased in patients with AH compared with normal livers ( P ≤ 0.01), chronic hepatitis C ( P ≤ 0.01), and HCV-induced cirrhosis ( P ≤ 0.01). Immunohistochemistry scores generated for Keratin7 and EpCAM demonstrated a good correlation with gene expression. Keratin7 gene expression correlated with liver failure as assessed by model for endstage liver disease score ( r = 0.41, P = 0.006) and Maddrey's discriminant function ( r = 0.43, P = 0.004). Moreover, Keratin7 (OR1.14, P = 0.004) and Prominin-1 (OR1.14, P = 0.002), but not EpCAM (OR1.16, P = 0.06), were identified as independent predictors of 90-day mortality. CART analysis generated an algorithm based on the combination of Keratin7 and EpCAM gene expression that stratified three groups of patients with high, intermediate, and low short-term mortality (89%, 33%, and 6%, respectively; area under the receiver operating curve 0.73, 95% confidence interval 0.60–0.87). Keratin7 expression provided additional discrimination potential to the age, bilirubin, international normalization ratio, creatinine (ABIC) score. Conclusion: LPC markers correlate positively with severity of liver disease and short-term mortality in AH patients. This study suggests that LPC proliferation may be an important feature of AH pathophysiology.
T cells reactive to an inducible heat shock protein induce disease in toxin-induced interstitial nephritis.
Authors: R A Weiss, M P Madaio, J E Tomaszewski, C J Kelly
Journal: The Journal of Experimental Medicine (1994)

T cells reactive against immunodominant regions of inducible heat shock proteins (HSPs) have been identified in the chronic inflammatory lesions of several experimental autoimmune diseases. Since HSPs are known to be induced by a number of renal tubular epithelial cell toxins associated with chronic interstitial nephritis, we investigated the relevance of HSP expression and T cell reactivity to HSP70 in a model of progressive inflammatory interstitial nephritis. Chronic administration of cadmium chloride (CdCl2) to SJL/J mice induces HSP70 expression in renal tubular cells 4-5 wk before the development of interstitial mononuclear cell infiltrates. CdCl2 also induces HSP70 expression in cultured tubular epithelial cells from SJL/J mice. CD4+, TCR-alpha/beta+ T cell lines specific for an immunodominant HSP peptide are cytotoxic to heat stressed or CdCl2-treated renal tubular cells. Such HSP-reactive T cells mediate an inflammatory interstitial nephritis after adoptive transfer to CdCl2-treated mice at a time when immunoreactive HSP70 is detectable in the kidneys, but before the development of interstitial mononuclear cell infiltrates. T cells isolated from the nephritic kidneys of mice treated with CdCl2 for 13 wk are also cytotoxic to heat shocked or cadmium-treated tubular cells. These kidney-derived T cells additionally induced interstitial nephritis after passive transfer, indicating their pathogenic significance. Our studies strongly support a role for HSP-reactive T cells in CdCl2-induced interstitial nephritis and suggest that the induction of HSPs in the kidney by a multitude of "non-immune" events may initiate or facilitate inflammatory damage by HSP-reactive lymphocytes.
301. Safe and Effective Treatment of Ovarian Cancer Models Using Targeted Adenovirus Vector Delivery and Selective Expression of Tumor Necrosis Factor
Authors: Selva R. Murugesan, Masaki Akiyama, David A. Einfeld, Thomas J. Wickham, C. Richter King
Journal: Molecular Therapy (2006)

Ovarian cancer is the fourth most common cancer among women, and despite advances in therapy most patients still die as a consequence of disease that is disseminated within the peritoneal cavity. Delivery of hTNFa gene to tumors using direct intra-tumoral injection of a non-replicating adenovector is a promising strategy for treatment for a variety of diseases. The relative abundance of the coxsackie and adenovirus receptor (CAR) in the mesothelial lining of the peritoneal space and paucity of CAR in tumors may limit on the use of un-targeted adenovectors administered to the peritoneal cavity. To enhance selectivity of TNFa exposure to the tumor we combined two approaches. We modified adneovector capsids to limit transduction of normal cells. We analyzed the ability of Ad5 based vectors in which the fiber and penton base binding interactions were deleted. To allow tumor uptake we incorporated a RGD-4C motif in the fiber knob (Ad**RGD) to target αvβ3/5 integrins receptors that are highly expressed in tumor and sparsely expressed in the epithelial layer of peritoneum. Ad**RGD vector exhibits effective gene transfer in a variety of ovarian cancer cell lines that we examined in vitro and in vivo. Importantly, the Ad**RGD vector has a capability to target ovarian tumor nodules and avoid infecting the normal mesothelial cells that line the intraperitoneal space of athymic nude mice following intraperitoneal (ip) administration. We have now added an additional level of control by placing the TNFa expression under the control of tumor selective promoters. These promoters were incorporated into the capsid-modified vector to confer the expression of human tumor necrosis factor alpha (hTNFa) therapeutic gene. We compared both constitutive (CMV or RSV) and tumor selective promoters (DF3, E2F or hTERT) for safety and efficacy in human ovarian cancer models. Vector containing capsid targeting combined with the DF3 promoter expression control was shown to reduce tumor burden in the human ovarian cancer models (Caov3 and Igrov1) following ip administration. The DF3 vector was well tolerated with no evidence of body weight changes, and limited exposure to systemic TNFa at the effective dose (1.2e11 pu/20g). Together, our data support a strategy of combining receptor targeting combined with expression control of TNFa as a potential gene delivery mechanism for ovarian cancer treatment.
Impact of Diabetes on Mortality After the First Myocardial Infarction
Authors: Heikki Miettinen, Seppo Lehto, Veikko Salomaa, Markku Mähönen, Matti Niemelä, Steven M Haffner, Kalevi Pyörälä, Jaakko Tuomilehto
Journal: Diabetes Care (1998)

OBJECTIVE To study diabetic and nondiabetic patients with their first myocardial infarction to determine overall 1-year mortality, out-of-hospital mortality, 28-day mortality of hospitalized patients, and 1-year mortality of 28-day survivors. RESEARCH DESIGN AND METHODS This study—based on the FINMONICA Myocardial Infarction Register, a part of the Finnish contribution to the WHO MONICA Project (World Health Organization Multinational Monitoring of Trends and Determinants of Cardiovascular Disease)—covered coronary heart disease (CHD) deaths and acute CHD events occurring during hospitalization among residents of Finland aged 25–64 years in three geographically defined areas. The study population comprised 620 diabetic and 3,445 nondiabetic patients who had their first myocardial infarction during the years 1988–1992. RESULTS The age- and area-adjusted mortality rates and hazard ratios (HRs) for diabetic versus nondiabetic patients (95% CI) were as follows: The 1-year mortality rate was 44.2% in diabetic men and 32.6% in nondiabetic men (HR, 1.38; 1.18−1.61) and 36.9% in diabetic women and 20.2% in nondiabetic women (HR, 1.86; 1.40−2.46); the out-of-hospital mortality rate was 28.3% in diabetic men and 22.4% in nondiabetic men (HR, 1.25; 1.03−1.52) and 10.4% in diabetic women and 11.0% in nondiabetic women (HR, 0.95; 0.58−1.54); the 28-day mortality rate of hospitalized patients was 14.4% in diabetic men and 8.8% in nondiabetic men (HR, 1.58; 1.15−2.18) and 21.7% in diabetic women and 7.8% in nondiabetic women (HR, 2.60; 1.71−3.95); and the 1-year mortality rate of 28-day survivors was 9.6% in diabetic men and 5.0% in nondiabetic men (HR, 1.97; 1.25−3.12) and 10.7% in diabetic women and 2.5% in nondiabetic women (HR, 4.17; 2.05−8.51). CONCLUSIONS The high mortality rate of diabetic patients after their first myocardial infarction and the high proportion of out-of-hospital deaths in this group imply that vigorous primary and secondary preventive measures should become an integral part of their medical care.