tbuckley/cabot-search huggingface dataset:
STUDIES OF HYPERTHYROIDISM
Authors: C. C. Speidel
Journal: The Journal of Experimental Medicine (1926)

Experimental hyperthyroidism in urodele larvae (Amblystoma) and anuran larvae (Rana, Bufo, and Hyla) is accompanied by definite changes in bile color. The normal pale green, or pale yellow-green, color of the full gall bladder changes progressively after thyroid administration to a brighter green, then emerald-green, and finally a very dark green. In several hundred observations no exceptions were noted. The bile pigment, biliverdin (and its derivatives), is elaborated from the hemoglobin of worn out erythrocytes. Thyroid administration induces an increased rate of erythrocyte destruction, and this is followed by an increased output of bile pigment. Other minor factors are mentioned which may to a limited extent modify the color of the bile. Erythrocyte destruction occurs largely by enucleation, cytoplasmic segmentation, and fragmentation, and is probably widespread in the body. Many fragments and senile red cells collect in the liver. During the later stages of thyroid treatment the macrophages become conspicuously active. They are especially abundant in the liver, the gut, and the gills. In addition to the hemoglobin eliminated after transformation into bile pigment, some is transported by macrophages through the gut lining, and to a less extent through the involuting gill epithelium, and thus eliminated from the body.
Primary and Secondary Kinase Genotypes Correlate With the Biological and Clinical Activity of Sunitinib in Imatinib-Resistant Gastrointestinal Stromal Tumor
Authors: Michael C. Heinrich, Robert G. Maki, Christopher L. Corless, Cristina R. Antonescu, Amy Harlow, Diana Griffith, Ajia Town, Arin Mckinley, Wen-Bin Ou, Jonathan A. Fletcher, Christopher D.M. Fletcher, Xin Huang, Darrel P. Cohen, Charles M. Baum, George D. Demetri
Journal: Journal of Clinical Oncology (2008)

Most gastrointestinal stromal tumors (GISTs) harbor mutant KIT or platelet-derived growth factor receptor alpha (PDGFRA) kinases, which are imatinib targets. Sunitinib, which targets KIT, PDGFRs, and several other kinases, has demonstrated efficacy in patients with GIST after they experience imatinib failure. We evaluated the impact of primary and secondary kinase genotype on sunitinib activity.Tumor responses were assessed radiologically in a phase I/II trial of sunitinib in 97 patients with metastatic, imatinib-resistant/intolerant GIST. KIT/PDGFRA mutational status was determined for 78 patients by using tumor specimens obtained before and after prior imatinib therapy. Kinase mutants were biochemically profiled for sunitinib and imatinib sensitivity.Clinical benefit (partial response or stable disease for > or = 6 months) with sunitinib was observed for the three most common primary GIST genotypes: KIT exon 9 (58%), KIT exon 11 (34%), and wild-type KIT/PDGFRA (56%). Progression-free survival (PFS) was significantly longer for patients with primary KIT exon 9 mutations (P = .0005) or with a wild-type genotype (P = .0356) than for those with KIT exon 11 mutations. The same pattern was observed for overall survival (OS). PFS and OS were longer for patients with secondary KIT exon 13 or 14 mutations (which involve the KIT-adenosine triphosphate binding pocket) than for those with exon 17 or 18 mutations (which involve the KIT activation loop). Biochemical profiling studies confirmed the clinical results.The clinical activity of sunitinib after imatinib failure is significantly influenced by both primary and secondary mutations in the predominant pathogenic kinases, which has implications for optimization of the treatment of patients with GIST.
Family Income Supplements and Development of Psychiatric and Substance Use Disorders Among an American Indian Population
Authors: Ann Bullock
Journal: JAMA (2010)

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
Presence of antigen-specific somatic allelic mutations and splice variants do not predict for immunological response to genetic vaccination
Authors: Jordan T Becker, Douglas G McNeel
Journal: Journal for ImmunoTherapy of Cancer (2013)

Antigen-specific anti-tumor vaccines have demonstrated clinical efficacy, but immunological and clinical responses appear to be patient-dependent. We hypothesized that naturally-occurring differences in amino acid sequence of a host's target antigen might predict for immunological outcome from genetic vaccination by presentation of epitopes different from the vaccine.Using peripheral blood cells from 33 patients who had been treated with a DNA vaccine encoding prostatic acid phosphatase (PAP), we sequenced the exons encoding PAP and PSA genes from somatic DNA to identify single nucleotide polymorphisms. In addition, mRNA was collected to detect alternative splice variants of PAP.We detected four synonymous coding mutations of PAP among 33 patients; non-synonymous coding mutations were not identified. Alternative splice variants of PAP were detected in 22/27 patients tested. The presence of detectable splice variants was not predictive of immunological outcome from vaccination. Immune responses to peptides encoded by these splice variants were common (16/27) prior to immunization, but not associated with immune responses elicited with vaccination.These results suggest that antigen-specific immune responses detectable after treatment with this genetic vaccine are specific for the host-encoded antigen and not due to epitope differences between the vaccine and a particular individual's somatic coding sequence.
Improved Survival in Asymptomatic Diabetic Patients With High-Risk Spect Imaging Treated With Coronary Artery Bypass Grafting
Authors: Paul Sorajja, Panithaya Chareonthaitawee, Navin Rajagopalan, Todd D. Miller, Robert L. Frye, David O. Hodge, Raymond J. Gibbons
Journal: Circulation (2005)

Background— The Bypass Angioplasty Revascularization Investigation trial demonstrated that symptomatic diabetics with multivessel coronary artery disease had a survival advantage with initial coronary artery bypass grafting (CABG) versus percutaneous coronary intervention (PCI). No published study has examined different treatments and outcome in asymptomatic diabetics. Methods and Results— This study group consisted of 826 asymptomatic diabetics (age 62±12 years; 76% men) without known coronary artery disease who had abnormal myocardial perfusion during stress single photon emission computed tomography (SPECT). SPECT images were classified as low-, intermediate-, and high-risk. Early revascularization (CABG or PCI ≤4 months after SPECT) was performed in 76 patients. Survival (follow-up, 5.3±3.3 years) was compared in patients treated with CABG, PCI, or medical therapy. Revascularization (CABG or PCI) was performed in 54 of 261 patients with high-risk scans and was independently associated with improved survival (χ 2 =4.55; P =0.03 after multivariate adjustment). Subset analysis demonstrated that the survival advantage was confined to patients treated with CABG (n =39), with a 5-year survival CABG at 85%, PCI at 72%, and medical therapy at 67% ( P =0.02 for 3 groups). Although CABG was associated with better survival, mortality remained high (3% per year). There was no survival advantage by treatment for patients with less-severe SPECT abnormalities. Conclusions— These nonrandomized data suggest that CABG improves survival in asymptomatic diabetic patients with high-risk SPECT, although revascularization was performed infrequently in these patients. These results parallel those of the Bypass Angioplasty Revascularization Investigation trial in symptomatic diabetic patients.
Effects of Dietary Protein and Carbohydrate Level on Cholesterolemia and Atherogenesis in Cockerels on a High-Fat, High-Cholesterol Mash
Authors: JEREMIAH STAME, RUTH PICK, LOUIS N. KATZ
Journal: Circulation Research (1958)

Decreased protein intake in the presence of a high-fat, high-cholesterol diet was found to produce marked aggravation of hypercholesterolemia and atherogenesis in cockerels. Sucrose was substituted for protein in this low protein diet. The effect of this diet is not due to sucrose since restoring the protein to a high level, while keeping the sucrose in the ration constant, had no such effect.
Diabetes and 30-Day Mortality From Peptic Ulcer Bleeding and Perforation
Authors: Reimar W. Thomsen, Anders Riis, Steffen Christensen, Mette Nørgaard, Henrik T. Sørensen
Journal: Diabetes Care (2006)

OBJECTIVE— Diabetes may influence the outcome of complicated peptic ulcer disease, due to angiopathy, blurring of symptoms, and increased risk of sepsis. We examined whether diabetes increased 30-day mortality among Danish patients hospitalized with bleeding or perforated peptic ulcers. RESEARCH DESIGN AND METHODS— This population-based cohort study took place in the three Danish counties of North Jutland, Viborg, and Aarhus between 1991 and 2003. Patients hospitalized with a first-time diagnosis of peptic ulcer bleeding or perforation were identified using the counties’ hospital discharge registries. Data on diabetes, other comorbidities, and use of ulcer-associated drugs were obtained from discharge registries and prescription databases. The Danish Civil Registry System allowed complete follow-up for mortality. The outcome under study was 30-day mortality in diabetic versus nondiabetic patients, adjusted for potential confounders. RESULTS— We identified 7,232 patients hospitalized for bleeding ulcers, of whom 731 (10.1%) had diabetes. The 30-day mortality among diabetic patients was 16.6 vs. 10.1% for other patients with bleeding ulcers. The adjusted 30-day mortality rate ratio (MRR) for diabetic patients was 1.40 (95% CI 1.15–1.70). We also identified 2,061 patients with perforated ulcers, of whom 140 (6.8%) had diabetes. The 30-day mortality among diabetic patients was 42.9 vs. 24.0% in other patients with perforated ulcers, corresponding to an adjusted 30-day MRR of 1.51 (1.15–1.98). CONCLUSIONS— Among patients with peptic ulcer bleeding and perforation, diabetes appears to be associated with substantially increased short-term mortality.
Growth factors in endothelial regeneration
Authors: N. P J Brindle
Journal: Cardiovascular Research (1993)

Journal Article Growth factors in endothelial regeneration Get access Nicholas P J Brindle Nicholas P J Brindle Department of Cardiology, University of Wales College of Medicine, Heath Park, Cardiff CF4 4XN, United Kingdom: Dr N P J Brindle. Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 27, Issue 7, July 1993, Pages 1162–1172, https://doi.org/10.1093/cvr/27.7.1162 Published: 01 July 1993 Article history Received: 17 July 1992 Accepted: 07 January 1993 Published: 01 July 1993
Host bone marrow-derived IL-12 enhances donor T cell engraftment in a mouse model of bone marrow transplantation
Authors: Katarzyna A Darlak, Ying Wang, Jian-Ming Li, Wayne AC Harris, Cynthia R Giver, Chunzi Huang, Edmund K Waller
Journal: Journal of Hematology & Oncology (2014)

Donor cell engraftment is critical for the success of allogeneic bone marrow transplants. Graft failure is a result of donor cells either failing to engraft initially or being eliminated at later time points. Donor cell engraftment is facilitated by donor T cells, which eliminate residual host hemato-lymphoid effector cells such as NK cells and T cells. We aimed to explore the role of host hematopoietic cell derived IL-12 on donor cell engraftment in a murine model of BMT. We established radiation chimeras by transplanting C57BL6/J (B6) mice with BM from either congenic B6 mice or IL-12p40 KO mice. These WT → WT or IL-12 KO → WT chimeras then underwent a secondary transplant with allogeneic (FVB) BM. Survival, engraftment, donor T cell expansion, cytokine production by donor T cells, as well as expression of stimulatory markers on donor T cells was analyzed. Mice whose residual host hematopoietic cells were capable of producing IL-12 had modestly higher survival, higher donor T cell engraftment, and significantly higher donor erythroid engraftment. We have also found that an increased number of donor T cells in IL-12 KO → WT chimeras have a regulatory phenotype, expressing FoxP3, producing lower levels of TNF-α, higher levels of IL-10, and expressing higher levels of ICOS as well as PD-1 on CD4+ T cells. To our knowledge, this is the first report of a beneficial role of IL-12 production by host cells in the context of bone marrow engraftment in a murine model of BMT. These findings support the clinical use of exogenous IL-12 for use in settings where graft failure is of concern.
NODULAR FORMS OF TUBAL DISEASE
Authors: Emil Ries
Journal: The Journal of Experimental Medicine (1897)

THE CONCLUSIONS AT WHICH WE ARRIVE ARE THE FOLLOWING: 1. Nodular enlargement of the tube can be caused by a number of different pathological conditions. 2. Clinical examination does not enable us to make a diagnosis of the pathological condition existing in an individual case of nodule of the tube. 3. The diagnosis of the nature of a tubal nodule can be made only with the microscope. 4. The conditions causing nodular enlargement of the tube are congenital or acquired, non-inflammatory or inflammatory. 5. Any one of these conditions can exist without the production of nodules. 6. The nodules can be found in all parts of the tube and-taking the peculiar anatomy of each part of the tube into account-show the same structure. 7. The enlargement can be caused by epithelial or epithelioid formations, connective or muscular tissue, by round-cell infiltrations or combinations of two or more of these. 8. The epithelial formations originate in the epithelium of a. the tubal mucous membrane (salpingitis pseudo-follicularis, adenomyoma originating in the tubal epithelium). b. the accessory tubes (intraparietal parasalpinx and hydro-parasalpinx). c. remnants of the Wolffian body (adenomyoma). 9. The epithelioid formations originate in the peritoneal endothelium (peritoneal growths under "relative heterotopy"). 10. The excess of formation of connective tissue is a consequence of inflammatory conditions of the tubal wall (salpingitis interstitialis, Zweifel). 11. The hypertrophy of the muscular tissue is a. non-inflammatory (adenomyoma). b. consequent upon inflammation-Kaltenbach's case (23). 12. The accumulations of round cells are direct evidence of inflammation: a. non-specific (salpingitis interstitialis disseminata, salpingitis abscedens); or b. specific (salpingitis tuberculosa or s. gonorrhoica). 13. The epithelioid formations can occur wherever pseudo-membranes cover organs lined with a serous coat. 14. Extra-uterine pregnancy (abdominal or tubal) produces epithelioid formations by causing pseudo-membranes to form-not by any irritation peculiar to the pregnancy.
IgE And Symptoms By Age 2 Years Predict FENO At Age 5-7 Years In A Low-Income Urban New York City Population
Authors: A. Divjan, M. Rosa, A.C. Just, B.J. Sheares, F.P. Perera, R.L. Miller, M.S. Perzanowski
Journal: Journal of Allergy and Clinical Immunology (2009)
Decreased miR-199 augments visceral pain in patients with IBS through translational upregulation of TRPV1
Authors: QiQi Zhou, Liuqing Yang, Scott Larson, Sapreet Basra, Shehzad Merwat, Alai Tan, Carlo Croce, G Nicholas Verne
Journal: Gut (2015)

<h3>Objective</h3> Many patients with irritable bowel syndrome IBS not only have abdominal pain but also may suffer from visceral hypersensitivity and heighted visceral nociception. Moreover, IBS has few effective therapeutic agents and mechanisms of disease are unclear. Our goals were to (i) identify microRNA (miRNA) expression, signalling and targets in human colon (controls; patients with IBS); (ii) verify in vitro, IBS-associated changes in miRNAs, especially miR-199, which is complementary to the transient receptor potential vanilloid type 1 (TRPV1) gene; and (iii) determine whether modulating the expression of miRNAs in vivo, especially miR-199, reverses associated changes and pathological hallmarks of visceral hypersensitivity via TRPV1 signalling. <h3>Design</h3> We evaluated 45 patients with diarrhoea-predominant IBS (IBS-D) and 40 controls with (1) visceral pain severity score and (2) colonoscopy with biopsies. miRNA expression was evaluated in human colon following miRNA array analysis. Luciferase assays were done to confirm relationships between miR-199 and TRPV1 expression. A rat model of visceral hypersensitivity was used to study miR-199 and its target gene (TRPV1) expression in dorsal root ganglion (DRG) and colon in vivo. <h3>Results</h3> Gut miR-199a/b expression in IBS-D was significantly decreased, which correlated directly with both increased visceral pain scores and TRPV1 expression. In vivo upregulation of miR-199a by intraperitoneal injection of lenti-miR-199a precursors decreased visceral hypersensitivity via diminished TRPV1 signalling. <h3>Conclusions</h3> Decreased colonic miR-199a/b correlates with visceral pain in patients with IBS-D. Similarly, reduced miR-199a expression in rat DRG and colon tissue is associated with heightened visceral hypersensitivity. In vivo upregulation of miR-199a decreases visceral pain via inhibition of TRPV1 signalling. Thus, miR-199 precursors may be promising therapeutic candidates for the treatment in patients with visceral pain.
Low Dosage and Long Treatment Duration of β-Lactam
Authors: Didier Guillemot, Claude Carbon, Beverley Balkau, Pierre Geslin, Hervé Lecoeur, Françoise Vauzelle-Kervroëdan, Gilles Bouvenot, Eveline Eschwége
Journal: JAMA (1998)

The spread of drug-resistant Streptococcus pneumoniae in the community is a public health problem in developed and developing nations, but whether antibiotic use is responsible for the increase in drug resistance is not known.To analyze the relationship between penicillin-resistant S pneumoniae (PRSp) pharyngeal carriage and characteristics of beta-lactam use.Observational study of children attending 20 randomly sampled schools.The Loiret, in the center of France.A total of 941 children, 3 to 6 years old.Pharyngeal carriage of S pneumoniae, antibiotic use, and medical events during the preceding 30 days. Pneumococcal penicillin G sodium minimal inhibitory concentrations and serotyping were performed.Medical illnesses and the use of antibiotics were not associated with PRSp carriage. However, oral beta-lactam use was associated with an increased risk of PRSp carriage (odds ratio [OR], 3.0; 95% confidence interval [CI], 1.1-8.3; P=.03). Children treated by low daily doses of an oral beta-lactam (defined as lower than clinical recommendations) had an increased risk of PRSp carriage, as compared with children who did not (OR, 5.9; 95% CI, 2.1-16.7; P=.002). A treatment of long duration (>5 days) with a beta-lactam was associated with an increased risk of PRSp carriage (OR, 3.5; 95% CI, 1.3-9.8; P=.02).Our results suggest that a low daily dose and a long duration of treatment with an oral beta-lactam contribute to the selective pressure in promoting pharyngeal carriage of PRSp.
Disease-Specific Hashtags for Online Communication About Cancer Care
Authors: Matthew S. Katz, Audun Utengen, Patricia F. Anderson, Michael A. Thompson, Deanna J. Attai, Claire Johnston, Don S. Dizon
Journal: JAMA Oncology (2015)

Case 3. In 2012, a young adult man with history of Klinefelter syndrome presented with intermittent chest pain and was found to have a 15-cm primary mediastinal NSGCT.He was treated with 4 cycles of VIP followed by resection of residual mediastinal mass, which revealed teratoma.In 2014, he was found to have leukocytosis (WBC, 44 000/μL [44.0 × 10 9 / L]).Bone marrow examination confirmed chronic-phase CML by morphologic characteristics, and a t(9;22)(q34;q11) was identified by chromosome analysis.The patient started treatment with dasatinib and achieved a hematologic response.To date, his BCR/ABL transcript declined appropriately from 55% to 9%.He continues to be in remission for his GCT.Discussion | There have been reports of chemotherapy-related Philadelphia-chromosome leukemias in patients with antecedent malignant neoplasms. 3Past treatments for GCT with cisplatin-etoposide-containing regimens or HDCT with carboplatin-etoposide have been linked to an increased risk of secondary acute leukemia 1,4 and solid tumors. 5A review of the literature reveals 7 cases of GCT with subsequent development of CML. 1,3,6 In this series, we present 3 cases of patients with GCT who achieved remission with chemotherapy and later developed BCR/ABL-positive CML.These findings raise the question of a causal relationship between etoposide and/or platinum-containing chemotherapy and the development of CML with t(9;22)(q34;q11).Etoposide-based chemotherapy in patients with GCT is leukemogenic.It is not clear whether combination chemotherapy with cisplatin and bleomycin contribute to this result.While its association with AML is well established, questions regarding the connection of etoposide and cisplatincontaining combination chemotherapy and secondary CML are posed herein.The relatively low risk of secondary leukemia in patients treated with potentially curative combination chemotherapy for GCT continues to be reassuring. 1 However, physicians should be aware of possible late toxic effects of these treatment regimens and the need for diligent follow-up in these patients.
Antibiotics and Coronary Heart Disease
Authors: F Javier Nieto
Journal: JAMA (2004)

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