tbuckley/cabot-search huggingface dataset:
Isolation and properties of the mixed lipid micelles present in intestinal content during fat digestion in man.
Authors: C M Mansbach, R S Cohen, P B Leff
Journal: Journal of Clinical Investigation (1975)

To evaluate better the physicochemical characteristics of human fat digestion, a method was developed which allowed characterization of the bile acid-lipid mixed micelles of the aqueous phase of post-prandial duodenal fluid. Duodenal fluid was collected after a 36-g fat breakfast for two 90-min periods and for 60 min after i.v. cholecystokinin and was ultracentrifuged at 15,400,000 g-min. The aqueous phase was isolated, passed through a 200-nm filter, and the mixed micelles were concentrated by an ultrafiltration procedure using a 1.5-nm filter. The 1.5-nm retentate was eluted from Sepharose 6B columns with 1.5-nm filtrate for both preequilibration fluid and eluent. 1.5-nm filtrate approximated the monomer concentrations. Each sample was assayed for bile acid, fatty acid, lecithin, lysolecithin, protein, cholesterol, and counterions (pH, Na+, K+, Ca2+). Constituents were concentrated only on the 1.5-nm filter. On gel permeation chromatography, coincident peaks were observed for bile acid, fatty acid, lysolecithin, and cholesterol; and were eluted with a Kav range of 0.50-0.68 (corresponding to a Stokes radius of 2.3-3.5 nm). An average density of 1.25 and coincident peaks of bile acid and fatty acid were found for the mixed micelles on sucrose density gradients. The regression lines of micellar fatty acid, lysolecithin, and cholesterol vs. bile acid gave a stoichiometry of 1.4 mol fatty acid, 0.15 mol lysolecithin, and 0.06 mol cholesterol for each mole of bile acid. Mixed micelles were homogeneous in composition. These results provide direct evidence for the existence of the postprandial mixed micelle and describe several of its physicochemical properties.
DNA Barcode <i>ITS</i> Effectively Distinguishes the Medicinal Plant <i>Boerhavia Diffusa</i> from Its Adulterants
Authors: Dhivya Selvaraj, Dhivya Shanmughanandhan, Rajeev Kumar Sarma, Jijo C. Joseph, Ramachandran V. Srinivasan, Sathishkumar Ramalingam
Journal: Genomics Proteomics & Bioinformatics (2012)

Boerhavia diffusa (B. diffusa), also known as Punarnava, is an indigenous plant in India and an important component in traditional Indian medicine. The accurate identification and collection of this medicinal herb is vital to enhance the drug's efficacy and biosafety. In this study, a DNA barcoding technique has been applied to identify and distinguish B. diffusa from its closely-related species. The phylogenetic analysis was carried out for the four species of Boerhavia using barcode candidates including nuclear ribosomal DNA regions ITS, ITS1, ITS2 and the chloroplast plastid gene psbA-trnH. Sequence alignment revealed 26% polymorphic sites in ITS, 30% in ITS1, 16% in ITS2 and 6% in psbA-trnH, respectively. Additionally, a phylogenetic tree was constructed for 15 species using ITS sequences which clearly distinguished B. diffusa from the other species. The ITS1 demonstrates a higher transition/transversion ratio, percentage of variation and pairwise distance which differentiate B. diffusa from other species of Boerhavia. Our study revealed that ITS and ITS1 could be used as potential candidate regions for identifying B. diffusa and for authenticating its herbal products.
Inhibition of AP-1 signaling by JDP2 overexpression protects cardiomyocytes against hypertrophy and apoptosis induction
Authors: Christian Hill, Alona Würfel, Jacqueline Heger, Bettina Meyering, Klaus-Dieter Schlüter, Martin Weber, Peter Ferdinandy, Ami Aronheim, Rainer Schulz, Gerhild Euler
Journal: Cardiovascular Research (2013)

AimsExpression and activity of the transcription factor AP-1 are enhanced during cardiac remodelling and heart failure progression. In order to test if AP-1 inhibition may limit processes contributing to cardiac remodelling, ventricular cardiomyocytes of mice with cardiac overexpression of the AP-1 inhibitor JDP2 were analysed under stimulation of hypertrophy, apoptosis, or contractile function.
Brief Communication: Ramipril Markedly Improves Walking Ability in Patients with Peripheral Arterial Disease
Authors: Anna A. Ahimastos, Adam Lawler, Christopher M. Reid, Peter A. Blombery, Bronwyn A. Kingwell
Journal: Annals of Internal Medicine (2006)

This article has been retracted. See Notice of Retraction. Background: Peripheral arterial disease (PAD) affects up to 12% of adults older than 50 years of age. Conventional therapies have only modest effects in improving symptoms. Objective: To examine the effects of angiotensin-converting enzyme inhibition on walking ability in patients with PAD. Design: Randomized, double-blind, placebo-controlled trial initiated in March 2003 and completed in January 2005. Setting: The Alfred Hospital, Melbourne, Australia. Participants: 40 older adults with symptomatic PAD and no history of diabetes or hypertension. Intervention: 10 mg of ramipril (n = 20) or placebo (n = 20) once daily for 24 weeks. All patients completed the trial. Measurements: Pain-free and maximum walking time were recorded during a standard treadmill test, and the standard Walking Impairment Questionnaire was administered. Results: After adjustment for the baseline pain-free walking time, mean pain-free walking time after ramipril treatment was 227 seconds (95% CI, 175 seconds to 278 seconds; P < 0.001) longer than that after placebo treatment. Similarly, maximum walking time improved by 451 seconds in the ramipril group (CI, 367 seconds to 536 seconds; P < 0.001) but did not change in the placebo group. Ramipril improved the Walking Impairment Questionnaire median distance score from 5% (range, 1% to 39%) to 21% (range, 12% to 58%; P < 0.001), speed score from 3% (range, 3% to 39%) to 18% (range, 8% to 50%; P < 0.001), and stair-climbing score from 17% (range, 4% to 80%) to 67% (range, 38% to 88%; P < 0.001). No adverse events were reported. Limitations: The sample size is modest, and the strict inclusion criteria limit the applicability of the results to patients with claudication and infrainguinal disease and those without diabetes. Conclusion: Ramipril improved pain-free and maximum walking time in some adults with symptomatic PAD.
Antiviral drugs should not be used to treat Bell's palsy, Cochrane analysis concludes
Authors: R. Dobson
Journal: BMJ (2009)

Antiviral drugs that are widely prescribed to treat Bell’s palsy are ineffective, new research from the Cochrane Database shows.

High quality evidence from randomised controlled trials of Herpes simplex antiviral drugs showed that they were no more effective than placebo, say the authors ( Cochrane Database of Systematic Reviews 2009;(4):CD001869, doi:10.1002/14651858.CD001869.pub4). They recommend that research should now focus on discovering other potential causes and treatments of the condition, which affects between 11 and 40 in every 100 000 people.

“These results cast doubt on research that suggests Herpes simplex causes the condition,” said the study’s …
Casein Kinase I Attenuates Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand–Induced Apoptosis by Regulating the Recruitment of Fas-Associated Death Domain and Procaspase-8 to the Death-Inducing Signaling Complex
Authors: Kamel Izeradjene, Leslie Douglas, Addison B. Delaney, Janet A. Houghton
Journal: Cancer Research (2004)

Abstract Tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) induces apoptosis in a wide variety of malignant cell lines, in contrast to normal cells, but with considerable heterogeneity in response. Death receptor–mediated apoptosis may be attenuated by a variety of different mechanisms, including phosphorylation-based signaling pathways. We have demonstrated that casein kinase I can attenuate TRAIL-induced apoptosis in human cell lines derived from colon adenocarcinoma (HT29 and HCT8) and pediatric rhabdomyosarcoma (JR1). Inhibition of casein kinase I (CKI) phosphorylation events in HT29, HCT8, and JR1 cells by CKI-7 dramatically increased apoptosis after exposure to TRAIL, in the absence of apoptosis induced by TRAIL treatment alone. CKI inhibition enhanced the recruitment of Fas-associated death domain and procaspase-8 to the death-inducing signaling complex after TRAIL treatment and enhanced cleavage of procaspase-8 at the death-inducing signaling complex. In HT29 cells studied further, rapid cleavage of caspase-8, caspase-3, Bid, and the caspase substrate poly(ADP-ribose) polymerase occurred when CKI-7 and TRAIL were combined. Overexpression of Bcl-2, Bcl-xL, or mutant DN-Fas-associated death domain protected HT29 cells from TRAIL-induced apoptosis in the presence of the CKI inhibitor. In addition, TRAIL combined with CKI-7 promoted the release of cytochrome c, Smac/DIABLO, HtrA2/Omi, and AIF from the mitochondria and down-regulated the expression of XIAP and c-IAP1. Small hairpin RNAs directed against CKI revealed that the CKIα isoform contributed significantly to the inhibition of TRAIL-induced apoptosis. These findings suggest that CKIα plays an antiapoptotic role through the generation of phosphorylated sites at the level of the death-inducing signaling complex, thereby conferring resistance to caspase cleavage mediated by TRAIL.
Up-regulation of HIF in experimental acute renal failure: Evidence for a protective transcriptional response to hypoxia
Authors: Christian Rosenberger, Samuel N. Heyman, Seymour Rosen, Ahuva Shina, Marina Goldfarb, Wanja Griethe, Ulrich Frei, Petra Reinke, Sebastian Bachmann, Kai-Uwe Eckardt
Journal: Kidney International (2005)
Inhibition of hepatitis B virus production associated with high levels of intracellular viral DNA intermediates in iron-depleted HepG2.2.15 cells
Authors: Philippe Chouteau, Jacques Le Seyec, Bénédicte Saulier-Le Dréan, Isabelle Cannie, Pierre Brissot, Gérard Lescoat, Christiane Guguen-Guillouzo, Philippe Gripon
Journal: Journal of Hepatology (2001)
Hyperthyroidism From Thyroid Metastasis of Pancreatic Adenocarcinoma
Authors: Margareta Eriksson
Journal: JAMA (1977)

A nontender goiter rapidly developed in a 54-year-old patient with suspected disseminated carcinoma. Thyroid function tests showed increased thyroxine, triiodothyronine resin uptake, free thyroxine index, and free thyroxine. Radioactive iodine uptake by the gland was near zero, and thyroid-stimulating hormone (TSH) was undetectable. Histologic examination of the thyroid before and after death showed invasion and disruption of the thyroid follicles by adenocarcinoma (pancreatic primary). Release of thyroglobulin by follicular disruption probably resulted in hyperthyroxinemia and suppression of TSH and radioactive iodine uptake, as occurs in subacute thyroiditis. (<i>JAMA</i>238:1276-1278, 1977)
GAS GANGRENE AND TETANUS
Authors: W. K. Hatch
Journal: BMJ (1915)

j per cent., and most recently in metlhod (1) sterile water.The urea and quinine hydrochloride requires a little longer to act, but its effect is more prolonged than that produced by novocain, otherwise thero is nothing to choose between them; whil&t for an intradermiiic injection, water alone is perfectly satisfactory.At first we were doubtful of the action of this anaesthetic on the vitality of tlle grafts, btit even whlen transferred direct to the wound they took perfectly, altlhoucgh as a matter of convenience in lhandling, we, as a rule, puit tlhem first into warm saline.Tbe advantages of a local over a general anaestlhetic for this purpose are obviotus.There is Ino need of an assistant, of previous preparation of the patient, or of moving the p)atient from his bed.In the eyes of the patient it appears a iuielh nmore triffinr btisiness-an imiportant point if it hias to be done frequiently, as in the case of large wounds, or repeated if the first grafts fail to take.Lastly, perlhaps, if one can skin-graft witlh no more trotuble than doitig a dressing, one will be inclined to graft even sm11all wNounds, wlicilh would lheal perfectly well witlh- out it, but in wlichl, nevertlheless, a weelk or ten days can tlhereby be saved.
Quantitation, tissue distribution and proliferation kinetics of kupffer cells in normal rat liver
Authors: Luc Bouwens, Marijke Baekeland, Ronald de Zanger, Eddie Wisse
Journal: Hepatology (1986)

In normal rat liver, Kupffer cells were unequivocally identified using peroxidase cytochemistry by light microscopy in semithin plastic sections. The Kupffer cell population was found to constitute 31% of the sinusoidal cells and by morphometry and serial sectioning, a mean absolute number of 14 to 20 × 106 Kupffer cells per g liver was calculated. The mean distribution of Kupffer cells in the liver lobules was 43% in the periportal, 28% in the midzonal and 29% in the central area of the lobule. Administration of latex particles labeled only 64% of all Kupffer cells, and in particular centrally located cells, showed a lower activity of latex uptake, even at overloading doses. Furthermore, the latter cells were of smaller size than periportal Kupffer cell profiles. The mean number and distribution of latex-labeled Kupffer cells did not change over a period of 3 months, indicating a long lifetime for these resident macrophages. This slow population turnover was supported by the observed small mitotic index, 0.06% after a 6 hr arrest by vinblastine, and by the small [3H]thymidine labeling index which did not change over a period of 3 weeks after administration of the label. It is proposed that the Kupffer cell population, under physiologic conditions, is a long-living and self-renewing population, the kinetics of which substantially differ from those of other sinusoidal cell types.
879-2 Does heart rate regularization with biventricular pacing itself enhance net cardiac function in heart failure patients with chronic atrial fibrillation?
Authors: Ilan Hay, Vojta Melenovsky, Barry J Fetics, Joshua Hare, Daniel Judge, Andrew Kramer, Craig Reister, Joe Pastore, Rick Conville, David A Kass, Ronald Berger
Journal: Journal of the American College of Cardiology (2004)
Cbfβ-SMMHC impairs differentiation of common lymphoid progenitors and reveals an essential role for RUNX in early B-cell development
Authors: Ya-Huei Kuo, Rachel M. Gerstein, Lucio H. Castilla
Journal: Blood (2007)

Abstract The core-binding factor (CBF)–associated leukemia fusion protein CBFβ-SMMHC impairs myeloid and lymphoid differentiation. By inhibiting RUNX function, the fusion oncoprotein predisposes specifically to acute myeloid leukemia in both patients and mouse models. We have shown that Cbfβ-SMMHC expression leads to a sustained reduction of circulating B lymphocytes in the mouse. In this study, we demonstrate that the activation of Cbfβ-SMMHC reduces pre–pro-B cells approximately 3-fold and pre-B cells more than 10-fold and that this differentiation block is cell-autonomous. The reduction of pre–pro-B cells coincided with an increase in apoptosis in this population. The number of common lymphoid progenitors (CLPs) were not affected; however, the expression of critical early B-cell factors Ebf1, Tcfe2a, and Pax5 was significantly reduced. In addition, Cbfβ-SMMHC reduced Rag1 and Rag2 expression and impaired V(D)J recombination in the CLPs. Furthermore, CLPs expressing Cbfβ-SMMHC also show inhibition of B cell–specific genes Cd79a, Igll1, VpreB1, and Blk. These results demonstrate that CBF/RUNX function is essential for the function of CLPs, the survival of pre–pro-B cells, and the establishment of a B lineage–specific transcriptional program. This study also provides a mechanistic basis for the myeloid-lineage bias of CBFβ-SMMHC–associated leukemia.
Spontaneously hypertensive rat vascular smooth muscle cells in culture exhibit increased growth and Na+/H+ exchange.
Authors: B C Berk, G Vallega, A J Muslin, H M Gordon, M Canessa, R W Alexander
Journal: Journal of Clinical Investigation (1989)

The cellular mechanisms responsible for abnormalities in spontaneously hypertensive rat (SHR) vascular smooth muscle cell (VSMC) growth and vasoreactivity are not defined. Because Na+/H+ exchange, which we have previously demonstrated in cultured VSMC, plays an essential role in mediating growth factor responses, we hypothesized that abnormalities in SHR growth regulation might be reflected in the activity of this transporter. To test this hypothesis, we studied DNA synthesis and Na+/H+ exchange (measured as the rate of amiloride-sensitive intracellular alkalinization or Na+ influx) in early subcultures (less than 6) of aortic VSMC from 12-wk-old SHR and Wistar Kyoto (WKY) animals. Serum-deprived SHR VSMC grew more rapidly in response to 10% serum with an increase in [3H]thymidine incorporation of 439% compared with 191% in WKY controls. Basal intracellular pH (pHi) values determined by fluorescent pH measurements were 7.37 +/- 0.04 and 7.27 +/- 0.03 (P less than 0.05) in early passage SHR and WKY, respectively. Acid recovery (initial pHi = 6.8) by SHR VSMC was faster than by WKY VSMC as measured by alkalinization (1.8 +/- 0.6 vs. 0.8 +/- 0.2 mmol H+/liter.min, P less than 0.05) or by amiloride-sensitive 22Na+ influx (14.5 +/- 1.2 vs. 4.0 +/- 0.5 nmol Na+/mg protein.min, P less than 0.05). In comparison to WKY cells early passage SHR VSMC exhibited 2.5-fold greater alkalinization and amiloride-sensitive 22Na+ influx in response to 100 nM angiotensin II. During serial passage, WKY cells acquired enhanced Na+/H+ exchange and growth rates so that by passage 6, these differences were no longer present. These findings in early cultures of SHR VSMC, removed from the in vivo neurohumoral milieu, suggest that increased Na+/H+ exchange in SHR may reflect alterations in Na+ homeostasis that might contribute to altered SHR VSMC function such as enhanced growth and vasoreactivity.
Abstract 3836: Regulation of class III PI3K by class I PI3K/Akt inhibits autophagy through phosphorylation of UVRAG
Authors: Shaokun Shu, Mei Sun, Donghwa Kim, Jin Q. Cheng
Journal: Cancer Research (2010)

Abstract It has been well documented that the class I PI3K (PI3KC1)/Akt pathway inhibits whereas class III PI3K (PI3KC3) induces autophagy. UVRAG forms a complex with Beclin1 and PI3KC3 leading to activation of autophagy process. In this study, we demonstrate that PI3KC1/Akt inhibits PI3KC3 kinase activity and autophagy induced by different stimuli, including mTOR inhibitor rapamycin, suggesting PI3KC1/Akt regulation of autophagy independent of mTOR. Further, Akt directly phosphorylates UVRAG on serine-509, which results in disruption of UVRAG-Beclin1-PI3KC3 complex, and inhibition of PI3KC3 and autophagy. Inhibition of PI3KC1 or depletion of Akt increases the ability of UVRAG to bind to Beclin 1. UVRAG-S509A, which is not phosphorylated by Akt, enhances whereas UVRAG-S509D, which mimics the phosphorylation by Akt, reduces the interaction between UVRAG and Beclin1. Notably, UVRAG-S509A abrogates the effect of Akt on PI3KC3 and autophagy. These findings establish the cross-talk between class I and class III PI3K and indicate that PI3KC1/Akt regulates autophagy through inhibition of PI3KC3 by phosphorylation of UVRAG. 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 3836.
QUANTITATIVE STUDIES OF THE VIRUS-HOST RELATIONSHIP IN CHIMPANZEES AFTER INAPPARENT INFECTION WITH COXSACKIE VIRUSES
Authors: Lisbeth M. Kraft, Joseph L. Melnick
Journal: The Journal of Experimental Medicine (1953)

Eight chimpanzees were fed and/or inoculated with a single Coxsackie (C) virus or combinations of different ones. The responses in terms of complement-fixing (c-f) antibodies to 6 to 10 such viruses were measured throughout periods of 1 to 2 years. Although the animals usually responded with rises in homologous antibodies after the feeding or the inoculation of viruses of special immunological types, a variable number of heterologous c-f antibodies were observed to increase significantly at the same time. When immune animals were challenged with homologous virus, they failed to become virus carriers again and no rises in neutralizing antibodies were detected. However, the challenge usually resulted in a boost in the titer of the homologous c-f antibody and often of heterotypic c-f antibodies. This was particularly striking in those chimpanzees in which the c-f antibody had fallen below a detectable level. In contrast to this, the infection of chimpanzees with agents outside the Coxsackie family (poliomyelitis viruses and Egyptian strains of West Nile virus) failed to influence the level of Coxsackie antibodies even during the periods when c-f antibodies to these non-Coxsackie viruses were rapidly rising.
Effects of chronic octreotide treatment on renal changes during cirrhosis in rats
Authors: Thomas E.N Jonassen, Sten Christensen, Anne-Mette Sørensen, Niels Marcussen, Allan Flyvbjerg, Frederik Andreasen, Jørgen S Petersen
Journal: Hepatology (1999)

We examined the effect of a new long-acting release formula (LAR) of the somatostatin analogue, octreotide, on development of sodium retention and functional and structural changes in the thick ascending limb ofHenle's loop (TAL) in rats with cirrhosis induced by common bile duct ligation (CBL). CBL and sham-operated control rats were treated withoctreotide-LAR (10 mg/kg bodyweight subcutaneously, as a singledose) or vehicle at the time of CBL or sham-CBL. The rats were instrumented with chronic catheters, and sodium balance and renal function were examined 4 weeks after CBL or sham operation. Octreotide-LAR treatment significantly inhibited sodium retention in CBL rats and prevented renalvasodilatation without changes in glomerular filtration rate (GFR). The natriuretic response to a test dose of furosemide (7.5 mg/kg body weight intravenously) was significantly increased in CBL rats, and when expressed in terms of natriuretic efficiency (mmol Na/mg furosemide in urine), thenatriuretic response was increased by 57% relative to sham-operatedcontrols. Stereological examination of kidneys demonstrated a 53% increase in the volume of the inner stripe of the outer medulla and a 108% increase in the volume of TAL epithelium in cirrhotic rats relative to controls. The increased natriuretic efficiency of furosemide as well as the hypertrophy of the inner stripe and the TAL in this renal zone were absent in CBL rats treated with octreotide-LAR. These results suggest that octreotide-LAR treatment inhibits sodium retention in cirrhotic rats, partly by inhibition of increased furosemide-sensitive sodium reabsorption in the TAL