tbuckley/cabot-search huggingface dataset:
Reversible Renal Failure Associated with Angiotensin-Converting Enzyme Inhibitors in Polycystic Kidney Disease
Authors: Arlene B. Chapman, Patricia A. Gabow, Robert W. Schrier
Journal: Annals of Internal Medicine (1991)

The renin-angiotensin-aldosterone system appears to play an important initiating role in the pathogenesis of hypertension in patients with autosomal-dominant polycystic kidney disease (ADPKD). Therefore, angiotensin-converting enzyme (ACE) inhibitors would appear to be appropriate therapy for hypertension in such patients. However, because ADPKD is a bilateral disorder, ACE-inhibitor therapy may worsen renal function, as occurs in patients with bilateral renal artery stenosis. We describe eight episodes of reversible acute renal deterioration in five patients with ADPKD, massive renal involvement, and chronic renal insufficiency. In all cases, ACE-inhibitor therapy either predisposed the patient to or precipitated the acute event. Two of the patients who had acute renal failure while receiving ACE-inhibitor therapy experienced a recurrence when rechallenged with such therapy. Furthermore, patients receiving combined therapy with an ACE inhibitor and a diuretic and patients who experience a cyst hemorrhage while receiving ACE inhibitor therapy are also at risk for reversible renal dysfunction. Caution is therefore recommended in using ACE inhibitors to treat hypertension in patients with ADPKD who are at high risk because of compromised renal function and massive cystic involvement.
COMPARISON OF THE EFFICACY AND SAFETY OF VARIOUS DIURETIC REGIMENS USED TO OVERCOME DIURETIC RESISTANCE IN ACUTE HEART FAILURE
Authors: Tien M. Ng, Erica Konopka, Alifiya F. Hyderi, Shenche Hshieh, Yuki Tsuji, Brian J. Kim, Song Y. Han, Duc H. Phan, Aaron I. Jeng, Mimi Lou, Uri Elkayam
Journal: Journal of the American College of Cardiology (2011)
Occurrence of a Cardiac Anomaly in One of Symmetrical Conjoined Twins
Authors: Dorothy E. Klein, Sidney Friedman
Journal: New England Journal of Medicine (1964)

THE occurrence of a congenital cardiac anomaly in 1 of monozygotic twins has been reported on numerous occasions.1 2 3 4 5 6 7 Although a wide variety of criteria have been used to determine the monozygosity of such twinships considerable doubt remains in some cases concerning their monovular origin. Gross asymmetries8 , 9 have also been described among conjoined twinships, 1 member being markedly different in size and development from the other. In equal or symmetrical conjoined twins, however, the presence of a cardiac anomaly in only 1 member of the twinship has been reported on only 1 previous occasion.7 The purpose of this report is to . . .
PERINEAL OPERATION FOR PERFORATIVE APPENDICITIS WITH ABSCESS IN THE CUL-DE-SAC.
Authors: E. M. SUTTON
Journal: JAMA (1898)

The literature on the surgical treatment of appendicitis is replete, and it is the consensus of opinion that, for ordinary cases of perforative appendicitis with abscess formation the incision over McBurney's point, or the extra-peritoneal operation from the side, reaching the abscess without entering the peritoneal cavity, with simple evacuation and drainage, only removing the appendix when possible to do so without causing general infection, are the best methods of procedure. In looking over the reports of cases it has not come to my knowledge that an operation reaching the appendix abscess, when located back of the bladder, below the small intestine, and in front of the rectum, has been operated on from the perineum. The difficulties of draining these cases through the abdominal incision and the avoidance of soiling the peritoneum are barriers which render the operation useless and fatal when attempted above, except when the operation is made
Regression of Coronary Atherosclerosis During Treatment of Familial Hypercholesterolemia With Combined Drug Regimens
Authors: John P. Kane
Journal: JAMA (1990)

We conducted a randomized, controlled trial in 72 patients with heterozygous familial hypercholesterolemia to test whether reducing plasma low-density lipoprotein levels by diet and combined drug regimens can induce regression of coronary lesions. Four hundred fifty-seven lesions were measured before and after a 26-month interval by computer-based quantitative angiography. The primary outcome variable was within-patient mean change in percent area stenosis. Mean low-density lipoprotein cholesterol levels decreased from 7.32 +/- 1.5 to 4.45 +/- 1.6 mmol/L. The mean change in percent area stenosis among controls was +0.80, indicating progression, while the mean change for the treatment group was -1.53, indicating regression (P = .039 by two-tailed t test for the difference between groups). Regression among women, analyzed separately, was also significant. The change in percent area stenosis was correlated with low-density lipoprotein levels on trial. We conclude that reduction of low-density lipoprotein cholesterol levels can induce regression of atherosclerotic lesions of the coronary arteries in patients with familial hypercholesterolemia. The anticipation of benefit from treatment applies to women and men alike.
GENDER AND RACIAL/ETHNIC DIFFERENCES IN SURVIVAL AFTER CARDIOPULMONARY RESUSCITATION FOR IN-HOSPITAL CARDIAC ARREST
Authors: Dhaval Kolte, Sahil Khera, Wilbert Aronow, Marjan Mujib, Chandrasekar Palaniswamy, Diwakar Jain, Sachin Sule, Sei Iwai, Paul Eugenio, Seth Lessner, Ali Ahmed, Gregg Fonarow, Julio Panza
Journal: Journal of the American College of Cardiology (2014)
Use of Exhaled Nitric Oxide Measurement to Identify a Reactive, at-Risk Phenotype among Patients with Asthma
Authors: Raed A. Dweik, Ronald L. Sorkness, Sally Wenzel, Jeffrey Hammel, Douglas Curran-Everett, Suzy A. A. Comhair, Eugene Bleecker, William Busse, William J. Calhoun, Mario Castro, Kian Fan Chung, Elliot Israel, Nizar Jarjour, Wendy Moore, Stephen Peters, Gerald Teague, Benjamin Gaston, Serpil C. Erzurum
Journal: American Journal of Respiratory and Critical Care Medicine (2010)

Rationale: Exhaled nitric oxide (FeNO) is a biomarker of airway inflammation in mild to moderate asthma. However, whether FeNO levels are informative regarding airway inflammation in patients with severe asthma, who are refractory to conventional treatment, is unknown. Here, we hypothesized that classification of severe asthma based on airway inflammation as defined by FeNO levels would identify a more reactive, at-risk asthma phenotype.Methods: FeNO and major features of asthma, including airway inflammation, airflow limitation, hyperinflation, hyperresponsiveness, and atopy, were determined in 446 individuals with various degrees of asthma severity (175 severe, 271 nonsevere) and 49 healthy subjects enrolled in the Severe Asthma Research Program.Measurements and Main Results: FeNO levels were similar among patients with severe and nonsevere asthma. The proportion of individuals with high FeNO levels (>35 ppb) was the same (40%) among groups despite greater corticosteroid therapy in severe asthma. All patients with asthma and high FeNO had more airway reactivity (maximal reversal in response to bronchodilator administration and by methacholine challenge), more evidence of allergic airway inflammation (sputum eosinophils), more evidence of atopy (positive skin tests, higher serum IgE and blood eosinophils), and more hyperinflation, but decreased awareness of their symptoms. High FeNO identified those patients with severe asthma characterized by the greatest airflow obstruction and hyperinflation and most frequent use of emergency care.Conclusions: Grouping of asthma by FeNO provides an independent classification of asthma severity, and among patients with severe asthma identifies the most reactive and worrisome asthma phenotype.
Disorganisation of intermediate filament structure in alcoholic and other liver diseases.
Authors: C Barbatis, J Morton, J C Woods, J Burns, J Bradley, J O McGee
Journal: Gut (1986)

The distribution of Mallory body antigens JMB1 and 2 was examined in 82 human fresh diagnostic needle liver biopsies and 28 necropsies by the indirect immunoperoxidase technique using 2 monoclonal antibodies (anti-JMB1 and 2) against Mallory bodies. The JMB1 antigen was detectable in bile duct epithelium and in hepatocytes of histologically normal livers. It was also found in all Mallory bodies in various hepatic disorders. This antigen was markedly increased in the cytoplasm of all liver cells in acute alcoholic hepatitis superimposed on alcoholic cirrhosis, in most cases of acute alcoholic hepatitis, and in severe fatty infiltration of the liver with or without Mallory body formation. Mallory bodies contained this antigen but the cytoplasm of Mallory body containing cells lacked JMB1. In normal liver the JMB2 antigen was localised on the cytoplasmic intermediate filament network of hepatocytes and bile duct epithelium; and almost all Mallory bodies also contained this antigen but the adjacent cytoplasm of these cells lacked JMB2. In severe alcoholic liver disease these antigens could not be detected in large zones of hepatocytes even when these hepatocytes did not contain Mallory bodies. It is evident that there is disorganisation of intermediate filament constituents in severe alcoholic liver disease.
Clinical Value of Ambulatory Blood Pressure
Authors: Giuseppe Mancia, Paolo Verdecchia
Journal: Circulation Research (2015)

This article reviews the clinical value of ambulatory blood pressure (BP) vis-à-vis the traditional BP measurements taken in the physician’s office or in the hospital. Mention is initially made that longitudinal studies conducted in the general population or in hypertensive cohorts have shown that ambulatory BP provides a more accurate prediction of outcome than office BP. Namely, that (1) the risk of cardiovascular events increases in a less steep fashion with office than with 24-hour mean BP, (2) the 24-hour BP-dependent prediction is maintained after adjustment for office BP values, and (3) among individuals with normal office BP, those with increased ambulatory BP (masked hypertension) have an increased prevalence of organ damage, a more frequent unfavorable metabolic profile and a higher risk of new onset sustained hypertension, diabetes mellitus, and cardiovascular events than those with normal ambulatory BP. It is further mentioned, however, that more recently similar observations have been made for individuals with high office but normal ambulatory BP (white coat hypertension) suggesting a complementary role of out-of-office and office BP values in the determination of patients’ prognosis. The evidence in favor of an independent prognostic value also of some within 24-hour BP phenomena (night BP reduction or absolute values, short-term BP variations, and morning BP surge) is then critically appraised for its elements of strength and weakness. Finally, whether the clinical advantages of ambulatory BP make this approach necessary for all patients with hypertension is discussed. The conclusion is that this is at present still premature because crucial evidence pro or against routine use of this approach in untreated and treated hypertensives is not yet available. It will be crucial for future studies to determine whether, compared with a treatment guided by office BP, a treatment tailored on ambulatory BP allows to improve prevention or regression of organ damage as well as protection from major cardiovascular complications to a degree that justifies the complexity and cost of the procedure.
The potentiation of warfarin anticoagulation by amiodarone.
Authors: A Hamer, T Peter, W J Mandel, M M Scheinman, D Weiss
Journal: Circulation (1982)

The potentiation of the anticoagulant effect of sodium warfarin by amiodarone is reported in 10 patients. Amiodarone appears to augment the depression of vitamin K-dependent coagulation factors caused by warfarin by an uncertain mechanism, and may lead to serious bleeding. The maintenance dose of warfarin should be halved when amiodarone and warfarin are prescribed together.
Critical Tumor Suppressor Function Mediated by Epithelial <i>Mig-6</i> in Endometrial Cancer
Authors: Tae Hoon Kim, Dong-Kee Lee, Sung-Nam Cho, Grant D. Orvis, Richard R. Behringer, John P. Lydon, Bon Jeong Ku, Adrienne S. McCampbell, Russell R. Broaddus, Jae-Wook Jeong
Journal: Cancer Research (2013)

Endometrial cancer is preceded by endometrial hyperplasia, unopposed estrogen exposure, and genetic alterations, but the precise causes of endometrial cancer remain uncertain. Mig-6, mainly known as a negative regulator of the EGF receptor, is an important mediator of progesterone signaling in the uterus, where it mediates tumor suppression by modulating endometrial stromal-epithelial communications. In this study, we investigated the function of Mig-6 in the uterine epithelium using a tissue-specific gene knockout strategy, in which floxed Mig-6 (Mig-6(f/f)) mice were crossed to Wnt7a-Cre mice (Wnt7a(cre+)Mig-6(f/f)). Wnt7a(cre+)Mig-6(f/f) mice developed endometrial hyperplasia and estrogen-dependent endometrial cancer, exhibiting increased proliferation in epithelial cells as well as apoptosis in subepithelial stromal cells. We documented increased expression of NOTCH1 and BIRC3 in epithelial cells of Wnt7a(cre+)Mig-6(f/f) mice and decreased expression of the progesterone receptor (PR) in stromal cells. Progesterone therapy controls endometrial growth and prevents endometrial cancer, but the effectiveness of progesterone as a treatment for women with endometrial cancer is less clear. We noted that the hyperplasic phenotype of Wnt7a(cre+)Mig-6(f/f) mice was prevented by progesterone treatment, whereas this treatment had no effect in PR(cre/+)Mig-6(f/f) mice where Mig-6 was deleted in both the epithelial and stromal compartments of the uterus. In contrast, activation of progesterone signaling in the stroma regulated proliferation and apoptosis in the epithelium via suppression of ERα signaling. In summary, our results establish that epithelial Mig-6 functions as a critical tumor suppressor that mediates the ability of progesterone to prevent the development of endometrial cancer.
Mesenchymal stem cells from the oral cavity and their potential value in tissue engineering
Authors: Antonio R. Sanz, Flavio S. Carrión, Alejandra P. Chaparro
Journal: Periodontology 2000 (2014)

Abstract Periodontal disease is one of the most common conditions affecting humans, and current treatment strategies, which focus on the removal and long‐term control of dental plaque, are generally successful in eliminating active disease and promoting tissue repair. However, regeneration of the supporting structures of the tooth remains an elusive goal and a challenge. The formation of new bone and cementum with supportive periodontal ligament is the ultimate objective, but current regeneration therapies are incapable of achieving this in a predictable way. The regeneration of periodontal tissue requires a combination of fundamental events, such as appropriate level and sequencing of regulatory signals, the presence of progenitor cells, an extracellular matrix or carrier and an adequate blood supply. Based on tissue‐engineering concepts, the regeneration process may be modulated by manipulating the signaling pathways of regulatory molecules, the extracellular matrix or scaffold, or the cellular components. The identification of mesenchymal stem cells from bone marrow started a new era in regenerative medicine. Tissue engineering using mesenchymal stem cells became a therapeutic option with several advantages, including high‐quality regeneration of damaged tissues without the formation of fibrous tissue, minimal donor‐site morbidity compared with autografts and a low risk of autoimmune rejection and disease transmission. The aim of this review was to describe the main sources of mesenchymal stem cells from tissues in the oral cavity and the potential of these cells in regenerative therapy. Special attention is paid to gingival tissue‐derived mesenchymal stem cells because they represent the most accessible source of stem cells in the human mouth.
Sport and Medicine — The New Epidemiology — In Praise of Tobacco
Authors: John Lister
Journal: New England Journal of Medicine (1954)

IT was a proud day for Britain and for the medical profession when Roger Bannister accomplished at Oxford what a whole world of milers have recently been bracing themselves to achieve first — the fourminute mile. As a physiologist and a medical student Bannister has a clear insight into the medical aspects of violent physical exertion. It is now generally agreed that strenuous exertion has no immediate ill effect on the healthy body, but it is more difficult to assess the delayed effects of exercises. Increased heart size is commonly found in men taking part in sports that entail . . .
A piece of my mind. Beginnings
Authors: C. Wolf-Gould
Journal: JAMA (1995)

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SUSTAINED RESTORATION OF LV FUNCTION IN A PORCINE ISCHEMIA-REPERFUSION INJURY MODEL USING HUMAN PLACENTAL MESENCHYMAL STEM CELLS AND MANGANESE-ENHANCED MRI
Authors: Rajesh Dash, Paul Kim, Yuka Matsuura, Fumiaki Ikeno, Jennifer Lyons, Xiaohu Ge, Scott Metzler, Ngan Huang, Patricia Nguyen, Joseph C. Wu, John Cooke, Pilar Luiz-Rozano, Robert Robbins, Michael McConnell, Alan Yeung, Phillip Harnish, Phillip Yang
Journal: Journal of the American College of Cardiology (2013)
Determination of spatial and temporal colonization of enteropathogenic<i>E. coli</i>and enterohemorrhagic<i>E. coli</i>in mice using bioluminescent in vivo imaging
Authors: Ki-Jong Rhee, Hao Cheng, Antoneicka Harris, Cara Morin, James B. Kaper, Gail Hecht
Journal: Gut Microbes (2011)

Infectious diarrhea is a major contributor of child morbidity and mortality in developing nations. Murine models to study the pathogenesis of infectious diarrhea caused by organisms such as enteropathogenic E. coli (EPEC) and enterohemorrhagic E. coli (EHEC) are not fully characterized. More emphasis has been placed on infection of mice with the murine specific pathogen Citrobacter rodentium. While these three organisms are genetically related they are not identical. Our goal was to better characterize the murine model of EPEC and EHEC infection by using bioluminescent bacteria to determine temporal and spatial colonization of these two human pathogens. EPEC and EHEC were transformed with a bacterial luciferase expression plasmid containing the constitutive OmpC promoter. C57BL/6 mice were orally inoculated with bioluminescent EPEC or EHEC and bacterial localization in the intestine was monitored ex vivo and in vivo by IVIS. At 3 days after infection, EPEC, EHEC and Citrobacter rodentium were all localized in the cecum and colon. EPEC colonization peaked at day 2-3 and was undetectable by day 7. The bioluminescent EPEC adheres to the cecum and colon of the mouse intestine. However, when EPEC infected mice were administered xylazine/ketamine for in vivo live imaging, the EPEC persisted at high densities for up to 31 days. This is the first report of a bioluminescent imaging of luciferase expressing EPEC in a mouse model.
A role of<i>FCER1A</i>and<i>FCER2</i>polymorphisms in IgE regulation
Authors: V. Sharma, S. Michel, V. Gaertner, A. Franke, C. Vogelberg, A. von Berg, A. Bufe, A. Heinzmann, O. Laub, E. Rietschel, B. Simma, T. Frischer, J. Genuneit, D. P. Potaczek, M. Kabesch
Journal: Allergy (2013)

Background Both FCER2 and FCER1A encode subunits of IgE receptors. Variants in FCER1A were previously identified as major determinants of IgE levels in genome-wide association studies. Methods Here we investigated in detail whether FCER2 polymorphisms affect IgE levels alone and/or by interaction with FCER1A polymorphisms. To cover the genetic information of FCER2, 21 single-nucleotide polymorphisms (SNPs) were genotyped by Illumina HumanHap300 BeadChip (5 SNPs) and the matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS; 14 SNPs) in at least 1303 Caucasian children (651 asthmatics) (ISAAC II/ MAGICS population); genotypes of two SNPs were imputed. Results SNP rs3760687 showed the most consistent effect on total serum IgE levels (b [SE] = −0.38 [0.16]; P = 0.016), while FCER2 polymorphisms in general were predominantly associated with mildly-to-moderately increased IgE levels (50th and 66th percentiles). Gene-by-gene interaction analysis suggests that FCER2 polymorphism rs3760687 influences IgE levels mainly in individuals not homozygous for the risk allele of FCER1A polymorphism rs2427837, which belongs to the major IgE-determining tagging bin in the population. Conclusion FCER2 polymorphism rs3760687 affects moderately elevated total serum IgE levels, especially in the absence of homozygosity for the risk allele of FCER1A SNP rs2427837.
Words and music
Authors: J. O. Drife
Journal: BMJ (1997)

As a senior house officer I performed with youthful colleagues for six nights on the Edinburgh Festival Fringe. According to a personal view that I wrote in 1974, it was an exhilarating but stressful experience and “one that we are keen to avoid repeating for quite some time.” Twenty three years on, we are preparing to try again.

Our first revue, though scrupulously non-medical, seemed to set a trend, and junior doctors became a familiar sight on the Fringe. The urge to perform, however, dies at registrar level. Indeed, for most doctors it ends much earlier. All candidates for medical …
THE BACTERIAL INDUCTION OF HOMOGRAFT SENSITIVITY
Authors: Felix T. Rapaport, A. S. Markowitz, Robert T. McCluskey
Journal: The Journal of Experimental Medicine (1969)

Immunization of rabbits with Group A Type 12 streptococcal cell membranes has elicited serum antibodies which have the ability to cause rapid rejection of skin allografts in guinea pigs. Intradermal injection of such antisera has resulted in skin reactions characterized by prominent polymorphonuclear leukocyte infiltrates, similar to those noted in the Arthus reaction. The combined use of membrane antisera and epinephrine has resulted in hemorrhagic necrosis of the skin of guinea pigs. The ability of membrane antisera to exert these effects appears to be dependent upon the presence in the host tissues of antigen(s) shared by or cross-reacting with streptococcal membrane antigens. Such cross-reacting antigens may have a group distribution in the outbred guinea pig population. The results highlight the potential biological importance of antigens present in the Group A streptococcal membrane in the induction of altered tissue reactivity in the mammalian host.