tbuckley/cabot-search huggingface dataset:
Dynamics of Intramural and Transmural Reentry During Ventricular Fibrillation in Isolated Swine Ventricles
Authors: Miguel Valderrábano, Moon-Hyoung Lee, Toshihiko Ohara, Angela C. Lai, Michael C. Fishbein, Shien-Fong Lin, Hrayr S. Karagueuzian, Peng-Sheng Chen
Journal: Circulation Research (2001)

The intramural dynamics of ventricular fibrillation (VF) remain poorly understood. Recent investigations have suggested that stable intramural reentry may underlie the mechanisms of VF. We performed optical mapping studies of VF in isolated swine right ventricles (RVs) and left ventricles (LVs). Nine RV walls were cut obliquely in their distal edge exposing the transmural surface. Six LV wedge preparations were also studied. Results showed that intramural reentry was present. In RV, 28 of 44 VF episodes showed reentry; 15% of the activation pathways were reentrant. Except for 4 episodes, reentry was transmural, involving subendocardial structures as the papillary muscle (PM) or trabeculae. In LV, reentry was observed in 27 of 27 VF episodes; 23% of the activations were part of reentrant pathways (P<0.05 compared with RV). All LV reentrant pathways were truly intramural (confined to the wall) and were frequently located at the PM insertion. In both ventricles, reentry was spatially and temporally unstable. Histological studies showed abrupt changes in fiber orientation at sites of reentry and wave splitting. Connexin 40 immunostaining demonstrated intramyocardial Purkinje fibers at sites of reentry in the PM root and around endocardial trabeculae. Our results confirm that reentry is frequent-but unstable-in the myocardial wall during VF. In RV, reentry is mostly transmural and requires participation of subendocardial structures. The LV has a greater incidence of reentry and is intramural. Anisotropic anatomic structures played key roles in the generation of wave splitting and in the maintenance of reentry.
Proactively Engaging Smokers Leads to Higher Quit Rates
Authors: Anita Slomski
Journal: JAMA (2014)

Using a proactive intervention to motivate smokers to quit resulted in higher cessation rates than the traditional model in which smokers request treatment or a clinician initiates it (Fu S et al. JAMA Intern Med. doi:10.1001/jamainternmed.2014.177 [published online March 10, 2014]).
Chronic Fatigue Syndrome Answers Sought
Authors: Tracy Hampton
Journal: JAMA (2006)

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
Phil Sokolof fights the 'fatting' of America
Authors: D. L. Breo
Journal: JAMA (1990)

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
Tumor Stromal Phenotypes Define VEGF Sensitivity—Letter
Authors: Gert G. Van den Eynden, Nigel C. Bird, Luc Y. Dirix, Rikke L. Eefsen, Zu-Hua Gao, Gunilla Høyer-Hansen, Martin Illemann, Ali W. Majeed, Peter Metrakos, Andrew R. Reynolds, Ben Vainer, Pieter-Jan van Dam, Steven J. Van Laere, Peter B. Vermeulen, Fernando Vidal-Vanaclocha, Pnina Brodt
Journal: Clinical Cancer Research (2014)

With great interest, we read the article “Tumor Stromal Architecture Can Define the Intrinsic Tumor Response to VEGF-Targeted Therapy” by Smith and colleagues (1) in which the response to VEGF-targeted therapy was linked to the vascular/stromal architecture of primary tumors.We previously described different histologic growth patterns (GP) of the tumor–liver interface in liver metastases (LM) of patients with solid tumors, including colorectal cancer (2, 3). LMs with a “desmoplastic” GP are encapsulated by a band of desmoplastic stroma. In the “pushing” GP, the tumor cells are separated from the hepatocytes by a thin layer of reticulin fibers. Both of these patterns show histologic features consistent with angiogenesis. However, in the “replacement” GP, tumor cells invade into the liver parenchyma and coopt sinusoidal blood vessels instead of using angiogenesis (2–4).Although Smith and colleagues (1) studied primary tumors, we note similarities between the two major vascular phenotypes they describe and the patterns of vascularization in LMs of the three GPs. Namely, the tumor-associated vasculature in the desmoplastic GP and, to a lesser extent in the pushing GP, consists of newly formed capillaries surrounded by well-developed stroma, akin to the “stromal vessel (SV)” phenotype described by Smith and colleagues On the other the vasculature of the replacement GP is comparable with the Smith “tumor vessel (TV)” phenotype. In animal models, Smith and colleagues observed that TV tumors were more sensitive to VEGF-targeted therapy than SV tumors, whereas in human metastastic colorectal cancer samples, the SV phenotype group had a poorer response to bevacizumab and FOLFIRI. In contrast with this, we reason that because the LMs of the replacement GP (which are akin to the TV phenotype) are nonangiogenic, they should be the least responsive to VEGF-targeted therapy.In conclusion, a phenotypic variability in the stroma akin to that described by Smith and colleagues (1) for primary tumors has been described by us for colorectal cancer liver metastases. Both findings highlight the potential influence of the tumor stroma architecture on the response to antiangiogenic therapy. In the continuing effort to personalize treatment for metastatic colorectal cancer, the questions of whether this phenotypic variability in LMs determines the outcome of VEGF-targeted therapy and the relative contributions of the primary tumor versus LMs phenotypes to this response, warrant further investigation.See the Response, p. 5141No potential conflicts of interest were disclosed.
Gastric bleeding in portal hypertension: Inflammatory or congestive?
Authors: I. James Sarfeh, A. Tarnawski
Journal: Hepatology (1986)

This paper reports the incidence and natural history of macroscopic gastritis in a series of 127 consecutive patients with portal hypertension of various aetiologies. Gastritis was observed endoscopically in 65 patients (51%) and was of two main types. Twenty eight patients had severe or persistent gastritis which caused clinically significant bleeding on 80 occasions and accounted for 25% of the bleeds from all sources. The remainder had mild gastritis. The presence of gastritis seemed to be independent of the severity of liver disease or the degree of rise of wedged hepatic venous pressure and there was no difference in age, sex, or drugs prescribed in patients with or without gastritis. The mean follow up period and the mean number of sclerotherapy treatments was significantly greater (p<0.005) in patients with gastritis. Full thickness gastric biopsies in seven surgical patients and 11 autopsy specimens showed dilated and tortuous submucosal veins. Endoscopic biopsies in 14 patients showed vascular ectasia in the mucosal layer which was in excess of the degree of inflammatory infiltrate. Gastritis occurred in patients with portal hypertension of all common aetiologies and the clinical and pathological evidence supports the contention that it reflects a congested gastric mucosa and should be renamed congestive gastropathy. As injection sclerotherapy improves survival from variceal bleeding congestive gastropathy may become more common. The response to conventional (‘anti-erosive’) therapy is poor and measures aimed at reducing the gastric portal pressure may be the only effective means of treating this condition.
Children's Socks
Authors: C. Philpott
Journal: BMJ (1960)

One prominent manifestation of mechanical activity in hair cells is spontaneous otoacoustic emission, the unprovoked emanation of sound by an internal ear. Because active hair bundle motility probably constitutes the active process of nonmammalian hair cells, we investigated the ability of hair bundles in the bullfrog9s sacculus to produce oscillations that might underlie spontaneous otoacoustic emissions. When maintained in the normal ionic milieu of the ear, many bundles oscillated spontaneously through distances as great as 80 nm at frequencies of 5–50 Hz. Whole-cell recording disclosed that the positive phase of movement was associated with the opening of transduction channels. Gentamicin, which blocks transduction channels, reversibly arrested oscillation; drugs that affect the cAMP phosphorylation pathway and might influence the activity of myosin altered the rate of oscillation. Increasing the Ca <sup>2+</sup> concentration rendered oscillations faster and smaller until they were suppressed; lowering the Ca <sup>2+</sup> concentration moderately with chelators had the opposite effect. When a bundle was offset with a stimulus fiber, oscillations were transiently suppressed but gradually resumed. Loading a bundle by partial displacement clamping, which simulated the presence of the accessory structures to which a bundle is ordinarily attached, increased the frequency and diminished the magnitude of oscillation. These observations accord with a model in which oscillations arise from the interplay of the hair bundle9s negative stiffness with the activity of adaptation motors and with Ca <sup>2+</sup>-dependent relaxation of gating springs.
Market penetration of new drugs
Authors: H McGavock, G D Johnston, C H Webb
Journal: BMJ (1994)

EDITOR, - Three letters1 comment on our article on the market penetration of new drugs in Northern Ireland.2 J P Griffin attacks our article as flawed in its conclusions without revealing the flaws.1 We did not state that it was “always the first medicine in the field which continues to be…the market leader.” We did not advocate that the search for better products in the same therapeutic class should not be pursued. We …
PRODUCTION OF MACROPHAGE MIGRATION INHIBITION FACTOR BY CONTINUOUS CELL LINES
Authors: David G. Tubergen, Joseph D. Feldman, E. M. Pollock, Richard A. Lerner
Journal: The Journal of Experimental Medicine (1972)

Macrophage migration inhibitory factor (MIF) was found in media of human and mouse lymphocyte and fibroblast cell lines that were continuously growing. Its release was dependent on activation of the cells to enter the mitotic cycle, particularly on cells in S phase. The greatest quantity of MIF was detected in supernatants of lymphocytes collected during S phase after the cells were synchronized in G1 and in supernatants of growing fibroblasts. When the latter were contact inhibited little or no MIF was found in media. MIF was also released into media of cells proliferating in homologous serum in the absence of fetal calf serum and into media lacking any protein. The MIF produced by lymphocyte lines eluted from Sephadex G-100 in the same fashion as MIF produced by the interaction of sensitized guinea pig cells and antigen. The results indicated that MIF is not a specific mediator of delayed hypersensitivity and cellular immunity and that MIF released by sensitized lymphocytes incubated with antigen merely reflects that fraction of cells activated by antigen to enter the mitotic cycle.
Does It Prevent Prematurity?
Authors: B P Sachs, S Hellerstein, R Freeman, F Frigoletto, J C Hauth
Journal: New England Journal of Medicine (1991)

PREVENTION of premature births is the most important challenge in obstetrics. Recently a device for monitoring uterine activity at home (the Genesis Home Uterine Activity Monitor [HUAM] system, Tokos Medical Group), coupled with daily contact between patients and medical personnel, was reported to prevent premature births at an average cost per patient of over $5,000.1 The Food and Drug Administration recently approved this system for the early detection of preterm labor in women who had had a previous preterm delivery. The agency did not approve this system of care for the prevention of premature births, however, and has made it . . .
Abstract 5234: Microenvironmental signals dictate disseminated tumor cells (DTCs) fate through regulation of TGFβII and p38α
Authors: Paloma Bragado, Yeriel Estrada, Maria Soledad Sosa, Denis M. Schewe, Carla Capobianco, Kateri Moore, Hernan G. Farina, Julio Aguirre-Ghiso
Journal: Cancer Research (2012)

Abstract Metastases develop from disseminated tumor cells (DTCs) years or even decades after primary tumor treatment. This is thought to be due to the ability of residual DTCs to remain dormant, but the mechanisms controlling this state are poorly understood. We have explored whether the target organ microenvironment where DTCs lodge can control their fate and the timing of DTCs dormancy in a HNSCC model. When injected in nude mice, HEp3-GFP cells form tumors with 100% efficiency and spontaneously disseminate to lungs (72% incidence) and bone marrow (BM) (28% incidence). Tracking of GFP-tagged DTCs showed that after ∼2 weeks the quiescent DTCs in lungs start to grow to form overt metastasis in 72% of mice. In contrast, those in the BM remain at constant numbers suggesting a dormant phenotype. Furthermore, DTCs isolated from lungs and expanded in culture (Lu-HEp3) display a high ERK/p38 signaling ratio and are tumorigenic when inoculated in vivo. Meanwhile in vitro expanded BM-HEp3-derived cell lines remain dormant when inoculated in vivo and are characterized by a low ERK/p38 activity ratio (predictive of quiescence for breast fibrosarcoma, squamous carcinoma and colon carcinoma cells) and by increased expression of the key dormancy transcription factors (TFs) Sharp1 and p53. In addition, treatment of THEp3 cells with BM conditioned media inhibits in vivo proliferation, activates TGFβ2 and p38α, and induces the expression of Sharp1 and p53. Moreover, inhibition of TGFβ signaling using a TGFβRI inhibitor, blocks p38 activation and downregulates Sharp1 and p53 in BM-HEp3 cells, suggesting that BM-HEp3 cells dormancy is functionally linked to TGFβ signaling. Importantly, TGFβ2, p38α or Sharp-1 knock down interrupted BM-HEp3 cell dormancy, while overexpression of p38α inhibits lu-HEp3 cells in vivo growth. In addition to that, systemic inhibition of p38α/β with SB203580 or TGFβRI/II with LY364947, dramatically accelerated lung metastasis as well as DTCs, micro- and macro-metastasis burden in growth restricted sites such as, spleen, liver or BM. We propose that reprogramming of DTCs into dormancy in growth restrictive microenvironments might induce a gene network activated by stress signaling mediated at least by TGFβ2 and p38α/β signaling. 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 5234. doi:1538-7445.AM2012-5234
Role of transforming growth factor β signaling and expansion of progenitor cells in regenerating liver
Authors: Arun Thenappan, Ying Li, Krit Kitisin, Asif Rashid, Kirti Shetty, Lynt Johnson, Lopa Mishra
Journal: Hepatology (2009)

Adult hepatic progenitor cells are activated during regeneration when hepatocytes and bile duct epithelium are damaged or unable to proliferate. On the basis of its role as a tumor suppressor and in the potential malignant transformation of stem cells in hepatocellular carcinoma, we investigated the role of key transforming growth factor beta (TGF-β) signaling components, including the Smad3 adaptor protein β2-Spectrin (β2SP), in liver regeneration. We demonstrate a streaming hepatocyte-specific dedifferentiation process in regenerating adult human liver less than 6 weeks following living donor transplantation. We then demonstrate a spatial and temporal expansion of TGF-β signaling components, especially β2SP, from the periportal to the pericentral zone as regeneration nears termination via immunohistochemical analysis. This expansion is associated with an expanded remaining pool of octamer 3/4 (Oct3/4)-positive progenitor cells localized to the portal tract in adult human liver from more than 6 weeks posttransplant. Furthermore, disruption of TGF-β signaling as in the β2SP (β2SP+/−) knockout mouse demonstrated a striking 2 to 4-fold (P < 0.05) expanded population of Oct3/4-positive cells with activated Wnt signaling occupying an alpha-fetoprotein (AFP)+/cytokeratin-19 (CK-19)-positive progenitor cell niche following two-thirds partial hepatectomy. Conclusion: TGF-β signaling, particularly β2SP, plays a critical role in hepatocyte proliferation and transitional phenotype and its loss is associated with activation of hepatic progenitor cells secondary to delayed mitogenesis and activated Wnt signaling. (HEPATOLOGY 2010.)
[785] RECOMBINANT FACTOR VIIA (RFVIIA) FOR ACTIVE VARICEAL BLEEDING IN PATIENTS WITH ADVANCED CIRRHOSIS: A MULTI-CENTRE RANDOMIZED DOUBLE-BLIND PLACEBO-CONTROLLED TRIAL
Authors: J. Bosch, D. Thabut, A. Albillos, N. Carbonell, J. Spicak, J. Massard, G. D'Amico, D. Lebrec, R. de Franchis, S. Fabricius, Y. Cai, F. Bendtsen
Journal: Journal of Hepatology (2007)
Psychosomatic Approach to Medical Rehabilitation
Authors: Cairns Aitken
Journal: Psychotherapy and Psychosomatics (1979)

The author records his views about the future of medical rehabilitation. He reports some of the evidence on which to advocate the psychosomatic approach for the management of all disease and injury prone to chronic morbidity. As the causes of distress are multiple, clinical service is required from a multiprofessional team. The success of outcome is to be judged in the social adaptation achieved, recognising that this is influenced by such intangible concepts as morale and motivation.
Follow-up of Rhesus-negative Primigravidae
Authors: W. Weiner, J. L. Hallum
Journal: BMJ (1950)

A case of classical acute porphyria occurring in a West African negro is described.Post-mortem and biochemical findings are included.The literature is briefly quoted.I am indebted to Dr. A. Kahan, under whose care the patient was admitted, for permission to publish the case and for his encouragement and advice; to Dr. N. Orchard
A rare cause of abdominal pain
Authors: C. Anderson, H. Colvin
Journal: BMJ (2010)

A 28 year old injecting drug user presented to the hospital with non-specific symptoms of abdominal pain and fever. Clinical examination showed diffuse abdominal tenderness, most prominent in the left upper quadrant, with localised guarding and rigidity. One month earlier he had presented with a septic iliofemoral vein thrombosis and was started on warfarin. A portable chest radiograph was limited but unremarkable and did not show subphrenic air. Blood tests showed anaemia, consistent with his previous admission, and raised inflammatory markers of white blood cell count 19.88×109/l and C reactive protein 77 mg/l. He underwent computed tomography of the abdomen (fig 1⇓).



Fig 1 Computed tomogram of the abdomen





### 1 What abnormality can be seen on computed tomography and what are the possible causes?

#### Short answer

A 6 cm low attenuation lesion can be seen in the posterior parenchyma of an enlarged spleen (fig 2⇓). A left pleural effusion was also present. The possible causes of a low attenuating splenic lesion include splenic infarction, haematoma, tumour, and complicated cyst. In this clinical scenario, splenic abscess is the most likely cause.



Fig 2 Computed tomogram of the abdomen showing a low attenuation lesion in the posterior parenchyma of an enlarged spleen (arrow) 



#### Long answer

Computed tomography …
Flumazenil in cirrhotic patients in hepatic coma: A randomized double-blind placebo-controlled crossover trial
Authors: Gilles Pomier-Layrargues, J. F. Giguère, J. Lavoie, P. Perney, S. Gagnon, M. D’Amour, J. Wells, Roger F. Butterworth
Journal: Hepatology (1994)

Previous reports have suggested that "endogenous" benzodiazepines could contribute to neural inhibition in hepatic encephalopathy. RO 15-1788 (flumazenil), a specific antagonist of brain benzodiazepine receptors, could thus reverse the neurological symptoms of hepatic encephalopathy. To test this possibility, we conducted a double-blind, placebo-controlled crossover trial of the efficacy of flumazenil in cirrhotic patients in hepatic coma. Seventy-seven cirrhotic patients in hepatic coma were evaluated. Fifty-six were excluded from the trial because of multiorgan failure or because coma was precipitated by prior use of benzodiazepines, and 21 patients were randomly assigned to the flumazenil group (11 patients) or the placebo group (10 patients). Treatment was administered intravenously as a 20-ml solution (placebo or 2 mg flumazenil); seven patients were crossed over. Clinical status was assessed blindly by two observers, using a modified Glasgow scale, every 15 min for 6 hr. Electroencephalogram tracings obtained before and after drug administration were evaluated blindly by two independent observers. Serum concentrations of benzodiazepines before treatment were measured by means of a fluorescence polarization immunoassay. Improvement in neurological symptoms was observed in six patients treated with flumazenil, whereas none in the placebo group showed improvement (p < 0.05; Fisher's exact test). Improvements in electroencephalogram tracings were demonstrated in four patients treated with flumazenil, compared with two patients in the placebo group (p = NS). Benzodiazepines were found in the serum of four patients treated with flumazenil (two responders and two nonresponders); all of these patients had received pharmaceutical benzodiazepines 4 to 6 days before the trial.(ABSTRACT TRUNCATED AT 250 WORDS)