tbuckley/cabot-search huggingface dataset:
What will a primary care led NHS mean for GP workload? the problem of the lack of an evidence base
Authors: L. L. Pedersen, B. Leese
Journal: BMJ (1997)

<h3>Abstract</h3> Ongoing negotiations on the general practitioner contract raise the question of remunerating general practitioners for increased workload resulting from the shift from secondary to primary care. A review of the literature shows that there is little evidence on whether a shift of services from secondary to primary care is responsible for general practitioners9 increased workload, and scope for making generalisations is limited. The implication is that general practitioners have little more than anecdotal evidence to support their claims of greatly increased workloads, and there is insufficient evidence to make informed decisions about remunerating general practitioners for the extra work resulting from the changes. Lack of evidence does not, however, mean that there is no problem with workload. It will be increasingly important to identify mechanisms for ensuring that resources follow workload.
Expression of high affinity binding sites for erythropoietin on L8057 cells, a mouse megakaryoblastic cell line, associated with cell differentiation
Authors: Takeshi Yoshida, Yoji Ishida, Hideki Sasaki, Tohru Inoue, Kohei Kaku, Toshio Kaneko
Journal: American Journal of Hematology (1992)

Abstract In this study, specific binding sites were examined for erythropoietin (EPO) on the mouse leukemic cell line, L8057. This cell line is megakaryoblastic in origin as evidenced by an enlargement of cell size, multinuclearity, intense activity of acetylcholinesterase, more expression of glycoprotein Ilb and IIIa antigen, and higher ploidy distribution after the treatment with 12‐o‐tetradecanoylphorbor‐13‐acetate (TPA). The original undifferentiated cells possessed a single class of low affinity binding sites for recombinant human (rh) EPO with a Kd of 3.5 nM. Following the treatment with TPA, high affinity binding sites (Kd; 440 pM) were expressed in addition to the low affinity sites. EPO stimulated the incorporation of 3 H‐leucine into TPA‐treated L8057 cells, and the maximal effect of EPO was observed at the same order as the Kd value of high affinity sites. The present data demonstrates that the expression of high affinity binding sites for EPO is associated with the differentiation of L8057 cells which have megakaryocytic characteristics. Furthermore, protein synthesis stimulated by EPO may be mediated through the high affinity sites.
Dermatology Mobile Applications
Authors: Elliot J. Coups, Lee M. Ritterband
Journal: JAMA Dermatology (2014)

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 Dermatology HomeNew OnlineCurrent IssueFor Authors Podcast 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) 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 Dermatology journal
Mortality of bereavement.
Authors: A W Ward
Journal: BMJ (1976)

The death rate of a group of 87 widowers and 279 widows was followed for two years from the death of their spouses. The life tables for England and Wales 1970-2 indicated that the expected number of deaths would be 6 men and 11 women. The actual numbers (9 men and 11 women, 5.5%) were not significantly different, though there were more widowers' deaths during the first six months of bereavement. There was no significantly greater mortality among those whose spouses had died in hospital; but when this had occurred the health of the second spouse was likely to have been poorer than that of those whose spouses had died at home.
P360 CHLOROQUINE FOR MAINTENANCE REMISSION OF AUTOIMMUNE HEPATITIS ESPECIALLY IN PATIENTS WITH REACTIVITY TO ANTI-SLA
Authors: D.R.B. Terrabuio, M.A. Diniz, C.P. Abrantes-Lemos, E.S. Mello, F.J. Carrilho, E. Cancado, F.G. Souza
Journal: Journal of Hepatology (2014)
Mechanisms of Sex Differences in TNFR2-Mediated Cardioprotection
Authors: Meijing Wang, Paul R. Crisostomo, Troy A. Markel, Yue Wang, Daniel R. Meldrum
Journal: Circulation (2008)

Background— TNFR1/TNFR2 signaling may mediate different cellular and molecular responses (injury versus protection) and the balance may be affected by sex hormones. Previous studies have shown that females have improved myocardial functional recovery, TNFR1 signaling resistance, and increased SOCS3 expression after acute ischemia/reperfusion when compared with males. However, it is unknown whether the TNFR2 pathway protects the myocardium from ischemia/reperfusion injury, and if so, whether sex differences exist in TNFR2-mediated cardioprotection. Therefore, we hypothesized that (1) TNFR2 mediates myocardial protection from ischemia/reperfusion through STAT3, SOCS3, and vascular endothelial growth factor in both sexes; and (2) TNFR2 elicits greater protective signaling in females compared with males. Methods and Results— Isolated male and female mouse hearts from TNFR2 knockout, TNFR1/2 knockout, and wild-type (C57BL/6J or B6129SF2/J; n=5 to 6/group) were subjected to 20 minutes ischemia followed by 60 minutes reperfusion. TNFR2 deficiency decreased postischemic myocardial recovery in both sexes but had a greater effect on females. The deleterious effects of TNFR2 ablation were associated with a decrease in mRNA and protein levels of SOCS3, STAT3, and vascular endothelial growth factor as well as an increase in myocardial interleukin-1-beta production in female hearts. However, a significant increase in JNK activation and interleukin-1-beta protein levels was noted in male TNFR2KO hearts after ischemia/reperfusion. Additionally, TNFR1/2 knockout decreased myocardial function in female hearts but not males. This observation was associated with a decrease in mRNA levels of SOCS3, STAT3, and vascular endothelial growth factor and an increase in myocardial p38 mitogen-activated protein kinase activation in females. Conclusions— Sex differences in the mechanisms of TNFR2-mediated cardioprotection occur by increasing STAT3, SOCS3, and vascular endothelial growth factor in females and by decreasing JNK in males.
Allergic airway disease is unaffected by the absence of IL-4Rα–dependent alternatively activated macrophages
Authors: Natalie E. Nieuwenhuizen, Frank Kirstein, Jaisubash Jayakumar, Babele Emedi, Ramona Hurdayal, William G.C. Horsnell, Andreas L. Lopata, Frank Brombacher
Journal: Journal of Allergy and Clinical Immunology (2012)
Ban free consultations and "two for one" deals on cosmetic procedures, say respondents to review
Authors: Z. Kmietowicz
Journal: BMJ (2012)

People who responded to a consultation on the regulation of cosmetic interventions in England have said that they would like to see a raft of changes, including that all consultations should be with a medical professional—preferably the surgeon doing the procedure—and not a sales adviser.

They would also like to see an end to free consultations, tighter controls on advertising, a two stage consent process, and better information on the after-effects of surgery, such as photographs of bruising and scarring.1

The call for evidence into cosmetic interventions was launched by the NHS’s medical director, Bruce Keogh, in August 2012 after the …
Conduction performance of collateral vessels induced by vascular endothelial growth factor or basic fibroblast growth factor
Authors: K Kondoh
Journal: Cardiovascular Research (2003)

In the present study, we delivered vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) gene to a rabbit model of hind limb ischemia utilizing an ex vivo method of gene transfer, and evaluated the functional performance of the developed collateral vessels.The left femoral artery of a male Japanese White rabbit was excised to induce limb ischemia, and a section of skin was resected for culture of auto-fibroblasts. Twenty days later, the VEGF gene, bFGF gene or beta-galactosidase gene (LacZ) was adenovirally transferred to the cultured auto-fibroblasts (5x10(6) cells), and the next day, a pair of specifically infected fibroblasts (total 1x10(7) cells) was injected via the left internal iliac artery of the same rabbit. Pairs of transferred genes into the fibroblasts were as follows: LacZ/LacZ (control group), VEGF/LacZ (VEGF group), bFGF/LacZ (FGF group) and VEGF/bFGF (combination group). Twenty-eight days after cell administration, collateral development and its function were evaluated.Calf blood pressure ratio, resting blood flow of the left iliac artery and capillary density of ischemic muscle showed similar degrees of angiogenic effects in the VEGF and FGF groups, which were significantly greater than those in the control group. On the contrary, angiographic score, collateral conductance and smooth muscle cell (SMC)-positive vessel density in the FGF group were significantly greater than those in the VEGF group. In the combination group, collateral conductance showed synergistic effects, and in vivo blood flow and smooth muscle cell-positive vessel density revealed additive effects of VEGF and bFGF.These findings suggested that bFGF-induced collateral development exceeded VEGF-induced collateral development in the induction of arteriogenesis, and that combined gene delivery of VEGF and bFGF produced additive or synergistic effects of collateral development as compared with the effects induced by transfer of each gene alone.
Call for national body to ensure blood transfusion safety
Authors: Z. Kmietowicz
Journal: BMJ (1998)

Doctors in Britain concerned about the safety of blood transfusions have called for a national unified body to be established that will oversee the whole process, from collection of blood from donors to the delivery of blood components to patients on wards.

The move follows the first annual report issued by the Serious Hazards of Transfusion (SHOT) scheme, which revealed that in the year ending September 1997, 94 hospitals reported a total of 169 instances of error, almost half (47%) of which were cases where patients had received a blood component intended for someone else. These resulted in one death and nine cases …
Hepatitis delta virus inhibits alpha interferon signaling
Authors: Paolo Pugnale, Valerio Pazienza, Kévin Guilloux, Francesco Negro
Journal: Hepatology (2008)

Abstract Hepatitis delta virus (HDV) can cause severe acute and chronic liver disease in patients infected with hepatitis B virus. Interferon-α (IFN-α) is the only treatment reported to be effective in chronic hepatitis delta, albeit in a minority of patients. The molecular mechanisms underlying resistance to therapy are unclear. IFN-α–induced activation of the Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling cascade is essential for the induction of an antiviral state. Interference of HDV with the JAK-STAT pathway could be responsible for the IFN-α resistance in chronic hepatitis delta patients. We analyzed IFN-α–induced signal transduction through the JAK-STAT pathway in human hepatoma cells transfected with the complete HDV genome. The expression of IFN-α–stimulated genes was investigated with reverse transcription real-time polymerase chain reaction (PCR). STATs and JAKs activations were examined by immunofluorescence and immunoblot. The IFN-α–stimulated genes coding for the antiviral proteins myxovirus resistance A, double-stranded RNA (dsRNA)-activated protein kinase and 2′,5′-oligoadenylate synthetase were down-regulated in HDV-transfected hepatoma cells in response to IFN-α treatment. HDV severely impaired the phosphorylation of both STAT1 and STAT2, thus preventing their accumulation in the nucleus. Furthermore, HDV blocked the IFN-α–stimulated tyrosine phosphorylation of IFN receptor-associated JAK kinase Tyk2, without affecting either the tyrosine phosphorylation of Jak1 or the expression of type I IFN receptor subunits. Conclusions: IFN-α–induced intracellular signaling is impaired in HDV-transfected human hepatoma cells. HDV subverts the effect of IFN-α by blocking Tyk2 activation, thereby resulting in selective impairment of activation and translocation to the nucleus of STAT1 and STAT2. Interference of HDV with IFN-α signaling could represent an important mechanism of viral persistence and treatment resistance. (Hepatology 2008.)
Progress Against Cancer Quackery
Authors: Roald N. Grant
Journal: JAMA (1961)

WITH THE PASSAGE of Senate Bill 194 by the California Legislature last year and similar acts in Kentucky and Nevada this year, those responsible for protecting the public health have for the first time been provided with an effective means of controlling cancer quackery at its base of operations in the local community. National agencies and others concerned with this problem have long held that action taken in the community where he lives can best protect the cancer patient from the mistreatment or delayed proper treatment which is inherent in quackery. As similar legislation is enacted by other states, and protection from cancer quackery increases, many lives will be saved and much needless suffering will be avoided. This important step forward was achieved only after years of painstaking effort by the Cancer Commission of the California Medical Association and many other interested groups and individuals. Among these, the American Cancer
β-Cell Autoimmunity, Genetic Susceptibility, and Progression to Type 1 Diabetes in Unaffected Schoolchildren
Authors: Petri Kulmala, Jukka Rahko, Kaisa Savola, Paula Vähäsalo, Minna Sjöroos, Antti Reunanen, Jorma Ilonen, Mikael Knip
Journal: Diabetes Care (2001)

Lettersnondiabetic siblings of type 1 diabetic patients and therefore correlated with plasma concentrations of Lp(a) and fibrinogen.Cases of hyponatremia have been correlated with inflammation ( 14) and increased plasma interleukin Ϫ6 concentration (15).These findings are consistent with our hypothesis of an association among inflammatory markers, oxidative stress, and susceptibility to type 1 diabetes.Moreover, the familiarly overactive NHE could be viewed independently as further evidence for the presence in these families of a redox disequilibrium in which oxidation seems to be dominant.
Anatomic correction of transposition of the great arteries: pre- and postoperative cardiac catheterization, with angiocardiography in five patients.
Authors: R M Freedom, J A Culham, P M Olley, R D Rowe, W G Williams, G A Trusler
Journal: Circulation (1981)

Six of eight patients survived anatomic correction of transposition of the great arteries and repair of associated cardiovascular anomalies at the Hospital for Sick Children, Toronto, Canada. Two of the six survivors also had tricuspid atresia, and continuity between the right atrium and the subaortic outlet chamber in these patients was provided by a valved external conduit, in addition to the arterial switch and coronary artery reimplantation. Five of the six patients have undergone complete postoperative clinical, hemodynamic and angiocardiographic investigation and form the basis of this communication. Our present indications for anatomic repair are discussed.
Valvotomy for Mitral Stenosis
Authors: C. Baker, R. C. Brock, M. Campbell, P. Wood
Journal: BMJ (1952)

Our interest in valvotomy for mitral stenosis extends back over several years, although it was not until Sep- tember, 1948, that our first patient was operated on.In June, 1950, we were able to report our experiences in nine patients, seven with successful operations (Baker, Brock, and Campbell, 1950).We are now able to report the immediate results on 100 patients treated by opera- tion, with a more detailed analysis and follow-up of the first 50, the last of whom was operated upon in May, 1951, so that all have been followed for six months, the majority for more than a year, and some for two to three years.Apart from two patients at the Johns Hopkins Hospital, Baltimore, the operations were done at either Guy's Hospital or the Brompton Hospital, and all by one surgeon.For the purpose of analysis and follow-up the two Baltimore cases have been omitted from the first 50.In previous papers we have followed common usage in writing of pulmonary or mitral " valvulotomy," but it is a valve and not a valvule that is divided, and we think the term " valvotomy " is more correct, even though it is still a hybrid formation.The operation really does more than splitting the commissures, for if the valve cusps are reasonably supple the operation may enable them to close better and more normally, but we have thought it better to reserve the term " valvoplasty " for more elaborate operations that may be possible in the future.
Comparison of biventricular dimensions and function between pediatric sickle‐cell disease and thalassemia major patients without cardiac iron
Authors: Antonella Meloni, Jon Detterich, Vasili Berdoukas, Alessia Pepe, Massimo Lombardi, Thomas D. Coates, John C. Wood
Journal: American Journal of Hematology (2012)

Patients with chronic anemia develop compensatory ventricular dilation, even when maintained on chronic transfusion regimens. It is important to characterize these effects to interpret pathological changes in cardiac dimensions and function introduced by iron overload and sickle cell vasculopathy. Our primary goal was to compare biventricular dimensions and function assessed by cardiovascular magnetic resonance (CMR) in pediatric, chronically‐transfused sickle‐cell disease (SCD) and thalassemia major (TM) patients who had normal cardiac iron levels. Moreover, we explored systematic sex differences in ventricular dimensions in both populations. We identified 261 studies suitable for analysis from 64 patients with SCD (34 females) and 49 patients with TM (20 females). All demographic and CMR parameters were inversely weighted by the number of exams. In both populations, males had larger left and right ventricular dimensions than females, with a more marked effect observed in patients with SCD. Compared to patients with TM, patients with SCD showed significantly greater biventricular dilation and left ventricular hypertrophy. This difference could not be explained by different hemoglobin levels, cardiac iron overload, and systolic blood pressure. The left ventricular (LV) ejection fraction (EF) for the males and the right ventricular (RV) EF for both the sexes were comparable between SCD and TM groups, while females with SCD had significantly lower LV EF than females with TM. Our results represent important baseline findings that place changes introduced by iron overload as well as systemic and pulmonary vasculopathy in proper context. Am. J. Hematol. 88:213–218, 2013. © 2012 Wiley Periodicals, Inc.
839-4 Treatment with antioxidant N-acetylcysteine reverses interstitial fibrosis in a mouse model of human hypertrophic cardiomyopathy mutation
Authors: Natalia Tsybouleva, Tripti Halder, Rajnikant Patel, Silvia Lutucuta, Gilberto De Freitas, Masakuni Ishiyama, Blase Carabello, Ali J Marian
Journal: Journal of the American College of Cardiology (2004)
Sequencing ancient calcified dental plaque shows changes in oral microbiota with dietary shifts of the Neolithic and Industrial revolutions
Authors: Christina J Adler, Keith Dobney, Laura S Weyrich, John Kaidonis, Alan W Walker, Wolfgang Haak, Corey J A Bradshaw, Grant Townsend, Arkadiusz Sołtysiak, Kurt W Alt, Julian Parkhill, Alan Cooper
Journal: Nature Genetics (2013)
Toxicity from Large Doses of Imipramine and an MAO Inhibitor in Suicidal Intent
Authors: Elliot D. Luby
Journal: JAMA (1961)

Amine oxidase inhibitors and imipramine (Tofrānil) are now widely used in the treatment of the depressive states. In many instances these agents are substituted for electroshock therapy. Inasmuch as they are given to many potentially suicidal patients, toxicity becomes a matter of utmost importance.  Occasionally imipramine and an MAO inhibitor may be combined or one may be substituted for the other in order to produce a more effective therapeutic response. Potentiation or addition of toxic and possibly lethal effects may become a serious practical matter and pose many problems in management. Recently clinical reports 1,2 have described the disastrous results of overdosage with a combination of imipramine and the MAO inhibitor, phenelzine (Nardil).  The present paper describes a case of serious toxicity in a patient taking excessive doses of a new MAO inhibitor, tranylcypromine (Parnate), and imipramine. Preliminary toxicity data in rats support clinical observation in this case of
Partial purification of human renin.
Authors: K Murakami, T Inagami, E Haas
Journal: Circulation Research (1977)

An affinity gel for the purification of renin was prepared by coupling pepstatin to aminohexylagarose gel. Partially purified human renin (Haas et al., Arch. Biochem. Biophys., 110, 534-543, 1965) was purified further by affinity chromatography on the pepstatin-aminohexyl-agarose gel, gel filtration on a Sephadex G-75 column, and ion exchange chromatography on a DEAE-cellulose column. Separation from a protease permitted further purification without progressive loss of activity. Three peaks of enzymatically active renin were obtained after the DEAE-cellulose chromatography, with specific activities ranging from 206 to 166 and 85 Goldblatt units/mg protein, respectively. The specific activity of 206 GU units/mg represents a 103,000-fold purification compared to the renin present in the first crude extract.