tbuckley/cabot-search huggingface dataset:
Abstract 87: Brainstem Reflex Score Within 24 Hours of Hospital Admission Predicts Survival Post Cardiac Arrest
Authors: Shaker M Eid, Umashankar Lakshmanadoss, Skon M Nazarian, Rafael Llinas, Dhananjay Vaidya, Kerry J Stewart, Nisha Chandra-Strobos
Journal: Circulation (2011)

Background: Post Arrest Prognosis continues to be based on the neurologic exam at &gt;72 hours. We investigated whether a novel, simple clinical tool at 24 hours could predict survival-to-discharge post cardiac arrest. Methods: Data was collected on 123 survivors of non-traumatic out-of-hospital cardiac arrest (age 63 ± 15, 62% males) according to Utstein guidelines. Daily neurologic examination was performed and a brainstem reflex score (BRS) was derived from five brainstem reflexes: 1) pupillary reflex, 2) corneal reflex, 3) cough/gag reflex, 4) oculocephalic reflex (doll's eye), and 5) spontaneous breathing. We assumed that each brainstem reflex has an equal impact and assigned one point for each reflex present, giving a range of the BRS from 0 (worst) to 5 (best). BRS ≥3 was tested for association with survival and good neurologic outcome (CPC 1+2). Univariate and multivariate logistic regression analysis were used for assessment of outcome predictors. Data are reported as percentage, mean and standard deviation or odds ratio. Results: Of 123 patients, 84 (68.3%) had a witnessed arrest, 43 (34.9%) received bystander CPR, 25 (20.3%) had VF/VT as their initial arrest rhythm and time to return of spontaneous circulation {ROSC} was 35.5 ± 32.3 min (95% CI 29.4 - 41.6). Also, 86 (69.9%) were sedated during the initial 24 hours, 53 (43.1%) received hypothermia and only 31 (25.2%) survived to discharge. Univariate analysis identified and multivariate analysis confirmed, as noted below, that BRS ≥3 at 24 hours is an accurate, early predictor of survival to discharge. Although BRS also emerged as a predictor of good neurologic outcome on univariate analysis (OR=5.17, 95% C.I. 1.88-14.24, p=0.001) this association was not confirmed on multivariate testing (OR=1.90, 95% C.I. 0.16-22.40, p=0.610). Conclusion: BRS is a simple clinical tool that can be universally used and appears to be highly predictive of survival to discharge. This observation needs to be tested in larger cohorts.
Abstract 1684: Histone deacetylase inhibition enhances Pemetrexed cytotoxicity through induction of apoptosis and autophagy in non-small cell lung cancer models
Authors: Daniela Trisciuoglio, Marianna Desideri, Teresa D. Luca, Marta D. Martile, Chiara Gabellini, Adriana Eramo, Ruggero D. Maria, Michele Milella, Donatella Del Bufalo
Journal: Cancer Research (2014)

Abstract Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related death worldwide. Pemetrexed (PEM), a multi-target folate antagonist, has demonstrated targeted efficacy in NSCLC histological subtypes characterized by low thymidylate synthase (TS, one of PEM's molecular targets) expression. Histone deacetylase inhibitors (HDACi) modulate the expression of multiple genes, including thymidylate synthase (TS), one of the main targets of Pemetrexed. Since high levels of TS have been linked to clinical resistance to Pemetrexed in non-small cell lung cancer (NSCLC), we investigated the molecular and functional effects of combined Pemetrexed and ITF2357, a class I/II HDACi currently in clinical trials as anti-cancer agents .ITF2357 reduced TS mRNA and protein expression, potentially affecting sensitivity to Pemetrexed. When the two drugs were used in combiation, their sequence of administration was critical in determining the pharmacologic response: in both NSCLC cell lines and LCSC, a strikingly synergistic reduction in cell viability was observed with the sequence Pemetrexed followed by ITF2357, in both adenocarcinoma and squamous cell carcinoma models. Cell death induced by the combination involved both apoptosis and autophagy. Genetic and pharmacological approaches provided an interesting link between these two pathways and showed that sequential Pemetrexed/ITF2357 causes a toxic form of autophagy with consequent activation of a caspase-dependent apoptotic program. In vivo experiments in NSCLC xenografts confirmed that sequential Pemetrexed/ITF2357 is feasible and results in increased inhibition of tumor growth and increased mice survival. Overall, this data provide a strong rationale for the clinical development of sequential schedules employing Pemetrexed followed by HDAC inhibition in NSCLC. Citation Format: Daniela Trisciuoglio, Marianna Desideri, Teresa De Luca, Marta Di Martile, Chiara Gabellini, Adriana Eramo, Ruggero De Maria, Michele Milella, Donatella Del Bufalo. Histone deacetylase inhibition enhances Pemetrexed cytotoxicity through induction of apoptosis and autophagy in non-small cell lung cancer models. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 1684. doi:10.1158/1538-7445.AM2014-1684
Some Peculiar Biological and Biochemical Properties of a Mouse Hepatoma induced by Chrysoidin. II. Metabolic Properties of the Hepatoma&lt;xref ref-type="fn" rid="FN1"&gt;2&lt;/xref&gt;
Authors: Zygmunt Albert, Marian Orłowski
Journal: JNCI Journal of the National Cancer Institute (1960)

The metabolism of slices of a transplanted hepatoma originally induced with chrysoidin (2,4′-azodianiline) in C57BL mice was compared with that of liver slices from normal animals of the same strain. The metabolism of the hepatoma is characterized by a high respiratory rate, a high anaerobic glycolytic rate, and a low aerobic glycolytic rate no different from that of normal liver. This metabolic behavior is indicative of a low Warburg ratio. High aerobic and anaerobic glycolytic rates were observed in other tumors examined, i.e., Crocker sarcoma 180, a spontaneous mammary adenocarcinoma of mice, a primary rat hepatoma, and a transplanted hamster hepatoma.
Abstract 1608: Profiling c-Met and EGFR kinase inhibitor resistance pathways in non-small lung cancer cells
Authors: Ryan D. Bomgarden, Ryan Jacobs, Jason Fong, David Moravec, Gregory M. Botting, Michael Blank, Rosa I. Viner, John C. Rogers, Neelu Puri
Journal: Cancer Research (2014)

Abstract Tyrosine kinase inhibitors (TKIs) against c-MET and EGFR have positive therapeutic effects in a subset of Non-Small Cell Lung Cancer (NSCLC) patients; however, their clinical efficacies are limited due to the development of TKI resistance. To determine mechanisms of TKI resistance, two NSCLC model cell lines H2170 and H358 were made resistant to the c-Met/EGFR TKIs SU11274, erlotinib or a combination of both by exposing the cells to progressively increasing concentrations of inhibitor. Initial characterization of these cell lines using phospho-specific antibodies showed that phospho-c-Met was found to be downregulated 4- and 1.5- fold in SU11274-resistant (SR) H2170 and SR H358 cells, respectively. Phospho-EGFR was found to be constitutively autophosphorylated (upregulated 19-fold) in erlotinib-resistant (ER) H2170 cells, but downregulated 6-fold in ER H358 cells. Interestingly, c-Met/EGFR downstream signaling proteins p-mTOR, p-p70S6K and p-ERK were found to be 2-4-fold upregulated, 2-fold upregulated and 2-5-fold upregulated, respectively, in ER H2170 and H358 cells. Phospho-p70S6K was also found to be upregulated 20-fold in SR H2170 cells. These results indicate that alternative signaling pathways may confer TKI resistance in these cell lines. To identify which signaling pathways may be responsible for TKI resistance, H358 parental and resistant cell lines were analyzed by mass spectrometry (MS). Differences in protein expression in cell lines treated with and without EGF and/or erlotinib were measured using higher multiplexing Thermo Scientific™ Tandem Mass Tag™ (TMT™) reagents. More than 1500 protein groups were identified and quantified using a Thermo Scientific™ Orbitrap™ Fusion™ platform with HCD-MS2 and MS3 fragmentation methods. Protein expression in ER H358 cells showed a marked increase in expression of DNA replication proteins, transcription factors, apoptosis inhibitors and some Ras-associated signal transduction pathways. To further investigate the mechanism of TKI resistance, phospho-peptide enrichment was also used in combination with TMT quantitation to profile changes in protein phosphorylation state. Overall, the combination of phospho-peptide enrichment coupled with higher multiplexing TMT and high resolution MS analysis enabled deeper global profiling of TKI resistance signaling pathways compared to previous studies without enrichment. Citation Format: Ryan D. Bomgarden, Ryan Jacobs, Jason Fong, David Moravec, Gregory M. Botting, Michael Blank, Rosa I. Viner, John C. Rogers, Neelu Puri. Profiling c-Met and EGFR kinase inhibitor resistance pathways in non-small lung cancer cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 1608. doi:10.1158/1538-7445.AM2014-1608
Abstract 12182: Brain-Derived Neurotrophic Factor Maintains Exercise Capacity and Mitochondrial Function in the Skeletal Muscle Through Ampk-Pgc1α Signaling
Authors: Shingo Takada, Shintaro Kinugawa, Shouji Matsushima, Wataru Mizushima, Arata Fukushima, Takaaki Furihata, Tomoyasu Kadoguchi, Takashi Yokota, Tadashi Suga, Koichi Okita, Hiroyuki Tsutsui
Journal: Circulation (2014)

Background: Brain-derived neurotrophic factor (BDNF), a member of neurotrophin family, exists not only in the brain but also in the skeletal muscle. We have demonstrated that its serum levels are decreased in heart failure (HF) and are correlated with exercise capacity, indicating that it may regulate skeletal muscle function. We thus determined its physiological role in exercise capacity and mitochondrial function of skeletal muscle by using the gene deletion both in vivo and in vitro. Methods and Results: Experiments were performed using male wild type (WT, n=8) and BDNF knockout (KO+/-) mice (n=8, 15 to 17 weeks). Body and organ weights, cardiac function assessed by echocardiography, and metabolic parameters including blood sugar, insulin, and lipid profiles did not differ between groups. Plasma BDNF level (15±1 vs. 22±1 pg/mL) as well as BDNF protein levels and phosphorylation of TrkB (tyrosine kinase receptor), BDNF binding receptor were significantly decreased in the skeletal muscle from BDNF KO+/- compared to WT mice (all p&lt;0.05). Citrate synthase (CS) (17±2 vs. 44±2 mM/min/μg protein, p&lt;0.05) and mitochondrial complex I and III activities were significantly decreased in BDNF KO+/-. Phosphorylation of AMPK and peroxisome proliferator-activated receptor γ co-activator 1α (PGC1α) levels were significantly lower in BDNF KO+/- by 20% and 25%, respectively (p&lt;0.05). The work (distance x body weight; 26±1 vs. 16±1 J, p&lt;0.05) and peak oxygen uptake (VO2; 162±4 vs. 136±3 mL/kg/min, p&lt;0.05) evaluated by treadmill test were significantly decreased in BDNF KO+/-. Treatment of BDNF KO+/- mice with a specific activator of AMPK (AICAR, 500 mg/kg/day, i.p. for 5 weeks) significantly improved the reduced work (22±1 J), peak VO2 (159±2 mL/kg/min), and CS activity (34±2 mM/min/μg protein) in the skeletal muscle. To further determine the direct role of BDNF in the regulation of mitochondrial function in vitro, knockdown of BDNF in C2C12 myotube by using siRNA decreased the phosphorylation of AMPK and PGC1α protein level of by 70% and 42%, respectively. Conclusions: BDNF plays an essential role in the maintenance of exercise capacity and the regulation of mitochondrial function in the skeletal muscle thought the AMPK- PGC1α signaling.
PPARβ/δ governs Wnt signaling and bone turnover
Authors: Carina Scholtysek, Julia Katzenbeisser, He Fu, Stefan Uderhardt, Natacha Ipseiz, Cornelia Stoll, Mario M Zaiss, Michael Stock, Laura Donhauser, Christina Böhm, Arnd Kleyer, Andreas Hess, Klaus Engelke, Jean-Pierre David, Farida Djouad, Jan Peter Tuckermann, Béatrice Desvergne, Georg Schett, Gerhard Krönke
Journal: Nature Medicine (2013)
Abstract 15623: Angiopoietin Like-2 Knockdown Worsens Pressure Overload-Induced Cardiac Dysfunction Despite Preserving Vascular Endothelial Integrity in Mice
Authors: Cécile Martel, Adeline Raignault, Carol Yu, Marc-Antoine Gillis, Natacha Duquette, Nathalie Thorin-Trescases, Christine Des Rosiers, Eric Thorin
Journal: Circulation (2014)

Background: High circulating levels of angiopoietin-like 2 (angptl2), a pro-inflammatory protein, have been associated with obesity, diabetes and atherosclerosis. In mice, angptl2 induces vascular inflammation and endothelial dysfunction, but the impact of angptl2 on cardiac function is still unknown. Since mechanical stress has been shown to promote angptl2 expression and tissue remodeling, we hypothesized that angptl2 could contribute to cardiac dysfunction and that knocking down angptl2 would be protective against pressure overload. Methods/Results: We investigated both cardiac and vascular endothelial functions in angptl2 knockdown mice (KD) versus wild-type (WT) littermates, in response to a 6-week pressure overload induced by transverse aortic constriction (TAC). While peripheral blood pressure was not affected by TAC, systolic pressure in the right carotid artery was increased by 60 % in WT, but only by 28 % in KD mice (p<0.05 vs. WT, n=8). In WT, but not in KD mice, carotid and posterior cerebral ...
Chronic Nonhealing Ulcerated Nodules in a Spanish Boy After Traveling
Authors: Maria Encarnacion Gomez Sánchez, Joaquin Bartolomé Alvarez, Silvia Herrera León
Journal: JAMA Dermatology (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 Dermatology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Dermatology journal
Congenital multiple clustered dermatofibroma
Authors: P. De Unamuno, Y. Carames, E. Fernandez-Lopez, A. Hernandez-Martin, C. Peña
Journal: British Journal of Dermatology (2000)

Multiple clustered dermatofibroma (MCD) is a rare tumour which usually appears during the first and second decades of life. We report a man in whom the MCD was congenital, although during the first few years of his second decade it extended to involve a broad zone on the left hip, gluteal region and upper thigh.
The fertile window
Authors: Kamran Abbasi
Journal: BMJ (2000)

A pregnancy theme runs through this week's BMJ —from the optimum interpregnancy interval for minimising maternal morbidity and mortality (p 1255) to diagnosing ectopic pregnancy (p 1235). Wilcox and colleagues also offer a fresh perspective on the definition of the fertile window (p 1259). Conventional wisdom speaks of six fertile days in an average woman's menstrual cycle, …
4Ig-B7H3: A target for monoclonal antibody (MoAb) therapy of human solid tumors
Authors: Hong Xu, Irene Cheung, Nai-Kong Cheung
Journal: Cancer Research (2008)

2139  Introduction: MoAb 8H9 specific for cell surface glycoprotein gp58 (Cancer Res 61:4048, 2001) is broadly reactive with human solid tumors, while restricted in its expression in normal tissues. The phase I study of intra-Ommaya 131I-8H9 has shown promise both in its efficacy and tolerability in patients with central nervous system (CNS) relapse (2007 AACR Annual Meeting LB-4). We now describe the biochemical characterization of the gp58 antigen.  Methods: gp58 was purified from LAN1 neuroblastoma cell extracts by 8H9-affinity chromatography, prepared using Pierce’s Protein G IgG Plus Orientation Kit. The 8H9 antigen-positive band from SDS-PAGE was analyzed by mass spectrometry. Transcript was measured by quantitative RT-PCR. In vitro binding kinetics was investigated by surface plasmon resonance using Biacore 2000. Protein was studied by Western analysis and immunohistochemistry.  Results: Two different peptides from mass spectrometric sequencing (MALDI-TOF-MS/MS) unequivocally identified the 8H9-reactive molecule as 4Ig-B7H3, the long and principal form of B7H3 in human tissues. Both 8H9 and MAB1027 (anti-B7H3 MoAb from RD 4Ig-B7H3 protein is only found in tumors, but not on most normal tissues. Non-specific background staining of normal tissues was much lower for 8H9 compared to MAB1027. By Biacore, association rate (kon) was lower for 8H9 [1.4x104 M-1sec-1] than MAB1027 [1.9x105 M-1sec-1], although both had a very slow and comparable dissociation rate (koff), 5.3x10-4 sec-1 and 2.2x10-4 sec-1 , for 8H9 and MAB1027, respectively.  Conclusions: 8H9 targets 4Ig-B7H3, a tumor-associated cell surface antigen which is known to inhibit NK and stimulate T-cells. Initial successes in patient studies support the clinical potential of antibody targeting of 4Ig-B7H3, especially for solid tumors metastatic to the CNS.
387. The Size of Sinusoidal Fenestrae Is a Critical Determinant of Hepatocyte Transduction after Adenoviral Gene Transfer
Authors: Tatsuya Nomoto, Takashi Okada, Kuniko Shimazaki, Toru Yoshioka, Mutsuko Sarukawa, Koichi Takeuchi, Hiroaki Mizukami, Takashi Matsushita, Ken-ichiro Katsura, Keiji Yamamoto, Akihiro Kume, Uichi Ikeda, Shigeo Ookawara, Yasuo Katayama, Keiya Ozawa
Journal: Molecular Therapy (2004)

Background: Our previous studies demonstrated that systemic expression of interleukin-10 (IL-10) decreased atherosclerosis through its anti-inflammatory property. IL-10 prevents the plaque formation in large arteries, but the protective effect on the arterial damage such as hypertensive arteriosclerosis has not yet been demonstrated. To further elucidate the involvement of the inflammatory regulation in the hypertensive arterial damage, we examined the preventive effect of this anti-inflammatory cytokine using the stroke-prone spontaneously hypertensive rats (SHR-SP) which suffer from arteriosclerosis and stroke spontaneously.
Microwave Therapy Warning
Authors: Jane E. Henney
Journal: JAMA (2000)

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 Elementary Manual of Physiology. For Colleges, Schools of Nursing, of Physical Education, and of the Practical Arts.
Authors: Russell Burton-Opitz
Journal: JAMA (1926)

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
Assessment of the role of etoposide (VP16) and cisplatin (CDDP) in chemotherapy (CT) for small cell lung cancer (SCLC): a meta-analysis with a methodology assessment.
Authors: Marianne Paesmans, Céline Mascaux, Thierry Berghmans, Fabrice Branle, Jean-Jacques Lafitte, Anne-Pascale Meert, Philippe Vermylen, Jean-Paul Sculier
Journal: European Respiratory Journal (1999)