tbuckley/cabot-search huggingface dataset:
Phylogenetic relationships within the Alcidae (Charadriiformes: Aves) inferred from total molecular evidence
Authors: V. L. Friesen, A. J. Baker, J. F. Piatt
Journal: Molecular Biology and Evolution (1996)

The Alcidae is a unique assemblage of Northern Hemisphere seabirds that forage by "flying" underwater. Despite obvious affinities among the species, their evolutionary relationships are unclear. We analyzed nucleotide sequences of 1,045 base pairs of the mitochondrial cytochrome b gene and allelic profiles for 37 allozyme loci in all 22 extant species. Trees were constructed on independent and combined data sets using maximum parsimony and distance methods that correct for superimposed changes. Alternative methods of analysis produced only minor differences in relationships that were supported strongly by bootstrapping or standard error tests. Combining sequence and allozyme data into a single analysis provided the greatest number of relationships receiving strong support. Addition of published morphological and ecological data did not improve support for any additional relationship. All analyses grouped species into six distinct lineages: (1) the dovekie (Alle alle) and auks, (2) guillemots, (3) brachyramphine murrelets, (4) synthliboramphine murrelets, (5) true auklets, and (6) the rhinoceros auklet (Cerorhinca monocerata) and puffins. The two murres (genus Uria) were sister taxa, and the black guillemot (Cepphus grylle) was basal to the other guillemots. The Asian subspecies of the marbled murrelet (Brachyramphus marmoratus perdix) was the most divergent brachyramphine murrelet, and two distinct lineages occurred within the synthliboramphine murrelets. Cassin's auklet (Ptychoramphus aleuticus) and the rhinoceros auklet were basal to the other auklets and puffins, respectively, and the Atlantic (Fratercula arctica) and horned (Fratercula corniculata) puffins were sister taxa. Several relationships among tribes, among the dovekie and auks, and among the auklets could not be resolved but resembled "star" phylogenies indicative of adaptive radiations at different depths within the trees.
TWO CARDIAC COMPRESSION TRIADS
Authors: CLAUDE S. BECK
Journal: JAMA (1935)

Lesions of the pericardium are generally difficult problems in diagnosis. Auenbrugger, Corvisart and Laënnec early recognized these difficulties. Osler not infrequently lamented his failure to recognize a lesion of the pericardium and it would seem that these problems in diagnosis still exist. The chief reason for failure in the diagnosis of pericardial lesions is the fact that the physiologic concept of acute and chronic compression of the heart has not found the place in applied medicine that it deserves. Clinically, almost all of the intrapericardial lesions express themselves, if they express themselves at all, by producing either acute or chronic compression of the heart. Some lesions of the pericardium are entirely silent; they produce no clinical signs whatever and clinical recognition of these silent lesions is not to be expected.<sup>1</sup>However, the important group of lesions—important because treatment is effective—produces either acute or chronic compression of the heart. In
Heart disease in diabetic patients is undertreated
Authors: David Spurgeon
Journal: BMJ (2004)

Patients with type 2 diabetes and symptoms of atherosclerotic disease were systematically undertreated with drugs known to be effective in reducing the risk of cardiovascular disease and mortality, “perhaps because of a ‘glucocentric’ view of diabetes,” according to a study published in the journal of the Canadian Medical Association ( CMAJ 2004;171:1189-92).

Most deaths among diabetic patients are caused by cardiovascular disease, yet the study, of data on 12 106 patients in Canada with type 2 diabetes (mean age 64 years, 55% men, mean follow up period of five years), showed that less than 25% received an antiplatelet drug or a statin …
Abstract LB-215: Inhibition of Polo-like kinase 4 as an anti-cancer strategy
Authors: Jacqueline Mason, Sam Wei, Xunyi Luo, Vincent Nadeem, Reza Kiarash, Ping Huang, Don Awrey, Genie Leung, Irina Beletskaya, Miklos Feher, Bryan Forrest, Radek Laufer, Peter Sampson, Sze-Wan Li, Yong Liu, Yunhui Lang, Henry Pauls, Tak Mak, James Guohua Pan
Journal: Cancer Research (2011)

Abstract Polo-like kinase 4 or PLK4 is a member of a conserved family of serine/threonine protein kinases that regulate multiple cellular processes, such as cell division and checkpoint regulation of mitosis. These kinases are often deregulated in cancer. PLK4 is the most structurally divergent PLK, localizes to centrosomes and is a critical regulator of centriole duplication. Over-expression of PLK4 leads to centrosome amplification and results in chromosome instability (CIN), a common characteristic observed in many types of cancers. We found that PLK4 is upregulated in breast cancer, specifically in the basal-like subtype. PLK4 expression is induced by hypoxia and suppressed by p53 in cancer cells. Consistent with this observation, PLK4 expression in cancer cells is upregulated when they are implanted and grown as xenografts in vivo. Furthermore, RNAi-mediated depletion of PLK4 inhibits the growth of cancer cells, but not normal cells (HMEC), in vitro, and tumor growth in vivo. Interestingly, siRNA knockdown of PLK4 sensitizes cancer cells to hypoxia. These findings suggest that targeting PLK4 may be a good therapeutic strategy in treating certain cancers. To this end, we initiated a discovery program that resulted in the identification of potent PLK4 inhibitors. These novel inhibitors are potent anti-prolifeartives, cause loss of mitotic checkpoint followed by apoptotic cell death, and suppress tumor growth in xenograft models. Mechanistically, inhibition of PLK4 suppresses phosphorylation of PLK4 and Histone H3, leads to failure of centrosome clustering and formation of multipolar spindles. Interestingly, breast cancer cell response to PLK4 inhibition appears to differ among subtypes of breast cancer cells and to be influenced by receptor and mutation status, such as ER and PTEN. Since multipolar division in cancer cells is not viable, due to massive missegregation of chromosomes, inhibition of PLK4 and formation of multipolar division followed by cell death may be a unique strategy for killing cancer cells. Implications of these findings in treating cancer will also be discussed. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-215. doi:10.1158/1538-7445.AM2011-LB-215
A morphometric and immunohistochemical study on angiogenesis of human metastatic carcinomas of the liver
Authors: N Terayama, T Terada, Y Nakanuma
Journal: Hepatology (1996)

To clarify the angiogenetic process and the origin of tumor vessels in human metastatic liver carcinomas.One hundred autopsy livers with metastatic carcinomas were studied by immunohistochemistry for von Willebrand factor, by lectin histochemistry for Ulex europaeus agglutinin I (UEA-I), and by morphometry of the density of tumor vessels in the liver metastases. In addition, tumor vessels were observed three-dimensionally in silicone rubber-injected livers with metastases.Tumor vessels in metastatic liver carcinomas were positive for von Willebrand factor and UAE-I agglutinin I receptor. Tumor vessels first appeared in liver metastases of 200 micron in diameter. The density of the tumor vessels in the metastases increased up to 3mm in diameter, and it remained stable over 3mm. Sinusoidal endothelial cells around the liver metastases were positive for these endothelial markers. Sinusoidal endothelial cells were frequently in continuity with vessels in the metastases. Silicone rubber-injected specimens showed that blood vessels arising from surrounding sinusoids entered into the metastases.The angiogenesis of liver metastases may progress stepwise as the metastases enlarge, and capillarization of sinusoidal endothelium around the liver metastases may occur. Tumor vessels of liver metastases may in part originate from sinusoidal endothelial cells neighboring the tumors.
Tissue engineering the retinal ganglion cell nerve fiber layer
Authors: Karl E. Kador, Ramon B. Montero, Praseeda Venugopalan, Jonathan Hertz, Allison N. Zindell, Daniel A. Valenzuela, Mohammed S. Uddin, Erin B. Lavik, Kenneth J. Muller, Fotios M. Andreopoulos, Jeffrey L. Goldberg
Journal: Biomaterials (2013)
The Professional Scene — Pollution Alarm — The Long and the Short
Authors: John Lister
Journal: New England Journal of Medicine (1971)

IT is no doubt true that the public is sometimes confused by the mystique that seems to surround certain professional practices. Many of these have been described as restrictive, and although the restrictions are intended to protect the clients or patients, the Monopolies Commission was asked by Mr. Harold Wilson during the last Parliament to advise on whether these so-called restrictive practices were operating for or against the public interest. Now, after 3 1/2 years of study, the Commission has reported1 to another government and has concluded that many of these practices are in fact undesirable. Rules prohibiting interprofessional partnerships, . . .
Guidelines to Evaluate Human Observational Studies for Quantitative Risk Assessment
Authors: Jelle Vlaanderen, Roel Vermeulen, Dick Heederik, Hans Kromhout
Journal: Environmental Health Perspectives (2008)

Careful evaluation of the quality of human observational studies (HOS) is required to assess the suitability of HOS for quantitative risk assessment (QRA). In particular, the quality of quantitative exposure assessment is a crucial aspect of HOS to be considered for QRA.
Abstract 707: Anti-SSTR antibodies can reverse neuroendocrine tumor cellular dedifferentiation induced by neutralizing EMT regulator miR-200c in pancreatic neuroendocrine tumor BON cells while increase cell death
Authors: Frank Leu, Minesh Nandi, Chung Wong
Journal: Cancer Research (2010)

Abstract Somatostatin receptors (SSTR) are antiproliferative and antisecretory receptors that belong to the Class A of the seven-transmembrane G-protein coupled receptors. SSTR is comprised of five major subtypes namely subtype 1, 2 (A and B), 3, 4 and 5. Recently, we reported that SST signaling serves as a determinant in neuroendocrine-mesenchymal transition (NMT), a process that is dependent on the TGF-beta - SST signaling axis. NMT is similar to the epithelial-mesenchymal transition (EMT), but it has the opposite cellular differentiation outcome in response to the TGF-beta treatment. For instance, TGF-beta promotes cell dedifferentiation in EMT but promotes cell differentiation in NMT. In epithelial cancers, the micro RNA 200c (miR-200c) has been shown to negatively regulate the zinc finger homeodomain enhancer-binding protein (ZEB1) (an E-cadherin's transcriptional repressor) and thus able to keep EMT invasiveness in check. In this study, we found that upon transient transfection of the miR-200c repressor (X-miR-200c made by Oligoengine Inc., designed by Todd Hauser) into BON cells, the X-miR-200c was able to drive NMT forward. In general, the X-miR-200c triggers the expression of tumor metastasis markers to change, such as ZEB1 protein increase coupled with E-cadherin protein decrease, these changes altogether lead to both Vimentin and Twist protein increase. Interestingly, our anti-SSTR 2, 3, and 5 antibodies derived from the extracellular loop 2 ectodomain region were able to reverse BON cells from the mesenchymal state back to the neuroendocrine state. Additionally, the wound gap healing assay demonstrated that the gap closes at a much slower rate (∼2.5x slower) in the presence of either anti-SSTR2 antibody or anti-SSTR5 antibody treatment than the isotype IgG treatment. Our results suggest that similar to EMT, the miR-200c is also involved in controlling the process of NMT and it is reversible in the presence of anti-SSTR2, 3 and 5 antibodies. Furthermore, we also found that these anti-SSTR antibodies examined can increase neuroendocrine tumor cell death that may or may not be dependent on the NMT reversal. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 707.
Efficacy of Sublingual Immunotherapy—Reply
Authors: Sandra Y. Lin, Catalina Suarez-Cuervo, Jodi Segal
Journal: JAMA (2013)

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
Mineral Dusts Directly Induce Epithelial and Interstitial Fibrogenic Mediators and Matrix Components in the Airway Wall
Authors: JIN DAI, BLAKE GILKS, KAREN PRICE, ANDREW CHURG
Journal: American Journal of Respiratory and Critical Care Medicine (1998)

Exposure to mineral dusts is associated with the development of chronic airflow obstruction, probably mediated in part by dust-induced fibrosis of the small airways. To investigate the mechanism of fibrosis, we exposed rat tracheal explants to amosite asbestos, iron oxide, or titanium dioxide. Explants were then maintained in air organ culture, and the expression of genes encoding for various mediators and matrix components assessed by reverse transcriptase–polymerase chain reaction (RT-PCR). At 7 d, all dusts produced significant increases in platelet-derived growth factor-A (PDGF-A) and transforming growth factor- β1 (TGF- β1) gene expression compared with control; asbestos and titanium dioxide produced increases in PDGF-B, and titanium dioxide increased TGF- α expression. Only asbestos caused increases in procollagen expression. No dust increased expression of tumor necrosis factor- α (TNF- α ), fibronectin, or tropoelastin. Elevations in these factors coincided temporally with transport of particles into the epithelium and then to the subepithelial space. By in situ hybridization, TGF- β gene expression was found in both the epithelium and subepithelial (interstitial) space, and PDGF-B and procollagen gene expression in the subepithelial space. Chemical analysis showed a small increase in hydroxyproline, a measure of collagen content, in asbestos-treated explants. We conclude that mineral dusts can induce airway wall fibrosis by directly upregulating proliferative and fibrogenic mediators as well as matrix components in the airway epithelium and interstitium, and that neither airspace nor circulating inflammatory cells are required for these effects. Different mineral dusts produce different patterns of reaction.
The SAMP1/Yit mouse: another step closer to modeling human inflammatory bowel disease
Authors: Warren Strober, Kazuhiko Nakamura, Atsushi Kitani
Journal: Journal of Clinical Investigation (2001)

, Kosiewicz andher colleagues (1) provide valuable clin-ical data and the first systematicimmunologic study of the SAMP1/Yitmouse, a murine model of sponta-neous gastrointestinal inflammationthat bears remarkable similarity tohuman Crohn’s disease. The mousestrain used has its origin in strainsdeveloped in the early 1980s for a verydifferent purpose. Hoping to study thegenetics of aging, Takeda et al. inter-bred AKR mice to generate senescence-prone or senescence-resistant sublines,including the short-lived strain SAMP1(2). In the 1990s, Matsumoto et al.established a new subline of theSAMP1 mouse with spontaneous skinulcerations (3). The SAMP1/Yit strain,which arose from SAMP1, no longerundergoes accelerated senescence, butit exhibits the novel phenotype ofspontaneous intestinal inflammation.Genetic analysis in the present reportshows that approximately 40% of thepolymorphic alleles in the SAMP1/Yitgenome differ from the original AKRstrain, indicating that genetic materialfrom one or more other strains wasintroduced into this line at some pointin the SAMP1/Yit pedigree. Regardlessof the origin of these unexpected alle-les, SAMP1/Yit is now an inbred strainof great promise for the study ofCrohn’s disease pathogenesis.As described initially by Matsumotoet al. (3), the intestinal lesions in theSAMP1/Yit mouse strain consist of dis-continuous inflammatory lesionsoccurring mainly in the terminal ileum,and to a lesser extent the cecum, whichare more or less similar to those occur-ring in Crohn’s disease. These lesionsconsist of an extensive infiltration ofCD3
An Evaluation of Methods of Assessing Impaired Awareness of Hypoglycemia in Type 1 Diabetes: Response to Pedersen-Bjergaard et al.
Authors: Jacqueline Geddes, Brian M. Frier
Journal: Diabetes Care (2007)

We thank Pedersen-Bjergaard et al. (1) for their comments regarding our study (2). In our study, the ability of three methods (Gold et al. [3], Clarke et al. [4], and Pedersen-Bjergaard et al. [5]) to identify impaired awareness of hypoglycemia (IAH) in people with type 1 diabetes was evaluated. The method that was initially described by Pedersen-Bjergaard et al. (5) required patients to respond to the question, “Can you feel when you are low?” and asked them to select …
Adoption of new surgical technology
Authors: Charles B Wilson
Journal: BMJ (2006)

<h3>Objectives</h3> To examine current practices, attitudes and levels of confidence related to advance care planning (ACP) in patients with chronic obstructive pulmonary disease (COPD) among healthcare professionals working in Ireland. This will inform future clinical guidance development. <h3>Methods</h3> A cross-sectional survey of healthcare professionals. <h3>Results</h3> There were 143 participants (109 general practitioners, 25 nurses, 7 physiotherapists and 2 consultant physicians). The majority (82%, n=117) cared for patients with COPD weekly, but only 23% (n=33) had initiated ACP with a patient with COPD over the previous 6 months. Overall, 59% (n=85) answered ≥6 of 8 general knowledge questions correctly. Participants demonstrated positive attitudes towards ACP (mean score 3.6/5.0), but confidence levels were low (2.2/4.0). Most thought ACP was appropriate for patients with severe or very severe COPD (71%, n=101%, and 91%, n=130, respectively) but were unsure or felt that it was not appropriate for those with mild–moderate COPD. However, almost all participants (97%, n=139) stated that if a patient expressed a desire to have ACP discussions, they would comply. Topics most likely to be discussed related to diagnosis and treatment options. Death and end-of-life issues were rarely discussed. The death of a family member or friend and participation in support groups were identified as new 'triggers' for initiating ACP. <h3>Conclusions</h3> Targeted education to improve general knowledge and confidence levels among healthcare professionals, together with initiatives to increase public awareness of ACP so that patients themselves might be more inclined to start the discussion, may help increase the uptake of ACP for this patient group.
Wartime Precautions for Diabetics
Authors: R. D. Lawrence
Journal: BMJ (1940)

TIIE BRIATISH rec9rded by Hartfall, Garland, and Goldie (1937).Our case of agranulocytosis (Ellman and Lawrence, 1935) was unfor- tLnately fatal: purpura haemorrhagica was also present.We have not had any further case of this type since adopting the above-mentioned principle of using great caution when the blood sedimentation rate has become normal.Albuminuria was often met with when the larger doses were employed.It proved transient, and was not associated with other evidence of kidney damage.It was not considered an indication for stopping the treatment.
Abstract 3858: Gains in FGF19 are predictive of response to the fibroblast growth factor receptor (FGFR) small molecule tyrosine kinase inhibitor BGJ 398 <i>in vitro</i>
Authors: Richard S. Finn, Alex Aleshin, Danyun Zhao, Lee Anderson, Charles Ginther, Judy Dering, Michael Shi, Diana Graus Porta, Roanld W. Busuttil, Dennis J. Slamon
Journal: Cancer Research (2012)

Abstract Background: Hepatocellular carcinoma (HCC) is a leading cause of cancer death world-wide. Sorafenib, a multi-targeted small molecule inhibitor of the vascular endothelial growth factor (VEGF) receptor and other kinases is the only approved systemic agent in advanced HCC. Despite multiple studies defining the molecular heterogeneity of HCC, clinical trials of new agents do not pre-select for predictive markers. The fibroblast growth factor (FGF) receptor consists of 4 receptor tyrosine kinases and over 20 ligands. Differential expression and activation of these receptors and ligands have been implicated in oncogenesis and the pathogenesis of HCC (Sawey 2011). BGJ398 is a selective small molecule tyrosine kinase inhibitor of the FGFR family of receptors 1-4. Given the molecular diversity of HCC, we hypothesized that there would be a subset of HCC that would be more dependent on FGFR inhibition and used cell line models to identify predictive markers of response to BGK 398. Methods: 20 human HCC cell lines were used. In vitro dose response curves were generated using direct cell count assays over 6 days. IC 50 values were calculated from the dose response curves. Genomic data on the cell lines was derived using the Agilent 105K CGH platform. These data were analyzed in the context of the sensitivity data to BGJ 398. Western blot analysis was performed for effects of BGJ398 on phospho-FRS2Δ (tyr-196), a downstream signaling molecule for FGFR activation. Flow cytometry was performed for effects of BGJ 398 on the cell cycle and apoptosis. Results: There was differential sensitivity to BGJ 398 across the HCC cell lines. 3 cell lines were identified as having IC 50 values less than 1 μM versus the remaining cell lines which were all &amp;gt;1 uM. When analyzed in the context of the CGH data, all 3 cell lines had gains in FGF 19 of log2 ratio of 0.9 to 2.6. BGJ inhibited FRS2α activation in all cell lines tested. Flow cytometry revealed the BGJ induced cell cycle arrest in sensitive lines without significant apoptosis. Conclusions: Gains in FGF19 are predictive for growth inhibitory effects of BGJ398 in human HCC cell lines in vitro and provide rationale for patient selection in clinical trials. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3858. doi:1538-7445.AM2012-3858