tbuckley/cabot-search huggingface dataset:
The "five minute" consultation: effect of time constraint on verbal communication.
Authors: M O Roland, J Bartholomew, M J Courtenay, R W Morris, D C Morrell
Journal: BMJ (1986)

In a study in which patients were allocated non-systematically to surgeries booked at 5, 7.5, and 10 minute intervals 623 consultations were taperecorded. In surgeries booked at longer intervals doctors used the extra time to take a fuller history from their patients. In surgeries booked at 10 minute intervals doctors spent more time explaining the patient's problem, explaining the proposed management, and in discussing prevention and health education, these increases not being evident in surgeries booked at 7.5 minute intervals.
Development of a Scleroderma-like Illness during Therapy with L-5-Hydroxytryptophan and Carbidopa
Authors: Esther M. Sternberg, Melvtn H. Van Woert, Simon N. Young, Ib Magnussen, Herman Baker, Serge Gauthier, C. Kirk Osterland
Journal: New England Journal of Medicine (1980)

A scleroderma-like illness developed in a patient treated with L-5 hydroxytryptophan (L-5HTP) and carbidopa for intention myoclonus. The patient had high plasma kynurenine levels that remained high when the L-5HTP-carbidopa combination was discontinued, However, levels rose futher on drug rechallenge, suggesting that the drug unmasked an abnormality in one of the enzymes that catabolize kynurenine. Plasma kynurenine was also determined to be high in seven of 15 patients wth idiopathic scleroderma, but not in eight patients with intention myoclonus treated with L-5HTP and a decarboxylase inhibitor and in whom scleroderma did not develop or in 10 patients with Parkinson's disease treated wth L-dopa and carbidopa. Our data and studies in the literature suggest that two factors may be important in the pathogenesis of some scleroderma-like illness: high plasma serotonin and the abnormality associated with elevated kynurenine.
Repolarization inhomogeneities in ventricular myocardium change dynamically with abrupt cycle length shortening.
Authors: D S Rosenbaum, D T Kaplan, A Kanai, L Jackson, H Garan, R J Cohen, G Salama
Journal: Circulation (1991)

BACKGROUND In single heart cells, abrupt changes in stimulation rate elicit complex alterations in repolarization. The effects of rate change on dispersion of repolarization, however, have not been well characterized. METHODS AND RESULTS To determine the effects of abrupt cycle length (CL) shortening on spatial inhomogeneity of repolarization in a syncytium of ventricular cells, 124 action potentials were simultaneously recorded from Langendorff-perfused guinea pig hearts using high-resolution optical mapping with voltage-sensitive dye. The distribution of ventricular action potential durations (APDs) mapped during each cardiac cycle was used to calculate mean APD and repolarization dispersion index (DI), defined as the variance of the distribution. After abruptly shortening CL from 500 to 300 msec, mean APD declined exponentially in normoxic controls (by 23 +/- 3 msec, p less than 0.0001). This response was characterized by beat-to-beat oscillations of APD that were synchronized at all ventricular sites. After 30 minutes of hypoxia, mean APD decreased from 175.0 +/- 13.3 to 76 +/- 25.7 msec. However, during hypoxia, abrupt CL shortening lowered mean APD by only an additional 6 +/- 6 msec, and APD oscillations were no longer synchronized throughout the ventricle. In controls, beat-to-beat DI decreased significantly (-51.0 +/- 6.8%, p less than 0.01) by the sixth post-CL shortening beat and then recovered (by 15-20 beats). In contrast, DI failed to decrease during hypoxia (+7.1 +/- 23%). Two mechanisms for the transient decline of DI in controls were identified: synchronous APD oscillations and transient diminution of the apical-to-basal ventricular APD gradient. CONCLUSIONS These data demonstrate that inhomogeneity of ventricular repolarization, as measured by DI, changes dynamically with CL shortening. Furthermore, the hypoxic ventricle does not attenuate DI after abrupt CL shortening and thereby lacks a physiological response expected to diminish vulnerability to arrhythmias.
Maggie's Centres
Authors: Edwin Heathcote
Journal: BMJ (2006)

There is something profoundly depressing about the spaces in which we experience our most momentous, traumatic, emotional, and joyous moments.Hospitals, the buildings in which we are born and sometimes experience the birth of our own children, in which we may die, and in which, as a rapidly ageing population, we will be spending an increasingly large proportion of our lives, are grim.It was the grinding spiritual and aesthetic poverty that spurred Maggie Keswick Jencks into thinking there must be an alternative.Her legacy is an extraordinary collection of centres throughout the United Kingdom that attempt to lift the soul not only through the sympathetic professional advice and listening of the trained oncology nurses who staff them but through architecture, through the redemptive power of space, light, and sculptural form.There are no great claims being made for this approach.Architecture does not and cannot heal cancer.Much research has linked views of trees, greenery, the sky, and natural light with quicker healing, but most of it is common sense: people feel better in nice spaces.I once heard a beautiful story.A man lies in a hospital bed but can't see out of the window at the end of the room so the fellow in the bed next to the window tells him all about what he sees.He tells him about the life on the street, the children playing, the girls walking by, the women hanging out their washing, about the traffic, the clouds and the changing weather.Dropping in and out of consciousness it is these images that keep him alive but sadly the occupant of the window bed dies.Though upset, his friend thinks at least he'll now get the bed by the window, which he does.He is amazed to see that the window looks out on to a blank brick wall.
Mathematical modifications fail to improve CPK estimates of extent of infarct.
Authors: C R Roe, C F Starmer, F R Cobb
Journal: Circulation (1977)

To the Editor:In 1971, Shell and co-workers' presented a mathematical model for estimating the extent of myocardial infarction from serial serum CPK measurements.These calculated estimates were compared to estimates of infarct size based on depletion of enzyme activity from myocardium.These depletion estimates of the extent of injury were considered to represent an equivalent of anatomic injury.There was no pathological confirmation of this assumption.The model, therefore, compares estimates of damage from enzyme activity measurements in serum to estimates based on disappearance of en- zyme activity from myocardium.During the intervening five years several modifications have been introduced.2 3 Each of these methods involves the following basic formula Serum Enzyme Estimate of foT f(t)dt Kw BW Myocardial Injury CPKD KRIn this formula, f(t) represents the enzyme appearance function which is the amount of CPK in ml of the body distribution volume dE at time, t, and is defined as f(t) =-+ KdE.E(t) is the enzyme
Inhibition of c-Met Reduces Lymphatic Metastasis in RIP-Tag2 Transgenic Mice
Authors: Barbara Sennino, Toshina Ishiguro-Oonuma, Brian J. Schriver, James G. Christensen, Donald M. McDonald
Journal: Cancer Research (2013)

Abstract Inhibition of VEGF signaling can promote lymph node metastasis in preclinical models, but the mechanism is not fully understood, and successful methods of prevention have not been found. Signaling of hepatocyte growth factor (HGF) and its receptor c-Met can promote the growth of lymphatics and metastasis of some tumors. We sought to explore the contributions of c-Met signaling to lymph node metastasis after inhibition of VEGF signaling. In particular, we examined whether c-Met is upregulated in lymphatics in or near pancreatic neuroendocrine tumors in RIP-Tag2 transgenic mice and whether lymph node metastasis can be reduced by concurrent inhibition of VEGF and c-Met signaling. Inhibition of VEGF signaling by anti-VEGF antibody or sunitinib in mice from the age of 14 to 17 weeks was accompanied by more intratumoral lymphatics, more tumor cells inside lymphatics, and more lymph node metastases. Under these conditions, lymphatic endothelial cells, like tumor cells, had strong immunoreactivity for c-Met and phospho-c-Met. c-Met blockade by the selective inhibitor, PF-04217903, significantly reduced metastasis to local lymph nodes. Together, these results indicate that inhibition of VEGF signaling in RIP-Tag2 mice upregulates c-Met expression in lymphatic endothelial cells, increases the number of intratumoral lymphatics and number of tumor cells within lymphatics, and promotes metastasis to local lymph nodes. Prevention of lymph node metastasis by PF-04217903 in this setting implicates c-Met signaling in tumor cell spread to lymph nodes. Cancer Res; 73(12); 3692–703. ©2013 AACR.
EXCESSIVE GOLF FOLLOWED BY MUSCULOSPIRAL PALSY
Authors: Cornelius C. Wholey
Journal: JAMA (1922)

A man, aged 35, consulted me because of severe pain which would come on as soon as he lay down, and which disturbed his sleep. The pain was located to the left of the spine over the lower part of the neck. The peculiarity of the pain was that it would largely disappear when the patient was up and about his work, but, no matter what position he lay in, it would continue. Examination revealed a pronounced weakness involving all of the extensor muscles of the left upper extremity. The ability to extend the wrist against resistance was very weak. In fact, the wrist was held in a partially wrist-drop position. Extension of the fingers, and at the elbow, and at the shoulder were proportionately weak. The hand grip was also very much reduced in strength. There was a similar weakness in the power of supinating the forearm. Testing for
Pathogenesis of lipid metabolism disorder in hepatitis C: Polyunsaturated fatty acids counteract lipid alterations induced by the core protein
Authors: Hideyuki Miyoshi, Kyoji Moriya, Takeya Tsutsumi, Seiko Shinzawa, Hajime Fujie, Yoshizumi Shintani, Hidetake Fujinaga, Koji Goto, Toru Todoroki, Tetsuro Suzuki, Tatsuo Miyamura, Yoshiharu Matsuura, Hiroshi Yotsuyanagi, Kazuhiko Koike
Journal: Journal of Hepatology (2010)
Case of Fracture op the Coronoid Process of the Ulna
Authors: W. Gillard
Journal: BMJ (1846)

the river, enjoying good bealth, and free from every indication of relapse of his disorder.The marginal figure represents the liga-i9 ture as preserved by me since its removal; .it will serve to shew the exact ditnension of the circle that compressed the artery, as well as the size of the ligature employed.The advantage of using a small
P5-13-01: Survival Outcome with Bevacizumab: Activation of the Phosphatidylinositol-3 Kinase (PI3K) Pathway Due to PIK3CA Mutations or PTEN Loss Makes a Difference.
Authors: M Vidal, S Di Cosimo, D Torrejon, C Saura, P Gómez-Pardo, J Pérez-Garcia, E Muñoz-Couselo, M Bellet, G Sanchez-Olle, Mattos-Arruda L De, M Oliveira, J Tabernero, J Baselga, J Cortes
Journal: Cancer Research (2011)

Abstract Background The PI3K pathway is known to regulate the transcription of Vascular Endothelial Growth Factor (VEGF) in endothelial and cancer cells. The inhibition of VEGF is the rationale behind the development therapy with anti-angiogenics. We investigated the activation of PI3K pathway, defined as PTEN loss and/or PIK3CA mutations, and the relationship with survival in metastatic breast cancer patients treated with the anti-VEGF monoclonal antibody bevacizumab. Patients and methods: Records for patients with HER2 negative metastatic breast cancer (MBC), treated with bevacizumab from July 2005 to June 2010, and with known PI3K status were reviewed. Univariate and multivariate analysis were performed using SPSS 15.0. Results: A total of 40 patients — 26 with and 14 without PI3K activation — were identified. Median age was 47 years (range 27–79). Median overall survival (OS) was 41.23 months (CI 95%: 27.29 — 55.18) and 66.23 months (CI 95%: 61.04 — 71.42) in patients with and without PI3K activation, respectively (p=0.04). Among patients with PI3K activation, OS was 34.13 months (CI 95%: 22.40 — 45.86) and 43.43 months (CI 95%: 26.9 — 59.97) in cases with PIK3CA mutations and PTEN loss, respectively. As compared to patients without PI3K activation, patients with PI3KCA mutations but not patients with PTEN loss showed a significant worse outcome (p=0.006 and p=0.3, respectively). In the multivariate analysis including grade, hormone receptor and Ki67 status, and total lines of treatment, the activation of PI3K activation proved to be an independent prognostic factor (p=0.03). Conclusions: The activation of the PI3K pathway is significantly associated with decreased OS of MBC patients treated with bevacizumab. Prospective evaluation of PI3K activation on VEGF signaling with differential implication of PI3KCA and PTEN loss is warranted. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P5-13-01.
Monocyte Chemotactic Protein-1 Secreted by Primary Breast Tumors Stimulates Migration of Mesenchymal Stem Cells
Authors: R.M. Dwyer, S.M. Potter-Beirne, K.A. Harrington, A.J. Lowery, E. Hennessy, J.M. Murphy, F.P. Barry, T. O'Brien, M.J. Kerin
Journal: Clinical Cancer Research (2007)

Abstract Purpose: Major barriers to effective adenovirus-based gene therapy include induction of an immune response and tumor-specific targeting of vectors. The use of mesenchymal stem cells (MSC) as systemic delivery vehicles for therapeutic genes has been proposed as a result of their combined ability to home in on the tumor site and evade the host immune response. This study is aimed at investigating factors mediating homing of human MSCs to breast cancer primary cultures and cell lines in vitro and in vivo. Experimental Design: Fluorescently labeled MSCs were given to mice bearing breast cancer xenografts, and tumor tissue was harvested to detect MSC engraftment. MSC migration in response to primary breast tumors in vitro was quantified, and chemokines secreted by tumor cells were identified. The role of monocyte chemotactic protein-1 (MCP-1) in cell migration was investigated using antibodies and standards of the chemokine. Serum MCP-1 was measured in 125 breast cancer patients and 86 healthy controls. Results: Engrafted MSCs were detected in metastatic breast tumors in mice after systemic administration. There was a significant increase in MSC migration in response to primary breast tumor cells in vitro (6-fold to 11-fold increase). Tumor explants secreted a variety of chemokines including GROα, MCP-1, and stromal cell–derived factor-1α. An MCP-1 antibody caused a significant decrease (37-42%) in MSC migration to tumors. Serum MCP-1 levels were significantly higher in postmenopausal breast cancer patients than age-matched controls (P &amp;lt; 0.05). Conclusions: These results highlight a role for tumor-secreted MCP-1 in stimulating MSC migration and support the potential of these cells as tumor-targeted delivery vehicles for therapeutic agents.
Use of Adenoviral Vectors to Target Chemotherapy to Tumor Vascular Endothelial Cells Suppresses Growth of Breast Cancer and Melanoma
Authors: Pingchuan Li, Yanzheng Liu, Jonathan Maynard, Yucheng Tang, Albert Deisseroth
Journal: Molecular Therapy (2010)

To target chemotherapy to tumor vascular endothelial cells (TVECs), we created the AdTie2RprCDFibknob−RGD+ vector by inserting into an AdEasy adenoviral vector (Ad) backbone: (i) the cytosine deaminase (CD) gene driven by the Tie2 receptor promoter (Tie2Rpr) into the E1 region of Ad; (ii) mutations that reduce binding of the fiber knob to the Coxsackie adenovirus receptor (CAR); and (iii) the RGD peptide into the H1 loop of fiber for binding to the αVβ3 integrin receptors on TVECs. To reduce uptake of the AdTie2RprCDFibknob−RGD+ by reticuloendothelial (RE) and liver cells, we intravenously (i.v.) injected Hetastarch and low-dose Ad (one million vector particles (VPs)) prior to i.v. injection of a therapeutic dose (one billion VPs) of the AdTie2RprCDFibknob−RGD+ vector. This treatment induced regressions of N202 breast cancer and B16 melanoma without toxicity to normal tissues. We showed that the tumor regression was induced by infection of the TVECs and not by the infection of tumor cells by the AdTie2RprCDFibknob−RGD+ vector. To target chemotherapy to tumor vascular endothelial cells (TVECs), we created the AdTie2RprCDFibknob−RGD+ vector by inserting into an AdEasy adenoviral vector (Ad) backbone: (i) the cytosine deaminase (CD) gene driven by the Tie2 receptor promoter (Tie2Rpr) into the E1 region of Ad; (ii) mutations that reduce binding of the fiber knob to the Coxsackie adenovirus receptor (CAR); and (iii) the RGD peptide into the H1 loop of fiber for binding to the αVβ3 integrin receptors on TVECs. To reduce uptake of the AdTie2RprCDFibknob−RGD+ by reticuloendothelial (RE) and liver cells, we intravenously (i.v.) injected Hetastarch and low-dose Ad (one million vector particles (VPs)) prior to i.v. injection of a therapeutic dose (one billion VPs) of the AdTie2RprCDFibknob−RGD+ vector. This treatment induced regressions of N202 breast cancer and B16 melanoma without toxicity to normal tissues. We showed that the tumor regression was induced by infection of the TVECs and not by the infection of tumor cells by the AdTie2RprCDFibknob−RGD+ vector.
REMOVAL OF A FOREIGN BODY INTRODUCED INTO THE UTERINE CERVICAL CANAL TO PREVENT CONCEPTION
Authors: Aimé Paul Heineck
Journal: JAMA (1913)

Foreign bodies are sometimes introduced into the uterine cavity for the purpose of terminating an undesired pregnancy. Most frequently, they are employed in the absence of any legitimate indication. These foreign bodies are responsible for a certain number of punctured and perforating wounds of the body and of the cervix of the uterus, inflicted by way of the vaginal canal. Some foreign bodies also have been inserted into the cervical canal to be retained more or less permanently; some of these devices are introduced and retained in the uterine cervical cavity merely to prevent conception. That their value as such is debatable, is amply demonstrated by what follows: I have lately removed from the uterine cavity of several patients referred to me by other physicians a device which had been introduced into the uterine cervical canal with the positive assurance that conception was impossible as long as the "Jentsch self-retaining
Effects of topical budesonide and levocabastine on nasal symptoms and plasma exudation responses in seasonal allergic rhinitis
Authors: C. Svensson, M. Andersson, L Greiff, L‐O. Blychert, C. G. A. Persson
Journal: Allergy (1998)

This study compares the effects of two topical nasal treatments for allergic rhinitis, budesonide and levocabastine, on symptom development during seasonal pollen exposure. Additionally, the protective effects of drug treatments on allergen‐challenge‐induced responses (symptoms and microvascular exudation of plasma) are examined late into the pollen season. Forty‐four patients with seasonal allergic rhinitis to birch pollen participated in this single‐blind, randomized, and placebo‐controlled study. Topical nasal treatment with either levocabastine (200 p.g b.i.d.: n = 16), budesonide (200 μg b.i.d.; n = 16), or placebo ( n = 12) was instituted before the start of the pollen season and continued for 5 weeks until the end of the birch pollen season. The participants kept diaries for scores of nasal and ocular symptoms. Nasal allergen challenges with increasing doses of a birch pollen extract (10 2 , 10 3 and lC SQ‐U) were carried out both before, when patients were asymptomatic and without treatment, and late into the pollen season. A nasal lavage followed each challenge, and the lavage fluid levels of albumin were measured as an index of the acute inflammatory response of the allergic mucosa. The birch pollen season was rather mild, producing only small increases in nasal symptoms. Budesonide treatment reduced the total nasal symptoms compared to placebo (P&lt;0.01) and to levocabastine (P&lt;0.05), while levocabastine treatment did not differ significantly from placebo. Ocular symptoms and use of rescue medication did not differ between placebo and the active treatments. At the end of the pollen season, both treatments reduced allergen‐challenge‐induced nasal symptoms compared to placebo (P&lt;0.01). Only budesonide reduced allergen‐challenge‐ induced increments of albumin levels in postchallenge nasal lavage fluids (P&lt;0.05, in comparison with placebo). The results suggest that budesonide reduces both seasonal and allergen‐challenge‐induced nasal symptoms, while levocabastine is effective against allergen‐challenge‐induced symptoms also during the season. In addition, the topical steroid treatment, but not the antihistamine, inhibits the inflammatory exudation evoked by allergen challenge in patients with active seasonal disease.
Shall The Journal be Removed to Washington?-Reply
Authors: B. F. Hart
Journal: JAMA (1891)

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Predictors for lymph node metastasis in T1 colorectal cancer
Authors: J. Suh, K. Han, B. Kim, C. Hong, D. Sohn, H. Chang, M. Kim, S. Park, J. Park, H. Choi, J. Oh
Journal: Endoscopy (2012)

It is critical that the risk of lymph node metastasis (LNM) is evaluated for determining the suitability of endoscopic resection for T1 colorectal cancer (CRC). Reported risk factors for LNM in completely resected T1 CRC are deep submucosal invasion, grade 3, angiolymphatic invasion, and budding. The aim of the present study was to identify the histopathologic factors associated with LNM in T1 CRC.The study involved 435 patients with T1 CRC treated by endoscopic or surgical resection between January 2001 and April 2010 at the National Cancer Center, Korea. The 435 patients were classified into two groups - those undergoing surgical resection (n = 324) and those undergoing endoscopic resection (n = 111). In the surgically resected group, details regarding depth of submucosal invasion, angiolymphatic invasion, tumor grade, budding, and background adenoma (BGA) were evaluated with respect to presence or absence of LNM. In the endoscopically resected group, the results of follow-ups and additional salvage surgeries were studied.In the surgically resected group, LNM was detected in 42 patients (13.0 %). Grade 3, angiolymphatic invasion, budding, and the absence of BGA were identified as factors associated with LNM in univariate and multivariate analyses (P < 0.05). Among the 50 patients in the endoscopically resected group with high risk, three were diagnosed as being LNM-positive during the follow-up period. There was no LNM in the endoscopically resected group with low risk.Grade 3, angiolymphatic invasion, budding, and the absence of BGA are the risk factors that predict LNM in patients with T1 CRC. In cases where endoscopically resected T1 CRC has no risk factor, cautious follow-up could be recommended. However, if the tumor has any risk factor, additional surgical resection should be considered.