tbuckley/cabot-search huggingface dataset:
Hemodynamic Correlates of Blood Pressure Across the Adult Age Spectrum
Authors: Gary F. Mitchell, Na Wang, Joseph N. Palmisano, Martin G. Larson, Naomi M. Hamburg, Joseph A. Vita, Daniel Levy, Emelia J. Benjamin, Ramachandran S. Vasan
Journal: Circulation (2010)

Systolic blood pressure and pulse pressure are substantially higher in older adults. The relative contributions of increased forward versus reflected pressure wave amplitude or earlier arrival of the reflected wave to elevated pulse pressure remain controversial.We measured proximal aortic pressure and flow, forward pressure wave amplitude, global wave reflection, reflected wave timing, and pulse wave velocity noninvasively in 6417 (age range, 19 to 90 years; 53 women) Framingham Heart Study Third Generation and Offspring participants. Variation in forward wave amplitude paralleled pulse pressure throughout adulthood. In contrast, wave reflection and pulse pressure were divergent across adulthood: In younger participants, pulse pressure was lower and wave reflection was higher with advancing age, whereas in older participants, pulse pressure was higher and wave reflection was lower with age. Reflected wave timing differed modestly across age groups despite considerable differences in pulse wave velocity. Forward wave amplitude explained 80 (central) and 66 (peripheral) of the variance in pulse pressure in younger participants (<50 years) and 90 and 84 in the older participants (≥ 50 years; all P<0.0001). In a stepwise model that evaluated age-pulse pressure relations in the full sample, the late accelerated increases in central and peripheral pulse pressure were markedly attenuated when variation in forward wave amplitude was considered.Higher pulse pressure at any age and higher pulse pressure with advancing age is associated predominantly with a larger forward pressure wave. The influence of wave reflection on age-related differences in pulse pressure was minor.
Shifts in dietary carbohydrate-lipid exposure regulate expression of the non-alcoholic fatty liver disease-associated gene PNPLA3/adiponutrin in mouse liver and HepG2 human liver cells
Authors: Lei Hao, Kyoko Ito, Kuan-Hsun Huang, Sudathip Sae-tan, Joshua D. Lambert, A. Catharine Ross
Journal: Metabolism (2014)
Refractory pretibial myxoedema with response to intralesional insulin‐like growth factor 1 antagonist (octreotide): downregulation of hyaluronic acid production by the lesional fibroblasts
Authors: M. Shinohara, Y. Hamasaki, I. Katayama
Journal: British Journal of Dermatology (2000)

Journal Article Refractory pretibial myxoedema with response to intralesional insulin‐like growth factor 1 antagonist (octreotide): downregulation of hyaluronic acid production by the lesional fibroblasts Get access M. Shinohara, M. Shinohara Department of Dermatology, Nagasaki University School of Medicine, 1‐7‐1 Sakamoto, Nagasaki 852‐8102, Japan Search for other works by this author on: Oxford Academic Google Scholar Y. Hamasaki, Y. Hamasaki Department of Dermatology, Nagasaki University School of Medicine, 1‐7‐1 Sakamoto, Nagasaki 852‐8102, Japan Search for other works by this author on: Oxford Academic Google Scholar I. Katayama I. Katayama Department of Dermatology, Nagasaki University School of Medicine, 1‐7‐1 Sakamoto, Nagasaki 852‐8102, Japan Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 143, Issue 5, 1 November 2000, Pages 1083–1086, https://doi.org/10.1046/j.1365-2133.2000.03850.x Published: 01 November 2000
Analysis did not account for cluster randomisation
Authors: G. Maclennan, C. Ramsay, J. M Grimshaw, M. K Campbell
Journal: BMJ (2000)

EDITOR—We congratulate Chapman et al for their paper on prevention of dog bites in children.1 The study was a cluster randomised trial; schools were allocated to intervention or control groups, and data were collected at the level of the individual schoolchild. The analysis did, however, not account for cluster randomisation. The assumption of …
Abstract 1396: FGFR1-induced radioresistance of Panc02 pancreatic tumor cells is decreased by SSR128129 treatment <i>in vitro</i> and <i>in vivo</i>
Authors: Claudine Tardy, Genevieve Gueguen, Sandrine Mazoyer, Gaëlle Morin, Severine Planel, Corentin Herbert, Christine Toulas, Elisabeth Cohen-Jonathan Moyal, Paul Schaeffer, Françoise Bono
Journal: Cancer Research (2010)

Abstract We have previously established the important role of FGF-2 pathways in tumor cell radioresistance. Although radiotherapy is commonly used in the treatment of pancreatic carcinomas which are known to express FGF and FRGFR, the role of FGFR pathways in radioresistance of pancreatic tumor has not yet been studied. We established a new syngenic mouse model of orthotopic pancreatic xenograft of Panc02 cells transfected with hFGFR1-receptor (Panc02-FGFR1). Whereas the in vitro radioresistance of the parental cell line (Panc02) was not affected by the addition of the specific FGF-receptor antagonist SSR128129, Panc02-FGFR1 radioresistance was significantly decreased by treating cells with SSR128129 (1 µM) 4 hours before irradiation (mean inactivation dose [MID] was 6.1±0.2 Gy in control PancO2-FGFR1 versus 4.2±0.2 Gy in SSR128129 treated cells, P&amp;lt;0.001). Orthotopic injection of Panc02-FGFR1 cells in syngeneic C57B6 mice led to rapid growth of pancreatic tumors. While SSR128129 (30 mg/kg/d) was ineffective on the tumor growth, this compound significantly decreased microvessel density in Panc02-FGFR1 tumors (104.7±14.6 vs 136.6±10.3 vessels/field, P&amp;lt;0.001). Local irradiation (2×2.5 Gy) of tumor-bearing animals previously treated for 1 week with SSR128129, led to a strong decrease of tumor size (40% decrease, P&amp;lt;0.05) one week after radiotherapy, whereas the tumor size of untreated animals was not affected by irradiation. The effect of SSR128129 on microvessel density was not affected by radiotherapy. Together, these data show that inhibiting FGFR pathways leads to a major radiosensitization of pancreatic tumors in vitro and in vivo. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. 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 1396.
Acetylator phenotype in spontaneous SLE and rheumatoid arthritis.
Authors: D H Lawson, D A Henry, J Lowe, P Reavey, J A Rennie, A Solomon
Journal: Annals of the Rheumatic Diseases (1979)

Acetylator phenotype was determined in 22 patients with spontaneous systemic lupus erythematosus and the proportion of 'slow' acetylators compared with that obtained in a group of patients with rheumatoid arthritis and a group of healthy controls. 73% of the SLE group were designated 'slow' compared with 72% of the rheumatoid group and 64% of the control group. These differences were not significant.
Renal Acidification Defect in Diabetic Ketoacidosis
Authors: CHARLES C. BAILEY
Journal: Annals of Internal Medicine (1980)

Letters1 February 1980Renal Acidification Defect in Diabetic KetoacidosisCHARLES C. BAILEY JR., M.D., ROBERT W. STEINER, M.D.CHARLES C. BAILEY JR., M.D.Search for more papers by this author, ROBERT W. STEINER, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-92-2-263_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Oh and colleagues (1) reported a series of patients in whom hyperchloremic metabolic acidosis developed during the recovery phase of diabetic ketoacidosis. They speculated that elevated renal excretion of beta-hydroxybutyrate anion could have been responsible for loss of potentially regenerated bicarbonate and maintenance of a normal anion gap. Alternatively, Fisher (2) has suggested that hyperchloremic metabolic acidosis could result from proximal tubule bicarbonate wasting secondary to hypophosphatemia. We have documented a transient renal acidification defect that may have contributed to the development of hyperchloremic metabolic acidosis in a patient with insulin-treated diabetic ketoacidosis.A 27-year-old white woman...References1. OHCARROLLGOLDSTEINFEIN MHDI. Hyperchloremic acidosis during the recovery phase of diabetic ketosis. Ann Intern Med. 1978;89:925-7. LinkGoogle Scholar2. FISHER A: Hyperchloremic acidosis and diabetic ketoacidosis. Ann Intern Med. 1979;90:722-3. Letter. LinkGoogle Scholar3. HAMMEKEBEARLEEGOLDSTEINHALPERIN MRRMM: Hyperchloremic metabolic acidosis in diabetes mellitus: a case report and discussion of the pathophysiologic mechanisms. Diabetes. 1978;27:16-20. CrossrefMedlineGoogle Scholar4. GIAMMARCOGOLDSTEINHALPERINSTINEBAUGH RMMB: Renal tubular acidosis during therapy for diabetic ketoacidosis. Can Med Assoc J 1975;112:463-6. MedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Mercy Hospital and Medical Center San Diego, CA 92103 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 February 1980Volume 92, Issue 2_Part_1Page: 263-263KeywordsAcidosisAnionsBicarbonatesExcretionInsulin Issue Published: 1 February 1980 PDF DownloadLoading ...
Rowland James Williams
Authors: James H S Wakelin
Journal: BMJ (2006)

served in the Royal Army Medical Corps in Normandy, Belgium, and Rhodesia before joining his brother in general practice in Bellshill in industrial Lanarkshire.After retirement in 1978 he did locum work.He was chairman of Lanarkshire Medical Committee for 12 years.In addition to an avid interest in politics, sport, crosswords, and puddings, he supplied family, friends and neighbours with plants annually, and grew show chrysanthemums, winning many prizes locally and nationally.He was chairman of the Scottish Chrysanthemum and Dahlia Society for many years.David survived cancer three times.
Two types of BCR interactions are positively selected during leukemia development in the Eμ-TCL1 transgenic mouse model of CLL
Authors: Stefano Iacovelli, Eva Hug, Sara Bennardo, Marcus Duehren-von Minden, Stefania Gobessi, Andrea Rinaldi, Mirza Suljagic, Daniel Bilbao, Giulia Bolasco, Julia Eckl-Dorna, Verena Niederberger, Francesco Autore, Simona Sica, Luca Laurenti, Hongsheng Wang, Richard J. Cornall, Stephen H. Clarke, Carlo M. Croce, Francesco Bertoni, Hassan Jumaa, Dimitar G. Efremov
Journal: Blood (2015)
Mesenchymal origin of hepatic stellate cells, submesothelial cells, and perivascular mesenchymal cells during mouse liver development
Authors: Kinji Asahina, Shirley Y. Tsai, Peng Li, Mamoru Ishii, Robert E. Maxson, Henry M. Sucov, Hidekazu Tsukamoto
Journal: Hepatology (2008)

The knowledge concerning fetal hepatic stellate cells (HSCs) is scarce, and their cell lineage and functions are largely unknown. The current study isolated fetal liver mesenchymal cells from a mouse expressing β-galactosidase under the control of Msx2 promoter by fluorescence-activated cell sorting (FACS) and surveyed marker genes by microarray analysis. Based on the location and immunostaining with conventional and newly disclosed markers, we have identified three distinct populations of fetal liver mesenchymal cells expressing both desmin and p75 neurotrophin receptor (p75NTR): HSCs in the liver parenchyma; perivascular mesenchymal cells expressing α-smooth muscle actin (α-SMA); and submesothelial cells associated with the basal lamina beneath mesothelial cells and expressing activated leukocyte cell adhesion molecule (ALCAM) and platelet-derived growth factor receptor α. A transitional cell type from the submesothelial cell phenotype to fetal HSCs was also identified near the liver surface. Mesothelial cells expressed podoplanin and ALCAM. Ki-67 staining showed that proliferative activity of the submesothelial cells is higher than that of mesothelial cells and transitional cells. Using anti-ALCAM antibodies, submesothelial and mesothelial cells were isolated by FACS. The ALCAM+ cells expressed hepatocyte growth factor and pleiotrophin. In culture, the ALCAM+ cells rapidly acquired myofibroblastic morphology and α-SMA expression. The ALCAM+ cells formed intracellular lipid droplets when embedded in collagen gel and treated with retinol, suggesting the potential for ALCAM+ cells to differentiate to HSCs. Finally, we demonstrated that fetal HSCs, submesothelial cells, and perivascular mesenchymal cells are all derived from mesoderm by using MesP1-Cre and ROSA26 reporter mice. Conclusion: Fetal HSCs, submesothelial cells, and perivascular mesenchymal cells are mesodermal in origin, and ALCAM+ submesothelial cells may be a precursor for HSCs in developing liver. (HEPATOLOGY 2009.)
Metabolic and genetic characterization of prediabetic states. Sequence of events leading to non-insulin-dependent diabetes mellitus.
Authors: H Beck-Nielsen, L C Groop
Journal: Journal of Clinical Investigation (1994)

Non-insulin-dependent diabetes mellitus (NIDDM)' is pheno- typically heterogenous and may therefore not be explained by one simple pathophysiological mechanism.Despite the heterog- enous nature of the disease, the major form as discussed in this review is linked to overweight, arterial hypertension, dyslipidemia, and macroangiopathy (coronary heart disease), all condi- tions which become more common with aging (1).This form of NIDDM seems to be growing worldwide in the footsteps of Westernized life style.Around 3% in the Western world suffers from the disease, but in subjects 60 yr and older, the prevalence is as high as 10-20% (2).In certain ethnic populations as the Pima Indians and the Nauruans the prevalence approaches 40% (2).Therefore, NIDDM imposes an enormous burden on the health care system all over the world.In general, the goals of treatment are achieved in only a small subset of patients, but nevertheless progression of macro- angiopathy is a more severe problem than worsening of glyce- mia.The overall mortality rate in patients with NIDDM is two to three times higher than in control subjects, primarily due to excess mortality of coronary heart disease (2).Of note, -40% of patients already suffer from clinical macroangiopathy at diag- nosis, indicating that these complications may not be secondary to the diabetic state itself, but rather a part of the NIDDM syndrome, also referred to as Syndrome X or "The Insulin Resistance Syndrome" (1).Resistance to the action of insulin on glucose metabolism in skeletal muscle has been proposed as the inherited basis for this syndrome and since insulin resistance is observed several decades before the onset of hyperglycemia an early detection can open the prospect of intervention in order to prevent the disease process (4-7).The present review discusses the metabolic and genetic background of NIDDM together with the current knowledge of the sequence of events leading to NIDDM.
A Transforming Growth Factor-β Receptor–Interacting Protein Frequently Mutated in Human Ovarian Cancer
Authors: Wei Ding, Qian Tang, Virginia Espina, Lance A. Liotta, David T. Mauger, Kathleen M. Mulder
Journal: Cancer Research (2005)

Ovarian carcinomas, particularly recurrent forms, are frequently resistant to transforming growth factor-beta (TGF-beta)-mediated growth inhibition. However, mutations in the TGF-beta receptor I and receptor II (TbetaR-I and TbetaR-II) genes have only been reported in a minority of ovarian carcinomas, suggesting that alterations in TGF-beta-signaling components may play an important role in the loss of TGF-beta responsiveness. Using laser-capture microdissection and nested reverse-transcription-PCR, we found that km23, which interacts with the TGF-beta receptor complex, is altered at a high frequency in human ovarian cancer patients. A novel form of km23, missing exon 3 (Deltaexon3-km23), was found in 2 of 19 tumor tissues from patients with ovarian cancer. In addition to this alteration, a stop codon mutation (TAA --> CAC) was detected in two patients. This alteration results in an elongated protein, encoding 107-amino-acid residues (Delta107km23), instead of the wild-type 96-amino-acid form of km23. Furthermore, five missense mutations (T38I, S55G, T56S, I89V, and V90A) were detected in four patients, providing a total alteration rate of 42.1% (8 of 19 cases) in ovarian cancer. No km23 alterations were detected in 15 normal tissues. Such a high alteration rate in ovarian cancer suggests that km23 may play an important role in either TGF-beta resistance or tumor progression in this disease. In keeping with these findings, the functional studies described herein indicate that both the Deltaexon3-km23 and S55G/I89V-km23 mutants displayed a disruption in binding to the dynein intermediate chain in vivo, suggesting a defect in cargo recruitment to the dynein motor complex. In addition, the Deltaexon3-km23 resulted in an inhibition of TGF-beta-dependent transcriptional activation of both the p3TP-lux and activin responsive element reporters. Collectively, our results suggest that km23 alterations found in ovarian cancer patients result in altered dynein motor complex formation and/or aberrant transcriptional regulation by TGF-beta.
Multinucleate epidermal cells in non-neoplastic dermatoses
Authors: SHUNJI KIMURA, HITOSHI HATANO
Journal: British Journal of Dermatology (1978)

Multinucleate epidermal cells (MEC) originated from keratinocytes were observed histologically in 92 of 197 cases of non-neoplastic dermatoses, such as lupus erythematosus (26 of 70), lichenoid eruptions (26 of 47), Hailey-Hailey disease (5 of 5), psoriasis vulgaris (20 of 49) and so on. Most of these cells had two nuclei, and a few had three nuclei. MEC usually showed perinuclear bands of eosinophilic material which also showed positive staining for epidermal fibres (tonofilaments). In all cases of Hailey-Hailey disease, close correlation between formation of MEC and dyskeratotic tendency was observed. From these findings, it is concluded that the mechanism of formation of MEC in these dermatoses may be similar to that of Bowen's disease, in which dyskeratotic tonofilaments become entangled with the spindles of the mitotic apparatus so that normal cell division cannot take place. It seems likely that MEC are a manifestation not only of malignant dyskeratosis but also of benign one.
Nedocromil sodium reduces allergen‐induced plasma extravasation in the guinea pig nasal mucosa by inhibition of tachykinin release
Authors: P. Javdan, M. Figini, C. Emanueli, P. Geppetti
Journal: Allergy (1995)

The effect of topically applied (10 microliters) nedocromil sodium (NS) and sodium cromoglycate (CS) on the plasma extravasation induced by local application of ovalbumin (5%, 10 microliters) into the respiratory nasal mucosa of sensitized guinea pigs pretreated with the neutral endopeptidase inhibitors, phosphoramidon, was studied. Topical NS (220 nmol, 10 microliters) reduced by 57% the Evans blue dye extravasation caused by local application of ovalbumin into the nasal mucosa, whereas CS (220 nmol, 10 microliters) was without effect. The tachykinin NK1 receptor antagonist CP-99994 (2 mumol/kg, i.v.) reduced by 45% the plasma extravasation induced by antigen challenge. The combination of NS and CP-99994 did not increase further the inhibition caused by NS alone. Plasma extravasation evoked by instillation of bradykinin (50 nmol), which causes this response by releasing tachykinins from sensory nerves, was markedly reduced by NS, but not by CS. Plasma extravasation evoked by installation of substance P, which acts directly on the endothelial cells, was not affected by NS. We conclude that the reduction by NS of the plasma extravasation induced by antigen challenge in the nasal mucosa of sensitized guinea pigs is due to the inhibition of tachykinin release from sensory nerve endings.
Inhibition of pacing-induced coronary dilation by aminophylline
Authors: J. LAMMERANT, I. BECSEI
Journal: Cardiovascular Research (1975)

In closed-chest anaesthetized dogs, aminophylline was infused into the left circumflex coronary artery at a rate of 250 mug/min. When the heart rate was lower than 100 beats/min, infusion did not modify the left circumflex coronary blood flow and resistance. When the heart rate was elevated to an average of 153 +/- 6 beats/min by right atrial pacing, infusion inhibited the increase in left circumflex coronary blood flow and decrease in coronary resistance. The pacing-induced increment in coronary blood flow was reduced by an average of 64% and the flow deficit was associated with a lowering of the coronary sinus blood oxygen tension. Since aminophylline is known to inhibit the coronary dilator action of exogenous adenosine, the results support the concept that adenosine resulting from the breakdown of adenine nucleotides is a mediator of the metabolic regulation of coronary blood flow.
Molecular Determinants of Agonist Discrimination by NMDA Receptor Subunits: Analysis of the Glutamate Binding Site on the NR2B Subunit
Authors: Bodo Laube, Hirokazu Hirai, Mike Sturgess, Heinrich Betz, Jochen Kuhse
Journal: Neuron (1997)

NMDA receptors require both L-glutamate and the coagonist glycine for efficient channel activation. The glycine binding site of these heteromeric receptor proteins is formed by regions of the NMDAR1 (NR1) subunit that display sequence similarity to bacterial amino acid binding proteins. Here, we demonstrate that the glutamate binding site is located on the homologous regions of the NR2B subunit. Mutation of residues within the N-terminal domain and the loop region between membrane segments M3 and M4 significantly reduced the efficacy of glutamate, but not glycine, in channel gating. Some of the mutations also decreased inhibition by the glutamate antagonists, D-AP5 and R-CPP. Homology-based molecular modeling of the glutamate and glycine binding domains indicates that the NR2 and NR1 subunits use similar residues to ligate the agonists' α-aminocarboxylic acid groups, whereas differences in side chain interactions and size of aromatic residues determine ligand selectivity.
Treatment escalation plans
Authors: M. H Mercer
Journal: BMJ (2009)

<h3>Abstract</h3> <b>Objectives</b> To compare the effectiveness of cognitive behaviour therapy delivered by telephone with the same therapy given face to face in the treatment of obsessive compulsive disorder. <b>Design</b> Randomised controlled non-inferiority trial. <b>Setting</b> Two psychology outpatient departments in the United Kingdom. <b>Participants</b> 72 patients with obsessive compulsive disorder. <b>Intervention</b> 10 weekly sessions of exposure therapy and response prevention delivered by telephone or face to face. <b>Main outcome measures</b> Yale Brown obsessive compulsive disorder scale, Beck depression inventory, and client satisfaction questionnaire. <b>Results</b> Difference in the Yale Brown obsessive compulsive disorder checklist score between the two treatments at six months was −0.55 (95% confidence interval −4.26 to 3.15). Patient satisfaction was high for both forms of treatment. <b>Conclusion</b> The clinical outcome of cognitive behaviour therapy delivered by telephone was equivalent to treatment delivered face to face and similar levels of satisfaction were reported. <b>Trial registration</b> Current Controlled Trials ISRCTN500103984[controlled-trials.com].