tbuckley/cabot-search huggingface dataset:
Effects of Methamphetamine Dependence and HIV Infection on Cerebral Morphology
Authors: Terry L. Jernigan, Anthony C. Gamst, Sarah L. Archibald, Christine Fennema-Notestine, Monica Rivera Mindt, Thomas L. Marcotte, Robert K. Heaton, Ronald J. Ellis, Igor Grant
Journal: American Journal of Psychiatry (2005)

The authors examined the separate and combined effects of methamphetamine dependence and HIV infection on brain morphology.Morphometric measures obtained from magnetic resonance imaging of methamphetamine-dependent and/or HIV-positive participants and their appropriate age- and education-matched comparison groups were analyzed. Main effects of age, HIV infection, methamphetamine dependence, and the interactions of these factors were examined in analyses of cerebral gray matter structure volumes.Independent of the effect of age, HIV infection was associated with reduced volumes of cortical, limbic, and striatal structures. There was also some evidence of an interaction between age and HIV infection such that older HIV-positive participants suffered disproportionate loss. Methamphetamine dependence was surprisingly associated with basal ganglia and parietal cortex volume increases, and in one of these structures-the nucleus accumbens-there appeared to be a larger effect in younger methamphetamine abusers. Neurocognitive impairment was associated with decreased cortical volumes in HIV-positive participants but with increased cortical volumes in methamphetamine-dependent participants.These results suggest significant brain structure alterations associated with both HIV infection and methamphetamine dependence. The regional patterns of the changes associated with these factors were distinct but overlapping, and the effects on brain volumes were opposing. Although the results of the present study provide little information about the specific mechanisms leading to the unexpected methamphetamine effects, they may be related to glial activation or neuritic growth, both of which have been associated with methamphetamine exposure in animal studies. These results have implications for the interpretation of brain morphological findings in methamphetamine-dependent, HIV-positive individuals, a group whose numbers are unfortunately increasing.
Advances in sonographic scoring of rheumatoid arthritis
Authors: Sarah Ohrndorf, Marina Backhaus
Journal: Annals of the Rheumatic Diseases (2012)

Accurate assessment of disease activity and joint damage in rheumatoid arthritis (RA) is important for monitoring treatment efficiency and for prediction of the outcome of the disease. Therefore, a reliable imaging method needs to be used. Musculoskeletal ultrasound (US) is a sensitive method for the detection of both early inflammatory soft tissue lesions (eg, synovitis, tenosynovitis, and bursitis) and early bone lesions (eg, erosions) in arthritic joint diseases and correlates well with MRI. Several musculoskeletal US scores are used for monitoring RA disease activity. Different qualitative (0/1) and semiquantitative (0–3) systems and quantitative measurements are used. The semiquantitative four-grade system developed by Skudlarek <i>et al</i>, which evaluates joint effusion, synovial thickening, bone erosion and power Doppler activity, is used most often. The new seven-joint ultrasound (US7) score is the first US sum score system which combines soft tissue (synovitis and tenosynovitis/paratenonitis) and destructive lesions (erosions) in a composite scoring system. The US7 score provides a fast overview of disease activity in daily rheumatological practice. This article reviews different US scores and sum scoring systems and current and proposed activity in this field.
Evaluation of disease activity in rheumatic patients by leucocyte adhesiveness/aggregation.
Authors: S Berliner, M Fried, D Caspi, A Weinberger, M Yaron, J Pinkhas, M Aronson
Journal: Annals of the Rheumatic Diseases (1988)

Previous work has shown that leucocyte adhesiveness/aggregation (LAA), as measured by the leukergy test, correlates well with disease severity in rheumatic patients. As LAA is probably a manifestation of the acute phase reaction various components of the acute phase reaction were measured in order to identify the best marker of disease activity. In addition to LAA, the following variables were measured in 79 patients with various rheumatic diseases and in 10 controls: white blood cell and platelet counts, erythrocyte sedimentation rate, haptoglobin, fibrinogen, C reactive protein, albumin, globulin, caeruloplasmin, alpha 1, alpha 2, beta, and gamma globulin, and haemoglobin concentrations. Patients were graded according to the state of their disease as mild, moderate, or severe. The extent of leucocyte adhesiveness/aggregation in peripheral blood proved to be the best laboratory variable for the grading of disease activity. Correct grading was obtained in 63% of the patients by means of the LAA, compared with 48% with C reactive protein, 41% with caeruloplasmin, 40% with haptoglobin, and 32% with haemoglobin. It is suggested that LAA of the peripheral blood during inflammation may be used as a reliable marker of disease severity.
Use of gene-modified virus-specific T lymphocytes to control Epstein-Barr-virus-related lymphoproliferation
Authors: C.M Rooney, C.Y.C Ng, S Loftin, C.A Smith, C Li, R.A Krance, M.K Brenner, H.E Heslop, C.M Rooney, M.K Brenner, M.K Brenner, R.A Krance, H.E Heslop
Journal: The Lancet (1995)
Restoration of cerebrovascular CO2 responsivity by glutamine synthesis inhibition in hyperammonemic rats.
Authors: H Takahashi, R C Koehler, T Hirata, S W Brusilow, R J Traystman
Journal: Circulation Research (1992)

Hyperammonemia increases brain glutamine levels, causes astrocytic swelling, and depresses cerebral blood flow (CBF) responsivity to CO2. Methionine sulfoximine (MSO) inhibition of glutamine synthetase activity, known to be enriched in astrocytes, prevents ammonia-induced increases in brain glutamine and water content. We tested the hypothesis that inhibition of glutamine accumulation restores CBF responsivity to CO2 during acute hyperammonemia. Pentobarbital-anesthetized rats treated with either vehicle or MSO (150 mg/kg i.p.) received a 6-hour intravenous infusion of either sodium or ammonium acetate. With subsequent induction of hypercapnia, CBF increased from 113 +/- 14 (mean +/- SEM) to 194 +/- 9 ml/min per 100 g in control rats but was unchanged from 107 +/- 13 to 79 +/- 10 ml/min per 100 g in hyperammonemic rats. Treatment with MSO in hyperammonemic rats restored the CBF response to hypercapnia (from 73 +/- 8 to 141 +/- 14 ml/min per 100 g). With induction of hypocapnia, CBF decreased from 114 +/- 11 to 88 +/- 11 ml/min per 100 g in control rats but increased from 112 +/- 13 to 142 +/- 19 ml/min per 100 g in hyperammonemic rats. Treatment with MSO in hyperammonemic rats did not fully restore the response to hypocapnia but prevented the paradoxical increase in CBF (from 80 +/- 8 to 80 +/- 8 ml/min per 100 g). In control rats, MSO did not affect CO2 responsivity. Treatment with MSO prevented ammonia-induced increases in intracranial pressure. Hyposmotic-induced increases in brain water content and intracranial pressure attenuated the CBF response to hypercapnia but, unlike hyperammonemia, did not attenuate the response to hypocapnia. In contrast to hypercapnia, vasodilation in response to arterial hypotension was intact in hyperammonemic rats. We conclude that the grossly abnormal CBF responsivity to CO2 alterations during hyperammonemia is linked to glutamine accumulation rather than ammonia per se. Cerebral edema secondary to glutamine accumulation may contribute in part to abnormal CBF responses, although other aspects of astrocyte dysfunction are likely to be important.
Tumor Origin of Endothelial Cells in Human Neuroblastoma
Authors: Annalisa Pezzolo, Federica Parodi, Maria Valeria Corrias, Roberta Cinti, Claudio Gambini, Vito Pistoia
Journal: Journal of Clinical Oncology (2007)

Purpose Malignant cells are genetically unstable and prone to develop chemotherapy resistance, whereas tumor vasculature is usually of host origin and genetically stable. Tumor endothelial microvessels attract interest as therapeutic targets, but their genetic instability would curtail such approach. Here, we have investigated the tumor origin of endothelial microvessels in human neuroblastoma (NB). Materials and Methods Paraffin-embedded tissue sections from 10 MYCN-amplified tumors (six stage 4, three stage 3, and one stage 1) were studied. Endothelial cells (ECs) were detected by immunofluorescent staining for CD31 or CD105, and MYCN amplification was detected using fluorescence in situ hybridization (FISH). In xenografts of the HTLA-230 human NB cell line, human ECs were detected by CD31 staining, mouse ECs were detected by CD34 staining, and MYCN amplification and murine DNA were detected using FISH. Results MYCN-amplified ECs formed approximately 70% of tumor endothelial microvessels in two stage 4 tumors and 20% in one stage 3 tumor. Similar results were obtained after EC labeling with CD31 or CD105. Staining for alpha-smooth muscle actin in combination with MYCN FISH demonstrated that tumor-derived ECs were coated with pericytes. These vessels were functional because they contained RBCs. Approximately 70% of endothelial vessels from HTLA-230 xenografts stained for human CD31, but not murine CD34, and displayed MYCN amplification, thus proving their tumor origin. Conclusion NB-associated endothelial microvessels can originate from tumor cells, and this finding challenges the tenet that tumor vasculature is genetically stable. The possibility that NB-derived ECs are chemotherapy resistant warrants further investigation.
Prevention of sudden cardiac death in athletes: new data and modern perspectives confront challenges in the 21st century
Authors: Jonathan Drezner, Babette Pluim, Lars Engebretsen
Journal: British Journal of Sports Medicine (2009)

The sudden death of a young athlete on the playing field remains the most devastating medical event in sports. The tragic impact of these events compels sports medicine professionals and sport governing bodies to develop and implement effective preventive strategies. In this issue, the British Journal of Sports Medicine and the International Olympic Committee (IOC) partner to present the most current information relevant to sudden cardiac death (SCD) in athletes. First in a series of quarterly BJSM-IOC issues devoted to injury prevention and health protection in athletes, this issue is dedicated to preventing the worst injury of all: sudden death.

The objective of this issue is to highlight cardiovascular diseases in athletes through a compilation of commissioned reviews and original investigations authored by international experts in sports cardiology and sports medicine. The issue provides modern perspectives and recent data in the areas of epidemiology, diagnosis, screening and management.

Prevention of SCD in athletes remains one of the most debated topics in sports medicine. What is the most appropriate strategy to screen athletes for underlying cardiovascular disease? Does the presence of automated external defibrillators (AEDs) at athletic events effectively treat young athletes who experience sudden cardiac arrest (SCA)? The complexities surrounding these questions are addressed in several reports presented in this issue.

The screening debate is centred on the inclusion …
Comparative Genomic and Phylogenetic Analyses of Calcium ATPases and Calcium-Regulated Proteins in the Apicomplexa
Authors: Kisaburo Nagamune, L. David Sibley
Journal: Molecular Biology and Evolution (2006)

The phylum Apicomplexa comprises a large group of early branching eukaryotes that includes a number of human and animal parasites. Calcium controls a number of vital processes in apicomplexans including protein secretion, motility, and differentiation. Despite the importance of calcium as a second messenger, very little is known about the systems that control homeostasis or that regulate calcium signaling in parasites. The recent completion of many apicomplexan genomes provides new opportunity to define calcium response pathways in this group of parasites in comparison to model organisms.
Surgery of the Ambulatory Patient.
Authors: Lewis Kraeer. Ferguson
Journal: Annals of Internal Medicine (1942)

<h2>Abstract</h2> The ambulatory treatment of surgical lesions has many advantages. The requirements in equipment are not great; the personnel must include at least one other person besides the operator. A practical knowledge of surgical technique and asepsis is necessary. Procaine solution has distinct advantages as a local anesthetic and has been used in 87 per cent of 1000 operations. Vinethene is the general anesthetic of choice because of its rapid induction and recovery and relative freedom from postanesthetic difficulties. The scope of surgery in the ambulatory patient includes operations upon superficial tumors and cysts, repair of minor deformities, the care of infections, anal lesions, and fractures of the arm and lower leg. Practical suggestions have been made concerning the treatment of these lesions
Deletion of Peg10, an imprinted gene acquired from a retrotransposon, causes early embryonic lethality
Authors: Ryuichi Ono, Kenji Nakamura, Kimiko Inoue, Mie Naruse, Takako Usami, Noriko Wakisaka-Saito, Toshiaki Hino, Rika Suzuki-Migishima, Narumi Ogonuki, Hiromi Miki, Takashi Kohda, Atsuo Ogura, Minesuke Yokoyama, Tomoko Kaneko-Ishino, Fumitoshi Ishino
Journal: Nature Genetics (2005)
Renal impairment associated with non-steroidal anti-inflammatory drugs.
Authors: J Unsworth, S Sturman, J Lunec, D R Blake
Journal: Annals of the Rheumatic Diseases (1987)

We have compared the renal function on admission and discharge of 22 patients routinely admitted to our rheumatology ward. None had previously diagnosed renal failure. Of 11 patients in whom we stopped long term non-steroidal anti-inflammatory drug (NSAID) therapy, all showed a rise in creatinine clearance (Ccr) after three to 28 days. In contrast, a control group comprising 11 similar patients who continued to receive NSAIDs showed no significant change. Recent work has suggested that it is possible to identify patients at risk of developing nephrotoxic side effects with NSAIDs. Based on these criteria (but excluding age alone as a risk), six patients from the first group and 10 from the second group would have been without risk. We infer from this that asymptomatic, reversible impairment of renal function is common, and that the potential clinical benefit from the use of NSAIDs should be balanced against this predictable toxicity.
S13 Incidence And Risk Factors For The Development Of Hospital Acquired Pneumonia In Older Hospitalised Patients
Authors: L. Burton, R. Price, K. Barr, S. McAuley, J. Allen, A. Clinton, G. Phillips, C. Marwick, M. McMurdo, M. Witham
Journal: Thorax (2014)

<h3>Introduction and objectives</h3> Older people are at risk of hospital-acquired pneumonia (HAP). Few data exist on the incidence or risk factors for HAP in non-intensive care patients. Our aim was to determine the incidence and key risk factors for HAP in a sample of older people. <h3>Methods</h3> A prospective survey of people &gt;65 years admitted to Acute Medical, Medicine for the Elderly and Orthopaedic wards in NHS Tayside (Dundee, UK) over a 12 month period. HAP was defined in accordance with the European and Scottish National Prevalence Survey of Healthcare Associated Infection and Antimicrobial Prescribing, June 2011. Key analyses included: incidence of case-defined HAP, risk factors for development using Cox regression analysis and the percentage of clinically diagnosed HAP that met the diagnostic criteria for case-defined HAP. <h3>Results</h3> A total of 1302 patients were included in the survey, 539 (41%) male, and mean age 82 years (SD 8). Median length of hospital stay was 14 days (IQR 20). 157 episodes of HAP were suspected clinically in 143 patients (incidence 10.9%), but only 83 episodes (53% of total) in 76 patients met the diagnostic criteria (incidence 5.8%). Case fatality rate was 29% in patients with confirmed HAP, and 19% in patients with suspected but not confirmed HAP. Risk of HAP increased by 0.3% per day spent in hospital. Swallowing problems were the single most important risk factor; HR 3.7 (95% CI 2.2 to 6.1, p &lt; 0.001). <h3>Conclusion</h3> HAP is common but overdiagnosed in older hospitalised patients. Older patients with swallowing problems have a greater risk of developing HAP. Given the high mortality rate, knock on effects on antibiotic use and length of hospital stay, ways of preventing HAP would be of potential importance to health services.
The effects of gadolinium, a stretch-sensitive channel blocker, on diaphragm muscle
Authors: C Coirault, MP Sauviat, D Chemla, JC Pourny, Y Lecarpentier
Journal: European Respiratory Journal (1999)

Stretch-activated channels (SAC) have been identified in many cell types including striated muscles. In diaphragm muscle, the influence of SAC on the length-active tension relationship remains unknown. Patch clamp experiments were performed on single fibres (n = 10). In isolated diaphragm muscle from adult hamsters, the effects of gadolinium (Gd3+), the most potent inhibitor of SAC blocker, on tension response to stretch at baseline were studied (n = 10), after pretreatment of the muscle with 1 nmol isoproterenol (n = 10), 0.5 micromol forskolin (n = 6), or 0.1 mmol dibutyryl cyclic adenosine monophosphate (cAMP) (n = 10). Results were compared to those obtained in low [Na+]e (n = 10), Ca2+-free medium (n = 6) or after 5 micromol nifedipine (n = 8). Gd3+ reduced active tension measured over a range of initial muscle lengths in a concentration-dependent manner (10 and 50 micromol). In isolated fibres, mechanical stretch generated a membrane current that was sensitive to Gd3+. In muscles, lowering [Na+]e mimicked the effects of Gd3+, while no change in the length-tension relationship was observed in Ca2+-free medium or after nifedipine. Drugs which increase cAMP prevented the effects of Gd3+ on active tension. In the diaphragm, gadolinium-sensitive channels are activated during physiological changes in length and influence tension development. Moreover, cyclic adenosine monophosphate content modulates the effects of gadolinium on stretch-activated channels.
Amiodarone pulmonary toxicity: functional and ultrastructural evaluation.
Authors: F L Liu, R D Cohen, E Downar, J W Butany, J D Edelson, A S Rebuck
Journal: Thorax (1986)

Pulmonary function, chest radiographic appearances, and the cellular composition of bronchoalveolar lavage fluid were assessed in 13 patients who were receiving amiodarone treatment. Eight of the patients had developed clinical and radiological evidence of lung disease and five were symptom free. The proportions of lymphocytes (mean 8.6 (SD 6.9)) and neutrophils (mean 3.4 (3.3)) obtained by bronchoalveolar lavage were similar in patients with and without lung complications. Electron microscopic examination of alveolar macrophages showed intralysosomal inclusion bodies in all subjects, regardless of clinical state. There was no significant difference in the mean number of inclusion bodies per macrophage transection between those with and those without lung disease. The differential cell count in bronchoalveolar lavage fluid and the presence of macrophage inclusion bodies were therefore not useful as markers of disease activity. Among those who developed clinical and radiological evidence of lung disease, the cumulative drug dose per kilogram of body weight and the duration of treatment (mean 16.5 (SD 9.0) months) were significantly correlated with the degree of lung restriction as measured by total lung capacity and forced vital capacity. It is concluded that, while the severity of the restrictive pulmonary defect that is induced by amiodarone is largely dose related, the development of lung toxicity is to some extent idiosyncratic.
Closed Visceral Injuries of Abdomen and Thorax
Authors: John H. Kennedy
Journal: JAMA (1967)

When a wound penetrates the abdomen or thorax the presence of internal visceral injury must be assumed. On the other hand, "closed" visceral injuries of the abdomen and thorax constitute special problems because the clinical manifestations may be unimpressive early in the postinjury period, as has been emphasized by Simeone.<sup>1</sup>Later, when symptoms develop, a severe physiological derangement may already exist and may compromise the results of therapy. It is the purpose of this presentation (1) to emphasize the importance of precise physiological assessment in preparation of the patient before major surgery required as a result of trauma, (2) to define the frequency of this clinical problem in a general hospital, and (3) to cite specific cases as illustrations of principles in management. <h3>Initial Therapy and Assessment</h3> In a military evacuation system this function is carried out continuously in a triage area. Blood volume replacement is initially started with
Left Ventricular Muscle Mass and Elevated Heart Rate Are Associated With Coronary Plaque Disruption
Authors: Ulrich E. Heidland, Bodo E. Strauer
Journal: Circulation (2001)

Plaque disruption is the central pathophysiological mechanism underlying acute coronary syndromes and the progression of coronary atherosclerosis. There exists only scant information about the factors that are associated with its development. The aim of the current study was to analyze the contribution of hemodynamic forces in the pathogenesis of plaque disruption. Plaque disruption was diagnosed by coronary angiography of stenosed but not completely occluded coronary arteries.This study retrospectively analyzed 106 patients who underwent 2 coronary angiography procedures within 6 months. We investigated 53 patients with initially smooth stenoses who developed plaque disruption by the time of the second coronary angiogram and compared these patients with 53 age- and sex-matched individuals with smooth stenoses without angiographic signs of plaque disruption. The 2 groups were compared by analyzing central hemodynamics, echocardiographic measurements, and cardiovascular medication use. Logistic regression analysis identified positive associations between plaque disruption, left ventricular muscle mass >270 g, and a mean heart rate >80 bpm and a negative association with the use of beta-blockers.The associations documented by our investigation indicate that hemodynamic forces may play a crucial role in the pathogenesis of plaque disruption. These findings may help to identify patients who are at an increased risk of plaque disruption and who might gain benefit from pharmacological interventions aimed at reducing heart rate, for example, by the use of beta-blockers, or a reduction of left ventricular hypertrophy.
Vitamin A, β-Carotene, and the Risk of Cancer: A Prospective Study&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: A Paganini-Hill, A Chao, R K Ross, B E Henderson
Journal: JNCI Journal of the National Cancer Institute (1987)

A cohort of 10,473 residents of Leisure World, Laguna Hills, CA, who were initially free of cancer were followed from 1981 to 1986. A health survey questionnaire completed by all cohort members included usual frequencies of consumption of certain food items, including vegetables, fruits, dairy products, liver, and cereal, as well as specific information on brand and formulation of vitamin supplements containing vitamins A, C, or E. Pathologic diagnosis of incident cancer was confirmed in 643 persons (56 lung, 110 colon, 59 bladder, 93 prostate, 123 female breast, and 202 cancers of other sites). Our study found little indication that increased intake of vitamin A or beta-carotene from the diet or supplements protects against the development of cancer overall. Dietary vitamin A intake was highly associated with smoking status; 25% of current smokers were in the highest third of dietary vitamin A consumption versus 32% of past smokers and 36% of never-smokers. In males who never smoked there was some indication that cancer rates decreased with increasing vitamin A intake, but the results were not statistically significant.