tbuckley/cabot-search huggingface dataset:
Additive Protection of the Ischemic Heart Ex Vivo by Combined Treatment With δ-Protein Kinase C Inhibitor and ε-Protein Kinase C Activator
Authors: Koichi Inagaki, Harvey S. Hahn, Gerald W. Dorn, Daria Mochly-Rosen
Journal: Circulation (2003)

Background— Protein kinase C (PKC) plays a major role in cardioprotection from ischemia/reperfusion injury. Using an HIV-1 Tat protein–derived peptide to mediate rapid and efficient transmembrane delivery of peptide regulators of PKC translocation and function, we examined the cardioprotective effect of selective δ-PKC inhibitor (δV1-1) and ε-PKC activator (ψεRACK) peptides for ischemia/reperfusion damage in isolated perfused rat hearts. Furthermore, we examined the protective effects of these PKC isozymes in isolated perfused hearts subjected to ischemia/reperfusion damage using transgenic mice expressing these peptides specifically in their cardiomyocytes. Methods and Results— In isolated perfused rat hearts, administration of δV1-1 but not ψεRACK during reperfusion improved cardiac function and decreased creatine phosphokinase release. In contrast, pretreatment with ψεRACK but not δV1-1, followed by a 10-minute washout before ischemia/reperfusion, also improved cardiac function and decreased creatine phosphokinase release. Furthermore, administration of ψεRACK before ischemia followed by δV1-1 during reperfusion only conferred greater cardioprotective effects than that obtained by each peptide treatment alone. Both the δ-PKC inhibitor and ε-PKC activator conferred cardioprotection against ischemia/reperfusion injury in transgenic mice expressing these peptides in the heart, and coexpression of both peptides conferred greater cardioprotective effects than that obtained by the expression of each peptide alone. Conclusions— δ-PKC inhibitor prevents reperfusion injury, and ε-PKC activator mimics ischemic preconditioning. Furthermore, treatment with both peptides confers additive cardioprotective effects. Therefore, these peptides mediate cardioprotection by regulating ischemia/reperfusion damage at distinct time points.
Increased expression of the lactate dehydrogenase M subunit in myocardial regions with decreased thallium uptake
Authors: L. Lin, L. Kaijser, J. Liska, C. Sylven, A. Holmgren, K. Lindstrom, E. Jansson
Journal: Cardiovascular Research (1993)

Objective: In ischaemic heart disease, the heart muscle is subjected to repeated episodes of regional ischaemia or to a constant underperfusion. The purpose of the present investigation was to study the myocardial metabolic adaptation to this stress. Methods: Eighteen male patients with ischaemic heart disease were studied by biopsies taken from the left ventricular septum during bypass surgery. Citrate synthase, total lactate dehydrogenase and its H and M subunits, coenzyme Q10, and myoglobin were determined in all biopsies. Concentrations of ATP, ADP, and AMP were determined and energy charge calculated in the biopsies from the patients with ischaemic heart disease. Biopsies from the septal region of hearts obtained from brain dead kidney and liver donors were used as reference and preoperative myocardial thallium scintigraphy was performed in the patients with ischaemic heart disease to relate the myocardial biochemical markers to thallium uptake at the biopsy site. Results: Myocardial activities of citrate synthase as well as contents of coenzyme Q10 and myoglobin in patients with ischaemic heart disease were not different from those of the reference group, and no linear relation was found between these three markers on the one hand and thallium uptake on the other. The energy charge was directly related and the M subunit of lactate dehydrogenase inversely related to the thallium uptake. Conclusion: The results suggest an absence of adaptation to ischaemia in terms of increased myocardial oxidative capacity and 02 transport and storage capacity. Furthermore, it is indicated that a stressed energy metabolism with increasing severity of ischaemic heart disease enhances anaerobic metabolism and induces a shift in myocardial lactate dehydrogenase subunit fractions. Cardiovascular Research 1993;27:1300-1305
AN ENCOURAGING CASE OF LOCOMOTOR ATAXIA.
Authors: GUY HINSDALE
Journal: JAMA (1905)

The case of locomotor ataxia which I report is worthy of record, not because of any extraordinary feature of the disease, but on account of the remarkable improvement in the patient in a short space of time. <h3>Patient.</h3> —A man, J. C., aged 42, has been twice under my care. In 1899, when he first came under observation, he was engaged in the office of a large tanning establishment in Cincinnati. <h3>History.</h3> —His mother died of nervous prostration, and his father of apoplexy; he had been married 18 years but had no children, and his wife had had no miscarriages. He had been well and strong until five years before he first came under observation. He used alcohol and tobacco in moderation, and had had gonorrhea but denied syphilis. <h3>Examination.</h3> —The scalp was partly bald. The first symptom was attacks of abdominal pain, with vomiting and occasional diarrhea. These
Factors predicting outcome after unrelated donor stem cell transplantation in primary refractory acute myeloid leukaemia
Authors: C Craddock, M Labopin, S Pillai, J Finke, D Bunjes, H Greinix, G Ehninger, N-K Steckel, A R Zander, R Schwerdtfeger, S Buchholz, H-J Kolb, L Volin, A Fauser, E Polge, C Schmid, M Mohty, V Rocha
Journal: Leukemia (2011)
Endoscopic Tattoo Practice at a District General Hospital
Authors: D. Gavin, A. Sidwell, M. Scott, K. Dowler, J. Anderson, N. Shepherd, M. Lucarotti
Journal: Gut (2011)

<h3>Introduction</h3> Without placing an endoscopic tattoo it may be difficult to accurately relocate the site of pathology after removal (eg, polypectomy). The National Bowel Cancer Screening Program (BCSP) have published guidelines on tattoo practice for suspected malignant polyps.12 We aimed to test the null hypothesis: there is no difference in tattoo practice between BCSP and non-BCSP lower GI endoscopy. <h3>Methods</h3> All reports for lower GI endoscopy performed at our unit over a 3 year period were reviewed. All polyps greater than 10 mm in diameter were identified. Lesions identified clinically and reported as a carcinoma were excluded. Colonoscopies were grouped by indication; either BCSP or non-BCSP. Information was gathered on polypectomy practice, tattoo practice, polyp size and the incidence of a histological diagnosis of polyp cancer. Statistical analysis was performed using χ<sup>2</sup> with Yates correction. <h3>Results</h3> A total of 11 679 endoscopy reports were reviewed. A polyp &gt;10 mm in diameter was identified n 556 procedures, 145 in the BCSP (21.9%) and 411 in the non-BCSP (3.7%)(p&lt;0.0001). In the BCSP group 116 tattoos were placed (80% of procedures) while in the non-BCSP group 126 tattoos were placed (30.66% of procedures)(p&lt;0.0001). Excluding caecal and rectal lesion did not significantly alter the tattoo results (83.45% BCSP, 36.63% non-BCSP (p&lt;0.0001)). Polyp malignancy was diagnosed in 14 cases in the BCSP group (9.66%) and in 44 cases in the non-BCSP group (10.71%) (p=0.843). 10 of 14 polyp cancers were tattooed (71.42%) in the BCSP group. 14 of 44 polyp cancers in the non-BCSP group were tattooed (31.82%) (p=0.02). Polypectomy was performed in 142 (97.93%) cases in the BCSP group and in 316 (76.89%) cases in the non-BCSP group (p&lt;0.0001). <h3>Conclusion</h3> There is a difference in the management of colonic polyps in our unit. Polyps &gt; 10 mm were more likely to be treated at the index endoscopy and the site of the polyp or polypectomy was more likely to be tattooed if the procedure was performed within the BCSP. Current guidelines published by BCSP and JAG for tattooing of colonic polyps are broadly similar with no reference to polyp size. In our hospital BCSP practice seems to be following a separate BSG Polypectomy Guide3, which state that polyps &gt;10 mm should be tattooed, with superior results. This would suggest that BCSP and non-BCSP colonoscopy guidelines should be updated to improve tattoo practice. <h3>Competing interests</h3> None.
Withaferin A Causes FOXO3a- and Bim-Dependent Apoptosis and Inhibits Growth of Human Breast Cancer Cells <i>In vivo</i>
Authors: Silvia D. Stan, Eun-Ryeong Hahm, Renaud Warin, Shivendra V. Singh
Journal: Cancer Research (2008)

Abstract Withaferin A (WA) is derived from the medicinal plant Withania somnifera, which has been safely used for centuries in Indian Ayurvedic medicine for treatment of different ailments. We now show, for the first time, that WA exhibits significant activity against human breast cancer cells in culture and in vivo. The WA treatment decreased viability of MCF-7 (estrogen-responsive) and MDA-MB-231 (estrogen-independent) human breast cancer cells in a concentration-dependent manner. The WA-mediated suppression of breast cancer cell viability correlated with apoptosis induction characterized by DNA condensation, cytoplasmic histone–associated DNA fragmentation, and cleavage of poly-(ADP-ribose)-polymerase. On the other hand, a spontaneously immortalized normal mammary epithelial cell line (MCF-10A) was relatively more resistant to WA-induced apoptosis compared with breast cancer cells. The WA-mediated apoptosis was accompanied by induction of Bim-s and Bim-L in MCF-7 cells and induction of Bim-s and Bim-EL isoforms in MDA-MB-231 cells. The cytoplasmic histone–associated DNA fragmentation resulting from WA exposure was significantly attenuated by knockdown of protein levels of Bim and its transcriptional regulator FOXO3a in both cell lines. Moreover, FOXO3a knockdown conferred marked protection against WA-mediated induction of Bim-s expression. The growth of MDA-MB-231 cells implanted in female nude mice was significantly retarded by 5 weekly i.p. injections of 4 mg WA/kg body weight. The tumors from WA-treated mice exhibited reduced cell proliferation and increased apoptosis compared with tumors from control mice. These results point toward an important role of FOXO3a and Bim in regulation of WA-mediated apoptosis in human breast cancer cells. [Cancer Res 2008;68(18):7661–9]
Fruit‐pollen‐latex cross‐reactivity: implication of profilin (Bet v 2)
Authors: M.L. Díez‐Gómez, S. Quirce, M. Cuevas, C. Sánchez‐Fernández, G. Baz, F.J. Moradiellos, A. Martínez
Journal: Allergy (1999)

An association between allergy to fruits and latex, and between pollen and plant-derived food has been described. The cross-reactive structures responsible for these associations have not yet been completely elucidated.IgE reactivity to the recombinant allergens Bet v 1 and Bet v 2, different pollens, natural latex, papain, and bromelain was investigated in 29 patients with allergy to fruits or vegetables who lived in an area without birch trees.Exactly 79.3% of patients were allergic to grass pollen, and two of them had clinical allergy to latex. Serum IgE reactivity (CAP) to birch pollen was found in 65% of patients, to Bet v 2 in 51.7%, to Bet v 1 in 3.4%, to latex in 58.6%, to bromelain in 51.7%, and to papain in 17.2% of patients. All subjects with positive IgE to Bet v 2 had also reactivity to latex, grass, olive tree, birch, and mugwort pollens. The six patients not allergic to pollen did not show IgE reactivity to latex, Bet v 1, or Bet v 2. A significant correlation was found between CAP to latex with Bet v 2 (r=0.86, P<0.001), with birch (r=0.86, P<0.001), and with ryegrass (r=0.81, P<0.001). Immunoblotting using nine sera with positive CAP to birch pollen showed IgE-binding to a 15-kDa band that was recognized by antiprofilin monoclonal antibody. Bet v 2 CAP could be inhibited up to 52% by ryegrass and up to 23% by mugwort. CAP to latex was almost completely inhibited by ryegrass pollen with sera from five subjects without symptoms due to latex, whereas no inhibition was observed with serum from one patient with allergy to latex.Patients with allergy to plant-derived food and associated pollinosis showed a high frequency of IgE reactivity to Bet v 2, which may cause positive serum IgE determinations to latex and birch pollen due to the presence of cross-reactive epitopes. IgE reactivity to Bet v 2 may serve as an indicator of broad sensitization.
The efficacy of oral treatment with pramiconazole in pityriasis versicolor: a phase II a trial
Authors: J. Faergemann, J. Ausma, L. Vandeplassche, M. Borgers
Journal: British Journal of Dermatology (2007)

Conflicts of interest: This study was supported by Barrier Therapeutics. J.A. and L.V. are full‐time employees of Barrier Therapeutics. M.B. is a member of the scientific advisory board of Barrier Therapeutics. J.F. is clinical investigator; he is not a consultant for Barrier Therapeutics and he has no stocks in the company. Sir, the efficacy of pramiconazole (R126638) has recently been tested in a first series of patients with pityriasis versicolor. This chronic superficial fungal disease is usually located on the upper trunk, neck or upper arms. Under the influence of predisposing factors Malassezia changes in pityriasis versicolor from blastospores into hyphae.1 Pramiconazole is a broad‐spectrum antifungal belonging to the class of triazoles. In vitro and in vivo data have demonstrated activity against several dermatophytes and Malassezia spp.2 3–4 The aim of the present study was to evaluate the effects of a single dose of 200 mg of pramiconazole given orally during three consecutive days in a group of 19 patients with pityriasis versicolor.
Helicobacter pylori augments the acid inhibitory effect of omeprazole on parietal cells and gastric H+/K+-ATPase
Authors: W Beil
Journal: Gut (2001)

<h3>BACKGROUND</h3> In duodenal ulcer patients, intragastric acidity during omeprazole treatment is significantly lower before <i>Helicobacter pylori</i> eradication than after cure. <h3>AIMS</h3> To determine if<i>H pylori</i> enhances the acid inhibitory potency of omeprazole in isolated parietal cells and on H<sup>+</sup>/K<sup>+</sup>-ATPase. <h3>METHODS</h3> Rat parietal cells and pig gastric membrane vesicles enriched in H<sup>+</sup>/K<sup>+</sup>-ATPase activity were incubated with<i>H pylori</i> and the <i>H pylori</i> fatty acid <i>cis</i>9,10-methyleneoctadecanoic acid (MOA), and the inhibitory effects of omeprazole on parietal cell acid production, H<sup>+</sup>/K<sup>+</sup>-ATPase enzyme activity, and ATPase mediated proton transport were assessed. <h3>RESULTS</h3> In isolated parietal cells, <i>H pylori</i> and MOA increased the acid inhibitory potency of omeprazole 1.8 fold.<i>H pylori</i> did not affect the inhibitory potency of omeprazole on H<sup>+</sup>/K<sup>+</sup>-ATPase enzyme activity. In proton transport studies,<i> H pylori</i> (intact bacteria and sonicate) and MOA accelerated the onset of the inhibitory effect of omeprazole and enhanced the proton dissipation rate in response to omeprazole. <i>H pylori</i> itself increased proton permeability at the vesicle membrane. <h3>CONCLUSION</h3> Our results show that <i>H pylori</i> augments the acid inhibitory potency of omeprazole in parietal cells and enhances omeprazole induced proton efflux rate from gastric membrane vesicles. We suggest that omeprazole unmasks the permanent effect of<i>H pylori</i> on proton permeability at the apical parietal cell membrane, which is counteracted in the absence of a proton pump inhibitor by a reserve H<sup>+</sup>/K<sup>+</sup>-ATPase capacity.
Care of mentally ill people in the community
Authors: T Burns, K Goddard, R Bale
Journal: BMJ (1994)

about 0 4% of total per capita consumption of fresh, bought vegetables.3The maximum intake-achievable only if the dish was consumed raw daily-would contribute only 15% of the plasma cotinine concentration due to passive smoking by a typical non-smoker and 1-5% of the plasma cotinine concentration for the most exposed non-smokers (table).However, a typical non-smoker's actual average dietary nicotine intake produces only 0 7% of a typical non-smoker's cotinine dose from passive smoking.Dietary nicotine intake does not confound cotinine in body fluids as an index of passive smoking.
RELATION OF ANTIBODY AND ANTIGEN TO SERUM DISEASE SUSCEPTIBILITY
Authors: George M. Mackenzie, W. H. Leake
Journal: The Journal of Experimental Medicine (1921)

1. Studies on nineteen patients to whom foreign serum had been administered for therapeutic purposes are reported. Analysis of the results obtained by following the precipitin and precipitinogen in the circulation and comparing these factors with the time of appearance, intensity, and duration of the symptoms shows that the nineteen patients fall into three groups. 2. The first group includes eleven patients. These were good precipitin formers, they had severe serum disease, and the precipitinogen disappeared from the circulation near the time that the symptoms subsided. 3. The second group includes four patients who had little or no serum disease, in whose circulation little or no precipitin was demonstrable, and in whom the precipitinogen persisted in the circulation as long as the patients could be kept under observation-from 52 to 67 days. 4. The remaining four patients form a more or less distinctly intermediate group. 5. The results lend further support to the conception of serum disease as an antigen-antibody reaction. 6. The possibility that our results indicate a factor which may be important in the mechanism of natural immunity is discussed.
Points from Letters: Which arm squeezes the bag?
Authors: M Beckett
Journal: BMJ (1977)

<h3>Abstract</h3> MicroRNA dysregulation is a common feature of cancer and due to the promiscuity of microRNA binding this can result in a wide array of genes whose expression is altered. miR-106b is an oncomiR overexpressed in cholangiocarcinoma and its upregulation in this and other cancers often leads to repression of anti-tumorigenic targets. The goal of this study was to identify the miR-106b-regulated gene landscape in cholangiocarcinoma cells using a genome-wide, unbiased mRNA analysis. Through RNA-Seq we found 112 mRNAs significantly repressed by miR-106b. The majority of these genes contain the specific miR-106b seed-binding site. We have validated 11 genes from this set at the mRNA level and demonstrated regulation by miR-106b of five proteins. Combined analysis of our miR-106b-regulated mRNA data set plus published reports indicate that miR-106b binding is anchored by G:C pairing in and near the seed. Novel targets Kruppel-like factor 2 (KLF2) and KLF6 were verified both at the mRNA and at the protein level. Further investigation showed regulation of four other KLF family members by miR-106b. We have discovered coordinated repression of several members of the KLF family by miR-106b that may play a role in cholangiocarcinoma tumor biology. <h3>List of abbreviations</h3> MTT: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide DAPI: 4’,6-diamidine-2’-phenylindole dihydrochloride CLASH: Crosslinking, ligation, and sequencing of hybrids DR5: Death receptor-5 DMEM: Dulbecco’s Modified Eagle’s Medium FDR: False discovery rate FBS: Fetal bovine serum KLF: Kruppel-like factor LNA: Locked-nucleic acid qRT-PCR: Quantitative reverse-transcription PCR SDS-PAGE: Sodium dodecylsulfate-polyacrylamide gel electrophoresis UTR: Untranslated region
Bone-Marrow Transplantation in a Patient with Sickle-Cell Anemia
Authors: F. Leonard Johnson, A. Thomas Look, Jon Gockerman, Mary R. Ruggiero, Luciano Dalla-Pozza, Frederic T. Billings
Journal: New England Journal of Medicine (1984)

SICKLE-CELL anemia affects 1 in 600 of the U.S. black population and accounts for 80,000 deaths annually throughout the world.1 , 2 Current therapy is designed to prevent sickle-cell crises, but supportive care remains the only treatment available once they occur. Attempts to alter the expression of hemoglobin genes in β-thalassemia and sickle-cell anemia with the use of azacytidine have produced only transient effects.3 This report describes the conversion of sickle-cell anemia to sickle-cell trait by marrow transplantation (done for treatment of leukemia) in a child with both sickle-cell anemia and acute myeloblastic leukemia. It raises the possibility of using marrow transplantation . . .
Bone Disease in End-Stage Renal Failure
Authors: Marvin L. Daves
Journal: JAMA (1986)

<h3>To the Editor.—</h3> Congratulations on the CONTEMPO '85 issue. This annual offering of a year's update on medical progress is a luxury. I write, however, to differ with Dr Glassock's conclusion, in the nephrology section, that aluminum is a primary factor in the bone complications of end-stage renal disease. The knowledge that phosphate depletion alone<sup>2,3</sup>may cause rickets has been with us long enough to have been forgotten. Ingestion of aluminum hydroxide causes phosphate depletion.<sup>4</sup>Thus, aluminum may mediate rickets (and osteomalacia) by causing phosphate depletion, rather than by poisoning the osteocyte. Reduction in bone formation caused by aluminum toxicity, as claimed by Dr Glassock, would have just the opposite result to what is known to happen when elemental phosphorus, lead, bismuth,<sup>5</sup>or fluorine<sup>6</sup>is the toxin. In these poisonings it is the osteoclastic activity of the osteocyte, not its osteoblastic activity, that is inhibited. At
TCT-313 Characterization of Lesion Shape and Hemodynamic Forces Acting on Coronary Artery Atherosclerotic Plaques using Computational Flow Dynamics and Computed Tomography Data
Authors: Gilwoo Choi, Hyun-Jin Kim, Jun-Bean Park, Joo Myung Lee, Sethuraman Sankaran, Hiromasa Otake, Joon-Hyung Doh, Eun-Seok Shin, Charles A. Taylor, Bon-Kwon Koo
Journal: Journal of the American College of Cardiology (2014)