tbuckley/cabot-search huggingface dataset:
Aspects of MMR
Authors: K Schmidt
Journal: BMJ (2002)

Editor—Vaccination for measles, mumps, and rubella (MMR) is highly controversial.1 One of us (EE) found that some providers of complementary medicine have a negative attitude towards immunisation.2 We therefore evaluated and compared the response of professional homoeopaths, chiropractors, and general practitioners to an inquiry about MMR vaccination.

We obtained the email addresses of the three health professions from these websites: www.homeopath.co.uk/directory, www.chiro-online.com/interadcom, www.internetgp.com/gpsites/alphabet.htm. We also visited the private homepages of homoeopaths and chiropractors on the internet. We sent a letter in which a mother asked for advice about the MMR vaccination for her 1 year old child to all the addresses. We explained to all those who responded that the query was, in fact, part of a research project, giving them opportunity to withdraw their answers. The study was approved by the local ethics committee.

We contacted 168 homoeopaths, of whom 104 (72%) responded, 27 (26%) withdrawing their answers. We contacted 63 chiropractors, of whom 22 (44%) responded, six (27%) withdrawing their responses. No general practitioners responded. The table shows that only a few professional homoeopaths and a quarter of the chiropractors advised in favour of the MMR vaccination. Almost half of the homoeopaths and nearly a fifth of the chiropractors advised against it. 

These data suggest that some providers of complementary medicine are advising people against government policy. General practitioners, on the other hand, seem not respond at all to patients' emails on this delicate matter.
An Atlas of Midwifery.
Authors: Geo. M. White
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
Platelet-Activating Factor (PAF)-induced invasion involves a complex signaling cascade in vascular endothelial cells.
Authors: Dayanand D. Deo, T. William Axelrad, Jennefer Van Kirk, Paulo Ottino, Nicolas G. Bazan, Haydee E. P. Bazan, Jay D. Hunt
Journal: Cancer Research (2004)

3594   Platelet-activating factor (PAF), a potent phospholipid second messenger, promotes  in vivo  angiogenesis by stimulation of vascular endothelial cell migration and invasion, thus acting as a mediator of vascularization for tumor growth and metastasis. We have elucidated a complex signaling cascade upon stimulation of the G-protein-coupled, seven transmembrane PAF receptor in human umbilical vein endothelial cells (HUVEC). Activation of the PAF receptor induces specific, receptor-associated pertussis toxin-insensitive Gα q  protein stimulation of adenylate cyclase, increased levels of cAMP, and induction of PKA in HUVEC, all of which requires the activation of Gα q  protein coupled to the PAF receptor. The use of PAF receptor antagonists, as well as either inhibition of Gα q  protein or adenylate cyclase, attenuates phosphorylation of Src by PAF; indeed, there is an absolute requirement for PKA activation in the PAF-PAF receptor signaling to Src. We have previously demonstrated that both Src and JAK-2 phosphorylate STAT-3 in HUVEC in a temporally regulated fashion. Our recent studies show that the initial signal to STAT-3 through the PAF-PAF receptor signaling mechanism involves the activation of Gα q  protein, adenylate cyclase, and PKA, whereas the delayed and prolonged phosphorylation of STAT-3 by PAF is independent of these signaling intermediates. Activation of the Gα q  protein-coupled PAF receptor by PAF also stimulates the early phosphorylation of PLCβ3 and does not involve Src, while there is no requirement of G-proteins for the activation of PLCγ1 by the PAF-PAF receptor mechanism. The Src inhibitor PP1 attenuates the delayed activation of PLCγ1 by PAF, suggesting the importance of Src in the PAF-mediated activation of PLCγ1. The Gα q  protein-coupled PAF-PAF receptor-signaling cascade also phosphorylates FAK in a time dependent manner, and its activation is independent of the adenylate cyclase/PKA axis in HUVEC. Stimulation of the tyrosine phosphorylation of FAK by PAF-PAF receptor signaling cascade induces the binding of Src, p130 Cas , SHC, and paxillin to FAK in HUVEC. The biological consequence of this signaling cascade is the upregulation of mRNA levels for the matrix metalloproteinase  MT1-MMP  and the regulatory protein  TIMP-2 . The concomitant temporal increases in expression of MT1-MMP and TIMP-2 lead to conversion of latent proMMP2 to MMP2, resulting in increased capacity to degrade the extracellular matrix and migrate. Taken together, we demonstrate that PAF is an important intermediate in vascular remodeling during pathological angiogenesis.
Ventilatory Acclimatization to Moderate Hypoxemia in Man
Authors: J. A. Dempsey, H. V. Forster, G. A. Dopico
Journal: Journal of Clinical Investigation (1974)

This study has assessed the regulation of arterial blood and cerebrospinal fluid (CSF) pH and thereby their contribution to the control of breathing in normal man during various stages of ventilatory acclimatization to 3,100 m altitude. CSF acid-base status was determined: (a) from measurements of lumbar spinal fluid during steady-state conditions of chronic normoxia (250 m altitude) and at + 8 h and + 3-4 wk of hypobaric hypoxia; and (b) from changes in cerebral venous P(CO2) at + 1 h hypoxic exposure. After 3-4 wk at 3,100 m, CSF [H(+)] remained significantly alkaline to values obtained in either chronic normoxia or with 1 h hypoxic exposure and was compensated to the same extent ( approximately 66%) as was arterial blood [H(+)]. Ventilatory acclimatization to 3,100 m bore no positive relationship to accompanying changes in arterial P(O2) and pH and CSF pH: (a) CSF pH either increased or remained constant at 8 h and at 3-4 wk hypoxic exposure, respectively, coincident with significant, progressive reductions in Pa(CO2); (b) arterial P(O2) and pH increased progressively with time of exposure; and (c) in the steady-state of acclimatization to 3,100 m the combination of chemical stimuli present, i.e. Pa(O2) = 60 mm Hg, pHa and pH(CSF) = + 0.03-0.04 > control, was insufficient to produce the observed hyperventilation (Pa(CO2) = 32 mm Hg). It was postulated that ventilatory acclimatization to 3,100 m altitude was mediated by factors other than CSF [H(+)] and that the combination of chronic hypoxemia and hypocapnia of moderate degrees provided no mechanisms for the specific regulation of CSF [H(CO3) (-)] and hence for homeostasis of CSF [H(+)].
Prominent vascular endothelial proliferation in clinically aggressive neuroblastoma
Authors: R. Peddinti, R. Zeine, D. Luca, R. Seshadri, A. Chlenski, K. Cole, B. Pawel, H. Salwen, J. Maris, S. L. Cohn
Journal: Journal of Clinical Oncology (2007)

10611 Background: Tumor blood vessels are disorganized and vascular endothelial cell proliferation (VEP) has been identified as a poor prognosticator in many adult cancers. To determine the clinical significance of VEP in neuroblastoma (NB), we evaluated blood vessel architecture in tumor sections from 51 children diagnosed at Children's Memorial Hospital, Chicago (CMH) and in 154 NB tumors on a Tissue Microarray (TMA) constructed at Children's Hospital of Philadelphia (CHOP). Methods: H&amp;E-stained tumor sections were examined for the presence of structurally abnormal vessels and further characterized by immunostaining with anti-CD31 and von Willebrand factor (vWF) antibody to highlight endothelial cells. Tumors that contained vessels with disorganized walls and more than one endothelial cell layer were classified as VEP positive. Tumor sections that contained only thin walled vessels with no more than one layer of endothelial cells were classified as VEP negative. Associations between VEP and established clinico-pathologic features and outcome were assessed. Results: In the CHOP series, VEP was associated with high-risk group classification and MYCN amplification (p&lt;0.001 and p=0.006). In the CMH series only 5 of the 10 children with MYCN amplification had VEP but 4 of these 5 patients have died, while there were no deaths in the subset of patients with MYCN amplified tumors that lacked VEP (n=5). In both study groups, VEP was significantly associated with Schwannian stroma-poor histology (CMH series: p=0.008; CHOP series: p&lt;0.001) and decreased survival probability (CMH series: p=0.017; CHOP series: p= 0.014). Conclusions: The association between structurally abnormal vessels and poor outcome provides further support for the concept that angiogenesis plays an important role in determining the biologic behavior of NB tumors. Our results also indicate that angiogenesis is regulated differently in Schwannian stroma-rich versus stroma-poor NB tumors. Further studies investigating the activity of angiogenic inhibitors in children with clinically aggressive stroma-poor NB are warranted. No significant financial relationships to disclose.
The Insulin Treatment of Diabetes Mellitus.
Authors: A H Rowe
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
Review of<i>Prehospital Care of Neurologic Emergencies</i>
Authors: Christopher M. Franklin
Journal: JAMA Neurology (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 Neurology 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 Neurology journal
Small-molecule approach to block p53-MDM2 interaction as a cancer therapeutic strategy
Authors: Shaomeng Wang
Journal: Cancer Research (2008)

LB-144   Design of small-molecule antagonists to block the MDM2-p53 protein-protein interaction is being intensely pursued as a potentially attractive new cancer therapeutic strategy. Employing a structure-based approach, we have rationally designed MI-219 as an orally bioavailable and most potent and selective inhibitor of the MDM2-p53 interaction and have performed critical  in vitro  and  in vivo  evaluations of MI-219 as a potential new cancer therapy. MI-219 disrupts the MDM2-p53 interaction and activates the p53 pathway in cells with wild-type p53. Activation of p53 by MI-219 leads to cell cycle arrest in both normal and tumor cells and selective apoptosis in the latter. It activates p53 in normal mouse tissues with minimal p53 accumulation and is not toxic to animals, indicating that normal cells and tissues are intrinsically resistant to activation of p53 by an MDM2 inhibitor. MI-219 stimulates rapid but transient p53 activation in xenograft tumor tissues, resulting in inhibition of cell proliferation and induction of apoptosis, and complete tumor growth inhibition, consistent with the notion that established tumors remain persistently vulnerable to p53 tumor-suppressor function. Our study provides compelling evidence that pharmacological activation of p53 by blocking the MDM2-p53 interaction is a promising cancer therapeutic strategy and MI-219 warrants clinical evaluation as a new cancer therapy.
Abstract 14182: Identification of a Candidate Alternative Fuel Source in the Failing Heart Using Quantitative Mitochondrial Proteomics and Metabolomics
Authors: Gregory Aubert, Ling Lai, Marcus Kruger, David Pagliarini, Teresa C Leone, Thomas Braun, Daniel P Kelly
Journal: Circulation (2011)

Significant evidence suggests that derangements in mitochondrial fuel and energy metabolism contribute to the pathogenesis of heart failure (HF). To identify changes in mitochondrial proteins relev...
Abstract B105: Significance of BRCA mutation for the patients with pancreatic cancer
Authors: Alexey Kashintsev, Evgeny Imyanitov, Nikolai Kokhanenko, Aglaya Ievleva
Journal: Cancer Research (2015)

Abstract Background: Several independent reports have indicated the efficacy of DNA damaging therapy for the oncological patients with loss of homolog recombination in consequence of BRCA 1,2 or PALB2 germiline mutation. There are similar works about pancreatic cancer but the frequency and localization of defects in these genes and the results of chemotherapy are variable. Methods: From 2009 to 2012 years 257 patients with PAC were included in the study. The analysis of the Russian founder mutation BRCA1 5382insC is performed in 150 PAC: 116 pacients included accidentally and 34 – by the presence of kindred’s with oncology. We had compared our results with the control group of 1007 healthy people. Prevalence of BRCA2 6174delT were analyzed in 22 cases. For these two genes we used allele specific real-time PCR. Full exon sequencing of coding region of BRCA2, PALB2 was conducted on DNA samples extracted from 8 patients by the HRM-analysis. For the administration of chemotherapy (ChT) we estimated a performance status by ECOG scale and efficacy by the RECIST criteria. Results: Two patients had carriers of BRCA1 mutation and one – BRCA2 5197_5198delTC. In the control group only 1/1007 had BRCA1 allele. All patients with founder mutations had 2 or more kindred’s with oncology and 1 had carriers of BRCA1 5382insC. Defects in the PALB 2 were not identified. ChT was administered only for 1 patients with BRCA2 allele because only he had a 1 score for ECOG scale. He had a 4 line of ChT (FOLFIRINOX, cisplatin, chlorambucil, mitomicin) and only in last one there was stabilization of the process by RECIST criteria and decrease the level of CA 19-9 from 3810 to 547 U/ml. FTP was a 4,1 months and overall survival – 8,1. Conclusion: The frequency of BRCA1/2mutation carriers was rare for PAC but higher than in the general population and probability of detection was depended on familial history. It means that samples from patients with PAC whom had 2 or more relatives or kindred carrier of BRCA mutation should be selected for DNA analysis. The DNA crosslink agents are preferable for patients with BRCA mutation. Note: This abstract was not presented at the conference. Citation Format: Alexey Kashintsev, Evgeny Imyanitov, Nikolai Kokhanenko, Aglaya Ievleva. Significance of BRCA mutation for the patients with pancreatic cancer. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2015;75(13 Suppl):Abstract nr B105.
Abstract #1507: Development of an artificial zinc finger protein against human SNAIL protein
Authors: Rainelli Koumangoye, Burthia Booker, CharvannK. Bailey, Mukul Mittal, Smita Misra, Gautam Chaudhuri
Journal: Cancer Research (2009)

Development of DNA-binding proteins for the specific control of the functions of a transcription factor is one of the challenges for several research laboratories. The zinc finger proteins, which typically contain many fingers linked in a tandem fashion, are some of the most intensively studied DNA-binding proteins. The C2H2-type zinc finger is one of the most common DNA-binding motifs in eukaryotes. The SNAI family of transcriptional repressors is such a zinc-finger containing transcriptional repressors that are implicated in the metastatic transformation of human epithelial cancer cells. With the intent to develop a DNA-binding decoy polypeptide against one of SNAI family members, SNAIL, we selected the C-terminal zinc finger of this protein and created a heptamer of this finger. We chose this finger because it is unique among the other fingers and contains the nuclear localization signals. We designed this heptamer by the ligation of six complementary and antiparallel overlapping 5´-phosphorylated oligonucleotides followed by PCR amplifications of different polymers of the finger. We installed a Kozak ATG in front of the first finger and a stop codon at the end of the last finger by Gene SOEing. We cloned the gel-purified heptamer in pET100/D-TOPO and expressed this protein in Escherichia coliBL21 (DE3) cells. The purified recombinant protein is being characterized by EMSA for its affinity for binding to the promoters of several SNAIL-target genes in vitro. We also cloned the heptamer into p3XFLAG vector to express the FLAG-tagged protein in human breast cells. The in vivo expressed protein is being characterized for its ability to bind to SNAIL-target gene promoters by ChIP-DSL techniques as well as for its ability to alleviate repression of these genes by SNAIL. Our objective is to develop retroviral constructs with this artificial zinc finger protein to transfect rapidly growing pre-malignant breast and other cancer cells. This DNA-binding protein will bind specifically to the promoters of SNAIL-target genes e.g., E-cadherin, claudin 7, 15-PGDH etc. and block their repression by SNAIL, thus alleviating the metastatic transformation of these cells. Supported by the DOD-CDMRP IDEA Grant# W81XWH-06-1-0466 and the Susan G. Komen Breast Cancer Foundation grant# BCTR0707627 to GC.  Citation Information: In: Proc Am Assoc Cancer Res; 2009 Apr 18-22; Denver, CO. Philadelphia (PA): AACR; 2009. Abstract nr 1507.
Abstract #4460: The \#946;-Spectrin ELF and Smad3/Smad4 signaling play an important role in suppression of optic glioma
Authors: Kyi Soe, Zhongxian Jiao, Anan Said, Zhixing Yao, Wilma Jogunoori, Lopa Mishra, Bibhuti Mishra
Journal: Cancer Research (2009)

Transforming growth factor-beta (TGF-\#946;) represents a large family of growth and differentiation factors that mobilize complex signaling networks to regulate cellular differentiation, proliferation, motility, adhesion, and apoptosis. The adaptor protein ELF ( E mbryonic  L iver  F odrin; \#946;-Spectrin, non PH domain, isoform2 ) is a potent regulator of tumorigenesis through its ability to affect TGF-\#946; tumor suppressor function, specifically Smad3 and Smad4 signaling. Disruption of ELF results in loss of Smad3/Smad4 activation and, therefore, a disruption of the TGF-beta pathway. We have observed that  elf +/-   and  elf +/- /Smad3 +/-   mice develop visceromegaly and multiple cancers including nephroblastoma, hepatocellular carcinoma, and optic gliomas with phenotypic characteristics frequently observed in patients with Beckwith-Wiedemann syndrome (BWS), a hereditary human cancer overgrowth syndrome. Several reports document the association of optic gliomas as well as neural crest tumors with the development of BWS. These observations led us to pursue the function of ELF and the TGF-\#946; pathway in neural tumorigenesis and tumor suppression. Immunohistochemical labeling with p-Tau, PCNA, Cyclin A and CDK4 showed a substantial increase in expression in the neural tissue of  elf +/- /Smad4 +/-    mice compared to wild type control, indicating an escape from TGF-\#946; growth inhibition. Furthermore, the optic gliomas exhibited a marked loss in the expression of ELF when compared to normal tissues. Analysis of optic gliomas in the  elf +/- /Smad3 +/-   double heterozygous mice in comparison with reported characteristics of human gliomas was also analyzed. These results suggest that  elf +/-   and  elf +/- /Smad3 +/-   mice provide an important animal model for optic gliomas and provide insight into the role of the TGF-\#946; signaling pathway in the pathology of patients with BWS, as well as sporadic gliomas.   Citation Information:  In: Proc Am Assoc Cancer Res; 2009 Apr 18-22; Denver, CO. Philadelphia (PA): AACR; 2009. Abstract nr 4460.
Abstract 453: The S1p2 Receptor Is Expressed In Human Platelets,is Linked To The Rhoa-rho Kinase Pathway And Is Degraded By {micro}-calpain In Type 2 Diabetes
Authors: Voahanginirina Randriamboavonjy, Klaus Badenhoop, Rudi Busse, Ingrid Fleming
Journal: Circulation (2007)

Sphingosine-1-phosphate (S1P) is a bioactive lipid involved in multiple biological processes; it is stored in platelets and released upon activation. Although S1P is known to exert extracellular ef...