tbuckley/cabot-search huggingface dataset:
Cancer Care Shows Signs of Strain as Patients Live Longer
Authors: Mike Mitka
Journal: JAMA (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 HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Hepatic lipase gene therapy in hepatic lipase-deficient mice. Adenovirus-mediated replacement of a lipolytic enzyme to the vascular endothelium.
Authors: D Applebaum-Bowden, J Kobayashi, V S Kashyap, D R Brown, A Berard, S Meyn, C Parrott, N Maeda, R Shamburek, H B Brewer, S Santamarina-Fojo
Journal: Journal of Clinical Investigation (1996)

Hepatic lipase (HL) is an endothelial-bound lipolytic enzyme which functions as a phospholipase as well as a triacylglycerol hydrolase and is necessary for the metabolism of IDL and HDL. To evaluate the feasibility of replacing an enzyme whose in vivo physiologic function depends on its localization on the vascular endothelium, we have infused recombinant replication-deficient adenovirus vectors expressing either human HL (HL-rAdV; n = 7) or luciferase cDNA (Lucif-rAdV; n = 4) into HL-deficient mice with pretreatment plasma cholesterol, phospholipid, and HDL cholesterol values of 176 +/- 9, 314 +/- 12, and 129 +/- 9, respectively. After infusion of HL-rAdV, HL could be detected in the postheparin plasma of HL-deficient mice by immunoblotting and postheparin plasma HL activities were 25,700 +/- 4,810 and 1,510 +/- 688 nmol/min/ml on days 5 and 15, respectively. Unlike the mouse HL, 97% of the newly synthesized human HL was heparin releasable, indicating that the human enzyme was virtually totally bound to the mouse vascular endothelium. Infusion of HL-rAdV in HL-deficient mice was associated with a 50-80% decrease in total cholesterol, triglyceride, phospholipids, cholesteryl ester, and HDL cholesterol (P < 0.001) as well as normalization of the plasma fast protein liquid chromatography lipoprotein profile by day 8. These studies demonstrate successful expression and delivery of a lipolytic enzyme to the vascular endothelium for ultimate correction of the HL gene defect in HL-deficient mice and indicate that recombinant adenovirus vectors may be useful in the replacement of endothelial-bound lipolytic enzymes in human lipolytic deficiency states.
Targeting CCR2 or CD18 Inhibits Experimental In-Stent Restenosis in Primates
Authors: Christopher Horvath, Frederick G.P. Welt, Mark Nedelman, Patricia Rao, Campbell Rogers
Journal: Circulation Research (2002)

A central role for leukocytes in neointimal hyperplasia after arterial injury is suspected. However, the relative importance of neutrophils and monocytes in balloon or stent-induced injury are not well understood, and mechanistic targeting of leukocyte recruitment or function is crude. We determined the temporal and spatial distribution of different leukocytes after balloon and stent-induced injury in primate iliac arteries. Based on these data, we targeted neutrophil and monocyte recruitment selectively after angioplasty or stent implantation and demonstrated that monocyte-specific blockade achieved via blockade of the MCP-1 receptor CCR2, was effective at reducing neointimal hyperplasia after stenting. In contrast, combined neutrophil and monocyte blockade achieved by targeting the leukocyte β 2 -integrin β-subunit CD18 was required to reduce neointimal hyperplasia after balloon injury. Distinct patterns of leukocyte infiltration in balloon versus stent-injured arteries predict distinct mechanisms for antiinflammatory strategies targeting neutrophils or monocytes in primates and may assist design of effective clinical strategies for optimizing vascular interventions.
Inside Baseball—Reply
Authors: M. Therese Southgate
Journal: JAMA (2006)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Forecasting the Effects of Health Reform on US Physician Workforce Requirement
Authors: Jonathan P. Weiner
Journal: JAMA (1994)

This article provides an estimate of the effects of health reform on the US physician workforce requirement. Its basic methodology is to extrapolate current patterns of staffing within managed care plans to the reshaped health care system of the year 2000. In this analysis it is assumed that 40% to 65% of Americans will be receiving care from integrated managed care networks in the near future, and that all citizens will be covered by some type of health insurance. On the basis of these assumptions, this article forecasts that in the year 2000, (1) there will be an overall surplus of about 165000 patient care physicians; (2) the requirement and supply of primary care physicians will be in relative balance; and (3) the supply of specialists will outstrip the requirement by more than 60%. In summation, it appears that national health reform—based largely on an expansion of managed care networks—will have significant impact on the US physician workforce. Concerns have been raised by others that health system reform's shift toward more primary and preventive care will be stymied by workforce availability. This study underscores this concern to some degree. However, the evidence presented herein suggests that the issue is not so much a primary care provider shortage as a specialty care surplus. (<i>JAMA</i>. 1994;272:222-230)
Research bodies and industry should combine efforts to develop biomarkers for dementia
Authors: A. Gulland
Journal: BMJ (2008)

A report on mental health has called for medical research bodies and the drug industry to join forces to find biomarkers for the early identification of dementia.

The study, Mental Capital and Wellbeing , says that biomarkers are vital for the prompt detection and monitoring of dementia. Biomarkers are objective biological measures associated with the presence of a disease, increased risk, or response to treatment.

The report, published by Foresight, part of the Government Office for Science, aims to advise the government on how to achieve the best possible mental development and mental wellbeing in …
Abstract 2947: Evolving Patterns of Use of Aldosterone Inhibition in Chronic Heart Failure; A Report from Get with the Guidelines HF
Authors: Nancy M Albert, Clyde W Yancy, Li Liang, Adrian F Hernandez, Gregg C Fonarow
Journal: Circulation (2008)

Aldosterone inhibition (ALD-I) is recommended in pts with moderately severe to severe HF (i.e. hospitalized for HF) and reduced LVEF with serum creatinine [S.Cr] < 2.5 mg/dL- men/< 2.0 mg/dL - wome...
Comorbidity in elderly NSCLC patients
Authors: K Miyazaki
Journal: Thorax (2005)

Comorbidity in elderly NSCLC patientsWe read with interest the report by Janssen-Heijnen and associates on the effect of comorbidity on the treatment and prognosis of elderly patients with non-small cell lung cancer (NSCLC). 1 The authors concluded that the number of comorbid conditions had no significant influence on the treatment chosen for patients with non-localised disease.We share the authors' opinion that ''comorbidity had no independent prognostic effect''.In their report, the authors used the Charlson comorbidity index and analysed the number of comorbid conditions. 1 However, they did not examine the scoring system of the index.We would like to know why the authors did not use the scoring of the index, and whether the conclusion would be changed if the scoring system was used.In the original article by Charlson et al and other related studies, 2-5 ''angina pectoris'' was not evaluated as one of the cardiovascular comorbid diseases.However, Janssen-Heijnen et al 1 included ''angina pectoris'' as a comorbid disease although they did not describe it precisely.We consider this inclusion is reasonable, and we would appreciate hearing from the authors whether ''angina pectoris'' would be evaluated as one of the cardiovascular comorbid diseases in future studies to evaluate the effect on mortality, and what score it should be assigned.
Nathan and Oski’s Hematology of Infancy and Childhood
Authors: Paulette Mehta
Journal: JAMA (2009)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Severe loss of invariant NKT cells exhibiting anti–HTLV-1 activity in patients with HTLV-1–associated disorders
Authors: Kazuko Azakami, Tomoo Sato, Natsumi Araya, Atae Utsunomiya, Ryuji Kubota, Kenshi Suzuki, Daisuke Hasegawa, Toshihiko Izumi, Hidetoshi Fujita, Satoko Aratani, Ryoji Fujii, Naoko Yagishita, Hajime Kamijuku, Takuro Kanekura, Ken-ichiro Seino, Kusuki Nishioka, Toshihiro Nakajima, Yoshihisa Yamano
Journal: Blood (2009)
Intracellular Delivery of Functional Proteins via Decoration with Transporter Peptides
Authors: Zurab Siprashvili, Jason A Reuter, Paul A Khavari
Journal: Molecular Therapy (2004)

<h2>Abstract</h2> Despite numerous attractive intracellular targets, protein therapeutics have been principally confined to the extracellular space due to the lack of a straightforward way to deliver functional polypeptides to the cell interior. Peptide sequences facilitating intracellular protein delivery have been identified; however, current strategies to apply them require problematic steps, such as generation of new in-frame fusion proteins, covalent chemical conjugation, and denaturation. We have developed a new approach to protein transfer into cells and tissues that relies on single-step decoration by cysteine-flanked, arginine-rich transporter peptides. This approach facilitated cell and tissue delivery of a variety of functional proteins, including antibodies and enzymes. Decoration with transporter peptides thus provides an attractive general means of intracellular delivery of functional proteins <i>in vitro</i> and in tissue.
THE NATURE AND PATHOLOGY OF RADIATION SICKNESS
Authors: VIRGIL H. MOON
Journal: JAMA (1941)

It has been known for years that severe, sometimes fatal illness may develop in patients subjected to intensive irradiation. Weakness, nausea, vomiting, oliguria, bloody diarrhea, rapid feeble pulse, low blood pressure and profound prostration are prominent clinical features. Both the metabolism and the renal elimination of wastes are markedly reduced. It has been observed that exposure of the abdomen to roentgen rays caused signs of illness more often than exposure of other areas. Death results from circulatory failure resembling that produced by anaphylaxis, severe intoxications, burns or intestinal obstruction. Space is lacking to discuss the various theories offered as explanations and the extensive experimentation done in search for further evidence. Those interested in these matters are referred to reviews.<sup>1</sup>Hall and Whipple<sup>2</sup>and Warren and Whipple<sup>3</sup>noted that the manifestations after extensive irradiation were like those of heat burns but with this difference: The latter produce illness
1150 ASYMPTOMATIC INTERSTITIAL PULMONARY AFFECTION &amp; ABNORMAL CELLULAR REACTIONS IN NON CIRRHOTIC HCV PATIENTS
Authors: M.E. El Dousoky, M. El Badrawy, M. El Bendary, M. Abd El Salam, A. Soltan, A. El-Karef, A. El Said
Journal: Journal of Hepatology (2011)
New concepts in assessing sickle cell disease severity
Authors: John-John B. Schnog, Leroy R. Lard, Robert A. Rojer, Fey P. L. Van der Dijs, Frits A. J. Muskiet, Ashley J. Duits
Journal: American Journal of Hematology (1998)

Vasoocclusion leads to pain, chronic organ damage, and a decreased life expectancy in patients with sickle cell disease. Therapeutic options for sickle cell disease have usually been evaluated according to their capacity for reducing the frequency of vasoocclusive crises requiring clinical attention. However, the frequency of vasoocclusive crises is not representative for the rate of accumulating organ damage in most sickle cell patients. This implies that the frequency of vasoocclusive crises needn't correlate with disease severity and, although being of importance, cannot solely serve as a parameter of treatment efficacy. Therefore, additional new objective parameters are needed to effectively study the vasoocclusive process in sickle cell disease. Several studies show that intricate adhesive interactions between (red) blood cells, plasma components, and endothelium play a crucial role in the pathophysiology of sickle cell vasoocclusion, offering new potential parameters to effectively assess disease severity as well as new therapeutical targets in the near future. Whether these adhesive mechanisms involve the causes or the effects of vasoocclusion will be determined if their inhibition, by interventive measures, results in therapeutic benefits. Am. J. Hematol. 58:61–66, 1998. © 1998 Wiley-Liss, Inc.
Role of adenosine in delayed preconditioning of myocardium
Authors: G Baxter
Journal: Cardiovascular Research (2002)

Myocardial protection conferred by ischemic preconditioning occurs in a bimodal time course. The early cardioprotection wanes rapidly and is succeeded by a delayed phase of protection reducing infarct development, myocardial stunning and arrhythmias. This 'second window' of preconditioning may be evident for up to 72 h. The current mechanistic paradigm for delayed preconditioning against infarction invokes roles for several freely-diffusible molecules, generated during the preconditioning period, that act in autocrine and/or paracrine fashion as triggers of cellular adaptation. These include adenosine, nitric oxide, reactive oxygen species and bradykinin. A role for adenosine receptor activation as a proximal molecular mechanism leading to delayed preconditioning against infarction was established in 1994. Pharmacological adenosine receptor blockade during preconditioning abolishes the acquisition of delayed protection, while transient adenosine A1 or A3 receptor activation fully recapitulates protection against infarction (but not against stunning or arrhythmias) 24 h later. Although nitric oxide is a co-trigger of delayed preconditioning, A1 agonist-induced delayed protection is independent of nitric oxide production. Adenosine receptor activation causes the activation of a complex protein kinase signalling cascade and, putatively, the subsequent activation of gene transcription. The induction or post-translational regulation of several proteins is associated with A1 agonist-induced delayed protection. These include the mitochondrial manganese-conjugated superoxide dismutase, and the 27-kDa heat shock protein. Opening of KATP channels during the index ischaemic event is an obligatory downstream event mediating A1 and A3 agonist induced delayed protection. However, the mechanism of sub-acute regulation of KATP channels following adenosine receptor activation is unknown. Evidence for induction of inducible nitric oxide synthase as a distal mechanism of A1 agonist-induced delayed protection is equivocal.
IgE‐mediated allergy to recombinant human insulin in a diabetic
Authors: X Baur, J Bossert, F Koops
Journal: Allergy (2003)

A 63‐year‐old nonatopic female suffering from type II diabetes with severe local and systemic immediate‐type allergic reactions to injections of different recombinant human insulin products has been reported. Skin testing as well as IgE measurements not only proved immediate‐type sensitization to human insulin but also to porcine and bovine insulin which had never been administered and indicated immunological cross‐reactivity. Cross‐reactivity was proved by an IgE inhibition test. Independent of this reaction, the patient showed IgE‐mediated sensitization to protamine.
Like the perfect animal, there's no such thing as the perfect institution
Authors: Susanne Lohmann
Journal: Behavioral and Brain Sciences (2001)

Models of biological and political systems share in common an irreconcilable tension. They must extract the essential features of the system to make its workings comprehensible to the human observer, and yet the omitted underbrush is essential to the workings of the system. A good model accommodates both the workings of the system and the cognitive makeup of the observer.
Right Hemihepatectomy for Primary Hepatoma
Authors: A. Otaki, A. E. Read, J. Stubbs, H. Sculthorpe
Journal: BMJ (1960)

Ectromelia (mouse-pox) virus multiplying in mouse liver provides an excellent model for the study of the effect of a virus on the metabolism of its natural mammalian-host cell.In this host-virus system meta- bolic changes are accompanied by "unbalanced"* (purely cytoplasmic) growth of the cell.Some meta- bolic changes occurring in this system are compared with those occurring (a) in other virus-infected tissues: (b) in regenerating liver showing "balanced" (nuclear and cytoplasmic) growth; (c) in precancerous and cancerous livers showing abnormal growth; (d) in the livers of tumour-bearing animals; and (e) in the livers of embryonic and starved animals.No consistent pattern of changes of enzyme activities is observed in either virus-infected or neoplastic tissues, nor are the changes similar to those in the livers of embryonic or starved animals.A possible mechanism is suggested for the production of metabolic changes in virus-infected tissues.It is proposed that such changes occur as the result of more or less chance competition between virus nucleic acids and structurally similar host-cell nucleic acids which control, or form templates for, the synthesis of host enzymes.Some implications of this explanation are discussed with regard to various host-virus relationships.Since virus infection, metabolic change, and unbalanced cell growth may be associated, the hypothesis of nucleic-acid competition is considered in relation to neoplasia.Neoplastic transformation may involve a metabolic change and a change in surface character; both these changes clearly could be the result of a process similar to that occurring in virus infection.The lack of pattern in enzyme changes in various hepatic neoplasms may be the outcome of chance competitions between foreign nucleic acid and host-cell nucleic acid, some of which may be quite incidental to the underlying primary changes characteristic of neoplasia.Th's hypothesis is discussed in relation to the causation of tumours by known tumour-viruses and to " spontaneous " neoplasms, in whiclh at least some of the alterations involved may be due to nucleic-acid competitions.
Doctor wins seat in fight to save hospital
Authors: A. Gulland
Journal: BMJ (2001)

Richard Taylor, the doctor who took a parliamentary seat from a Labour minister in the battle to save his local hospital, has vowed that he will fight against the privatisation of the NHS.

Dr Taylor, a retired physician, caused the biggest upset of election night when he overturned a Labour majority of 6000 votes to take the seat of Wyre Forest in Worcestershire. He had fought his campaign to reverse the downgrading of Kidderminster Hospital, and it clearly captured the imagination of the electorate. Dr Taylor polled 28487 votes compared with sitting MP David Lock's 10857 votes.

Dr Taylor, who worked at the hospital for almost 25 …