tbuckley/cabot-search huggingface dataset:
T cell development. Precursors and inducer requirements of helper effector and feedback suppression inducer cell sets.
Authors: F W Shen, J S McDougal, J Bard, S P Cort
Journal: The Journal of Experimental Medicine (1981)

The surface phenotypes and differentiative history of specific helper-effector (HE) and specific feedback suppression-inducer (FBSI) cell sets were further defined in reference to the Qa-1 and I-J marker systems by culture of selected sets of cortisone-resistant nylon-purified thymocytes with antigen on primed macrophages. The generation of Ly-1:HE and Ly-1:FBSI cell sets required, in each case, two initiating sets: a precursor set and a differentiation-inducing set. Precursor sets were distinguished from inducer sets by genetic markers. Accordingly, HE cells, phenotype Ly-1:Qa-1-:I-J-, differentiated from Ly-123:Qa-1- cells in the presence of Ly-1:Qa-1+:I-J+ inducer cells; and FBSI cells, phenotype Ly-1:Qa-1+:I-J+, differentiated from Ly-123:Qa-1- in the presence of Ly-1:Qa-1+:I-J+ inducer cells. The Ly-123:Qa-1-precursors of HE and FBSI cells have been distinguished from one another previously but there is as yet no evidence whether differentiation of these precursor sets requires the same or different Ly-1:Qa-1+:I-J+ inducer sets.
Guidelines for Cardiovascular Risk Assessment and Cholesterol Treatment
Authors: Donald M. Lloyd-Jones, David C. Goff, Neil J. Stone
Journal: JAMA (2014)

As the chairs of the 2013 guideline panels on risk assessment and cholesterol treatment,1,2 we would like to clarify some statements made in 3 Viewpoint articles3- 5 and correct some misinterpretations or incorrect assumptions.
Removal of Gastrostomy Tubes-Reply
Authors: Jacob Korula
Journal: JAMA (1992)

In Reply.  —Mr Campbell and his colleagues report a case where a fatal outcome occurred in a patient with anoxic brain injury in whom the gastrostomy tube was cut, allowed to pass intestinally, and resulted in intestinal perforation and abscess formation. They suggest that PEG tubes that cannot be removed by external traction be endoscopically removed, especially in cases where abdominal surgery was previously performed.  Although the majority (98%) of evaluable patients in our study eliminated the internal component of the PEG tube intestinally, in one patient the internal bumper lodged at the pylorus and required endoscopic removal. A number of patients in our study had had abdominal surgery at the time the initial PEG tubes were placed and did not have problems with elimination when their PEG tubes were removed nonendoscopically. Thus, an occasional patient may require an alternative method for removal of the internal PEG component and prior
Benefits with Risks — Bush's Tax-Based Health Care Proposals
Authors: Robert D. Reischauer
Journal: New England Journal of Medicine (2007)

Interview with Senator Chuck Grassley and Congressman Pete Stark on President Bush’s tax-based health care proposals. (12:55)Download In his State of the Union address in January, President George W. Bush announced a major two-part health initiative that would create a new uniform tax deduction for all those obtaining health insurance and provide assistance to states that make basic private health insurance available to residents (see box). The first and primary proposal addresses the tax code's perverse and inequitable treatment of health care expenditures, seeking thereby to reduce the ranks of the uninsured.1 If adopted as proposed (a highly unlikely prospect), the initiative would take half a step toward a more equitable system, but it would have an . . .
P729PD-1/PD-L1 axis contributes to infarct size in ST elevation myocardial infarction
Authors: MJ Forteza, E De Dios, A Hervas, A Ruiz-Sauri, C Bonanad, F Chaustre, I Trapero, G Minana, FJ Chorro, V Bodi
Journal: Cardiovascular Research (2014)

Programmed death-1 (PD-1) and Programmed death-1 ligand (PD-L1) regulate immune response. Previous studies associate an immune deregulation in ST-elevation myocardial infarction STEMI. We recruited 100 patients with a first STEMI treated with reperfusion. In all patients PD-1 and PD-L1 expression was studied 24 h post-reperfusion in peripheral blood mononuclear cells (PBMCs), by means of flow cytometry and molecular biology. PD-1 and PD-L1 expression was serially analyzed in the first 20 patients before reperfusion and 24h, 96h and 30 days afterwards. Results were compared with 30 age- and sex-matched controls. Cardiac Magnetic Resonance was used to quantify infarct size 1-week after infarction. In a series of 8 swine with induced STEMI, PD-1 and PD-L1 expression was analyzed at baseline, 90 min after balloon inflation, 2 h and 24 h after reperfusion in PBMCs, and in swine hearts. Results were compared to 5 controls. In patients, in comparison with controls, a significant decrease of PD-1 expression [mRNA fold change 0.8 ± 0.3 vs. 1.2 ± 0.6] and an increase of PD-L1+ expression [mRNA fold change 2.7 ± 2.1 vs. 0.9 ± 0.5] was observed 24h after infarction in PBMCs (p <0.05). STEMI patients with large infarct size showed decreased PD-1 expression, PD-L1 did not changed (Figure 1). Both in patients and swine, showed a significant increase of PD-1 and PD-L1 expression before reperfusion. Swine hearts revealed a marked infiltration of PMBCs and a significant increase of PD-1 and PD-L1 expression in the infarcted area compared to controls (Figure 2)
Impaired Cardiac Baroreflex Sensitivity Predicts Response to Renal Sympathetic Denervation in Patients With Resistant Hypertension
Authors: Christine S. Zuern, Christian Eick, Konstantinos D. Rizas, Sarah Bauer, Harald Langer, Meinrad Gawaz, Axel Bauer
Journal: Journal of the American College of Cardiology (2013)
Health effects associated with smokeless tobacco: a systematic review
Authors: J A Critchley
Journal: Thorax (2003)

<b>Background:</b> It is believed that health risks associated with smokeless tobacco (ST) use are lower than those with cigarette smoking. A systematic review was therefore carried out to summarise these risks. <b>Methods:</b> Several electronic databases were searched, supplemented by screening reference lists, smoking related websites, and contacting experts. Analytical observational studies of ST use (cohorts, case-control, cross sectional studies) with a sample size of ⩾500 were included if they reported on one or more of the following outcomes (all cause mortality, oral and pharyngeal cancers, other cancers, cardiovascular diseases, dental diseases, pregnancy outcomes, surgical outcomes). Data extraction covered control of confounding, selection of cases and controls, sample size, clear definitions and measurements of the health outcome, and ST use. Selection, extraction and quality assessments were carried out by one or two independent reviewers. <b>Results:</b> A narrative review was carried out. Many of the studies lacked sufficient power to estimate precise risks, mainly due to the small number of ST users. Studies were often not designed to investigate ST use, and many also had major methodological limitations including poor control for cigarette smoking and imprecise measurements of exposure. Studies in India showed a substantial risk of oral or oropharyngeal cancers associated with chewing betel quid and tobacco. Studies from other regions and of other cancer types were not consistent. Few studies have adequately considered the non-cancer health effects of ST use. <b>Conclusions:</b> Chewing betel quid and tobacco is associated with a substantial risk of oral cancers in India. Most recent studies from the US and Scandinavia are not statistically significant, but moderate positive associations cannot be ruled out due to lack of power. Further rigorous studies with adequate sample sizes are required, especially for cardiovascular disease.
PROGRESSIVE HYPERMETROPIC ASTIGMATISM.Read before the Chicago Ophthalmological and Otological Society, Oct. 16, 1894.
Authors: WM. T. MONTGOMERY
Journal: JAMA (1894)

In his classical work upon accommodation and refraction of the eye, Professor Donders says: "Astigmatism is either congenital or acquired. If it be acquired it is to be looked upon clinically as another form of disease," etc. I think this is the opinion that almost universally prevails with oculists up to the present time, so far as hypermétropie astigmatism is concerned. It is a congenital defect and does not progress or change without traumatism, or the presence of some other disease. Until recently I have accepted this idea without question. It had been my custom in prescribing glasses for the correction of hypermetropie astigmatism, either simple or compound, to assure the patients that they would not have to change their glasses. Within the past few years, a number of cases have come under my observation which have caused me to modify the above statement, and to question whether or not
The Best Peak Expiratory Flow Is Flow-Limited and Effort-Independent in Normal Subjects
Authors: Claudio Tantucci, Alexandre Duguet, Pietro Giampiccolo, Thomas Similowski, Marc Zelter, Jean-Philippe Derenne
Journal: American Journal of Respiratory and Critical Care Medicine (2002)

Recently, it has been suggested that peak expiratory flow (PEF) may be determined by the wave speed flow-limiting mechanism. In six normal male subjects (age = 33 ± 8 years) performing expiratory forced vital capacity (FVC) maneuvers, a negative expiratory pressure (NEP) of −10 cm H2O was randomly applied at the beginning of maximal expiration to assess changes in PEF as compared with baseline. During FVC maneuvers, the expiratory effort was measured by changes in esophageal pressure (Pes), as either peak expiratory Pes−Pes at end expiratory lung volume (ΔPespeak) or maximal rate of rise of Pes (dPes/dtmax). In each experimental condition, at least three FVC maneuvers with comparable expiratory effort were selected for analysis for each subject. With similar ΔPespeak (107.2 ± 34.9 versus 111.7 ± 40.5 cm H2O) and dPes/dtmax (1181 ± 518 versus 1177 ± 546 cm H2O/second) PEF amounted to 10.84 ± 1.08 L/second and to 10.82 ± 1.03 L/second with and without NEP, respectively. These data show that PEF obtained by normal subjects to the best of their abilities (best PEF) does not increase with NEP and indicate that the best PEF is a flow-limited and effort-independent parameter, reflecting only lung and airways mechanics as the other subsequent maximal expiratory flows achieved during the FVC maneuver.
Possible transmission of malaria by renal transplantation.
Authors: I D Johnston
Journal: BMJ (1981)

in liver transaminase or alkaline phosphatase activity.Haemoglobin concen- tration fell from 14-2 g/dl to 12-8 g/dl with a rise in reticulocytes to 3 %.Intravascular haemolysis was confirmed by a positive methaemalbumin test, a raised plasma haemoglobin concentration at 0-26 g/l (normal range 0-01- 0 04 g/l), and a reduced haptoglobin concentration at 0 028 g/l (normal range
Distinct patterns of collagen gene expression are seen in normal and keloid fibroblasts grown in three-dimensional culture
Authors: None Sato, None Ishikawa, None Miyachi
Journal: British Journal of Dermatology (1998)

Journal Article Distinct patterns of collagen gene expression are seen in normal and keloid fibroblasts grown in three‐dimensional culture Get access M. Sato, M. Sato Department of Dermatology, Gunma University School of Medicine, 3–39–22 Showa‐machi, Maebashi, Gunma, Japan Sato E‐mail: madosato@sb.gunma‐u.ac.jp Search for other works by this author on: Oxford Academic Google Scholar O. Ishikawa, O. Ishikawa Department of Dermatology, Gunma University School of Medicine, 3–39–22 Showa‐machi, Maebashi, Gunma, Japan Search for other works by this author on: Oxford Academic Google Scholar Y. Miyachi Y. Miyachi Department of Dermatology, Gunma University School of Medicine, 3–39–22 Showa‐machi, Maebashi, Gunma, Japan Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 138, Issue 6, 1 June 1998, Pages 938–943, https://doi.org/10.1046/j.1365-2133.1998.02258.x Published: 01 June 1998
Entactin stimulates neutrophil adhesion and chemotaxis through interactions between its Arg-Gly-Asp (RGD) domain and the leukocyte response integrin.
Authors: R M Senior, H D Gresham, G L Griffin, E J Brown, A E Chung
Journal: Journal of Clinical Investigation (1992)

Entactin is an integral component of basement membranes that plays a major role in basement membrane assembly through its ability to bind avidly to both laminin and type IV collagen. Because neutrophil (PMN) interactions with entactin have not been examined, we investigated the ability of natural and recombinant entactin to mediate PMN adhesion and chemotaxis. With both forms of entactin, we observed that entactin-coated surfaces promoted PMN adhesion and that entactin stimulated PMN chemotaxis. The increase in adhesion to entactin over control was two to threefold whereas the chemotactic response to 15 ng/ml (1 x 10(-10) M) entactin was equivalent to the chemotactic response elicited with 1 x 10(-8) M formyl-methionyl-leucyl-phenylalanine (fMLP). HL-60 cells, after differentiation with dimethylsulfoxide, also demonstrated adhesion and chemotaxis to entactin. A synthetic peptide of the Arg-Gly-Asp (RGD) domain in entactin, SIGFRGDGQTC (S-RGD), mediated PMN adhesion and chemotaxis, and preexposure of PMN to S-RGD blocked PMN adhesion and chemotaxis induced by entactin without diminishing the adhesive and chemotactic activities of fMLP. In contrast, preexposure to peptides SIGFRGEGQTCA or SIGFKGDGQTCA had no effect. The findings with synthetic peptides were confirmed with a recombinant entactin mutant in which aspartic acid at residue 674 was replaced with glutamic acid, thus converting the RGD sequence of entactin to RGE. RGE-entactin was neither adhesive nor chemotactic for neutrophils. Monoclonal antibodies to the leukocyte response integrin (LRI) and the integrin-associated protein blocked entactin-mediated adhesion and chemotaxis whereas monoclonal antibodies to beta 1 and beta 2 integrins had no effect and PMN from an individual with leukocyte-adhesion deficiency adhered normally to entactin-coated surfaces. These data demonstrate that entactin mediates biologically and pathologically important functions of PMN through its RGD domain and that LRI, which has been shown previously to mediate RGD-stimulated phagocytosis, is also capable of mediating RGD-stimulated PMN adhesion and chemotaxis.
Biofeedback for Gastrointestinal Disorders: A Review of the Literature
Authors: PETER M. MARZUK
Journal: Annals of Internal Medicine (1985)

Although biofeedback has been applied to many gastrointestinal disorders, including reflux esophagitis, peptic ulcer disease, and irritable bowel syndrome, the limited number of reports precludes conclusions concerning its safety or efficacy in these disorders. Most studies have used biofeedback in the treatment of fecal incontinence. Uncontrolled trials have shown this procedure can reduce substantially the frequency of incontinence in 70% to 83% of patients at up to 1 to 2 years of follow-up. Biofeedback has been most successful in patients with a surgical cause for fecal incontinence, but recent data suggest the procedure may also be useful in diabetics. The few number of sessions required, its apparent safety, physiological appeal, and apparent success suggest biofeedback is a promising therapy for this disorder, but it remains inadequately tested.
Impact of poor-quality medicines in the ‘developing’ world
Authors: Paul N. Newton, Michael D. Green, Facundo M. Fernández
Journal: Trends in Pharmacological Sciences (2010)

Since our ancestors began trading several millennia ago, counterfeit and substandard medicines have been a recurring problem, with history punctuated by crises in the supply of anti-microbials, such as fake cinchona bark in the 1600s and fake quinine in the 1800s. Unfortunately this problem persists, in particular afflicting unsuspecting patients in 'developing' countries. Poor-quality drugs are a vital (but neglected) public health problem. They contribute to a 'crevasse' between the enormous effort in therapeutic research and policy decisions and implementation of good-quality medicines.
Hereditary Presacral Teratoma
Authors: Kendrick C. Davidson
Journal: JAMA (1977)

<h3>To the Editor.—</h3> In the article by Drs Anderson and Burke (237:39, 1977) entitled "Anterior Sacral Meningocele," they identified sacral and coccygeal bony defects associated with the presentation of meningoceles in the pelvis communicating with the spinal subarachnoid space. I would like to call attention to a recent article in<i>Radiology</i>(122:187, 1977) in which we report a pattern of hereditary presacral teratoma occurring in 26 of 105 family members in six unrelated families. Of those 26 patients with a palpable presacral mass on rectal examination, 19 ultimately came to surgery, and there was pathologic examination of their tumors. As with the patients described by Anderson and Burke, most of our patients (22 of 26) had constipation. Thirteen of the 26 had anal stenosis, and 25 of 26 showed a typical hook-shaped or large central sacrococcygeal bony defect. One of our patients died of meningitis because the subarachnoid space was
Abstract 2035: Activating transcription factor 2 (ATF2) controls tolfenamic acid-induced ATF3 expression via MAP kinase pathways
Authors: Seong-Ho Lee, Jae Hoon Bahn, Nichelle Whitlock, Seung J. Baek
Journal: Cancer Research (2011)

Abstract Tolfenamic acid (TA) is a non-steroidal anti-inflammatory drug associated with anti-tumorigenic and pro-apoptotic properties in animal and in vitro models of cancer. However, the underlying cellular mechanisms by which TA exerts its effects are only partially understood. Activating transcription factor 3 (ATF3) is a member of the ATF/CREB subfamily of the basic region-leucine zipper family and has been known as a tumor suppressor in human colorectal cancer cells. The present study was performed to observe whether ATF3 mediates TA-induced apoptosis and to elucidate the molecular mechanism of ATF3 transcription induced by TA. TA treatment and ectopic expression of ATF3 increased apoptosis whereas knockdown of ATF3 resulted in significant repression of TA-activated apoptosis. The TA treatment also induced ATF3 promoter activity. Internal deletion and point mutation of the predicted ATF/C/EBP binding site in ATF3 promoter abolished luciferase activation by TA. Overexpression of ATF2 resulted in significant increase of ATF3 promoter activity, and electrophoretic mobility shift assay identified this region as a core sequence to which ATF2 binds. TA treatment resulted in an increase of ATF2 phosphorylation, which was followed by a subsequent increase of ATF3 transcription. Knockdown of ATF2 abolished TA-induced ATF3 expression. We further provide evidence that TA leads to increases of phospho-p38 MAPK, JNK, and ERK levels. Inhibition of these pathways using selective inhibitors and dominant negative constructs ameliorated TA-induced ATF3 expression and promoter activities. The current study demonstrates that TA stimulates ATF3 expression and subsequently induces apoptosis. These pathways are mediated through phosphorylation of ATF2, which is mediated by p38 MAPK, JNK, and ERK-dependent pathways. 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 2035. doi:10.1158/1538-7445.AM2011-2035
Abstract 4671: Dual mutational changes of ALK gene fusion combined with EGFR or K-ras oncogenes in lung adenocarcinomas
Authors: Jieun Lee, Suk Hee Hong, Eun Kyung Jeon, Jung O. Kim, Seung Joon Kim, Young Kyoon Kim, Jae Gil Park, Sook-Whan Sung, Tae-Jung Kim, Jin Hyoung Kang
Journal: Cancer Research (2014)

Abstract Purpose The mutations of the EGFR, K-ras or ALK oncogenes are closely associated with tumorigenesis and progression of lung adenocarcinoma. Their mutational changes are known to be mutually exclusive, but double oncogenic mutations of ALK combined with EGFR or K-ras gene are rarely found. We analyzed the clinical impacts of double oncogenic mutations on clinical characteristics and treatment outcome, according to EGFR, K-ras, ALK mutation or triple negative (EGFR, K-ras, ALK wild) in lung adenocarcinomas. Patients and Methods For one hundred ninety six lung cancer patients conformed histologically as adenocarcinoma, we examined activating EGFR (exons 18 and 21) and K-ras (exon 2 and 3) mutations by direct nucleotide sequencing and. ALK gene rearrangements by FISH using break-apart probe. Among 196 patients, 86 patients (43.9%) were triple negative adenocarcinoma, 73 patients (37.2%) presented with activating EGFR mutation, 17 patients (8.7%) with ALK and 13 patients (6.6%) with K-ras mutation. Median age of 17 patients harboring ALK rearrangement was 54 years (range 25∼79), approximately 7 years younger than the patient population harboring EGFR or K-ras mutation (62 and 61 years, respectively). Fifteen patients (88.2%) had stage III or IV and 9 patients (52.9%) were never smoker. Platinum doublet chemotherapy or EGFR TKIs was administered for 14 patients initially presented as stage IV disease or recurred as metastatic disease after local treatment. The median PFS of the patients receiving platinum doublet chemotherapy and EGFR TKIs as first-line treatment was 5.67 months (range 2.97-20.9) and 3.58 months (range 3.53-3.63), respectively. Of 17 ALK-positive patients, dual oncogenic mutations of ALK together with either EGFR or K-ras were identified in 7 patients (3.6%). Six patients (85.7%) receiving platinum-doublet or EGFR TKI as initial treatment. showed partial response, and 1 patient (14.3%) showed stable disease. These seven patients are all alive at present. Conclusion Taken together, our data suggest the existence of dual oncogenic mutations in lung adenocarcinomas is not infrequent. We are undergoing the experiment for detection for circulating tumor cells harboring ALK rearrangements, EGFR or K-ras mutation in these patients' peripheral blood. Citation Format: Jieun Lee, Suk Hee Hong, Eun Kyung Jeon, Jung Oh Kim, Seung Joon Kim, Young Kyoon Kim, Jae Gil Park, Sook-Whan Sung, Tae-Jung Kim, Jin Hyoung Kang. Dual mutational changes of ALK gene fusion combined with EGFR or K-ras oncogenes in lung adenocarcinomas. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4671. doi:10.1158/1538-7445.AM2014-4671
Consoling Mrs Byrne
Authors: S. Breanndan Moore
Journal: JAMA (1990)

It was an unusually warm, sunny July day in 1968 that stretched into an equally beautiful balmy night in Dublin. The late evening sun slanted its yellow shafts through the tall windows of the old Mater Misericordiae Hospital wards, which faced out toward the distant, darkening Wicklow hills. A faint hum of conversation came from the wards as I slowly trudged along the dimly lit corridors toward St Agatha's Ward, where I had to talk with Mrs Byrne. I was not looking forward to the task. I had arrived at the hospital a week earlier to begin the first six months of my internship in surgery. My attending physician was a middle-aged surgeon known to everyone as Johnny (except to his face). He had operated on me when I was a child, and I had later come to appreciate his wit and wisdom during my years in medical school, when I attended his teaching clinics at the hospital. Johnny believed that a physician's education came primarily from dealing with patients and that the more academic aspects of training provided the scaffolding on which clinical experience was draped in ever-growing layers. He was a wonderful raconteur, and for him,