tbuckley/cabot-search huggingface dataset:
Corrigendum to “Peginterferon alfa-2b plus ribavirin for treatment of chronic hepatitis C in previously untreated patients infected with HCV genotypes 2 or 3” [J Hepatol 40 (2004) 939–999]
Authors: Stefan Zeuzem, Rolf Hultcrantz, Marc Bourliere, Tobias Goeser, Patrick Marcellin, Jose Sanchez-Tapias, Christoph Sarrazin, Joann Harvey, Clifford Brass, Janice Albrecht
Journal: Journal of Hepatology (2005)
Final Gifts: Understanding the Special Awareness, Needs, and Communications of the Dying
Authors: M. Eletta Morse
Journal: JAMA (1992)

InFinal Giftshospice nurses Callanan and Kelley have written  clear and eloquent guidebook  everyone who has been or will ever be close to someone who is dying—for families and friends, for health-care workers, for dying people themselves. In simple nontechnical language they tell us how to help another person approach dying and death and help us to understand the social, spiritual, and emotional needs of the dying person.  The early chapters provide the reader  brief review of the hospice philosophy of care and of Elizabeth Kubler-Ross' work on the stages of dying. These together provide the foundation for the authors' recommendations for care and for their theory of  death  developed in this book. Drawing on many years of practice as hospice nurses, Callanan and Kelley define the state of nearing death awareness as a special awareness of people, places and things that dying people
Potassium Chloride Treatment in Thallotoxicosis
Authors: JOHN P. PAPP
Journal: Annals of Internal Medicine (1969)

A 64-year-old man was treated for thallotoxicosis with oral potassium chloride while on a known normal salt and potassium diet. An increase in restlessness, agitation, and confusion was noted to occur concomitantly with a two- to threefold increase in thalliuresis. Marked clinical improvement occurred after 1 week of treatment. The various modes of treatment are reviewed. It is postulated that potassium chloride used in conjunction with dithiocarb, or dithizon, or both, may be the treatment of choice for thallotoxicosis.
Cerebroventricular calcitonin gene-related peptide inhibits rat duodenal bicarbonate secretion by release of norepinephrine and vasopressin.
Authors: H J Lenz, M R Brown
Journal: Journal of Clinical Investigation (1990)

Proximal duodenal bicarbonate secretion is an important factor in humans and animals protecting the mucosa against acid-peptic damage. This study examined the mechanisms responsible for the central nervous system regulation of duodenal bicarbonate secretion by calcitonin gene-related peptide (CGRP) in unrestrained rats. Cerebroventricular administration of rat CGRP significantly inhibited basal duodenal bicarbonate secretion as well as the stimulatory effects of vasoactive intestinal peptide, neurotensin, a luminal PGE1 analogue, misoprostol, and hydrochloric acid. The inhibitory effects of cerebroventricular CGRP were abolished by ganglionic blockade with chlorisondamine, significantly attenuated by noradrenergic blockade with bretylium, and enhanced by vagotomy. Inhibition of duodenal bicarbonate secretion induced by CGRP coincided with significant increases in plasma norepinephrine (NE) and vasopressin concentrations. The alpha adrenergic receptor antagonist, phentolamine, and the vasopressin V1 receptor antagonist, (1-deaminopenicillamine, 2-[O-methyl]Tyr, 8-Arg)-vasopressin, given intravenously reversed the central inhibitory effect of CGRP by approximately 50% each. Pretreatment of the animals with both phentolamine and the vasopressin antagonist completely abolished the central inhibitory effect of CGRP. Peripheral vasopressin and NE significantly decreased duodenal bicarbonate secretion, and their inhibitory effects were additive and prevented by phentolamine and the vasopressin antagonist, respectively. We conclude that cerebroventricular CGRP inhibits rat duodenal bicarbonate secretion by activation of sympathetic efferents and subsequent release of NE and vasopressin that act on alpha adrenergic and vasopressin receptors, respectively.
Prevalence and characteristics of disporportionate ventricular septal thickening in infants with congenital heart disease.
Authors: B J Maron, J E Edwards, J H Moller, S E Epstein
Journal: Circulation (1979)

Necropsy studies were performed in 125 infants, 2 years old or less, with a variety of congenital heart malformations. Disproportionate ventricular septal thickening (septal-to-left ventricular free wall thickness ratio greater than or equal to 1.3) was present in 31 (25%) of the 125 patients. In the majority of patients, an abnormal septal-to-free wall ratio did not appear to be a manifestation of genetically transmitted hypertrophic cardiomyopathy, since: 1) marked disorganization of septal myocardium (involving greater than or equal to 5% of the tissue section) was present in only five of the 31 patients with disproportionate septal thickening; and 2) echocardiographic studies in first degree relatives of four other patients with disproportionate septal thickening and normal septal architecture did not show asymmetric septal hypertrophy. The relatively high prevalence of septal-to-free wall ratios of 1.3 or greater in this population of infants with congenital heart disease appeared to be due in part to minor differerences in ventricular wall thicknesses (in patients with relatively thin absolute wall thicknesses) which may produce particularly large deviations from unity in septal-to-free wall ratio. Hence, 1) nongenetically transmitted disproportionate septal thickening is relatively common in infants with congenital heart diseases studied at necropsy: and 2) a septal-to-free wall ratio of greater than or equal to 1.3 cannot be used as the sole criterion for identifying associated hypertrophic cardiomyopathy in infants with other congenital heart diseases, particularly if marked absolute septal thickening is absent.
Prediction of Axillary Lymph Node Status in Breast Cancer Patients by Use of Prognostic Indicators
Authors: P. M. Ravdin, M. De Laurentiis, T. Vendely, G. M. Clark
Journal: JNCI Journal of the National Cancer Institute (1994)

Background: If axillary lymph node status of breast cancer patients could be accurately predicted from basic clinical information and from characteristics of their primary tumors, then many patients could be spared axillary lymph node dissection. Tumor size alone does not allow the identification of groups with very low or high risk of being axillary node positive. Purpose: Our goal was to investigate the possibility of using prognostic indicators to predict axillary node status of patients with primary breast cancer. Methods: Data from 26 683 patients from the National Breast Cancer Tissue Resource were used in this study. Patients in this dataset were randomly assigned to a training set (patient information used to construct predictive models) or a validation set (patient information used to prospectively evaluate predictive models). The records of a total of 11 964 case patients that had complete prognostic factors and pathologic data were analyzed: 5963 patients in the training set and 6001 patients in the validation set. All of the patients studied had tumors 5 cm or less in size and at least 15 axillary lymph nodes that had been examined. Data used for construction of the predictive models were available for all patients and included tumor size, number of nodes positive, patient age, quantitative estrogen receptor levels, quantitative progesterone receptor (PgR) levels, DNA flow cytometry-derived ploidy, and S-phase fraction. Logistic regression models were used to predict nodal status. Results: Multivariate predictive models were produced that used tumor size, patient age, S phase, and PgR as independent predictors. These models allowed iden-tification of patient risks of being node positive ranging from 6%–79% and as having 10 or more positive nodes ranging from less than 1% to slightly more than 30%. Conclusion: Addition of prognostic indicator information to tumor size can refine estimates of whether a patient is likely to be node positive. However, no patient subsets could be identified as having greater than 95% chance of being node negative or node positive. Implications: These predictive models cannot alleviate the necessity of axillary node dissection for staging of breast cancer patients in situations in which nodal status would affect therapeutic decisions. Subsets of patients could be identified who had a less than 5% chance of having 10 or more positive nodes. Thus, some patients could be spared axillary dissection if it was being performed solely to identify patients with this high-risk feature. [J Natl Cancer Inst 86:1771–1775, 1994]
Sleep Duration, Melatonin, and Breast Cancer: Compliment and Complement
Authors: Thomas C. Erren
Journal: Cancer Research (2006)

To the Editor: 

In an interesting study, Verkasalo et al. ( [1][1]) found some support for lower breast cancer risks in long sleepers in Finland. The authors appropriately embedded their discussion in the existing literature, insofar as they point to prior studies into possible links between long
Requirement for increased IL-10 in the development of B-1 lymphoproliferative disease in a murine model of CLL.
Authors: S Ramachandra, R A Metcalf, T Fredrickson, G E Marti, E Raveche
Journal: Journal of Clinical Investigation (1996)

Malignant B-1 cells derived from NZB mice, a murine model of spontaneous autoimmunity and B cell lymphoproliferative disease, produce significantly higher levels of IL-10 mRNA than normal B-1 or B cells. IL-10 may act as an autocrine growth factor for the expansion of malignant B-1 cells. In order to determine if elevated endogenous production of IL-10 was a required element for the malignant transformation of B-1 cells in NZB mice, backcross animals were studied for the linkage between elevated IL-10 expression and the presence of lymphoid malignancy. The phenotypes of aged (NZB x DBA/2)F1 x NZB animals were determined and a strong correlation was found between the elevated levels of IL-10 mRNA and the development of B-1 malignant clones. In contrast, an increased level of IL-10 message was not associated with elevated serum IgM or the presence of anemia or reticulocytosis which is mainly seen in response to autoantibody production. These results indicate that, at least in NZB, the autoimmunity and lymphoproliferation phenotypes are not linked genetically. IL-10 may enhance proliferation and the development of B-1 cell malignancy rather than antibody production by the B-1 cell subpopulation. Thus, IL-10 plays an important role in B-1 malignancies, and downregulation of IL-10 could be a likely site for intervention in B cell malignancies.
The effect of CpG-oligodeoxynucleotides with different backbone structures and 3' hexameric deoxyriboguanosine run conjugation on the treatment of asthma in mice*1
Authors: Y. Chang, Y. Kim, T. Kim, H. Park, H. Kang, S. Kim, J. Bahn, K. Min, S. Cho
Journal: Journal of Allergy and Clinical Immunology (2004)
Correlation of Regional Emphysema and Lung Cancer: A Lung Tissue Research Consortium-Based Study
Authors: Laurie A. Hohberger, Darrell R. Schroeder, Brian J. Bartholmai, Ping Yang, Christine H. Wendt, Peter B. Bitterman, Ola Larsson, Andrew H Limper
Journal: Journal of Thoracic Oncology (2014)
Dermatophyte pseudomycetoma: a case report
Authors: A.W.J. CHRN, J.W.L. KUO, J.-S. CHEN, C.-C. SUN, S.-F. HUANG
Journal: British Journal of Dermatology (1993)

Journal Article Dermatophyte pseudomycetoma: a case report Get access A.W.J. CHRN, A.W.J. CHRN Department of Dermatology, National Taiwan University Hospital, Taipei, Taiwan Search for other works by this author on: Oxford Academic Google Scholar J.W.L. KUO, J.W.L. KUO Department of Dermatology, National Taiwan University Hospital, Taipei, Taiwan Search for other works by this author on: Oxford Academic Google Scholar J.‐S. CHEN, J.‐S. CHEN Department of Dermatology, National Taiwan University Hospital, Taipei, Taiwan Search for other works by this author on: Oxford Academic Google Scholar C.‐C. SUN, C.‐C. SUN Department of Dermatology, National Taiwan University Hospital, Taipei, Taiwan Search for other works by this author on: Oxford Academic Google Scholar S.‐F. HUANG S.‐F. HUANG Department of Pathology, National Taiwan University Hospital, Taipei, Taiwan Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 129, Issue 6, 1 December 1993, Pages 729–732, https://doi.org/10.1111/j.1365-2133.1993.tb03342.x Published: 01 December 1993 Article history Accepted: 06 August 1993 Published: 01 December 1993
New concepts on the histogenesis of eccrine neoplasia from keratin expression in the normal eccrine gland, syringoma and poroma
Authors: L. Langbein, B. Cribier, P. Schirmacher, S. Praetzel-Wunder, B. Peltre, J. Schweizer
Journal: British Journal of Dermatology (2008)

Peripheral and luminal layers of eccrine sweat gland ducts are self-renewing structures. Proliferation is restricted to the lowermost luminal layer, but randomly scattered in the peripheral layer. Each layer exhibits differential expression of keratins K5/K14 and K6/K16. Keratin K1 occurs only in peripheral cells and the novel keratin K77 is specific for luminal cells.To investigate the expression of luminal (K77), peripheral (K1) and further discriminatory keratins in two eccrine sweat gland tumours: syringoma, thought to show differentiation towards luminal cells of intraepidermal sweat ducts and eccrine poroma, considered to arise from poroid cells, i.e. peripheral duct cells; and keratinocytes of the lower acrosyringium/sweat duct ridge differentiating towards cells of intradermal/intraepidermal duct segments.Paraffin-embedded sections were examined by immunohistochemistry using several keratin, smooth muscle actin and Ki-67 antibodies.We confirmed the ductal nature of syringomas. Despite drastic morphological alterations in both layers, their keratin patterns remained almost undisturbed compared with normal ducts. In eccrine poroma epidermal keratins K5/K14 were ubiquitously expressed in all poroid cells. Cell islands deviating morphologically from poroid cells contained epidermal keratins K1/K10. K77 expression was limited to luminal cells of intact duct structures within the tumours.Syringomas are benign tumours of luminal cells of the lowermost intraglandular sweat duct. Poroid precursor cells of poromas do not comprise peripheral duct cells nor do poromas differentiate towards peripheral or luminal duct cells. Instead, poroid cells consist only of keratinocytes of the lowermost acrosyringium and the sweat duct ridge and poromas tend to differentiate towards the cells of the upper acrosyringium.
Arteriovenous Fistula for Self-Treatment of Hemophilia
Authors: Sanders H. Berk
Journal: JAMA (1975)

To the Editor.—  I read the article by Drs. Leon N. Sussman and Harvey Lozman, Arteriovenous Fistula for Self-Treatment of Hemophilia (230: 437, 1974) with great interest. More than three years ago, Dr. Harold Greenberg and I reported the creation of an arteriovenous fistula for the administration of blood in a patient with von Willebrand disease and implied that this technique could be used for other intravenous medications when veins were not available ( N Engl J Med 285:787, 1971). I assume that Drs. Sussman and Lozman and the editors ofThe Journalmissed our article since it was not mentioned in the text or references. As pointed out previously by us, and now by Dr. Sussman and Dr. Lozman, the creation of an arteriovenous fistula for transfusion or intravenous medications can be a valuable procedure on selected patients.
Is "nitrofurantoin lung"on the increase?
Authors: A. D. L. Marshall, O. J. Dempsey
Journal: BMJ (2013)

Gupta and Trautner suggest using nitrofurantoin as prophylaxis for recurrent urinary tract infections (UTIs) in non-pregnant women.1 They mention the risk of pulmonary toxicity (“nitrofurantoin lung”) associated with prolonged treatment but suggest that this occurs after years of treatment.

In Grampian we have identified 13 patients in the past four years with nitrofurantoin lung, 12 of whom …
Modulation of very low density lipoprotein production and clearance contributes to age- and gender- dependent hyperlipoproteinemia in apolipoprotein E3-Leiden transgenic mice.
Authors: B J van Vlijmen, H B van 't Hof, M J Mol, H van der Boom, A van der Zee, R R Frants, M H Hofker, L M Havekes
Journal: Journal of Clinical Investigation (1996)

Apolipoprotein E3-Leiden (APOE*3-Leiden) transgenic mice have been studied to identify factors modulating chylomicron and VLDL remnant lipoprotein metabolism. Transient elevated levels of VLDL/LDL-sized lipoproteins occurred in these mice with maximal levels during the period of rapid growth (optimum at 45 d of age). After about 100 d of age, serum cholesterol and triglyceride levels stabilized to slightly elevated levels as compared to control mice. The expression of the APOE*3-Leiden transgene was not age-dependent. In young mice the in vivo hepatic production of VLDL-triglycerides was 50% increased as compared to older mice. This is sustained by in vivo VLDL-apo B turnover studies showing increased (75%) VLDL-apo B secretion rates in young mice, whereas the VLDL-apo B clearance rate appeared not to be age dependent. On a high fat/cholesterol diet, females displayed significantly higher cholesterol levels than males (10 versus 7.0 mmol/liter, respectively). Serum levels of VLDL/LDL sized lipoproteins increased upon administration of estrogens, whereas administration of testosterone gave the opposite result. As compared to male mice, in female mice the hepatic VLDL-triglyceride production rate was significantly elevated. Injection of estrogen in males also resulted in increased VLDL-triglyceride production, although not statistically significant. In vivo VLDL-apo B turnover experiments showed that the VLDL secretion rate tended to be higher in females. Although, the fractional catabolic rate of VLDL-apo B is not different between males and females, administration of estrogens in males resulted in a decreased clearance rate of VLDL, whereas administration of testosterone in females resulted in an increased clearance rate of VLDL. The latter presumably due to an inhibiting effect of testosterone on the expression of the APOE*3-Leiden transgene. We conclude that hyperlipidemia in APOE*3-Leiden transgenic mice is strongly affected by age via its effect on hepatic VLDL production rate, whereas gender influences hyperlipidemia by modulating both hepatic VLDL production and clearance rate.
Genotype distribution of hepatitis C virus in São Paulo, Brazil: Rare subtype found
Authors: Leda Bassit, Gabriela Ribeiro-Dos-Santos, Luiz C. Da Silva, Kioko Takei, Paula Villaça, Elias David-Neto, Dalton Chamone, Amadeo Sáez-Alquézar
Journal: Hepatology (1999)

Subtype FoundTo the Editor: Genotypes 1, 2, and 3 of the hepatitis C virus (HCV) are widely distributed throughout Western countries and the Far East ( Japan, China, Taiwan, Thailand).Types 5 and 6 are mainly confined to South Africa and Southeast Asia, respectively, in contrast to type 4, which is predominant in the Middle East and Central Africa. 1-3 To investigate the prevalence and distribution of HCV genotypes in Brazil, 348 subjects from four different populations were studied: 34 anti-HCV-positive blood donors, 23 hemophiliacs, 40 renal-transplant recipients, and 251 chronic hepatitis C (CH-C) patients.HCV genotyping was performed in serum samples of 239 (95%) out of 251 CH-C patients and of all blood-donor and hemophiliac samples by a reverse hybridization assay (Line Probe Assay -INNO-LiPA HCV or INNO-LiPA HCV II, second generation, Innogenetics, Ghent, Belgium), in which a reverse transcriptase-polymerase chain reaction (RT-PCR) product of the 5Јuntranslated region (5ЈUTR) is hybridized with probes from various HCV genotypes. 2Twelve samples, of the 251 sera from the CH-C patients, and all from the renal-transplant patients were tested by a serotyping assay (HCV Serotyping Assay 1-6, Murex Diagnostics, Dartford, UK). 2 The genotyping results of the 348 HCV isolates, on the basis of the line probe and/or serotyping assays, are shown in Table 1.Four different types were found, and their overall prevalence was 63% for type 1, 4.3% for type 2, 31.3% for type 3, and 0.3% for type 4. Four subjects revealed mixed infections: two cases within types (1a ϩ 1b in a renaltransplant recipient and 2a ϩ 2b in a CH-C patient), and two cases across types (1b ϩ 3a in a blood donor and in a CH-C patient).A similar distribution was observed for each of the four populations, as a general rule; the exceptions were genotypes 2 for the renal-transplant recipients and 3 for the hemophiliacs, whose frequencies were found to be approximately double (13%) and half (15%), respectively, their values in the other populations.Data available from other Brazilian regions, showed corroborating figures for 114 blood donors in Rio de Janeiro, Southeast (1a, 42%; 1b, 34%; and 3a, 20%), 2 and for 100 CH-C patients in Porto Alegre, South (type 1, 55%; and type 3, 37%). 4Moreover, as it is known, the current screening assays are based on epitopes derived from only genotypes 1a or 1b, causing variation in seroreactivity among different HCV genotypes. 5,6Therefore, the high prevalence hereby reported not only for genotypes 1a and 1b, but for others (3 in particular) should be of main concern and of much interest for research and development of serological screening assays.
Impact of risk stratification on outcome among patients with multiple myeloma receiving initial therapy with lenalidomide and dexamethasone
Authors: Prashant Kapoor, Shaji Kumar, Rafael Fonseca, Martha Q. Lacy, Thomas E. Witzig, Suzanne R. Hayman, Angela Dispenzieri, Francis Buadi, P. Leif Bergsagel, Morie A. Gertz, Robert J. Dalton, Joseph R. Mikhael, David Dingli, Craig B. Reeder, John A. Lust, Stephen J. Russell, Vivek Roy, Steven R. Zeldenrust, A. Keith Stewart, Robert A. Kyle, Philip R. Greipp, S. Vincent Rajkumar
Journal: Blood (2009)
Prospero-related homeobox 1 and liver receptor homolog 1 coordinately regulate long-term proliferation of murine fetal hepatoblasts
Authors: Akihide Kamiya, Sei Kakinuma, Masafumi Onodera, Atsushi Miyajima, Hiromitsu Nakauchi
Journal: Hepatology (2008)

During early to late-fetal liver development, bipotential hepatoblasts proliferate and differentiate into hepatocytes and cholangiocytes. The prospero-related homeobox 1 gene (Prox1) is expressed in hepatoblasts, and the inactivation of Prox1 causes defective early liver development, in particular, faulty migration of fetal hepatoblasts. Prox1 binds to another hepatocyte-enriched transcription factor, liver receptor homolog 1 (Lrh1), and suppresses its transcriptional activity. However, the molecular mechanism by which Prox1 and Lrh1 regulate the characteristics of fetal hepatic cells remains unknown. We investigated the contribution of Prox1 and Lrh1 in early liver development. Embryonic day 13 liver-derived CD45-Ter119-Dlk+ cells were purified as fetal hepatic stem/progenitor cells, and formation of colonies derived from single cells was detected under low-density culture conditions. We found that overexpression of Prox1 using retrovirus infection induced migration and proliferation of fetal hepatic stem/progenitor cells. In contrast, overexpression of Lrh1 suppressed colony formation. Prox1 induced the long-term proliferation of fetal hepatic stem/progenitor cells, which exhibited both high proliferative activity and bipotency for differentiation. Prox1 up-regulated expression of cyclins D2, E1, and E2, whereas it suppressed expression of p16(ink4a), the cdk inhibitor. In addition, overexpression of Prox1 significantly inhibited the proximal promoter activity of p16(ink4a).These results suggested that Prox1 and Lrh1 coordinately regulate development of hepatic stem/progenitor cells and that Prox1 induces fetal hepatocytic proliferation through the suppression of the promoter activity of p16(ink4a).