tbuckley/cabot-search huggingface dataset:
Full-thickness endoscopic resection of gastrointestinal cancer: from animal lab to humans
Authors: JR Armengol Miro, M Abu-Suboh Abadia, J Dot Bach, M Masachs Peracaula, J Armengol Bertroli, A Benages Curell, JC Salord, SV Kantsevoy
Journal: Endoscopy (2012)

Background: Endoscopic mucosal resection (EMR) and endoscopic submucosal dissection (ESD) are currently used for resection of early gastrointestinal (GI) tract cancer, limited to superficial layers of the gastric and colonic wall. These techniques are technically difficult, labor intensive and cannot be used when tumor cannot be lifted with submucosal injection and/or involves deeper layers of GI tract wall.
Sequence variants in the 3'-untranslated region of CRTH2 are associated with asthma and differentially influence the mRNA stability*1
Authors: P.S. Gao, R.A. Mathisas, S. Hsu, B. Plunkett, A. Togias, K.C. Barnes, C. Stellato, T.H. Beaty, S.K. Huang
Journal: Journal of Allergy and Clinical Immunology (2004)
Protection of the Arterial Internal Elastic Lamina by Inhibition of the Renin-Angiotensin System in the Rat
Authors: Wei Huang, François Alhenc Gelas, Mary J. Osborne-Pellegrin
Journal: Circulation Research (1998)

Abstract —Spontaneous rupture of the internal elastic lamina (IEL) occurs in some arteries of the rat during growth and aging. Inbred, normotensive, Brown Norway (BN) rats are particularly susceptible to rupture of the IEL, especially in the abdominal aorta (AA). Preliminary experiments showed that different angiotensin-converting enzyme (ACE) inhibitors protect against rupture of the IEL in the BN rat to a greater extent than hydralazine, suggesting a role of the renin-angiotensin system (RAS) in this phenomenon. To explore this possibility, we have treated male BN rats from 4.5 to 14 weeks of age with either enalapril or losartan (both at 1, 3, and 10 mg · kg −1 · d −1 ) or with the calcium antagonists mibefradil (at 3, 10, 30, and 45 mg · kg −1 · d −1 ) and amlodipine (at 30 mg · kg −1 · d −1 ). Systolic blood pressure (SBP) was measured weekly, and at the end of treatment we (1) recorded body and heart weights, (2) measured various parameters of the RAS in plasma, (3) quantified interruptions in the IEL on “en face” preparations of AA, and (4) quantified elastin, collagen, and cell proteins in the media of the thoracic aorta. Results showed that enalapril and losartan similarly decrease SBP and rupture of the IEL in the AA, suggesting that enalapril inhibits the latter via a decrease in the production of angiotensin II (Ang II) and not via another effect on ACE. The decrease in IEL rupture and in SBP, as well as the modifications in the parameters of the RAS, were all dose dependent. Mibefradil had little effect on the RAS and, at the highest doses, decreased SBP to an extent similar to that for enalapril at 3 mg · kg −1 · d −1 but did not significantly inhibit IEL rupture. Amlodipine decreased SBP, increased plasma renin concentration, and was without effect on IEL rupture. All treatments at the highest doses had a hypotrophic effect on the aortic media but differed in their effects on the heart, with enalapril and losartan decreasing and mibefradil and amlodipine increasing heart weight, suggesting that the inhibition of IEL rupture may be related to a cardiac hypotrophic effect. All these results, taken together, suggest that Ang II plays a role in the rupture of the IEL that is, in part, independent of SBP.
Cardiac Dysfunction and Noncardiac Dysfunction as Precursors of Heart Failure With Reduced and Preserved Ejection Fraction in the Community
Authors: Carolyn S.P. Lam, Asya Lyass, Elisabeth Kraigher-Krainer, Joseph M. Massaro, Douglas S. Lee, Jennifer E. Ho, Daniel Levy, Margaret M. Redfield, Burkert M. Pieske, Emelia J. Benjamin, Ramachandran S. Vasan
Journal: Circulation (2011)

Background— Heart failure (HF) is a clinical syndrome characterized by signs and symptoms involving multiple organ systems. Longitudinal data demonstrating that asymptomatic cardiac dysfunction precedes overt HF are scarce, and the contribution of noncardiac dysfunction to HF progression is unclear. We hypothesized that subclinical cardiac and noncardiac organ dysfunction would accelerate the manifestation of HF. Methods and Results— We studied 1038 participants of the Framingham Heart Study original cohort (mean age, 76±5 years; 39% men) with routine assessment of left ventricular systolic and diastolic function. Major noncardiac organ systems were assessed with the use of serum creatinine (renal), serum albumin (hepatic), ratio of forced expiratory volume in 1 second to forced vital capacity (FEV 1 :FVC ratio; pulmonary), hemoglobin concentration (hematologic/oxygen-carrying capacity), and white blood cell count (systemic inflammation). On follow-up (mean, 11 years), there were 248 incident HF events (146 in women). After adjustment for established HF risk factors, antecedent left ventricular systolic dysfunction (hazard ratio, 2.33; 95% confidence interval, 1.43 to 3.78) and diastolic dysfunction (hazard ratio, 1.32; 95% confidence interval, 1.01 to 1.71) were associated with increased HF risk. After adjustment for cardiac dysfunction, higher serum creatinine, lower FEV1:FVC ratios, and lower hemoglobin concentrations were associated with increased HF risk (all P &lt;0.05); serum albumin and white blood cell count were not. Subclinical dysfunction in each noncardiac organ system was associated with a 30% increased risk of HF ( P =0.013). Conclusions— Antecedent cardiac dysfunction and noncardiac organ dysfunction are associated with increased incidence of HF, supporting the notion that HF is a progressive syndrome and underscoring the importance of noncardiac factors in its occurrence.
Vitiligo and leprosy
Authors: W. H. Jopling
Journal: British Journal of Dermatology (1978)

Journal Article Vitiligo and leprosy Get access W. H. Jopling W. H. Jopling 33 Crown Lance Gardens, Crown Lane, London SW16 3HZ Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 99, Issue 1, 1 July 1978, Page 112, https://doi.org/10.1111/j.1365-2133.1978.tb01970.x Published: 01 July 1978
Analysis of distribution patterns of<i>Propionibacterium acnes</i>phylotypes and<i>Peptostreptococcus</i>species from acne lesions
Authors: H.H. Kwon, J.Y. Yoon, S.Y. Park, D.H. Suh
Journal: British Journal of Dermatology (2013)

The precise roles of Propionibacterium acnes and other anaerobic bacteria in the pathogenesis of acne are still unclear. Recent studies have shown that P. acnes can be further classified into several phylotypes with distinct phenotypes and virulence. Their distribution patterns in acne lesions have rarely been demonstrated.To analyse distribution patterns of P. acnes phylotypes and Peptostreptococcus species on the skin surface of patients with acne and healthy controls, and in comedones, papules and pustules from patients.A total of 370 samples from 95 patients with acne and 65 samples from 65 healthy controls were investigated. Three P. acnes phylotypes and three Peptostreptococcus species were identified by polymerase chain reaction primarily using type-specific primers.There was no significant difference in the microflora of the skin surface samples between patients with acne and healthy controls. In acne lesions, distribution patterns between skin surface and comedonal lesions were similar, but they were significantly different from those of both papules and pustules. In the inflammatory acne lesions, the proportion of type IA P. acnes was increased, while those of type IB and II were decreased. The proportion of Peptostreptococcus species was also increased significantly in the inflammatory lesions.At the precision of this qualitative study, our results do not provide any evidence that different phylotypes in the surface microflora might be important in triggering acne. However, type IA P. acnes and Peptostreptococcus species might be more closely associated with inflammatory acne lesions.
Hepatitis C virus RNA and antibody response in the clinical course of acute hepatitis C virus infection
Authors: Massimo Puoti, Antonella Zonaro, Antonella Ravaggi, Maria Grazia Marin, Filippo Castelnuovo, Elisabetta Cariani
Journal: Hepatology (1992)

Hepatitis C virus RNA, anti—hepatitis C virus immune response and biochemical markers of liver injury were investigated in 17 patients with acute non-A, non-B hepatitis. At the first observation, 1 to 3 wk from the clinical onset, all patients had hepatitis C virus RNA in their serum, and most (15 of 17) were positive for second-generation anti—hepatitis C virus enzyme immunoassay. Follow-up serum samples were available for 10 patients. The rate of recombinant immunoblot assay—confirmed anti—hepatitis C virus enzyme immunoassay reactivities increased from 67% in the first 3 wk to 86% after 21 wk. Elevated ALT levels were associated with hepatitis C virus RNA positivity in most of cases, but the viral nucleic acid was also detected in sera with normal or slightly increased enzyme values. None of the single antibodies tested were related to hepatitis C virus RNA positivity or to the clinical phase of the infection. Therefore hepatitis C virus RNA determination might provide important additional information as compared with anti—hepatitis C virus markers, allowing earlier diagnosis, discrimination of active infection and, possibly, prognostic evaluation. (HEPATOLOGY 1992;16:877–881.)
THE PRIMARY IMMUNE RESPONSE IN MICE
Authors: Philip D. McMaster, Robert E. Franzl
Journal: The Journal of Experimental Medicine (1968)

The effects of a single injection of a bacterial endotoxin on the cellular changes of a primary immune response to a standard dose of sheep red blood cells were studied in the spleens and mesenteric lymph nodes of mice. Daily histological comparisons of these organs in mice, injected with endotoxin, or with antigen, or both, showed that endotoxin given simultaneously with sheep red blood cells, as antigen, significantly enhanced all of the cellular changes that appear in the mesenteric lymph nodes and spleens of mice that form antibody when that antigen is given alone. First, in the white pulp of the spleens and cortical regions of the nodes, there appeared an early and excessive proliferation of the large pyroninophilic cells which seems to be responsible for the earliest formation of antibody, as judged by this work and that of others cited in the body of the paper. Polymorphonuclear cells invaded the spleens of these animals early after simultaneous challenge with antigen and endotoxin, and in far greater numbers than have ever been seen in mice given the same antigen without endotoxin. "Activated" germinal centers formed in the lymphoid tissue either 1 day before the appearance of antibody in the blood stream or on the same day, and they became larger than in the mice given antigen only. On the other hand, these specific and characteristic cellular changes failed to appear in mice prevented from forming any antibody at all by injections of endotoxin given 2 days before the antigenic challenge. These findings are discussed in the light provided by data from recent reports of others as well as in the light of the accompanying paper (1) which demonstrated not only the enhancement of antibody formation following simultaneous injections of antigen and endotoxin, as already known, but a totally unexpected, complete suppression of its formation when endotoxin was given 2 days before antigen.
Cardiac baroreflex function during postural change assessed using non-invasive spontaneous sequence analysis in young men
Authors: A. Steptoe, C. Vogele
Journal: Cardiovascular Research (1990)

The aim was to assess the value of baroreflex sensitivity estimates calculated from analyses of spontaneous systolic blood pressure and pulse interval sequences derived from continuous non-invasive finger blood pressure recordings during sitting and active standing.Continuous recordings of digital systolic blood pressure and pulse interval were obtained non-invasively using a Finapres FD5 during 5 min trials of sitting and standing.Subjects were healthy males aged 19-28, divided into those with "high" normal (n = 18) and "low" normal (n = 17) blood pressure.Recordings were scanned for spontaneous sequences of three or more cardiac cycles over which systolic blood pressure increased progressively in conjunction with prolonged pulse interval, or decreased while pulse interval became shorter. Regressions between blood pressure and pulse interval (r greater than 0.80) provided estimates of cardiac baroreceptor reflex control. Computations were carried out with concurrent blood pressure and pulse interval measurements, and with a delay or lag of one and two cycles between the two variables. Pulse interval was reduced from an average 870.3 ms sitting to 571.3 ms on standing. Mean baroreflex sensitivity while sitting averaged 17.5 ms.mm Hg-1 at a delay of one cycle, failing to 7.65 ms.mm Hg-1 with standing. The decrease in sensitivity was correlated with the change in pulse interval between trials. The number of sequences was also significantly reduced with standing as opposed to sitting. Three cycle sequences were most frequent, with a lesser number of sequences involving 4, 5, and 6 or more cycles. No significant differences between "high" and "low" normal blood pressure groups were observed.The analysis of spontaneous sequences from non-invasive recordings may provide useful information concerning cardiac baroreflex control in different postural and behavioural states. A lag of one cycle between systolic blood pressure and pulse interval may provide the most representative estimates of baroreflex sensitivity.
Identification of a Biphasic Role for Genistein in the Regulation of Prostate Cancer Growth and Metastasis
Authors: Lara H. El Touny, Partha P. Banerjee
Journal: Cancer Research (2009)

Abstract Considered a chemopreventive agent, the ability of genistein to modulate the progression of existing prostate cancer (CaP) is not clear. We show here that the consumption of genistein (250 mg/kg diet) by 12-week-old transgenic adenocarcinoma mouse prostate (TRAMP-FVB) mice harboring prostatic intraepithelial neoplasia lesions until 20 weeks of age induces an aggressive progression of CaP, as evidenced by a 16% increase in the number of well-differentiated and poorly differentiated prostates, coinciding with a 70% incidence of pelvic lymph node (LN) metastases as opposed to 0% and 10% in 0 and 1,000 mg/kg groups, concomitant with elevated osteopontin (OPN) expression in prostates and LNs. Equivalent nanomolar (500 nmol/L) concentrations of genistein recapitulated these effects in human PC3 CaP cells as evidenced by increased proliferation, invasion, and matrix metalloproteinase-9 (MMP-9) activity (∼2-fold), accompanied by an up-regulation of OPN expression and secretion, compared with vehicle-treated cells. A pharmacologic dose (50 μmol/L) decreased proliferation, invasion, and MMP-9 activity (&amp;gt;2.0-fold) concomitant with OPN reduction. Upon OPN knockdown by short hairpin RNA, genistein was no longer effective in up-regulating PC3 cell proliferation, invasion, and MMP-9 activation, which were significantly reduced in the absence of OPN, highlighting the requirement for OPN in mediating the effects of genistein. Proliferation, invasion, and OPN levels were also nonsignificantly induced by genistein in the presence of ICI 182,780 or wortmannin, indicating a dependence on phosphatidylinositol 3-kinase and estrogen signaling. Our results suggest the presence of a biphasic regulation of CaP growth and metastasis by genistein, warranting careful examination of the effects of genistein on hormone-dependent cancers in a chemotherapeutic setting. [Cancer Res 2009;69(8):3695–703]
Can tasks be inherently boring?
Authors: Evan Charney
Journal: Behavioral and Brain Sciences (2013)

Abstract Kurzban et al. argue that the experiences of “effort,” “boredom,” and “fatigue” are indications that the costs of a task outweigh its benefits. Reducing the costs of tasks to “opportunity costs” has the effect of rendering tasks costless and of denying that they can be inherently boring or tedious, something that “vigilance tasks” were intentionally designed to be.
Localization of Tc-99m MDP in a Ureteral Tumor
Authors: MAKOTO KATSURAGI, HIROMI NISHIHARA, SEIJI MOTOMURA
Journal: Clinical Nuclear Medicine (1993)

Extraosseous uptake of Tc-99m MDP in tumors, such as in breast or lung cancer, is sometimes recognized; in ureteral tumors, however, accumulation has not yet been documented. A case of ureteral tumor that showed tracer uptake is presented. Plain CT and histopathologic examination demonstrated tiny calcifications in the tumor. It was presumed that hypermetabolism of calcium-phosphate in the tumor caused tracer uptake.
Increased FDG Uptake Along Dermatome on PET in a Patient With Herpes Zoster
Authors: Charles Egan, Eugene Silverman
Journal: Clinical Nuclear Medicine (2013)

This is a 66-year-old female patient being treated for diffuse large B-cell lymphoma. She reported to her physician in late January 2012 with a left flank pruritic painful rash. She was diagnosed with herpes zoster and treated with antiviral medication. Her chemotherapy regimen was delayed due to the zoster infection. In March 2012, the patient underwent a PET/CT as a lymphoma surveillance scan prior to reinstituting the chemotherapy treatment. As an incidental finding, the PET showed increased metabolic activity in a dermatomal distribution along the left flank, which corresponded to the patient's zoster infection.
Culture, Psychosomatics and Substance Abuse: The Example of Body Image Drugs
Authors: Gen Kanayama, James I. Hudson, Harrison G. Pope Jr.
Journal: Psychotherapy and Psychosomatics (2012)

Patterns of illicit drug use vary widely around the world. For example, one recent survey [1] found lifetime cannabis use among 41.9% of respondents in New Zealand, but only 6.6% of respondents in Italy and 1.5% in Japan. Cocaine was reported by 16.2% of respondents in the USA, versus 4.1% in Spain and 0.0% in the People's Republic of China. Favored drugs of abuse may also rank differently within different countries. Japan, for instance, has experienced three major epidemics of methamphetamine abuse over the last 50 years [2, 3], but shows a low prevalence of many other forms of drug abuse that are widespread elsewhere [4]. Clearly, factors such as drug availability, government enforcement policies and national healthcare systems contribute to these figures, but one must also acknowledge the critical role of culture [5]. Culture influences not only attitudes towards illicit drug use in general, but also which particular drugs people choose to use; a drug effect sought by one population might have little appeal for another. As one example of this little-studied issue, we explore here a form of drug abuse that is strikingly asymmetric across cultures: the use of ‘body image drugs’ such as anabolic-androgenic steroids (AAS).
<i>DDEF1</i> Is Located in an Amplified Region of Chromosome 8q and Is Overexpressed in Uveal Melanoma
Authors: Justis P. Ehlers, Lori Worley, Michael D. Onken, J. William Harbour
Journal: Clinical Cancer Research (2005)

Abstract Purpose: The molecular pathogenesis of uveal melanoma is poorly understood but is usually accompanied by amplification of chromosome 8q, suggesting the activation of one or more oncogenes. We recently identified a gene expression profile that distinguishes low-grade from high-grade melanomas. In this profile, a cluster of genes at chromosome 8q was overexpressed in high-grade tumors, providing an opportunity to search for potential oncogenes in this region. Experimental Design: Gene expression microarray analysis was done on 25 primary uveal melanomas. Microarray comparative genomic hybridization (CGH), quantitative PCR, and immunohistochemistry were done on a subset of these tumors. Cell motility was measured using a wound-healing assay. Results: In melanomas analyzed for microarray gene expression and CGH, gain of chromosome 8q correlated most strongly with expression of DDEF1, a gene located at 8q24. In contrast, the nearby MYC oncogene exhibited no significant change in expression. Confirming the microarray findings, DDEF1 mRNA levels and protein expression were significantly higher in high-grade melanomas. Furthermore, ectopic expression of DDEF1 in low-grade melanoma cells resulted in a significant increase in cell motility, a feature of high-grade metastasizing cells. Conclusions: These findings suggest that DDEF1 overexpression may be a pathogenetically relevant consequence of chromosome 8q amplification, which commonly occurs in high-grade uveal melanomas. We conclude that DDEF1 may act as an oncogene in this cancer, and it may be a useful diagnostic marker and therapeutic target.
PCI vs Optimal Medical Therapy - The Other Side of the Coin: Medication Adherence
Authors: Cüneyt Koçaş, Okay Abaci, Veysel Oktay, Ugur Coskun, Cem Bostan, Ahmet Yildiz, Alev Arat Ozkan, Tevfik Gurmen, Murat Ersanli
Journal: Journal of the American College of Cardiology (2013)
Abstract 4272: Hexastatin is a potent therapeutic agent for targeting tumor angiogenesis and tumor growth
Authors: Sudhakar Akulapalli, Chandra Shekhar Boosani, Archana Laknaur, Venugopal Gunda
Journal: Cancer Research (2011)

Abstract Peptides or short protein domains derived from the extracellular matrix are reported to possess anti-tumor properties. In the present study, one such molecule “Hexastatin or [α6(IV)NC1]” a non-collagenous domain of α6 chain of type (IV) collagen was derived from the carboxy terminal and was found to inhibit tumor growth, but the mechanism by which it inhibits the growth of solid tumors has not been reported yet. In the present study, we identified that the biological functions of hexastatin are attributed to its binding to different cell surface integrins. We identified that hexastatin binds to α3β1, αVβ3 and α5β1 integrins and inhibits p38-MAPK signaling. Hexastatin competes with human vascular endothelial cells in binding to α1β1 integrins on type IV collagen, and or with α5β1/αVβ3 integrins on fibronectin/vitronectin matrix, thus inhibiting endothelial migration and tube formation. Interestingly, p38-MAPK phosphorylation was not inhibited in α3 and β3 integrin null endothelial cells upon treatment with Hexastatin which confirms that the antiangiogenic functions of Hexastatin are possibly mediated through α3β1 and αVβ3 integrins. While both the integrins (α3β1 and α5β1) are required for the inhibition of tube formation by Hexastatin in endothelial cells, only α3β1 integrin was found to regulate endothelial cells migration. In addition we also demonstrate that Hexastatin inhibits tumor growth, tumor angiogenesis and circulating endothelial cells in-vivo. These in-vitro and in-vivo findings indicate that α3β1 and αVβ3 integrins are critical for Hexastatin mediated inhibition of angiogenic signaling and tumor progression. Collectively, our findings demonstrate that hexastatin is a potent therapeutic agent for targeting tumor angiogenesis and tumor growth. 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 4272. doi:10.1158/1538-7445.AM2011-4272