tbuckley/cabot-search huggingface dataset:
Abstract 336: Blockade of CCN6 (WISP3) activates growth factor-independent survival and resistance to anoikis in human mammary epithelial cells
Authors: Wei Huang, Maria E. Gonzalez, Kathy Toy, Mousumi Banerjee, Celina G. Kleer
Journal: Cancer Research (2010)

Abstract CCN6 is a secreted cysteine rich matricellular protein (36.9 kDa) that exerts growth inhibitory functions in breast cancer. Reduction or loss of CCN6 protein has been reported in invasive carcinomas of the breast with lymph node metastasis and in inflammatory breast cancer. However, the mechanism by which CCN6 loss promotes breast cancer growth remains to be defined. In the present study we developed lentiviral mediated shRNA knockdown of CCN6 in nontumorigenic mammary epithelial cells MCF10A and HME. We discovered that CCN6 knockdown protects mammary epithelial cells from apoptosis and activates growth factor-independent survival. In the absence of exogenous growth factors, CCN6 knockdown was able to promote growth under anchorage independent conditions and triggered resistance to detachment-induced cell death (anoikis). Upon serum starvation, CCN6 knockdown was sufficient for activation of the phosphatidylinositol 3-kinase/Akt pathway. Growth factor-independent cell survival was stunted in CCN6 knockdown cells when treated with either human recombinant CCN6 protein or the phosphatidylinositol 3-kinase inhibitor LY294002. Targeted inhibition of Akt isoforms revealed that the survival advantage rendered by CCN6 knockdown requires specific activation of Akt-1. The relevance of our studies to human breast cancer is highlighted by the finding that low CCN6 protein levels are associated with upregulated expression of phospho-Akt-1 (Ser473) expression in 21% of invasive breast carcinomas. These results enable us to pinpoint one mechanism by which CCN6 controls survival of breast cells mediated by the PI3K/Akt-1 pathway. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 336.
The Insulinopathies
Authors: Kenneth H. Gabbay
Journal: New England Journal of Medicine (1980)

DURING the past quarter-century, studies of the insulin molecule have elucidated details of its biosynthesis, structure, and function. These studies of insulin, a two-chain peptide hormone with a molecular weight of 6000, have provided a framework for the understanding of the clinical correlates of abnormalities of the insulin molecule and its precursors, and a model for the study of other peptide hormones and proteins.Insulin is synthesized as a larger single-chain precursor, pre-proinsulin, which is processed to proinsulin and then to the biologically active molecule, insulin.1 Figure 1 shows the proinsulin molecule, consisting of the A and B chains of insulin, connected . . .
THE SALIVARY GLANDS AND THE MECHANISM OF THIRST
Journal: JAMA (1931)

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 Publications 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 2023 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
Of red cell bondage
Authors: W. B. Shelley
Journal: JAMA (1983)

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 Publications 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 2023 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
Sex Steroids and the Construction and Conservation of the Adult Skeleton
Authors: B. L. Riggs
Journal: Endocrine Reviews (2002)

Here we review and extend a new unitary model for the pathophysiology of involutional osteoporosis that identifies estrogen (E) as the key hormone for maintaining bone mass and E deficiency as the major cause of age-related bone loss in both sexes. Also, both E and testosterone (T) are key regulators of skeletal growth and maturation, and E, together with GH and IGF-I, initiate a 3- to 4-yr pubertal growth spurt that doubles skeletal mass. Although E is required for the attainment of maximal peak bone mass in both sexes, the additional action of T on stimulating periosteal apposition accounts for the larger size and thicker cortices of the adult male skeleton. Aging women undergo two phases of bone loss, whereas aging men undergo only one. In women, the menopause initiates an accelerated phase of predominantly cancellous bone loss that declines rapidly over 4–8 yr to become asymptotic with a subsequent slow phase that continues indefinitely. The accelerated phase results from the loss of the direct restraining effects of E on bone turnover, an action mediated by E receptors in both osteoblasts and osteoclasts. In the ensuing slow phase, the rate of cancellous bone loss is reduced, but the rate of cortical bone loss is unchanged or increased. This phase is mediated largely by secondary hyperparathyroidism that results from the loss of E actions on extraskeletal calcium metabolism. The resultant external calcium losses increase the level of dietary calcium intake that is required to maintain bone balance. Impaired osteoblast function due to E deficiency, aging, or both also contributes to the slow phase of bone loss. Although both serum bioavailable (Bio) E and Bio T decline in aging men, Bio E is the major predictor of their bone loss. Thus, both sex steroids are important for developing peak bone mass, but E deficiency is the major determinant of age-related bone loss in both sexes.
Fifteen Trainees in Each Hundred Rejected
Journal: JAMA (1941)

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 Publications 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 2023 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
Normal mouse intestinal mucus release requires cystic fibrosis transmembrane regulator–dependent bicarbonate secretion
Authors: Mary Abigail S. Garcia, Ning Yang, Paul M. Quinton
Journal: Journal of Clinical Investigation (2009)

The mechanisms underlying mucus-associated pathologies in cystic fibrosis (CF) remain obscure.However, recent studies indicate that CF transmembrane conductance regulator (CFTR) is required for bicarbonate (HCO 3 -) transport and that HCO 3 -is critical for normal mucus formation.We therefore investigated the role of HCO 3 -in mucus secretion using mouse small intestine segments ex vivo.Basal rates of mucus release in the presence or absence of HCO 3 -were similar.However, in the absence of HCO 3 -, mucus release stimulated by either PGE 2 or 5-hydroxytryptamine (5-HT) was approximately half that stimulated by these molecules in the presence of HCO 3 -.Inhibition of HCO 3 -and fluid transport markedly reduced stimulated mucus release.However, neither absence of HCO 3 -nor inhibition of HCO 3 -transport affected fluid secretion rates, indicating that the effect of HCO 3 -removal on mucus release was not due to decreased fluid secretion.In a mouse model of CF (mice homozygous for the most common human CFTR mutation), intestinal mucus release was minimal when stimulated with either PGE 2 or 5-HT in the presence or absence of HCO 3 -.These data suggest that normal mucus release requires concurrent HCO 3 -secretion and that the characteristically aggregated mucus observed in mucin-secreting organs in individuals with CF may be a consequence of defective HCO 3 -transport.
Contributing Member Omitted
Journal: JAMA (1966)

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 Publications 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 2023 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
Air Pollutants and the Facilitation of Cancer Metastasis
Authors: A. Richters, K. Kuraitis
Journal: Environmental Health Perspectives (1983)

Studies have been carried out to determine whether the inhalation of ambient levels of nitrogen dioxide (NO2), a common air pollutant, could influence the frequency of blood-borne cancer cell metastasis to the lungs. B16 mouse melanoma cells were used as an in vivo test model. the results have indicated that animals inhaling ambient levels of NO2 developed a significantly higher number of melanoma nodules in their lungs than the animals inhaling filtered air. Thus, a new concept for the action of air pollutants is proposed. The question is raised whether similar events are taking place in urban human populations.
Antibiotiki, Moscow
Journal: JAMA (1965)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications 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) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 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
Scientific Exhibit
Journal: JAMA (1965)

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 Publications 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 2023 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
Reproductive toxicology. m-Nitrobenzoic acid.
Authors: Robert Chapin, Dushyant Gulati, Ester Hope, Leta Barnes, Tim Hart, Susan Russell, K Poonacha
Journal: Environmental Health Perspectives (1997)

NO2 10 C OH m-Nitrobenzoic acid (MNB) is widely used in explosive and dyestuff industries and also as a chemical intermediate in organic syn- theses.In a 90-day prechronic study, both F344 rats and B6C3F1 mice exposed to high concentrations of MNB exhibited tes- ticular atrophy and reduced sperm count.This RACB study using Swiss CD-1 mice was performed as a follow-up to that origi- nal observation.Data from a 2-week doserange-finding study (Task 1) were used to set exposure concentrations for the Task 2 continuous cohabitation study at 0.35, 0.75, and 1.5% in feed.Based on mean feed consumption and body weight, the estimated daily dosages were approximately 0.5, 1.3, and 2.8 g/kg/day.During Task 2, four, three, two, and three animals died from causes ranging from lymphoma to ruptures to partner- inflicted wounds to a variety of infections.There was no clear relationship to MNB exposure.During Task 2, postpartum dam weights in the middle and high dose groups were approximately 5 to 8% and approximately 12 to 14% lower than con- trols, respectively.Male body weights were reduced only at the high dose by approxi- mately 9%.Daily feed consumption was increased by approximately 10% at the high dose.Reproductive performance was impaired during Task 2. Mice in the middle and high dose groups delivered approximately 10 and 27% fewer pups per litter, respectively.At the high dose, there were 14% fewer litters
Jacqueline Kennedy Onassis Reservoir, Central Park, New York City
Journal: JAMA Internal Medicine (2018)

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 Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast Publications 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) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 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 Internal Medicine journal
THE SUBCUTANEOUS INJECTION OF PARAFFIN FOR THE CORRECTION OF DEFORMITIES OF THE NOSE.
Authors: F. GREGORY CONNELL
Journal: JAMA (1903)

The surgical use of paraffin as a prosthetic measure is a recent advancement in the surgical art and consequently is in a more or less experimental stage of development. The first instance in which it was used in an attempt to remedy a defect in the human anatomy dates back but a few years, and while the number of cases in the literature is increasing rapidly, they are still so few in number that every operation of this character should be reported. It is only by a careful classification and study of a large number of cases that we may be enabled to arrive at a definite conclusion as to the merits and demerits of the method, as a recognized surgical procedure. The attempts at improvement which terminate unsatisfactorily are of even more import than are the cases which result favorably. The temptation is to report the successful operations and to postpone
Abstract 11670: Presence of Dissociated Pulmonary Vein Activity After Isolation Depends on Fibrillatory Excitation in Pulmonary Vein
Authors: Takashi Kaneshiro, Hitoshi Suzuki, Yoshiyuki Matsumoto, Minoru Nodera, Yoshiyuki Kamiyama, Yasuchika Takeishi
Journal: Circulation (2014)

Background: Circumferential pulmonary vein (PV) isolation has been widely accepted as catheter ablation for atrial fibrillation (AF). Dissociated PV activity (DPVA) may appear after PV isolation, however, the electrophysiological property and clinical implication of DPVA have not been revealed. Methods and Results: The study subjects were consecutive 37 patients (62±8 years, 28 men) with drug-refractory AF who underwent successful PV isolation. Electrophysiological property of left atrium (LA) and PV during and after PV isolation were investigated. Excluded 21 PVs without LA-PV connection before procedure, all of 112 PVs with successful isolation were analyzed. DPVA appeared in 14 PVs (13%) after PV isolation, from left superior PV in 7 (50%), right superior PV in 5 (36%) and left inferior PV in 2 (14%). Mean cycle length (CL) of DPVA was 5180±3080 ms. DPVA appeared in 9 of 37 PVs (24%) without existence of AF, but in 5 of 75 PVs (7%) with existence of AF during procedure (P=0.008). There was the tendency that the CL of DPVA was shorter with existence of AF compared to that without existence of AF (3792±1815 vs. 6682±3041 ms, P=0.08), and the suppression of DPVA was observed by over drive pacing inside of PV with PV capture in several cases. There was not significant relationship between the presence of DPVA and AF recurrence with 2-month blanking period after PV isolation. Conclusions: The presence of DPVA after PV isolation depended on the existence of AF during procedure, but was not significantly related to the AF recurrence after PV isolation. The long CL and suppressive maneuver with PV over drive pacing suggested the vulnerability of DPVA. Thus, these findings suggest that passive and/or spontaneous fibrillatory excitation in PV might suppress the automatic activity of myocardial sleeves in PV.
Abstract 555: Loss of function Cbl-c mutations in solid tumors
Authors: Silvano R. Daniels, Stephen C. Kales, Mariya Liyasova, Marion M. Nau, Phil E. Ryan, Jeffrey E. Green, Stanley Lipkowitz
Journal: Cancer Research (2018)

Abstract Receptor Tyrosine Kinase (RTK) signaling, which is essential for cellular growth and proliferation, can lead to malignant transformation and tumorigenesis when aberrantly activated. Cbl proteins (Cbl, Cbl-b, and Cbl-c) are a conserved family of RING finger (RF) ubiquitin ligases (E3) that negatively regulate the activity of several tyrosine kinases such as the EGFR. Cbl mutations have recently been identified in 5% of human myeloid neoplasms, with a majority of mutations clustered within the RF and linker domains. Cbl-c is the most recently identified Cbl protein and is exclusively expressed in epithelial cells. We recently identified a novel cDNA isolated from a mouse mammary tumor in the C3(1) Large T Antigen transgenic mouse model. This mutant cDNA encodes a protein that has a deletion in the RF domain of Cbl-c, thereby resembling known Cbl family mutations associated with myeloid neoplasias. Genomic analyses of both parental and transgenic lines show no evidence of germline mutation, suggesting that this mutation is most likely somatic. The mutant Cbl-c protein enhances transformation of NIH 3T3 cells when co-transfected with SV40 Large T Antigen. In overexpression studies, this mutant Cbl-c fails to mediate ubiquitination of activated EGFR and acts in a dominant negative manner to prevent ubiquitination of activated EGFR by wildtype Cbl proteins. Datamining also reveals Cbl-c mutations associated with human solid tumors. Cell-based analyses demonstrate a similar loss of E3 function in some of these human mutations. These data collectively suggest that, like Cbl mutations in myeloid neoplasms, loss of function Cbl-c mutants may also contribute to the pathogenesis of solid tumors in murine models and in humans. Citation Format: Silvano R. Daniels, Stephen C. Kales, Mariya Liyasova, Marion M. Nau, Phil E. Ryan, Jeffrey E. Green, Stanley Lipkowitz. Loss of function Cbl-c mutations in solid tumors [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 555.