tbuckley/cabot-search huggingface dataset:
Calcitonin Has a Vasopressin-like Effect on Aquaporin-2 Trafficking and Urinary Concentration
Authors: Richard Bouley, Hua A.J. Lu, Paula Nunes, Nicolas Da Silva, Margaret McLaughlin, Ying Chen, Dennis Brown
Journal: Journal of the American Society of Nephrology (2010)

The most common cause of hereditary nephrogenic diabetes insipidus is a nonfunctional vasopressin (VP) receptor type 2 (V2R). Calcitonin, another ligand of G-protein–coupled receptors, has a VP-like effect on electrolytes and water reabsorption, suggesting that it may affect AQP2 trafficking. Here, calcitonin increased intracellular cAMP and stimulated the membrane accumulation of AQP2 in LLC-PK1 cells. Pharmacologic inhibition of protein kinase A (PKA) and deficiency of a critical PKA phosphorylation site on AQP2 both prevented calcitonin-induced membrane accumulation of AQP2. Fluorescence assays showed that calcitonin led to a 70% increase in exocytosis and a 20% decrease in endocytosis of AQP2. Immunostaining of rat kidney slices demonstrated that calcitonin induced a significant redistribution of AQP2 to the apical membrane of principal cells in cortical collecting ducts and connecting segments but not in the inner stripe or inner medulla. Calcitonin-treated VP-deficient Brattleboro rats had a reduced urine flow and two-fold higher urine osmolality during the first 12 hours of treatment compared with control groups. Although this VP-like effect of calcitonin diminished over the following 72 hours, the tachyphylaxis was reversible. Taken together, these data show that calcitonin induces cAMP-dependent AQP2 trafficking in cortical collecting and connecting tubules in parallel with an increase in urine concentration. This suggests that calcitonin has a potential therapeutic use in nephrogenic diabetes insipidus.
Inhibition of Estrogen-dependent Breast Cancer Growth by a Reaction Product of α-Fetoprotein and Estradiol
Authors: Herbert I. Jacobson, James A. Bennett, Gerald J. Mizejewski
Journal: Cancer Research (1990)

ABSTRACTReaction of picomolar quantities of human or rodent a-fetoprotein(AFP) with inuminolar quantities of 17/3-estradiol (E2) generates a product of unknown structure, designated AFP/E2, that inhibits estrogen-stimulated growth of mouse uterus. We describe herein the effect ofrodent AFP/Ej on the in vivo growth of two estrogen-dependent breastcancers, the MCF-7 human breast cancer and the MTW9A rat mammarycancer. Both cancers were grown as xenografts under the kidney capsuleof cyclosporine-immunosuppressed male HDI , mice. In addition, theMTYV9Atumor was grown as a homograft in syngeneic ovariectomizedWistar-Furth female rats. Estrogen support was provided by s.c. SilasticE2 implants. Injecting  that was generated by incubating 1.0 n%of AFP with 0.5 Mgof Â£2for l h at room temperature resulted in cessationof growth and, in most cases, regression of MCF-7 tumor xenografts. Italso produced regression of MTW9A tumor homografts and significantlyinhibited growth of MTW9A xenografts. Treatment with AFP alone orE2 alone did not inhibit growth of these tumors. The data suggest thatAM'/I j has a unique property which causes attenuation or shut-down ofthe biochemical reactions through which estrogen-dependent tumorgrowth is mediated.INTRODUCTIONAFP3 is a glycoprotein that is secreted primarily by the fetalliver and yolk sac. It is a major protein component of mammalian fetal plasma, but after parturition the concentrationrapidly dwindles to negligible levels. AFP is also synthesizedby certain tumors and is secreted into the plasma, where itspresence renders it useful as a marker for those malignancies.We have previously reported that E2 interacts with AFP togenerate a somatostatic growth factor (1). Incubating 0.5 ng E2(1840 pmol) with 1.0 ng AFP (14 pmol) in 0.1 ml vehicle for 1h at room temperature generated a potent inhibitory growthfactor designated AFP/E2 which upon i.p. administration toimmature mice or adult ovariectomized mice disabled the response of uterine tissue to estrogen (1-3). Increases in uterineweight and in epithelial mitotic index were substantially andequally restricted below those elicited by injection of E2 alone,indicating that the inhibitory effect was on estrogen-stimulatedcell proliferation. Injection of E2or moxestrol at l h after  treatment initiated no uterine growth, indicating that  produced a uterine refractory state that persisted for at least1 h. AFP from mouse, rat, and human were all activable by E2to an antiuterotrophic product (4). Separate but simultaneousinjections of AFP and E2 or of AFP alone were not growthinhibitory. Only AFP and E2 premixed for 1 h at or near theconcentrations described above generated the antiuterotrophicproduct.The above findings indicate that  can behave as anantiestrogen. Over one third of human breast cancers are re-Received4/3/89;revised9/7/89;accepted10/12/89.
Investigations of Remedies
Authors: C. G. K. Sharp
Journal: BMJ (1946)

<h3>Abstract</h3> The genus <i>Torovirus</i> (subfamily <i>Torovirinae</i>, family <i>Coronaviridae</i>, order <i>Nidovirales</i>) encompasses a range of species that infect domestic ungulates including cattle, sheep, goats, pigs and horses, causing an acute self-limiting gastroenteritis. Using the prototype species equine torovirus (EToV) we performed parallel RNA sequencing (RNA-seq) and ribosome profiling (Ribo-seq) to analyse the relative expression levels of the known torovirus proteins and transcripts, chimaeric sequences produced via discontinuous RNA synthesis (a characteristic of the nidovirus replication cycle) and changes in host transcription and translation as a result of EToV infection. RNA sequencing confirmed that EToV utilises a unique combination of discontinuous and non-discontinuous RNA synthesis to produce its subgenomic RNAs; indeed, we identified transcripts arising from both mechanisms that would result in sgRNAs encoding the nucleocapsid. Our ribosome profiling analysis revealed that ribosomes efficiently translate two novel CUG-initiated ORFs, located within the so-called 5’ UTR. We have termed the resulting proteins U1 and U2. Comparative genomic analysis confirmed that these ORFs are conserved across all available torovirus sequences and the inferred amino acid sequences are subject to purifying selection, indicating that U1 and U2 are functionally relevant. This study provides the first high-resolution analysis of transcription and translation in this neglected group of livestock pathogens. <h3>Importance</h3> Toroviruses infect cattle, goats, pigs and horses worldwide and can cause gastrointestinal disease. There is no treatment or vaccine and their ability to spill over into humans has not been assessed. These viruses are related to important human pathogens including severe acute respiratory syndrome (SARS) coronavirus and they share some common features, however the mechanism that they use to produce subgenomic RNA molecules differs. Here we performed deep sequencing to determine how equine torovirus produces subgenomic RNAs. In doing so, we also identified two previously unknown open reading frames “hidden” within the genome. Together these results highlight the similarities and differences between this domestic animal virus and related pathogens of humans and livestock.
Lymphoid follicles in chronic lung diseases
Authors: Koshika Yadava, Benjamin J Marsland
Journal: Thorax (2013)

Lymphoid follicles (LFs) can be induced in the lung on infection or chronic inflammation; however, their relevance and contribution to protective immunity or pathogenesis is poorly understood. Recent advances from clinical studies and animal models have shed some light on the mechanisms that trigger and facilitate the development of LFs. As we grasp a better understanding of their development and their relevance to disease, the potential value in targeting pulmonary LFs with novel therapeutics will become evident.
TCT-731 Switching from Clopidogrel to Prasugrel in Patients Undergoing Coronary Stent Implantation
Authors: Guido Parodi, Benedetta Bellandi, Vincenzo Comito, Renato Valenti, Nazario Carrabba, Rossella Marcucci, Angela Migliorini, Erica Ramazzotti, Rosanna Abbate, David Antoniucci
Journal: Journal of the American College of Cardiology (2012)
Gene for the human T cell differentiation antigen Leu-2/T8 is closely linked to the kappa light chain locus on chromosome 2.
Authors: V P Sukhatme, A C Vollmer, J Erikson, M Isobe, C Croce, J R Parnes
Journal: The Journal of Experimental Medicine (1985)

We have mapped the gene encoding the T cell differentiation antigen Leu-2/T8 to human chromosome 2 by hybridization of a Leu-2/T8 complementary DNA clone to DNA from a panel of mouse-human cell hybrids. In situ hybridization further localizes the gene to the 2p1 region in close proximity to the Ig kappa light chain gene. The Leu-2/T8 gene translocates with C kappa to chromosome 8 in a Burkitt lymphoma line carrying a t(2;8) translocation. These data support the hypothesis that Leu-2/T8 is the human homologue of the mouse Lyt-2,3 antigen.
Studies on the control of sodium excretion in experimental uremia
Authors: Raymond G. Schultze, Howard S. Shapiro, Neal S. Bricker
Journal: Journal of Clinical Investigation (1969)

A study of the mechanisms governing the high rate of sodium excretion per nephron characteristic of patients with chronic renal disease has been made in dogs. A "remnant kidney" was produced by 85% infarction of the left kidney while the right kidney was left intact. A bladder-splitting procedure allowed simultaneous measurement of glomerular filtration rate and the rate of sodium excretion by each kidney. The animals were fed a constant known amount of sodium chloride and 0.1 mg of 9 alpha-fluorohydrocortisone twice daily throughout the study. In a group of dogs fed 3 or 5 g of salt per day, sodium excretion by the remnant kidney averaged 6.5 muEq/min while the intact kidney was present and 53.7 muEq/min when the animals became uremic after the intact kidney was removed. The increased sodium excretion per nephron by the remnant organ often occurred within 18 hr after contralateral nephrectomy and persisted despite experimentally induced acute reductions in the glomerular filtration rate to below prenephrectomy levels. A second group of animals studied in the same manner but receiving 1 g of salt per day or less failed to develop a natriuresis after contralateral nephrectomy despite high grade uremia. Thus an increased impermeable solute load per nephron was not a regulatory factor in the production of the natriuresis. The increased rate of sodium excretion per nephron in uremia resembles that after saline loading in that it may occur without an increase in glomerular filtration rate or a reduction in mineralocorticoid stimulation. It follows that an additional factor or factors must be involved in the genesis of the natriuresis. In contrast to the natriuresis that is seen in normal animals subjected to saline loading, these uremic animals were found not to have a detectable increase in extracellular fluid volume or blood volume in the presence of high fractional sodium excretion rates. Sodium excretion in response to a small salt load by the remnant organ in uremia was 30% greater than the response of both kidneys in the preuremic state despite a markedly reduced total GFR. These data are consistent with the view that the volume control mechanism becomes more responsive in uremia.
Outpatient treatment with subcutaneous histamine dihydrochloride in combination with interleukin-2 and interferon-α in patients with metastatic renal cell carcinoma: results of an open single-armed multicentre phase II study
Authors: F. Donskov, H. von der Maase, R. Henriksson, U. Stierner, P. Wersäll, H. Nellemann, K. Hellstrand, K. Engman, P. Naredi
Journal: Annals of Oncology (2002)
Sale of Non-Health-Related Goods From Physicians' Offices
Authors: None Council on Ethical and Judicial Affairs, American Medical Association
Journal: JAMA (1998)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Journals JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2024 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Correlation of urine type I collagen-cross-linked N telopeptide levels with bone scintigraphic results in prostate cancer patients
Authors: Nobuyoshi Fukumitsu, Mayuki Uchiyama, Yutaka Mori, Shuuichi Yanada, Takashi Hatano, Hiroshi Igarashi, Kouichi Kishimoto, Jojiro Nakada, Akiko Yoshihiro, Junta Harada
Journal: Metabolism (2002)
Host-Cell Antigen Potentiated by Incomplete Growth Cycle of Influenza Virus
Authors: O Haller, J Lindenmann
Journal: JNCI Journal of the National Cancer Institute (1975)

Lysis of Ehrlich ascites tumor cells in mice was induced with the Hong Kong influenza A-strain HKH virus not previously adapted to the tumor. Despite high pathogenicity of HKH, mice not genetically resistant to the lethal action of myxoviruses survived the actue phase of oncolysis. Virus infection of tumor cells resulted in high titers of hemagglutinin with low infectivity which indicated incomplete virus growth. Serial passages of HKH in Ehrlich ascites tumors failed. HKH oncolysates induced solid antitumor immunity in several mouse strains, including those fully susceptible to the virus. The immunizing power of HKH oncolysates could be abolished by mouse antibody against egg-grown HKH (H3, N2) but not by antiserum raised aganist TUR virus (Havl, Nav3).
Durable Complete Remission Induced by Cetuximab Monotherapy in a Patient Infected With HIV and Diagnosed With Recurrent Squamous Cell Carcinoma of the Head and Neck
Authors: Paul G. Rubinstein, Valerie Lindgren, Suman Setty, Mike Yao, Kristen B. Pytynia, James A. Radosevich, ShriHari S. Kadkol, Lawrence E. Feldman
Journal: Journal of Clinical Oncology (2010)
Expression of interleukin 2 receptors and binding of interleukin 2 by gamma interferon-induced human leukemic and normal monocytic cells.
Authors: F Herrmann, S A Cannistra, H Levine, J D Griffin
Journal: The Journal of Experimental Medicine (1985)

Gamma interferon induced surface expression of interleukin 2 (IL-2) receptors on normal human monocytes and the monocytoid cell lines U937 and HL60. These receptors were detected by anti-IL-2 receptor monoclonal antibodies, and U937 IL-2 receptors were indistinguishable from T lymphocyte IL-2 receptors by immunoprecipitation. Also, U937 IL-2 receptors bound biologically active IL-2. These results suggest a role for monocyte IL-2 receptors in T cell/monocyte interaction during an immune response.
Soluble Triggering Receptor Expressed on Myeloid Cells and the Diagnosis of Pneumonia
Authors: Sébastien Gibot, Aurélie Cravoisy, Bruno Levy, Marie-Christine Bene, Gilbert Faure, Pierre-Edouard Bollaert
Journal: New England Journal of Medicine (2004)

The diagnosis and treatment of bacterial pneumonia in patients who are receiving mechanical ventilation remain a difficult challenge. The triggering receptor expressed on myeloid cells (TREM-1) is a member of the immunoglobulin superfamily, and its expression on phagocytes is specifically up-regulated by microbial products. The presence of soluble TREM-1 (sTREM-1) in bronchoalveolar-lavage fluid from patients receiving mechanical ventilation may be an indicator of pneumonia.
Possible involvement of CD14+ CD16+ monocyte lineage cells in the epidermal damage of Stevens-Johnson syndrome and toxic epidermal necrolysis
Authors: M. Tohyama, H. Watanabe, S. Murakami, Y. Shirakata, K. Sayama, M. Iijima, K. Hashimoto
Journal: British Journal of Dermatology (2011)

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are characterized by keratinocyte apoptosis and necrosis, resulting in epidermal detachment. Although monocytes abundantly infiltrate the epidermis in SJS/TEN skin lesions, the properties and functions of these cells have not been fully examined.To determine the properties of monocytes infiltrating into the epidermis in SJS/TEN.Immunostaining of skin sections was performed to examine the membrane markers of monocytes infiltrating into skin lesions.Immunostaining of cryosections from 11 SJS/TEN skin lesions revealed numerous CD14+ monocytes located along the dermoepidermal junction and throughout the epidermis. The cells coexpressed CD16, CD11c and HLA-DR. CD14+ CD16+ cells were identified in very early lesions without epidermal damage, suggesting that their infiltration is a cause, rather than a result, of epidermal damage. Moreover, these cells expressed CD80, CD86 and CD137 ligand, indicative of their ability to facilitate the proliferation and cytotoxicity of CD8+ T cells. CD16+ cells infiltrating the epidermis and detected at the dermoepidermal junction were immunostained and counted in paraffin-embedded skin sections obtained from 47 patients with drug rash manifested as TEN, SJS, maculopapular-type rash or erythema multiform-type rash. The number of CD16+ monocytes infiltrating the epidermis increased significantly, depending on the grade of epidermal damage.These findings suggest that the appearance of CD14+ CD16+ cells of monocyte lineage plays an important role in the epidermal damage associated with SJS/TEN, most probably by enhancing the cytotoxicity of CD8+ T cells.
More research is needed into the effects on injury of substitute and interchange rules in team sports
Authors: John Orchard
Journal: British Journal of Sports Medicine (2011)

There is a viewpoint that changes to the rules and scheduling of modern cricket need the blessing of the Board of Control for Cricket in India (BCCI), such is the financial dominance that India has in this sport. Twenty-20 cricket did not become a prominent form of the game until India won the 2007 T20 World Cup in South Africa; suddenly, it was the potential saviour of the sport just as the Indian Premier League was born. Although an injury prevention argument has been made for the introduction of substitutes in Test cricket,1 the traditionalist view is that cricket should remain a unique sport where substitutes are not permitted for the specialist positions in the game (batting, bowling and wicketkeeping). If this traditionalist view is ever reversed, historians may look back on a hamstring injury to Zaheer Khan, India's fast bowler, on the opening day of the 2011 first Test against England as one of the major catalysts. The much anticipated series between England and India turned out to be a major disappointment for those who love a close contest. The issue of whether cricket will finally join every other team sport on the planet in allowing substitutes or interchanges (for injury or performance reasons) now finally has some traction.2 Not only did Zaheer's injury handicap the Indians in the first Test, the fact that the remainder of India's first-choice bowling attack needed to be ‘overbowled’ in this Test to make up for their missing strike bowler possibly affected their performance for the remainder of the summer. We already …
The Hypoxia Hilton: recollections of a visit, with a postscript by J W Severinghaus on mechanisms of acute mountain sickness
Authors: J G Jones
Journal: Journal of the Royal Society of Medicine (2002)

During a training fellowship thirty years ago at the Cardiovascular Research Institute (CVRI) in San Francisco, I joined an expedition led by Professor John Severinghaus. Its purpose was to study pulmonary complications of acute hypoxia after a one-day ascent, by helicopter and hike, from sea level to the summit of White Mountain, 14 246 feet (4342 m) above sea level1, on the California—Nevada border.

Originally a physicist at the Massachusetts Institute of Technology, Severinghaus became a physician then chief of anaesthesia research in the University of California at CVRI. He invented the first reliable PO2 and PCO2 blood gas analysis systems, which are now used routinely in hospitals throughout the world. His research into the control of breathing, altitude physiology and oximetry continue to the present day. Before I joined the expedition he tested my ventilatory drive with a vital capacity breath of 15% CO2 in nitrogen2 (i.e. no oxygen). For what seemed like ages nothing happened. I gazed at the posters on the walls of his laboratory and continued to breathe normally into the spirometer. Then, suddenly, it was like the first huge breath that I experienced in an iron lung, but at 40 breaths per minute. The spirometer bell leapt out of the water. Severinghaus was expressionless. Then I lost consciousness.
The B Lymphocyte Adaptor Molecule of 32 kD (Bam32) Regulates B Cell Antigen Receptor Signaling and Cell Survival
Authors: Hiroaki Niiro, Akito Maeda, Tomohiro Kurosaki, Edward A. Clark
Journal: The Journal of Experimental Medicine (2002)

The B lymphocyte–associated adaptor protein 32 kD in size (Bam32) is expressed at high levels in germinal center (GC) B cells. It has an NH2-terminal src homology 2 (SH2) domain which binds phospholipase C (PLC)γ2, and a COOH-terminal pleckstrin homology (PH) domain. Thus, Bam32 may function to integrate protein tyrosine kinase (PTK) and phosphatidylinositol 3-kinase (PI3K) signaling pathways in B cells. To further define the role Bam32 plays in B cells, we generated Bam32-deficient DT40 cells. These Bam32−/− cells exhibited lower levels of B cell antigen receptor (BCR)-induced calcium mobilization with modest decreases in tyrosine phosphorylation of phospholipase C (PLC)γ2. Moreover, BCR-induced activation of extracellular signal-regulated kinase (ERK), c-jun NH2-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) pathways was impaired in Bam32−/− cells but not the activation of Akt-related pathways. Activation of downstream transcription factors such as nuclear factor of activated T cells (NF-AT) and nuclear factor of κ binding (NF-κB) was also impaired in Bam32−/− cells. Furthermore, Bam32−/− cells were more susceptible to BCR-induced death. Taken together, these findings suggest that Bam32 functions to regulate BCR-induced signaling and cell survival most likely in germinal centers.
Five years of experience with hydroxyurea in children and young adults with sickle cell disease
Authors: Alina Ferster, Parvine Tahriri, Christiane Vermylen, Geneviève Sturbois, Francis Corazza, Pierre Fondu, Christine Devalck, Marie F. Dresse, Walter Feremans, Kathleen Hunninck, Michele Toppet, Pierre Philippet, Chris Van Geet, Eric Sariban
Journal: Blood (2001)