tbuckley/cabot-search huggingface dataset:
673. Injection of Progenitor Cells from the Bone Marrow or Esophagus Prevents Irradiation-Induced Esophagitis
Authors: YunYun Niu, Michael W. Epperly, Hongmei Shen, Joel S. Greenberger
Journal: Molecular Therapy (2004)

To demonstrate whether progenitor or stem cells exist in esophagus, which can prevent irradiation-induced esophagitis, esophageal stem cells were isolated from C57BL/6J mice using a side population (SP) technique used in the isolation of hematopoietic stem cells. To determine whether hematopoietic or esophageal stem cells migrated to areas of esophageal damage, C57BL/6J mice were irradiated to 29 Gy to the esophagus and injected with whole bone marrow as well as esophageal SP cells from GFP+ transgenic mice. Mice were sacrificed 14 days later, the esophagus removed, and green foci were detected in the esophagus, indicating that the donor cells migrated and proliferated in the esophagus. To determine whether injections of whole bone marrow cells protected against irradiation-induced damage to the esophagus, groups of C57BL/6J mice were irradiated to 29 Gy and then injected intravenously (IV) with whole bone marrow isolated from GFP+ mice (1×106, 5×105, 1×105, or 5×104 bone marrow cells per mouse), and followed for development of esophagitis. The results demonstrated a significant increase in survival in mice that were injected with either 1×106 or 5×105 whole bone marrow cells. GFP+ esophageal squamous cells were identified in the transplanted groups demonstrating that cells from whole bone marrow replace damaged squamous cells preventing the development of esophagitis. To demonstrate that esophageal SP cells repopulated the esophagus of irradiation damaged mice, C57BL/6J mice were irradiated to 29 Gy to the esophagus and injected IV with 1000 GFP+ esophageal SP cells and followed for development of esophagitis. Mice injected with GFP+ esophageal SP cells survived and did not develop esophagitis. In contrast, non-injected mice died of esophagitis. The results demonstrate that esophageal SP cells can prevent lethal irradiation-induced esophageal damage. It is also suggested that bone marrow stem or progenitor cells may provide a resource for treating esophageal irradiation injury.
Withdrawal of Troglitazone and Cisapride
Authors: Jane E. Henney
Journal: JAMA (2000)

The FDA wishes to inform physicians of the removal from the market of troglitazone (Rezulin, Parke-Davis/Warner-Lambert Co, Morris Plains, NJ), a treatment for type 2 diabetes mellitus, and cisapride (Propulsid, Janssen Pharmaceutica Inc, Titusville, NJ), a treatment for severe heartburn.
Abstract P184: Effects of Sodium and Potassium Supplementation on Blood Pressure and Arterial Stiffness in Untreated (Pre)Hypertensives on a Low-Sodium, Low-Potassium Diet
Authors: Lieke Gijsbers, James Dower, Marco Mensink, Johanna M Geleijnse
Journal: Circulation (2014)

Introduction: We performed a 12-week randomized placebo-controlled crossover study to examine the effects of sodium and potassium supplementation on blood pressure (BP) and arterial stiffness in untreated (pre)hypertensive individuals on a low-sodium, low-potassium diet. Methods: During the study, subjects were on a fully controlled diet that provided on average 2.4 g/d of sodium (equals 6 g/d of salt) and 2.2 g/d of potassium. After a 1-week run-in period, 37 subjects received capsules with supplemental sodium (3 g/d, equals 7.5 g/d of salt), supplemental potassium (3 g/d), or placebo, for four weeks each (not separated by wash-out), in random order. Fasting office BP, 24-h ambulatory BP, and measures of arterial stiffness (SphygmoCor®) were assessed at baseline and after each treatment. Results: Subjects had a mean pre-treatment BP of 145/81 mmHg and 68% (25 of 37) had systolic BP (SBP) ≥140 mmHg. In 36 subjects who completed the study, sodium supplementation increased urinary sodium by 97.6 mmol/24h (2.2 g/d) and potassium supplementation increased urinary potassium by 62.9 mmol/24h (2.5 g/d), compared to placebo (Table). Sodium supplementation significantly increased office BP by 7.5/3.3 mmHg, 24-h BP by 7.0/2.1 mmHg and central BP by 8.5/3.6 mmHg. Potassium supplementation significantly reduced 24-h BP by 4.0/1.7 mmHg. Measures of arterial stiffness did not change. Conclusion: Increasing the intake of sodium has a strong adverse effect on BP in untreated (pre)hypertensive individuals. Increased potassium intake, however, lowers BP even when people are on a reduced sodium diet. Short-term changes in sodium and potassium intake have little effect on arterial stiffness. Trial registration: ClinicalTrials.gov Identifier: NCT01575041
Identification of a key molecule for hepatic metastasis of human pancreatic carcinoma by a novel quantitative metastasis model with NOD/SCID/ GCNULL (NOG) mice
Authors: Hiroshi Suemizu, Makoto Monnai, Yasuyuki Ohnishi, Norikazu Tamaoki, Masato Nakamura
Journal: Cancer Research (2005)

Proc Amer Assoc Cancer Res, Volume 46, 2005

5675 

Conventional cancer metastasis models using nude mice or SCID mice are inadequate due to residual immunity in recipient animals. We developed a new reliable assay system for hepatic metastasis using NOD/SCID/γcnull (NOD/ShiJic- scid with γcnull, NOG) mice. We evaluated hepatic metastasis abilities of the human pancreatic cancer cell lines by this xeno-transplantation model. Hepatic metastases were examined at autopsy within 6 weeks after cell suspensions were intrasplenically transplanted. Seven human pancreatic cancer cell lines (MIApaCa-2, AsPC-1, PANC-1, Capan-1, Capan-2, BxPC-3 and PL45) form diverse metastatic foci in the liver of the mice with cell dose dependency in the 4 logarithmic digit range. Capan-2 and PL45 showed no metastasis with even 10^5 cells. On the other hand, MIApaCa-2, AsPC-1 and PANC-1 metastasized only with 10^2 cells in 71.4% (5/7), 57.1% (4/7) and 37.5% (3/8) of the mice, respectively. Hepatic metastases of Capan-1 and BxPC-3 were apparent in 50% (5/10) of NOG mice after transplantation (1×10^3 cells), and in 12.5% (1/8) of NOG mice after transplantation (1×10^4 cells). Thus, we characterized in vivo metastatic properties of human pancreatic cancer cell lines with statistical reliability, and could use this property as a parameter for gene expression profiling. To identify genes involved in hepatic metastasis of pancreatic cancer cells, we established a highly metastatic subline of BxPC-3 (LM-BxPC-3) by a single transplantation from a few liver metastatic foci of the parental BxPC-3 cells with the poor metastatic ability. Then, the gene expression profiles of over 47,000 transcripts (Affymetrix, Human Genome U133 Plus 2.0 Array) were compared in these cell lines. Forty-five genes were upregulated or downregulated more than 4-fold in the LM-BxPC-3 cell line compared with the parental line. We confirmed the reliability of microarray data concerning 6 genes and 3 novel genes encoding a hypothetical protein by RT-PCR in the LM-BxPC-3 and parental line. We examined a correlation between up-, or downregulated 9 gene expression and in vivo hepatic metastatic properties in 7 human pancreatic cancer cell lines. The S100A4 gene expression correlates closely with hepatic metastasis ability, which was evaluated using a quantitative metastasis model with NOG mice, but the expressions of other genes was not correlated with metastatic ability. These results suggested that the S100A4 was a key molecule for hepatic metastasis of pancreatic cancer. This quantitative metastasis model will help us to search and develop new cancer-therapeutic approaches with novel drug against this key molecule.
Severe Acute Pancreatitis
Authors: Stephen Piwinski
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
An Introduction to the Mind in Health and Disease.
Authors: Viner N
Journal: JAMA (1925)

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
Complement facilitates early prion pathogenesis
Authors: Michael A. Klein, Pascal S. Kaeser, Petra Schwarz, Heiko Weyd, Ioannis Xenarios, Rolf M. Zinkernagel, Michael C. Carroll, J. Sjef Verbeek, Marina Botto, Mark J. Walport, Hector Molina, Ulrich Kalinke, Hans Acha-Orbea, Adriano Aguzzi
Journal: Nature Medicine (2001)
Abstract 668: Inhibition of DNA Methyltransferase Inhibits the Ang II-Induced Increase in Blood Pressure, Vascular Remodeling and Target Organ Damage
Authors: Methode Bacanamwo, Mukaila Akinbami, Dahai Wang, Gary H Gibbons
Journal: Circulation (2007)

Growth signals stimulate DNA methyltransferase (DNMT) expression through extracellular signal-regulated kinases 1/2 (ERK1/2) pathway and that inhibition of ERK1/2 signaling results in repression of DNMT expression and activation of expression of some DNMT-repressed genes. Angiotensin II (Ang II) has been shown to stimulate ERK1/2 signaling in resistance arteries. We hypothesized that Ang II stimulates DNMT expression resulting in methylation and repression of antihypertensive genes such as 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2) and that blocking DNMT activity may inhibit Ang II-induced hypertension, vascular remodeling, and target organ damage. C57BL/6J (C57) mice were treated with the specific DNMT inhibitor 5′-aza-2′-deoxycytidine (aza-CdR, 1 mg/kg/day) intraperitoneally for 3 consecutive days before subcutaneous Ang II infusion for 28d at a pressure dose of 0.7 mg/kg/day using Alzet osmotic minipumps. Systolic blood pressure was monitored during this period and tissues were harvested to determine vascular wall thickness, cardiac hypertrophy, and expression and methylation of 11β-HSD2 in arteries and the kidneys. Ang II infusion induced a more than 2-fold increase in DNMT1 expression (n=6, p≤ 0.05). Moreover, blocking DNMT1 activity significantly inhibited the Ang II-induced increase in systolic and diastolic blood pressure (from 102 ± 3 to138 ± 7 for saline-treated vs. 101 ± 4 to 105 ± 6 mm Hg for aza-CdR-treated mice, n=8, p≤ 0.01 for saline vs.aza-CdR in the presence of Ang II treatment). In addition, expression of 11β-HSD2 was inhibited by Ang II treatment. However, expression of 11β-HSD2 was found to be above the background observed in absence of Ang II when Ang II treatment was associated with DNMT activity blockade. Methylation-specific PCR indicated that 11β-HSD2 was methylated in the arteries and kidneys but its Ang II-dependency is still to be determined. Finally when DNMT activity was inhibited, the Ang II-induced increase cardiac hypertrophy (heart/body weight) and wall/lumen ratio in the carotid arteries were significantly inhibited (n= 8, p≤ 0.05). These results suggest that DNA methylation plays a critical role in the coordinate regulation of genes involved in the pathogenesis of hypertension and vascular remodeling.
Functional genetics – an approach to mechanisms in Alzheimer’s disease
Authors: Mikko Hiltunen
Journal: Molecular Neurodegeneration (2013)

Background Alzheimer’s disease (AD) is the most common neurodegenerative disorder in the world. As the aging population continues to increase globally, treatment of AD and other age-associated neurodegenerative diseases is becoming increasingly important, not only from a human point of view, but also from an economic perspective. In recent years, several attempts have been made to find novel susceptibility genes and pathways relevant for AD. Particularly genome-wide association (GWA) and meta-analysis-based studies have identified several risk variants in different genes, which significantly associate with AD. The subsequent mechanistic characterization of the identified risk genes is extremely important as it may pave the way for the development of new biomarkers and intervention approaches.
ANURIA FOLLOWING RETROGRADE PYELOGRAPHY
Authors: H M BURROS, V H BORROMEO, D SELIGSON
Journal: Annals of Internal Medicine (1958)

Case Reports1 March 1958ANURIA FOLLOWING RETROGRADE PYELOGRAPHYHARRY M. BURROS, M.D., V. H. J. BORROMEO, M.D., DAVID SELIGSON, SC.D., M.D.HARRY M. BURROS, M.D.Search for more papers by this author, V. H. J. BORROMEO, M.D.Search for more papers by this author, DAVID SELIGSON, SC.D., M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-48-3-674 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptSince 1897, retrograde pyelography has been used in studying diseases of the genitourinary tract. This is the method of choice for studying patients who are sensitive to contrast material given intravenously. We have studied a patient in whom unique sensitivity resulted from contrast media administered in retrograde fashion. Review of the urologic literature has revealed no similar case.CASE REPORTA 35 year old man was referred on April 23, 1955, to the urologic service of the Graduate Hospital of the University of Pennsylvania for study because he had been passing red blood cells in his urine following back injury.... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: HARRY M. BURROS, M.D.; V. H. J. BORROMEO, M.D.; DAVID SELIGSON, SC.D., M.D.*Received for publication August 13, 1956.From the Departments of Urology and Biochemistry, Graduate Hospital and Graduate School of Medicine, University of Pennsylvania, Philadelphia.Requests for reprints should be addressed to Harry M. Burros, M. D., Medical Tower, 255 South Seventeenth Street, Philadelphia 3, Pennsylvania. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byReflex Anuria Following Retrograde Pyelography: A Case Report and Literature ReviewARF after retrograde pyelography: a case report and literature reviewRoentgen diagnosis of the kidney and the ureterAbsorption of Contrast Material from the Urinary Tract During Retrograde PyelographyDRIP INFUSION PYELOGRAPHY: A STUDY OF 300 CASES IN A GERIATRIC POPULATIONAnuria Following Retrograde PyelographyUrinary Blockade after Bilateral CatheterizationIntravenous Urography in the Patient with Renal InsufficiencyUreteral Obstruction Following Retrograde Catheterization 1 March 1958Volume 48, Issue 3 Page: 674-676 Keywords Biochemistry Catheters Edema Graduate medical education Hospital medicine Pyelography Red blood cells Urea Urine Urology ePublished: 1 December 2008 Issue Published: 1 March 1958 PDF downloadLoading ...
Clinical use of an intra-operative RT-PCR assay for the detection of metastases in sentinel lymph nodes of breast cancer patients at the Institut Jules Bordet
Authors: I. Veys, J. C. Schobbens, S. Majjaj, D. Noterman, V. Filippov, N. Sirtaine, V. Durbecq, P. Bourgeois, J. M. Nogaret, D. Larsimont
Journal: Journal of Clinical Oncology (2008)

11100 Background: A molecular assay (GeneSearch™ BLN Assay, Veridex, LLC), CE marked and approved by the FDA, has been in clinical use at our institution for over 18 months to intra-operatively detect metastases ≥0.2 mm in the sentinel lymph nodes (SLNs) in breast cancer patients. After a small validation study (N=78, sensitivity = 92.3%, specificity = 96.9%) the assay was adopted as the only intra-operative SLN test used at the Institut Jules Bordet. This is the first report of the post-market assay performance. Methods: One SLN per patient is cut into approximately 2 mm sections. Alternating sections are processed fresh in the BLN assay. The assay detects mRNA expression of mammaglobin and CK19. Predetermined cutoffs are set to detect metastases ≥0.2 mm. The BLN Assay results are used to make intra-operative decisions for same surgery axillary lymph node dissections (ALND). The remaining alternating sections of the SLN are examined later by permanent section H&E. Results: Since August 2006, the BLN Assay has been used for intra-operative ALND decision-making on 100 patients. The assay intra-operatively detected all 15 H&E-positive SLNs. The assay was in agreement with 93% of the H&E-negative SLNs (79 of 85) and was positive when H&E was negative for 6 SLNs. One of these 6 SLNs had a 0.3 mm size metastasis detected by IHC alone. The average turn around time for the assay was 39 minutes for all 100 patients, and was 35 minutes for the second 50 patients. Conclusions: The BLN Assay results shows high correlation to permanent section H&E results that take 2–3 days, and its timing permits same-surgery ALND when nodes are found positive for metastases. In clinical use, agreement of assay results and permanent section H&E results (94%, 94/100) is similar to the agreement found in an earlier validation study (96.2%, 75/78). Perfect agreement is not expected since the two tests are evaluating different sections of the node. The BLN Assay is beneficial to our patients by reducing the need for second surgeries while being practical and cost effective for the institution to perform. Author Disclosure Employment or Leadership Consultant or Advisory Role Stock Ownership Honoraria Research Expert Testimony Other Remuneration Veridex Veridex
Long-Term Malignant Hematopoiesis in Human Acute Leukemia Bone Marrow Biopsies Implanted in Severe Combined Immunodeficiency Mice
Authors: Faezeh Legrand, Ibrahim Khazaal, Michel Peuchmaur, Odile Fenneteau, Hélène Cavé, Pierre Rohrlich, Etienne Vilmer, Bruno Péault
Journal: Blood (1997)
Price Blame Game
Authors: Brian Vastag
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 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
Abstract MP34: In Praise of Demanding Parenting: The Effects of Parenting Style and Poverty on Obesity Risk in Children: Evidence from a Nationally Representative Sample
Authors: Lisa Kakinami, Tracie Barnett, Gilles Paradis
Journal: Circulation (2014)

Background: One-quarter of children are already overweight or obese when they enter preschool, underscoring a critical need to improve our understanding of childhood determinants of health, including both sociodemographic (such as poverty) and social-familial influences (such as parenting style), as well as how these determinants may interact with one another. Objective: To examine the effects of parenting style on the risk of obesity in youth and determine if poverty is a mediator or moderator for this association. Methods: Participants (age 0-11) were from the National Longitudinal Survey of Children and Youth (NLSCY), a representative cross-sectional survey of youth collected bi-annually (1994-2008) throughout Canada. Factor analysis identified 4 parenting styles consistent with Baumrind’s theory of authoritative (demanding and responsive), authoritarian (demanding but not responsive), permissive (responsive but not demanding), and negligent (not demanding and not responsive) parenting control prototypes. Multivariable logistic regression assessed the risk of a child being obese (BMI percentile ≥ 97.7 th compared to age- and sex-specific WHO growth curves) based on parenting style after adjusting for age, sex, parental education, immigration status, family functioning score, birth order, and maternal age. Analyses were stratified by age (younger: 2-5 years of age, n=19,026; school-age: 6-11 years of age, n=18,551) due to age-related differences in parenting styles. Mediation or moderation by poverty (household income &lt; low income cut-offs adjusted for household size and geographic region) was assessed. Analyses used sampling and bootstrap weights. Results: Younger children’s parents were primarily authoritative (42%, n=7357), followed by negligent (22%, n=3763), permissive (20%, n=3436), and authoritarian (16%, n=4470). Parenting styles in school-age children were similar (authoritative: 32%, n=7195, negligent: 31%, n=5586, permissive: 22%, n=3850, authoritarian: 15%, n=1920). In multivariable analyses, compared to authoritative parenting, younger and school-age children with authoritarian parents were 30% (95% CI: 1.1-1.5, p=0.0002) and 37% (CI: 1.1-1.7, p=0.006) more likely to be obese, respectively. In younger children, poverty moderated this association: authoritarian and negligent parenting was associated with 39% (CI: 1.2-1.6, p&lt;0.0001) and 28% (CI: 1.1-1.5, p=0.002) increased risk of obesity, respectively, only among the children not living in poverty. In school-age children, poverty was not a mediator or moderator. Conclusions: Parenting style is associated with a child’s risk of obesity but is moderated by poverty in younger children. Successful strategies to combat childhood obesity need to reflect the independent and interactive effects of sociodemographic and social-familial influences on health especially in early childhood.