tbuckley/cabot-search huggingface dataset:
Effect of cold water immersion on repeated cycling performance and limb blood flow
Authors: J Vaile, C O'Hagan, B Stefanovic, M Walker, N Gill, C D Askew
Journal: British Journal of Sports Medicine (2010)

The purpose of the present study was to compare the effects of cold water immersion (CWI) and active recovery (ACT) on resting limb blood flow, rectal temperature and repeated cycling performance in the heat. Ten subjects completed two testing sessions separated by 1 week; each trial consisted of an initial all-out 35-min exercise bout, one of two 15-min recovery interventions (randomised: CWI or ACT), followed by a 40-min passive recovery period before repeating the 35-min exercise bout. Performance was measured as the change in total work completed during the exercise bouts. Resting limb blood flow, heart rate, rectal temperature and blood lactate were recorded throughout the testing sessions. There was a significant decline in performance after ACT (mean (SD) −1.81% (1.05%)) compared with CWI where performance remained unchanged (0.10% (0.71%)). Rectal temperature was reduced after CWI (36.8°C (1.0°C)) compared with ACT (38.3°C (0.4°C)), as was blood flow to the arms (CWI 3.64 (1.47) ml/100 ml/min; ACT 16.85 (3.57) ml/100 ml/min) and legs (CW 4.83 (2.49) ml/100 ml/min; ACT 4.83 (2.49) ml/100 ml/min). Leg blood flow at the end of the second exercise bout was not different between the active (15.25 (4.33) ml/100 ml/min) and cold trials (14.99 (4.96) ml/100 ml/min), whereas rectal temperature (CWI 38.1°C (0.3°C); ACT 38.8°C (0.2°C)) and arm blood flow (CWI 20.55 (3.78) ml/100 ml/min; ACT 23.83 (5.32) ml/100 ml/min) remained depressed until the end of the cold trial. These findings indicate that CWI is an effective intervention for maintaining repeat cycling performance in the heat and this performance benefit is associated with alterations in core temperature and limb blood flow.
Massive Plasmodium falciparum visceral sequestration: a cause of maternal death in Africa
Authors: P. Castillo, C. Menéndez, A. Mayor, C. Carrilho, M.R. Ismail, C. Lorenzoni, F. Machungo, N. Osman, L. Quintó, C. Romagosa, C. Dobaño, P.L. Alonso, J. Ordi
Journal: Clinical Microbiology and Infection (2012)
Predicting sarcoma-patients response to trabectedin treatment with molecular markers detected by immunohistochemistry.
Authors: Juan Carlos Tercero, Jose Jimeno, Nerea Martinez, Santiago Montes-Moreno, Socorro M. Rodriguez-Pinilla, Margarita Sanchez-Beato
Journal: Clinical Cancer Research (2008)

B8   Trabectedin (Yondelis ® , ET-743) is a marine anticancer agent that has been shown to induce long lasting objective remissions and tumor control in a subset of patients with pretreated/resistant soft tissue sarcoma. Drug induced tumor control is achievable in a group of such patients, but there is no clear identification of the molecular features that correlate with clinical sensitivity/resistance to Trabectedin. Trabectedin binds in the minor groove of DNA, blocks transcription factors activity, and traps protein from the nucleotide excision repair system affecting cellular cell cycle. Different studies performed in cell lines treated with the drug and others correlating DNA polymorphisms and RNA levels with drug response, suggest several markers implicated in DNA repair or other relevant cancer genes, that could be useful in predicting patients treatment response to Trabectedin.  To test this hypothesis we analyze the expression of potential biomarkers of sensitivity to Trabectedin implicated in DNA repair (XPG, XPA, ERCC1, BRCA1, BRCA2, ATM, DNA-PK, CHK 1, CHK2 and RAD51) or cell cycle (P21, P16, RCC1, P53, MDM2, DNA-PRIM, DNA-polA and CDK7) in a group of 177 sarcoma samples from patients treated with Trabectedin, using immunohistochemical detection on Tissue Microarrays (TMAs). Correlation with clinical variables (PFS and OS) was performed using conventional biostatistical tools.  Estimated OS of the whole series at 12 months was 49,1% (95% CI (41,4%-56,8%) and estimated PFS at 6 months was 36% (95% CI (29%-43,1%)).  Preliminary data suggests that XPG, BRCA1 and 2, and RAD51 could help to predict the outcome in sarcoma patients treated with Trabectedin. The most remarkable findings were a clear trend associating of low levels of BRCA2 expression, with better  OS at 12 months (59.5%; 95% CI (47.2%-71.9%)  vs . 36.3%; 95% CI (14.3%-58.3%) p: 0.0795); association of low expression of RAD51, with longer  PFS at 6 months (45.4%; 95% CI (34.7%-56.1%), vs. 30.0%; 95% CI (1.6%-58.4%); p: 0.0624) and a statistical significant association between high levels of XPG protein expression with an increment in the median of PFS (3.7 m (95% CI: 2.6-6.4) vs 7.1 m (95% CI: 3.5-27.3); p= 0.0411).  In conclusion, immunohistochemical evaluation of these markers allows routine analysis of tumor DNA repair efficiency in clinical pathology laboratories and provides potential immunohistochemical markers predictive of treatment response to Trabectedin.
Chloroethylnitrosourea treatment induces growth inhibition, shifts the pool of methyl and targets methylation of PP2A in melanoma cells
Authors: Samuel Guénin, Laurent Schwartz, Daniel Morvan, Maurice Israel, Jean-Claude Madelmont, Aicha Demidem
Journal: Cancer Research (2006)

4690  Chloroethylnitrosourea (CENU) chemotherapy is used in the treatment of melanoma. Its main target is DNA. Few studies relate to CENU-induced effects on metabolism and signaling pathway in tumor cells escaping cell death. We provide evidence that CENU treatment induces growth inhibition by altering the methyl group distribution in the nucleus and in the cytoplasm. This alteration resulted in the methylation of protein phosphatase 2A (PP2A). Methods: The effect of CENU on metabolism and cell signaling was investigated in B16 melanoma cell culture by: cell proliferation, cell cycle, protein content, protein analysis using Western Blot, and methylation of protein and DNA using methionine labeling with 14C. To confirm the regulation of PP2A, we used okadaic acid (OA), an inhibitor of PP2A. CENU-treated cells were exposed to OA (5nM) for 48 hours during the growth inhibition phase. Results: Cell proliferation in response to CENU can be summarized in two phases: a growth inhibition phase (GI) characterised by an alteration of cell cycle, an increase in protein content and a growth recovery phase (GR) with delayed cell proliferation. First, we showed that during the GI phase, there is an increase in the incorporation of L-[14CH3]-methionine into the cytoplasmic and nuclear proteins (fold 7 and 13 respectively, vs control). During this phase, there was an increase of PP2A expression and methylation of the catalytic subunit of PP2A (+35%) and a decreased expression of PAkt (-65%), Akt (-30%) and c-Myc (-57%). OA prevents the methylation of PP2A resulting into an increase of these oncoproteins expression. Moreover OA disrupted beta tubulin expression. To confirm the link between CENU and PP2A methylation, we were able to show that the adjunction of OA during the GI phase resulted in an increase in cell proliferation. Second, during the GR phase, there was a modification of the methylation pattern, consistent with a decrease in the methylation of the cytoplasm but a persistent methylation of the DNA. However PP2A methylation was maintained (+65%) as well as the lower expression of PAkt (-15%) and c-Myc (-29%) whereas Akt expression returned to baseline level. The lack of Akt activation was associated with the decrease in cell proliferation rate and the decreased c-Myc expression. The expression of these oncoproteins provided new data on cell signaling under CENU treatment such as Akt activation and c-Myc down-regulation that correlate with reduced tumor cell survival. Conclusion: The cytostatic effect of the CENU appeared to be a consequence of the methylation of PP2A which in turn down regulates c-Myc, P-Akt and Akt. It is probable that the methylation of PP2A is a prime target for drug discovery. Thus these data may have implications in the understanding of the responses to chemotherapy and in the clinical management of anti-cancer drugs.
Combination of Tyrosine Kinase Inhibitor with β-Catenin/CBP Modulator C82 Reverses TKI Resistance, Eradicates Quiescent CML Stem/Progenitors Cells, and Overcomes MSC-Associated Microenvironmental Protection
Authors: Hongsheng Zhou, Po Yee Mak, Hong Mu, Duncan H Mak, Hiroyuki Kouji, Marina Konopleva, Jorge E. Cortes, Michael Andreeff, Bing Z Carter
Journal: Blood (2014)
300 million years of conserved synteny between chicken Z and human chromosome 9
Authors: Indrajit Nanda, Zhihong Shan, Manfred Schartl, Dave W. Burt, Michael Koehler, Hans-Gerd Nothwang, Frank Grützner, Ian R. Paton, Dawn Windsor, Ian Dunn, Wolfgang Engel, Peter Staeheli, Shigeki Mizuno, Thomas Haaf, Michael Schmid
Journal: Nature Genetics (1999)
Assessment of clinical parameters associated with mutational status in metastatic malignant melanoma: a single-centre investigation of 141 patients
Authors: M. Schlaak, A. Bajah, T. Podewski, N. Kreuzberg, W. von Bartenwerffer, E. Wardelmann, S. Merkelbach-Bruse, R. Büttner, C. Mauch, P. Kurschat
Journal: British Journal of Dermatology (2013)

Background Inhibitors of the mutated, constitutively activated BRAF protein have shown efficacy in the treatment of metastatic melanoma in clinical trials. Mutation analysis especially of the BRAF, NRAS and KIT genes is essential to identify patients suitable for targeted therapies and has been introduced into routine patient care. Objectives To correlate mutational status with clinical parameters including age, skin type, number of melanocytic naevi, primary tumour location, chronic sun damage and exposure to ultraviolet (UV) irradiation. The overall aim was to define subgroups with an increased or decreased likelihood of gene mutations. Additionally, the impact of activating BRAF mutations on clinical course was investigated. Methods In a single-centre, retrospective approach, mutation analysis was performed on patients with metastatic malignant melanoma. Clinical parameters were correlated with molecular findings. The total sun-burden score was assessed using a validated standardized questionnaire. Results The analysis included 141 patients with metastatic melanoma. Forty-four per cent of patients had activating BRAF mutations and were significantly younger than patients with wild-type BRAF or with NRAS mutations. KIT mutations were detected in only 3% of the patients. BRAF-mutated melanomas developed preferentially in intermittently sun-exposed areas of the body, and patients had significantly more melanocytic naevi. Once patients had progressed into stage IV disease, survival times were identical for those with BRAF-mutated and BRAF wild-type tumours. Conclusions Mutations of the BRAF gene are correlated with younger age, a higher number of melanocytic naevi and a tumour location in intermittently UV-exposed skin. Signs of chronic photodamage are not indicative of mutational status. Patients with metastatic melanoma with BRAF mutations showed a nonsignificant tendency to progress later to stage IV disease, but once metastases were present the prognosis was identical to that with BRAF wild-type tumours.
Abstract 91: Aspects on Resuscitation in the Coronary Interventional Catheter Laboratory.
Authors: Henrik Wagner, Bjarne Madsen Hardig, Matthias Gotberg, Jan Harnek, Goran K Olivecrona
Journal: Circulation (2010)

Introduction: Mechanical chest compressions during prolonged cardiac arrest situations, where normal advanced life support efforts fails, using continued percutaneous coronary intervention has been...
Abstract 4323: Mortality Associated With Proton Pump Inhibitors Following Percutaneous Coronary Interventions With Drug Eluting Stents
Authors: Joseph M Sweeny, Annapoorna Kini, Paul Muntner, Madhavi Jakkula, Michael Farkouh, Samin Sharma
Journal: Circulation (2009)

Background: Proton pump inhibitors (PPIs) are frequently co-administered with aspirin and clopidogrel as gastrointestinal prophylaxis following percutaneous coronary interventions (PCI). PPIs have ...
Abstract MP89: Cardiovascular and Stroke Mortality in Asian Americans (2003-2010)
Authors: Powell O Jose, Ariel T Frank, Kristopher I Kapphahn, Benjamin A Goldstein, Karen Eggleston, Mark R Cullen, Latha P Palaniappan
Journal: Circulation (2014)

Background: Asian Americans are a rapidly growing racial/ethnic group in the United States. Our current understanding of Asian American cardiovascular disease mortality patterns is distorted by the aggregation of distinct subgroups, which masks the heterogeneity of cardiovascular disease and survival among diverse Asian American subgroups. Objective and Design: We examined cardiovascular disease and stroke mortality rates for the six largest Asian American subgroups (Asian Indian, Chinese, Filipino, Japanese, Korean, and Vietnamese) from 2003-2010. U.S. death records were used to identify race/ethnicity and cause of death by ICD-10 coding (I00-I09, I11, I13, I20-I69). Standardized mortality ratios (SMR), relative SMRs (rSMRs), and proportional mortality ratios (PMR) were calculated for each sex and ethnic group relative to Non-Hispanic Whites (NHW). Results: 15,943,806 death records were examined. Asian Indian men and women and Filipino men had higher relative SMRs and PMRs for all cardiovascular disease and ischemic heart disease compared to NHWs and other Asian subgroups. Every female Asian subgroup except Koreans had higher rSMRs and PMRs for rheumatic heart disease compared to NHWs. Relative SMRs and PMRs were lower for heart failure but higher for hypertensive heart disease and all cerebrovascular disease including both ischemic and hemorrhagic stroke for men and women in every Asian subgroup compared to NHW men and women, respectively. Conclusions: The variation in cardiovascular disease and stroke mortality patterns among diverse Asian American subgroups calls to attention the need for more research to help direct more specific treatment and prevention efforts, especially in hypertension and stroke, to reduce health disparities for this rapidly growing population.
The old and the new
Authors: Colin Douglas
Journal: BMJ (2001)

In a crowded lift in a fairly important building in London's political village there was a momentary drama. The doors closed, the lift lurched upwards, then dropped a few inches. Assorted apparatchiks and policy wonks glanced at each other nervously. A squat, square middle-aged man looked upwards, shook his head and murmured, “Bloody winding engineers.” I laughed, but no one else did.

He was vaguely familiar—an MP and former miner—and definitely old Labour. I remembered where I'd met him first. We …
Sex Differences in Mortality After Coronary Artery Bypass Graft Surgery
Authors: Robert H Habib, Anoar Zacharias, Thomas A Schwann, Christopher J Riordan, Samuel J Durham, Aamir Shah
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
Bill Banning Late-term Abortion Now in the Senate
Authors: Laura Buchholz
Journal: JAMA (2015)

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
Synthetic siRNA targeting heat shock protein 105 induces the apoptosis of various cancer cells both in vitro and in vivo.
Authors: Seiji Hosaka, Tetsuya Nakatsura, Yasuharu Nishimura, Hideo Baba
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

5515 

We previously reported that the heat shock protein 105 (HSP105), identified by a serological analysis of the recombinant cDNA expression library (SEREX) using the serum from a pancreatic cancer patient, was overexpressed in various human tumors and the testis in adult human tissues by immunohistochemical analysis. In the present study, to elucidate the biological function of HSP105 protein in cancer cells, we first established NIH3T3 cells overexpressing murine HSP105 (NIH3T3-HSP105). The NIH3T3-HSP105 cells acquired resistance to apoptosis induced by heat shock or doxorubicin. The siRNA-mediated suppression of HSP105 protein expression induced apoptosis in human cancer cells but not in fibroblasts. By the combination of siRNA introduction and doxorubicin or heat shock treatment, apoptosis was synergistically induced in a human colon cancer cell line, HCT116 cells. In vivo , siRNA inoculation into a human gastric cancer cell line KATO-3 tumor established in the flank of an NOD SCID mouse suppressed the tumor growth. This siRNA-induced apoptosis was mediated through caspases, but not p53 tumor suppressor protein, even though the HSP105 protein was bound to wild type p53 protein in HCT116 cells. These findings suggest that the constitutive overexpression of HSP105 in cancer cells is therefore involved in malignant transformation by protecting tumor cells from apoptosis. HSP105 may thus be a novel target molecule for cancer therapy and the treatment regimen using synthetic siRNA to suppress the expression of HSP105 protein may therefore provide a new strategy for cancer therapy.
Israel to increase fluoridated drinking water
Authors: J. Siegel-Itzkovich
Journal: BMJ (1998)

Nearly all Israelis will be drinking fluoridated water within the next few years after a Knesset (parliamentary) committee passed a regulation requiring all cities and towns with over 5000 residents to build fluoridation plants.

The Knesset's labour and social affairs committee has finally resolved an issue that has been causing arguments between the health ministry and municipalities for a decade. Until now, the ministry …
Influenza pandemic planning in Europe
Authors: W J Paget
Journal: Eurosurveillance (2001)

The World Health Organization strongly recommends that all countries prepare in advance multidisciplinary pandemic plans to prevent and control the next influenza pandemic. We carried out a survey of influenza surveil-lance methods among members of the European Influenza Surveillance Schemes, EISS, which included a set of questions on pandemic planning. All but one of the countries have a pandemic plan or are in the process of producing one. A coordination of these different national plans at a European level would probably contribute to their improved impact and efficiency.
Combined soluble receptor for advanced glycation endproducts (sRAGE) with cytotoxic chemotherapy effectively reduces metastatic tumor growth in a spontaneous mammary tumor model through modulation of cell proliferation and apoptosis
Authors: Kathie-Ann P. Joseph, Pinglan Wan, Yan Lu, Wu Qu, Ann-Marie Schmidt
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

4624 

INTRODUCTION: The receptor for advanced glycation endproducts (RAGE) has been implicated in tumor growth. Blockade of RAGE has previously been shown to halt the progression of breast tumors in an early intervention murine model of breast cancer through modulation of cell proliferation and increased apoptosis. High doses of a RAGE antagonist, soluble or (s)RAGE (100 μg), the extracellular ligand-binding domain of the receptor, have previously been shown to significantly reduce metastatic tumor growth. We hypothesize that the addition of sRAGE in doses lower than the maximally therapeutic dose to standard chemotherapeutic agents for metastatic breast cancer may enhance the effectiveness of monotherapy in a murine metastatic breast cancer model. METHODS: Female MMTV transgenic mice (age, 12-16 weeks) were divided into four groups: (1) Control group-no treatment, (2) doxorubicin (DOX) 2 mg/kg IP weekly (3) sRAGE 20 μg IP daily and (4) DOX 2 mg/kg IP weekly and sRAGE 20 μg IP daily for 4 weeks. The mice were sacrificed and tumors harvested on treatment day 35. Tumors were weighed, measured and lung surface metastases counted. RESULTS: There was a significant reduction in primary tumor weight between the control (n=9) and the combination (sRAGE/DOX) groups (n=6) (5.3g v. 3.9g) (p<0.05). The average tumor weight of the DOX alone group (n=6) was 3.4 (p<0.05) and for the sRAGE alone group(n=10) was 4.4g (p= NS). Additionally, there was a significant reduction in lung metastases in the DOX alone group compared to controls (23.2 vs 82.7, p < 0.05) and even further reduction in lung metastases in the combination group (15.4 vs. 82.7, p < 0.05). Additionally, there was a significant reduction in %PCNA positive cells in the combination group as well as a significant increase in TUNEL staining compared with controls as measured in the primary tumors. CONCLUSIONS: Although low dose sRAGE alone did not appear to have a significant effect on primary tumor growth in this metastatic model, the addition of sRAGE to doxorubicin enhanced the suppression of local tumor growth and lung metastases. Further, the addition of sRAGE to doxorubicin enhanced the effectiveness of this standard chemotherapy agent. The mechanism by which RAGE antagonism suppresses primary tumor growth and lung metastases appears to be through modulation of tumor cell proliferation and apoptosis.
Re: Long-Term Outcomes in Patients with Muscle-Invasive Bladder Cancer After Selective Bladder-Preserving Combined-Modality Therapy: A Pooled Analysis of Radiation Therapy Oncology Group Protocols 8802, 8903, 9506, 9706, 9906, and 0233
Authors: Ofer N. Gofrit
Journal: European Urology (2015)
391. Targeted Delivery of Adenovirus Expressing eNOS to the Endothelium In Vivo Lowers Blood Pressure in Hypertensive Rats
Authors: W H Miller, M J Brosnan, D Graham, A J Frater, K M Channon, S M Danilov, P N Reynolds, A H Baker, A F Dominiczak
Journal: Molecular Therapy (2004)