tbuckley/cabot-search huggingface dataset:
Platelet-derived growth factor receptors on macrovascular endothelial cells mediate relaxation via nitric oxide in rat aorta.
Authors: L D Cunningham, P Brecher, R A Cohen
Journal: Journal of Clinical Investigation (1992)

The effects of platelet-derived growth factor (PDGF) were studied in isolated rings of rat aorta contracted submaximally to phenylephrine. The BB isoform of PDGF elicited relaxation in rings with endothelium and further contraction in rings without endothelium. Both the endothelium-dependent relaxation and endothelium-independent contraction occurred at concentrations known to induce PDGF receptor-mediated responses in cultured cells. Furthermore, the relaxation was isoform specific. This conclusion is supported by the unique ability of PDGF-BB to induce endothelium-dependent relaxations, as well as by studies showing isoform specific, concentration-dependent desensitization of PDGF-BB relaxation. The relaxation induced by PDGF-BB was prevented by N omega-nitro-L-arginine. It was also observed that endothelium-independent contractions to the AB and AA isoforms of PDGF were less than those to PDGF-BB. Contrary to the widely held view that PDGF receptors are not present on the endothelium of macrovessels, these studies provide evidence for an endothelium-dependent, nitric oxide mediated relaxation of rat aorta caused by PDGF via PDGF beta beta-receptors.
EXPERIMENTAL LOCAL BLADDER EDEMA CAUSING URINE REFLUX INTO URETER AND KIDNEY
Authors: John Auer, Lloyd D. Seager
Journal: The Journal of Experimental Medicine (1937)

Experimental infiltration of the intravesical ureter of the normal bladder in the living, anesthetized animal with magnesium sulfate or physiological salt solution caused a reflux of urine into the ureter in 6 out of 18 guinea pigs (33 per cent); in 22 out of 27 rabbits (81 per cent), and in 14 out of 17 dogs (82 per cent). The vesical pressure necessary to produce this experimental reflux is low and ranges between 2 and 12 mm. of Hg; hydrostatic pressure of the bladder contents often sufficed to drive urine into the kidney pelvis. After an experimental reflux had occurred, increased vesical pressure often failed to raise the level of the regurgitant column in the ureters of rabbit and dog: these higher pressures had rendered an incompetent valve competent. Control pressures ranging between 8 and 40 mm. of Hg without a preceding infiltration, caused no reflux in the great majority of dogs. The amount of infiltrated fluid necessary to produce reflux varied from 0.2 cc. in the guinea pig to 0.5 to 2 cc. in dog. Spontaneous regurgitation, that is regurgitation without a preceding infiltration, was seen in 4 guinea pigs, 4 rabbits and 2 dogs. Antiperistalsis of the ureters, that is a wave of contraction passing from the bladder to the kidney, was never seen in our animals with experimental reflux. Biopsy of the bladder in rabbit and dog showed edema of the ureterovesical valves after infiltration in most of our animals. Hemorrhages into the submucosa in the neighborhood of the ureteral valves were observed in some. The bladders of 3 rabbits, exhibiting spontaneous reflux without infiltration showed pouting, edematous lips of the ureterovesical orifices. The cause of experimental regurgitation is a non-obstructive edema of the vesical valve; this edema renders the valve flap more rigid and therefore incompetent at relatively low intravesical pressures. Higher intravesical pressures may again render the incompetent valve competent. The experimental results are applied to the human subject because the urinary bladder of dog and of man are quite similar in structure and function. Reasons are presented suggesting that the described type of reflux may cause pyelitis and pyelonephritis.
p38-MAPK Induced Dephosphorylation of α-Tropomyosin Is Associated With Depression of Myocardial Sarcomeric Tension and ATPase Activity
Authors: Susan Vahebi, Asuka Ota, Manxiang Li, Chad M. Warren, Pieter P. de Tombe, Yibin Wang, R. John Solaro
Journal: Circulation Research (2007)

Our objective in work presented here was to understand the mechanisms by which activated p38α MAPK depresses myocardial contractility. To test the hypothesis that activation of p38 MAPK directly influences sarcomeric function, we used transgenic mouse models with hearts in which p38 MAPK was constitutively turned on by an upstream activator (MKK6bE). These hearts demonstrated a significant depression in ejection fraction after induction of the transgene. We also studied hearts of mice expressing a dominant negative p38α MAPK. Simultaneous determination of tension and ATPase activity of detergent-skinned fiber bundles from left ventricular papillary muscle demonstrated a significant inhibition of both maximum tension and ATPase activity in the transgenic-MKK6bE hearts. Fibers from hearts expressing dominant negative p38α MAPK demonstrated no significant change in tension or ATPase activity. There were no significant changes in phosphorylation level of troponin-T3 and troponin-T4, or myosin light chain 2. However, compared with controls, there was a significant depression in levels of phosphorylation of α-tropomyosin and troponin I in fiber bundles from transgenic-MKK6bE hearts, but not from dominant negative p38α MAPK hearts. Our experiments also showed that p38α MAPK colocalizes with α-actinin at the Z-disc and complexes with protein phosphatases (PP2α, PP2β). These data are the first to indicate that chronic activation of p38α MAPK directly depresses sarcomeric function in association with decreased phosphorylation of α-tropomyosin.
Regression of Electrocardiographic Left Ventricular Hypertrophy During Antihypertensive Therapy and Reduction in Sudden Cardiac Death
Authors: Kristian Wachtell, Peter M. Okin, Michael H. Olsen, Björn Dahlöf, Richard B. Devereux, Hans Ibsen, Sverre E. Kjeldsen, Lars H. Lindholm, Markku S. Nieminen, Kristian Thygesen
Journal: Circulation (2007)

Background— Sudden cardiac death (SCD) occurs more often in patients with ECG left ventricular (LV) hypertrophy. However, whether LV hypertrophy regression is associated with a reduced risk of SCD remains unclear. Methods and Results— The Losartan Intervention for End Point Reduction in Hypertension (LIFE) study included 9193 patients 55 to 80 years of age with essential hypertension and ECG LV hypertrophy by gender-adjusted Cornell product (CP) (RaVL+SV 3 [+6 mm in women]) · QRS duration&gt;2440 mm · ms) and/or Sokolow-Lyon voltage (SLV) (SV 1 +RV 5/6 &gt;38 mm). During follow-up (mean, 4.8 years), 190 patients (2%) experienced SCD. In time-dependent Cox analyses, absence of in-treatment LV hypertrophy was associated with a decreased risk of SCD: every 1-SD-lower in-treatment CP (1050 mm · ms) was associated with a 28% lower risk of SCD (hazard ratio [HR], 0.72; 95% CI, 0.66 to 0.79) and 1-SD-lower SLV (10.5 mm) with a 26% lower risk (HR, 0.74; 95% CI, 0.65 to 0.84). After adjustment for time-varying systolic and diastolic blood pressures, treatment allocation, age, gender, baseline Framingham risk score, ECG strain, heart rate, urine albumin/creatinine ratio, smoking, diabetes, congestive heart failure, coronary heart disease, atrial fibrillation, and occurrence of myocardial infarction, atrial fibrillation, heart failure, and noncardiovascular death, both in-treatment CP and SLV remained predictive of SCD: each 1-SD-lower CP was associated with a 19% lower risk of SCD (HR, 0.81; 95% CI, 0.73 to 0.90) and 1-SD-lower SLV with an 18% lower risk (HR, 0.82; 95% CI, 0.70 to 0.98). Absence of in-treatment LV hypertrophy by both SLV and CP was associated with a 30% lower risk of SCD (HR, 0.70; 95% CI, 0.54 to 0.92). Conclusions— Absence of in-treatment ECG LV hypertrophy is associated with reduced risk of SCD independently of treatment modality, blood pressure reduction, prevalent coronary heart disease, and other cardiovascular risk factors in hypertensive patients with LV hypertrophy.
Moonlighting: Wax Without the Wane
Authors: John L. Seymour
Journal: JAMA (1964)

<h3>To the Editor:—</h3> To put the lie to the $25,000 quote, very few financially established physicians—none to my knowledge—make extra money by taking night call in the hospital in which they have practice privileges, or in any other hospital. If the opportunity is there, why don't they take advantage of it and rake in the shekels? Because to most of us in medicine, there are some things in life more important than a few extra dollars. Medical educators, your gun-barrel vision becomes you not. You may be sailing full steam into the future, but you have neglected to pull up the anchor.
Lessons from Evidence-Based Operating Room Management in Balancing the Needs for Efficient, Effective and Ethical Healthcare
Authors: Allyson C. Rosen, Franklin Dexter
Journal: The American Journal of Bioethics (2009)

"Lessons from Evidence-Based Operating Room Management in Balancing the Needs for Efficient, Effective and Ethical Healthcare." The American Journal of Bioethics, 9(4), pp. 43–44 Acknowledgments Allyson C. Rosen is supported by a K award (K01AG025157) and the Sierra-Pacific MIRECC (Mental Illness Research, Education, and Clinical Center), Department of Veteran Affairs, VA Palo Alto Health Care System. Financial disclosure statement: FD receives no funds personally other than his salary from the State of Iowa, including no travel expenses or honoraria, and has tenure with no incentive program.
NOVEL QUANTITATIVE FLUOROPERFUSION ASSESSMENT OF THE PHYSIOLOGIC SIGNIFICANCE OF CORONARY STENOSES DURING DYNAMIC CINE FLUOROSCOPY
Authors: Omair Khwaja Yousuf, Jeffrey Trost, Takuya Sakaguchi, Hisato Takemoto, Jingwu Yao, Satoshi Kimura, Takashi Ichihara, Albert Lardo, Joao Lima, Richard George
Journal: Journal of the American College of Cardiology (2014)
"PEMPHIGUS SOLITAPJUS CICATRISANS."
Authors: TWISTON DAVIES
Journal: British Journal of Dermatology (1941)

Journal Article “PEMPHIGUS SOLITAPJUS CICATRISANS.” Get access TWISTON DAVIES TWISTON DAVIES Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology and Syphilis, Volume 53, Issue 6, 1 June 1941, Pages 187–190, https://doi.org/10.1111/j.1365-2133.1941.tb10549.x Published: 01 June 1941
ERα-Dependent E2F Transcription Can Mediate Resistance to Estrogen Deprivation in Human Breast Cancer
Authors: Todd W. Miller, Justin M. Balko, Emily M. Fox, Zara Ghazoui, Anita Dunbier, Helen Anderson, Mitch Dowsett, Aixiang Jiang, R. Adam Smith, Sauveur-Michel Maira, H. Charles Manning, Ana M. González-Angulo, Gordon B. Mills, Catherine Higham, Siprachanh Chanthaphaychith, Maria G. Kuba, William R. Miller, Yu Shyr, Carlos L. Arteaga
Journal: Cancer Discovery (2011)

Most estrogen receptor α (ER)-positive breast cancers initially respond to antiestrogens, but many eventually become estrogen-independent and recur. We identified an estrogen-independent role for ER and the CDK4/Rb/E2F transcriptional axis in the hormone-independent growth of breast cancer cells. ER downregulation with fulvestrant or small interfering RNA (siRNA) inhibited estrogen-independent growth. Chromatin immunoprecipitation identified ER genomic binding activity in estrogen-deprived cells and primary breast tumors treated with aromatase inhibitors. Gene expression profiling revealed an estrogen-independent, ER/E2F-directed transcriptional program. An E2F activation gene signature correlated with a lesser response to aromatase inhibitors in patients' tumors. siRNA screening showed that CDK4, an activator of E2F, is required for estrogen-independent cell growth. Long-term estrogen-deprived cells hyperactivate phosphatidylinositol 3-kinase (PI3K) independently of ER/E2F. Fulvestrant combined with the pan-PI3K inhibitor BKM120 induced regression of ER(+) xenografts. These data support further development of ER downregulators and CDK4 inhibitors, and their combination with PI3K inhibitors for treatment of antiestrogen-resistant breast cancers.
Living Alone After Myocardial Infarction
Authors: Robert B. Case
Journal: JAMA (1992)

To determine if the presence of a disrupted marriage or living alone would be an independent prognostic risk factor for a subsequent major cardiac event following an initial myocardial infarction.Prospective evaluation in the placebo wing of a randomized, double-blind drug trial in patients with an enzyme-documented acute myocardial infarction who were admitted to a coronary care facility. Data for living alone and/or a marital disruption were entered into a Cox proportional hazards model constructed from important physiologic and nonphysiologic factors in the same database.Multicenter trial in a mixture of community and academic hospitals in the United States and Canada.All consenting patients who were 25 to 75 years of age and without other serious diseases were enrolled (placebo, N = 1234) within 3 to 15 days of the index infarction and followed for a period of 1 to 4 years (mean, 2.1 years). Nine hundred sixty-seven patients were followed for 1.1 years and 530 for 2.2 years.Recurrent major cardiac event (either recurrent nonfatal infarction or cardiac death).Living alone was an independent risk factor, with a hazard ratio of 1.54 (95% confidence interval, 1.04 to 2.29; P less than .03). Using the Kaplan-Meier statistical method for calculation, the recurrent cardiac event rate at 6 months was 15.8% in the group living alone vs 8.8% in the group not living alone. Risk remained significant throughout the follow-up period (P = .001). A disrupted marriage was not an independent risk factor.Living alone but not a disrupted marriage is an independent risk factor for prognosis after myocardial infarction when compared with all other known risk factors.
Abstract B29: Improving the identification of beneficial mimotopes using a representative tumor-specific T cell receptor.
Authors: Jill E. Slansky, Jonathan D. Buhrman
Journal: Cancer Research (2013)

Abstract Vaccination with peptide mimotopes is a promising strategy to improve antitumor immunity. Mimotopes function by eliciting increased numbers of T cells that cross-react with the native tumor antigen. Using a high affinity tumor-specific T cell clone (CT), we have identified a panel of mimotopes for the dominant antigen (AH1) of a mouse colon tumor cell-line (CT26) that elicits a range of tumor protection when used in vaccines. Ex vivo evaluation of the TCRs of T cells initiated by mimotopes that protect against tumor challenge revealed increased representation of a Vβ8.3/Jβ2.6 motif: a small hydrophobic amino acid, followed by a large polar residue, and the tyrosine of the Jβ2.6. Clonotypes with this motif were also identified within the AH1-specific T cell repertoire of naturally responding TIL and following vaccination with the AH1 antigen. This motif was not found in the original CT clone. One particular clone with the motif made up nearly 8.5% of all Vβ8.3 sequences identified following immunization with mimotopes. Thus, we tested the hypothesis that this ‘representative’ TCR improves the frequency of discovery of efficacious mimotopes for cancer immunotherapy relative to the high affinity CT clone in the CT26 model. We have demonstrated that this is the case by screening genetically encoded peptide libraries. These results have important implications when considering the optimal T cells responding to tumor antigens and the improved identification of mimotopes for cancer immunotherapy. Citation Format: Jill E. Slansky, Jonathan D. Buhrman. Improving the identification of beneficial mimotopes using a representative tumor-specific T cell receptor. [abstract]. In: Proceedings of the AACR Special Conference on Tumor Immunology: Multidisciplinary Science Driving Basic and Clinical Advances; Dec 2-5, 2012; Miami, FL. Philadelphia (PA): AACR; Cancer Res 2013;73(1 Suppl):Abstract nr B29.
EXSUFFLATION BELT
Authors: William Fraimow
Journal: JAMA (1960)

An apparatus for use in treating pulmonary emphysema was designed to assist respiration in both the inspiratory and the expiratory phases. Air was supplied by an intermittent positive pressure breathing (IPPB) device in such a way that it flowed alternately into the patient's airways (inspiratory phase) and into an inflatable belt strapped about his body at the level of the diaphragm (expiratory phase). The apparatus was used initially on 27 patients with obstructive emphysema secondary to anthracosilicosis. Measurements of minute ventilation, tidal volume, expiratory flow rate, carbon dioxide excretion, arterial oxygen saturation, and the pCO<sub>2</sub>and pH of the blood showed that little, if any, objective improvement in the patients could be ascribed to the addition of the inflatable belt. Subjective improvement was reported by most patients, who thought they could breathe better.
Treatment of cardiac arrhythmias with phenytoin
Authors: J. D. Eddy, S. P. Singh
Journal: BMJ (1969)

Phenytoin was given intravenously in 37 patients with cardiac arrhythmias-21 had acute myocardial infarction and 16 had other conditions. There was a favourable response in 18 of the 21 cases with acute myocardial infarction, with a return to sinus rhythm in six of the nine cases with supraventricular arrhythmias, and a return to sinus rhythm in 10 of the 12 cases of ventricular arrhythmias, the remaining two showing a significant reduction in the number of ventricular extra-systoles.In the second group of 16 cases which had various causes there was a satisfactory response in only six. Digitalis played no part in producing any of the arrhythmias. Phenytoin was used orally for suppressing and preventing abnormal rhythm in five patients, and three of these responded favourably. The number of patients treated orally is too small to draw any definite conclusion.
One in four NHS trusts in England fail hygiene standards
Authors: Rebecca Coombes
Journal: BMJ (2008)

More than a quarter of NHS trusts in England have failed to meet one or more hygiene standards set by the Healthcare Commission.

Of the 103 trusts (26% of the total of 391 trusts) that failed on at least one of three core hygiene standards in 2007-8, 40 had slipped back from better performance the previous year.

The area where the greatest number of trusts struggled was in the decontamination of reusable medical devices. Seventy trusts failed to meet this standard. Thirty five trusts could not say that they had complied with standards on …
Th1 cytokines, programmed cell death, and alloreactive T cell clone size in transplant tolerance
Authors: Koji Kishimoto, Sigrid Sandner, Jaime Imitola, Masayuki Sho, Yongsheng Li, Peter B. Langmuir, David M. Rothstein, Terry B. Strom, Laurence A. Turka, Mohamed H. Sayegh
Journal: Journal of Clinical Investigation (2002)

The Th1 cytokines IL-2 and IFN-γ, which inhibit T cell proliferation and promote activation induced cell death, may be required to diminish alloreactive T cell numbers and to foster tolerance across full allogeneic barriers. However, we hypothesized that these cytokines might be dispensable when the alloreactive T cell clone size is relatively small, as is seen in recipients of minor-mismatched grafts. We show that alloreactive T cell clone size of C57BL/6 mice against multiple minor-mismatched 129X1/sv mice was ∼4–9-fold smaller than that against MHC-mismatched BALB/c mice. In the MHC-mismatched combination, CD28-B7 blockade by CTLA4Ig induced long-term graft survival in wild-type recipients, but this treatment was ineffective in IFNγ–/– or IL-2–/– recipients. In contrast, in the minor-mismatched combination, CTLA4Ig induced long-term allograft survival in wild-type, IFNγ–/–, and IL-2–/– recipients. Bcl-xL transgenic animals, which are defective in "passive" T cell death, are likewise sensitive to the effects of CTLA4Ig only in the setting of the minor-mismatch grafts. Therefore, the alloreactive T cell clone size is an important determinant affecting the need for Th1 cytokines and T cell death in tolerance induction. These data have implications for the design of tolerance strategies in transplant recipients with varying degrees of MHC mismatching.
On the Means by Which Uterine Haemorrhage Is Suppressed without Artificial Assistance
Authors: T. Radford
Journal: BMJ (1847)

UTERINE HEMORRHAGE.143 0left eye, and that he could not raise the lid, and that he could scarce feel his left cheek or the scalp of his head, which felt as he stated as if .asleep.Can we for a moment doubt that this attack was of the nature of apoplexy;, in its mildest form perhaps, but nevertheless dependent on a lesion of some portion of the encephalic *apparatus.It would be idle in the absence of all proof, to speculate upon the particular spot in the brain in which this lesion had occurred; it is more than probable, however, that the base of the brain must be the spot, but whetherin the thalamus, corpus striatum, pons Varolii, or any other portion having relation to the roots of these nerves, it is useless to speculate upon.
Pathways to Quality Inpatient Management of Hyperglycemia and Diabetes: A Call to Action
Authors: Boris Draznin, Janice Gilden, Sherita H. Golden, Silvio E. Inzucchi
Journal: Diabetes Care (2013)

Currently patients with diabetes comprise up to 25–30% of the census of adult wards and critical care units in our hospitals. Although evidence suggests that avoidance of hyperglycemia (&amp;gt;180 mg/dL) and hypoglycemia (&amp;lt;70 mg/dL) is beneficial for positive outcomes in the hospitalized patient, much of this evidence remains controversial and at times somewhat contradictory. We have recently formed a consortium for Planning Research in Inpatient Diabetes (PRIDE) with the goal of promoting clinical research in the area of management of hyperglycemia and diabetes in the hospital. In this article, we outline eight aspects of inpatient glucose management in which randomized clinical trials are needed. We refer to four as system-based issues and four as patient-based issues. We urge further progress in the science of inpatient diabetes management. We hope this call to action is supported by the American Diabetes Association, The Endocrine Society, the American Association of Clinical Endocrinologists, the American Heart Association, the European Association for the Study of Diabetes, the International Diabetes Federation, and the Society of Hospital Medicine. Appropriate federal research funding in this area will help ensure high-quality investigations, the results of which will advance the field. Future clinical trials will allow practitioners to develop optimal approaches for the management of hyperglycemia in the hospitalized patient and lessen the economic and human burden of poor glycemic control and its associated complications and comorbidities in the inpatient setting.