tbuckley/cabot-search huggingface dataset:
Colonoscopy: A Survey of its Value in a Teaching Hospital Surgical Unit<sup>1</sup>
Authors: Martin Jourdan, Max Rendall, Ian McColl
Journal: Journal of the Royal Society of Medicine (1981)

A survey has been undertaken of the diagnostic, therapeutic and economic value of colonoscopy in a teaching hospital surgical unit. Provided it is undertaken in conjunction with a good clinical history and double contrast barium enema, colonoscopy provides a high yield of information bearing upon the patient's subsequent management. Therapeutic polypectomy was undertaken in 21% of examinations. Its value in acute colonic disease is discussed, and the importance of training colonoscopists for the future is emphasized.
MtDNA D310insTC variant in tumorigenesis of ovarian serous carcinoma
Authors: Felix Aikhionbare, K Kumaresan, Sharifeh Mehrabi, Edward Partridge
Journal: Cancer Research (2007)

AACR Annual Meeting-- Apr 14-18, 2007; Los Angeles, CA

3532 

Approximately 80-90% of ovarian tumors arise from the surface epithelium of the ovary and the serous tumors are by far the most common subtype of the epithelial ovarian tumors. Although old age and a positive family history are associated risk factors, the molecular events that underlie the development and progression of the various subtypes and stages of epithelial ovarian cancer is not completely understood. The goal of this study was to assess the significance of the mitochondrial DNA sequence variants associated with the different histologic subtypes and stages of epithelial ovarian cancer.

A total of 102 frozen epithelial ovarian tumor tissue samples of serous, endometrioid and mucinous subtypes and stages were selected based on the criteria outlined by the International Federation of Gynecology and Obstetrics (FIGO). High-resolution restriction endonucleases and PCR-based sequencing analysis were used to assess the mtDNA sequence variants spanning 3.3 kb fragment that comprised the D-Loop, 12S rRNA- tRNAphe, tRNAval,, tRNAser , tRNAasp, tRNAlys, ATPase 6 ATPase 8, cytochrome oxidase I and II genes.

Notably, the incidence of mtDNA instability at np 303-315 were found in 97% of our study samples. Interestingly, a high frequency, 81% (13/16) of TC insertion at np 310 was found only in cystadenomas, 3/3; borderline, 4/4; stage IA, 2/2; stage IB, 0/3 and matched normal tissues, 4/4 of the ovarian serous subtype. Our findings suggest that mitochondrial DNA sequence variant, TC insertion at np 310, in combination with the mtDNA instability at np 303-315, may play a potential role in the tumorigensis of ovarian serous carcinoma.
Abstract 9411: Deterioration of Myocardial Infarction in Mice Infected with Periodontal Pathogens, Aggregatibacter Actinomycetemcomitans
Authors: Tomoya Hanatani, Jun-Ichi Suzuki, Masahito Ogawa, Norio Aoyama, Yuichi Izumi, Yasunobu Hirata, Ryozo Nagai, Mitsuaki Isobe
Journal: Circulation (2011)

Introduction Chronic inflammation plays a fundamental role in coronary heart disease (CHD). Periodontal disease is a common infectious disease among adults and is a potential source of systemic inflammation. However, the effect of periodontal infection on CHD has not been proven. Hypothesis We assessed the hypothesis that periodontopathic bacteria influence myocardial infarction (MI). Methods We surgically implanted a chamber into the subcutaneous tissue of each male mouse. Two weeks after the chamber implantation, Aggregatibacter actinomycetemcomitans (A.a., n = 8), which is a major periodontal bacteria, or PBS (n = 6) was injected into the chamber once a week. One week later, MI was induced by permanent ligation of the left anterior descending coronary artery. Seven days after the operation, the ischemic hearts and blood samples were obtained. Results The plasma level of anti-A.a. antibody was statistically higher in the A.a.-infected mice than in the vehicle control mice (100.3 ± 20.3-fold vs. control, p &lt; 0.05). Seven days after the experimental ischemia, infarction area of the infected mice by A.a. was significantly larger compared to that in the control mice (p &lt; 0.05). The infarction area/ischemic myocardium ratio was 0.37 ± 0.04 in the A.a.-infected mice, while the infarction area/ischemic myocardium ratio of the control mice was 0.20 ± 0.06. Conclusions The experimental infection of periodontal bacteria could deteriorate left ventricular remodeling after MI.
Abstract 18354: Chronic Pressure-Dependent Cardiac Unloading With a Novel Intra-Atrial Shunt (V-Wave Device) in an Ovine Model of Ischemic Heart Failure: Evidence for Shunt-mediated Improvements in Function and Survivability
Authors: Carlos L del Rio, Patrick I McConnell, Yaacov Nitzan, Yukie Ueyama, Pamela Kloepfer, Bradley L Youngblood, Robert George, Meni Jacoby, Robert L Hamlin, Orna Oz, Gad Keren, Stefan Verheye, William T Abraham
Journal: Circulation (2013)

Introduction: Progressive elevations in left-ventricular (LV) filling pressures, as occurring during heart failure (HF), increase myocardial energy demand and facilitate maladaptive remodeling. We hypothesized that chronic selective left-atrial unloading can mitigate LV remodeling and functional deterioration in HF. Hence, we studied a novel intra-atrial device designed to act as a selective/pressure-dependent one-way (left-to-right) shunt, implanted in sheep with chronic ischemic HF. Methods: Sheep (45 ± 2 Kg) underwent serial/selective coronary embolizations resulting in chronic left HF (EF: 65±1 to 36±1%, LVIDd: 3.5±0.1 to 4.9±0.1 cm; P&lt;0.05). Subsequently, sheep were instrumented via a thoracotomy with indwelling catheters into the pulmonary artery, the left atrium, and the right atrium/superior vena cava in order to monitor pressures and oxygen saturations. The animals were assigned either to serve as controls (CTRL, n = 7) or had the V-Wave device (n = 14) deployed into the fossa ovalis. After recovery, valved-shunt patency (via Fick’s method), mean atrial/pulmonary pressures, and LV function (echocardiography) were evaluated weekly for up to 12 weeks. Results: The deployed shunts acutely lowered left-atrial pressures (LAP, 17±1 to 14±1 mmHg, P&lt;0.05) without increasing right-atrial/pulmonary-artery pressures. Implanted shunts were patent for the duration of the study (mean Qp/Qs: 1.17±0.03 vs 0.76±0.03 in CTRL, P&lt;0.05). Chronically, shunt-treated sheep had improved LV loading/function when compared to controls, which progressively deteriorated; over the 12-week study, treated sheep had lower filling pressures (LAP: 14±1 vs. 22±2 mmHg in CTRL, P&lt;0.05) and preserved LV function (EF: 42±3 vs. 25±2% in CTRL, P&lt;0.05) . Notably, the 12-week survival in treated animals was 93%, while only 57% of the untreated controls survived the monitoring period. Conclusion: The V-Wave device, a novel intra-atrial shunt designed to selectively unload the left-heart in a pressure-dependent manner, lead to chronically reduced filling pressures, preserved right-sided pressures, and improved LV function in a clinically-relevant chronic model of ischemic heart failure.
Abstract 4855: Long-term Effect of Efonidipine Therapy on Plasma Aldosterone and Left Ventricular Mass Index in Patients With Essential Hypertension
Authors: Takayoshi Tsutamoto, Keizo Nishiyama, Masayuki Yamaji, Chiho Kawahara, Masanori Fujii, Takashi Yamamoto, Minoru Horie
Journal: Circulation (2009)

Background. Aldosterone (ALD) breakthrough often occurs and is an important issue during long-term treatment with angiotensin-converting enzyme inhibitors (ACE-I) and angiotensin receptor blockers (ARB). Previous studies showed that ALD breakthrough the incidence of ALD breakthrough was between 22–53% after 12 months. Recently, it has been reported that efonidipine, a T-type and L-type calcium channel blocker, decreases plasma levels of ALD. However, long-term effects of efonidipine on plasma levels of ALD and left ventricular mass index (LVMI) remain unknown in patients with hypertension. Methods and Results. Sixty stable outpatients with essential hypertension who had received amlodipine and ACE-I or ARB for more than one year were randomized to two groups [amlodipine group (n=30): continuous amlodipine treatment at a stable dose; efonidipine group (n=30): amlodipine (5mg/day) was changed to efonidipine at a dose of 40mg/day]. There was no difference in the baseline characteristics including LVMI and plasma levels of ALD between two groups. In the amlodipine group, there were no significant changes in blood pressure, LVMI or plasma levels of ALD during 18 months. In the efonidipine group, blood pressure did not change after replacement of amlodipine by efonidipine, although there was a significant decrease in plasma levels of ALD after 6 months and the decrease of ALD was sustained for 18 months (106±49 pg/mL at baseline, 76±30 pg/mL at 6 months, 79±43 pg/mL at 9 months, 77±34 pg/mL at 18 months) and plasma ALD level eventually increased again in only 2 patients (7% aldosterone breakthrough). In addition, LVMI was significantly decreased after 18 months (121±25 vs. 114±21 g/m2, p&lt;0.05). There was a significant correlation between changes in LVMI and % changes of ALD in the efonidipine group (r=0.427, p=0.018). Conclusion. These findings indicate that the effect of efonidipine on suppression of plasma ALD was sustained for at least 18 months and that long-term efonidipine therapy decreases LVMI in patients with essential hypertension
Abstract 3195: Quantification of Endothelial Cell Apoptosis in Pulmonary Arterial Hypertension Using Tc99m-Annexin V
Authors: Eileen M Rattigan, Marija Sedlar, Elizabeth DelGiacco, Kazue Okajima, John Hoppin, Lynne L Johnson
Journal: Circulation (2007)

Background - Pulmonary artery hypertension (PAH) is usually detected late in its course. Early detection may allow for the earlier initiation of disease-modifying therapies. Endothelial cell (EC) apoptosis is an early event that leads to unrestrained EC growth and subsequent smooth muscle cell proliferation. We tested the hypothesis that these early apoptotic changes may be detected non-invasively using Tc99m-labeled Annexin V (Tc99m-ANX) in the monocrotaline (MCT)-induced PAH rat model. Methods - To document disease course, 54 MCT treated Sprague Dawley rats (60mg/kg) were compared to 18 controls; 5– 6 treated rats and 3 controls were sacrificed weekly over 6 weeks for gross pathology and histopathologic sectioning. PA pressures were estimated by echocardiography. EC apoptosis was detected by caspase staining in arterioles smaller than 50 microns and quantified by random sampling. A second group of 16 rats were treated with MCT and underwent serial non-invasive SPECT imaging. They were injected with 55.5 MBq of Tc99m-ANX and imaged by HiSPECT at baseline (before MCT) and weekly for 6 weeks. Quantification of Tc99m-ANX uptake was assessed by biodistribution and by region of interest (ROI) analyses of SPECT images using MIP Tool. Results - See table below. Quantitative pulmonary tracer uptake peaked at day 14, correlated with peak positive caspase staining and preceded hemodynamic changes and RVH. Tc99m-ANX pulmonary uptake seen at later time points corresponded to caspase positive inflammatory cells in a dense intra-alveolar infiltrate. Conclusions - EC apoptosis can be detected in vivo with Tc99m-ANX during the early development of PAH in MCT treated rats before the onset of any detectable changes in pulmonary pressures or changes in RV architecture. Data Summary
Effects of the Jamison-Farabee consent decree: due process protection for involuntary psychiatric patients treated with psychoactive medication
Authors: W A Hargreaves, M Shumway, E J Knutsen, A Weinstein, N Senter
Journal: American Journal of Psychiatry (1987)

The Jamison-Farabee consent decree in California mandates an outside psychiatrist's review of involuntary medication of state hospital patients. Patients' rights advocates presumably hoped the decree would facilitate more frequent medication refusal, while clinicians predicted the procedure would impair patient care. Outside review led to only a 1.1% rate of medication denial; half of the patients involved deteriorated afterward. Examination of a sample of patients subject to the decree and two comparable samples 1 year and 10 years earlier suggests that patients' successful medication refusal was no more frequent after implementation of the decree and that the procedure had negligible effects on patient care or outcome for patients not denied medication.
Cyclin D1 Promotes Survival and Chemoresistance By Maintaining ATR and CHEK1 Signaling in TP53-Deficient Mantle Cell Lymphoma Cell Lines
Authors: Suchismita Mohanty, Thai Tran, Natalie Sandoval, Atish Mohanty, Victoria Bedell, Jun Wu, Charles Warden, Anna Scuto, Joyce Collins, Dennis D. Weisenburger, Vu N. Ngo
Journal: Blood (2014)
GRN163 and GRN163L, telomerase template antagonists, inhibit the growth of human hepatoma in vivo.
Authors: Meta W. Djojosubroto, Allison C. Chin, Ning Go, Ellen Wunder, David B. Karpf, K. Lenhard Rudolph
Journal: Cancer Research (2004)

Proc Amer Assoc Cancer Res, Volume 45, 2004

2416 

Continuous proliferation of tumor cells requires telomerase activity to maintain telomere length and to stabilize chromosomes. Since treatment options are very limited for hepatocellular cancer (HCC), and since HCC is characterized by critically short telomeres, telomerase inhibition represents a new therapeutic option for this tumor type. In this study the efficacy of telomerase inhibition for the treatment of human HCC was tested using 2 thio-phosphoramidate oligonucleotide compounds (GRN163 and its lipid-conjugated form, GRN163L) directed against the RNA template region of telomerase. The tumor forming capacity of the human hepatoma cell line (Hep3B) was followed in a xenotransplant model of subcutaneous tumor cells injected in nude mice (NMRI nu/nu). GRN163L or GRN163 was given intraperitoneally five times a week for a period of 4 weeks; treatment was started when subcutaneous tumors became detectable. Both compounds significantly inhibited tumor growth in nude mice, correlating with improved survival. The reduced tumor growth with the telomerase inhibitors was dose-dependent and suggests that GRN163L is more potent. No obvious toxicity was noted throughout the treatment period with either compound. TRAP assay demonstrated an approximately six-fold reduction (p=0.04) in telomerase activity in the tumors of treated mice. BrdU staining revealed reduced proliferation (20.5%, p=0.007) and TUNEL assay showed increased apoptosis in the tumors from the treated mice compared to the control mice. These data demonstrate the significant potential of the specific telomerase inhibitors GRN163L and GRN163 as a new treatment option for human HCC. Efficacy of combination therapy with telomerase inhibitors (GRN163 or GRN163L) and chemotoxic agents will also be presented.
Abstract #3775: Mechanistic studies of AV370, a potent FGFR3 antagonistic antibody
Authors: Ailin Bai, William Winston, Kristan Meetze, Sriram Kollipara, Jin-Kyeung Woo, Nhi Vo, Monica Kosmatka, Lyne Breault, Solly Weiler, Omar Kabbarah, Andrea Boudrow, Kelly Connolly, Michael DiPrima, Hamid Tissire, Jinwei Jiang, Jeno Gyuris, Zhigang Weng
Journal: Cancer Research (2009)

AACR Annual Meeting-- Apr 18-22, 2009; Denver, CO

The t(4;14)(p16.3;q32) translocation found in approximately 15% of patients with multiple myeloma leads to aberrant expression of 2 putative oncogenes, MMSET (a histone methyltransferase) and FGFR3 (a receptor tyrosine kinase). Patients carrying the t(4:14) translocation have a poor prognosis. Previous studies have demonstrated the oncogenic potential of FGFR3 in t(4:14) multiple myeloma, therefore targeting this receptor tyrosine kinase represents an attractive therapeutic opportunity in this patient population. Monoclonal antibodies have been developed to specifically block FGFR3 signaling in response to ligand stimulation. However, some of the tumors that harbor the t(4;14) translocation also carry mutations in FGFR3 that render the receptor constitutively active or hypersensitive to ligand stimulation. Whether antibody treatment is effective on tumors expressing mutant FGFR3 needs to be evaluated in preclinical models. The antagonistic anti-FGFR3 antibody, AV370 potently inhibits ligand-induced proliferation of FDCP cells expressing wild type FGFR3. AV370 also binds to mutant FGFR3 receptor with high affinity and inhibits the proliferation of FDCP cells driven by some mutant variants of the receptor. When tested in xenograft models using multiple myeloma cell lines, AV370 also significantly inhibited the growth of the OPM-2 xenograft that carries the K650E mutation in FGFR3. Although K650E mutation is thought to constitutively activate the receptor, we demonstrated that the tyrosine phosphorylation of this mutant receptor can be further stimulated by its ligands and AV370 could inhibit its tyrosine phosphorylation both in vitro and in vivo. Both cell surface and total FGFR3 level in OPM-2 cells were markedly reduced upon incubation with AV370. A profound receptor dowregulation in OPM-2 xenografts was also observed within 8 hours and the receptor downregulation sustained for at least 72 hours following a single dose of AV370 treatment. Similar receptor downregulation was also observed in another multiple myeloma cell line that carries a different activating mutation. Inhibition of receptor phosphorylation and induction of receptor downregulation by AV370 could bring therapeutic benefits to multiple meyloma patients with t(4:14) translocation.

Citation Information: In: Proc Am Assoc Cancer Res; 2009 Apr 18-22; Denver, CO. Philadelphia (PA): AACR; 2009. Abstract nr 3775.
Prostanoids from tumor cells induce Arginase I in tumor associated suppressor myeloid cells, that block T cell function
Authors: Paulo C. Rodriguez, David Quiceno, Jovanny Zabaleta, Juan B. Ochoa, Augusto C. Ochoa
Journal: Cancer Research (2005)

5305  Alterations in the immune response of patients with cancer have been described for several decades. Tumor associated suppressor myeloid cells (TAMC) produce high amounts of arginase I, which depletes L-Arginine in the microenvironment, inhibits CD3ζ expression and blocks T cell proliferation. However, the mechanisms of arginase induction I in TAMC are poorly understood. The aim of this study was to characterize the mechanisms of induction of arginase I in 3LL tumors. The results show that arginase I induction in the TAMC is independent of cytokine produced by T cells, as shown by a similar arginase I expression in tumor bearing SCID mice and wild type C57BL/6. In contrast, TAMC co-cultured with 3LL cells or 3LL supernatants maintained the expression of arginase I. 3LL cells constitutively express COX-1 and COX-2 and produce high levels of PGE2, which can induce arginase I in macrophages. Blocking of PGE2 partially prevented arginase I induction. Furthermore, inhibition of COX-2, but not COX-1, using pharmacological agents or siRNA probes completely blocked arginase I induction by 3LL cells both in vitro and in tumor bearing mice. Use of PGE2 analogs suggested that signaling through EP4 receptor plays an important role on the arginase I induction. Altogether the data suggest that the production of prostanoids, including PGE2, by tumor cells are important in the arginase I induction in tumors.
Relationship Between Bacterial Infection of Hepatobiliary System and Common Bile Duct Obstruction in Man
Authors: L R FREEDMAN, I S GOLDENBERG
Journal: JAMA (1963)

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
Doctors' Work: The Legacy of Sir William Osler
Authors: H. S. Meyer
Journal: JAMA (2003)

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 alternative treatment for postcholecystectomy Mirizzi’s syndrome: cystic duct balloon dilation
Authors: Bülent Odemis, Erkin Oztaş, Muhammet Akpınar, Serkan Torun, Ufuk Kuzu, Ertugrul Kayacetin
Journal: Endoscopy (2015)

Postcholecystectomy Mirizzi's syndrome is an extremely rare condition that is caused by a stone in the cystic duct remnant. Remnant cystic duct calculus could be due to either a retained stone or recurrence of a stone [1]. A 68-year-old woman with jaundice, fever, and abdominal pain was admitted to our hospital. She had been diagnosed with type-1 Mirizzi's syndrome 8 months previously and had undergone laparoscopic cholecystectomy. Laboratory studies at our hospital revealed the following results: leukocyte count 27 430, alanine aminotransferase 88 U/L, aspartate aminotransferase 173 U/L, gamma glutamyl transferase 484 U/L, lactate dehydrogenase 624 U/L, total serum bilirubin 7.36 mg/dL, and direct serum bilirubin 5.67 mg/dL.
Dominance of Furosemide for Loop Diuretic Therapy in Heart Failure
Authors: Behnood Bikdeli, Kelly M. Strait, Kumar Dharmarajan, Chohreh Partovian, Steven G. Coca, Nancy Kim, Shu-Xia Li, Jeffrey M. Testani, Usman Khan, Harlan M. Krumholz
Journal: Journal of the American College of Cardiology (2013)