tbuckley/cabot-search huggingface dataset:
Very low density lipoproteins in intestinal lymph: role in triglyceride and cholesterol transport during fat absorption
Authors: Robert K. Ockner, Faith B. Hughes, Kurt J. Isselbacher
Journal: Journal of Clinical Investigation (1969)

The role of nonchylomicron very low density lipoproteins (VLDL, S(f) 20-400) in the transport of triglyceride and cholesterol was studied during lipid absorption. Various long chain fatty acids were infused intraduodenally in the form of mixed fatty acid-mono-olein-taurocholate micelles; control animals received saline or taurocholate. As compared with controls, all fatty acids (palmitic, oleic, linoleic) resulted in significant increases in chylomicron (S(f) > 400) triglyceride. In addition, palmitic acid resulted in a twofold increase in VLDL triglyceride, whereas with the absorption of oleic or linoleic acid VLDL triglyceride did not change significantly. Differences in triglyceride fatty acid composition between chylomicrons and VLDL were observed during lipid absorption. Although the absolute amount of endogenous cholesterol in intestinal lymph was not significantly affected by lipid absorption under these conditions, its lipoprotein distribution differed substantially among the lipid-infused groups. During palmitate absorption, VLDL cholesterol was similar to that in the taurocholate-infused controls, and was equal to chylomicron cholesterol. In contrast, during oleate and linoleate absorption the VLDL cholesterol fell markedly, and was less than half of the chylomicron cholesterol in these groups. The half-time of plasma survival of VLDL cholesterol-(14)C was found to be twice that of chylomicron cholesterol-(14)C. These studies demonstrate that dietary long chain fatty acids differ significantly in their effects upon the transport of triglyceride and cholesterol by lipoproteins of rat intestinal lymph. These findings, together with the observed differences in rates of removal of chylomicrons and VLDL from plasma, suggest that variations in lipoprotein production at the intestinal level may be reflected in differences in the subsequent metabolism of absorbed dietary and endogenous lipids.
Human Erythrocytes Covered with Magnetic Core–Shell Nanoparticles for Multimodal Imaging
Authors: Mathieu Laurencin, Nithavong Cam, Thomas Georgelin, Olivier Clément, Gwennhael Autret, Jean‐Michel Siaugue, Christine Ménager
Journal: Advanced Healthcare Materials (2013)

Surface functionalization of human red blood cells (hRBCs) with fluorescent and magnetic silica core-shell nanoparticles is used to design a carrier suitable for multimodal imaging with a long circulating time. The coated magnetic hRBCs show no hemolytic activity, while the advantage of the affinity of proteins for silica allows a further coating. As a service to our authors and readers, this journal provides supporting information supplied by the authors. Such materials are peer reviewed and may be re-organized for online delivery, but are not copy-edited or typeset. Technical support issues arising from supporting information (other than missing files) should be addressed to the authors. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
Floods in Darfur prompt precautions against epidemic
Authors: Peter Moszynski
Journal: BMJ (2005)

Record levels of rainfall have added to the misery of the millions of people displaced by the Darfur crisis, raising concerns of a big increase in cases of malaria and the risk of an outbreak of cholera in the flooded camps, the World Health Organization has warned.

The organisation has launched new measures to control the diseases, arguing it is of ‘paramount importance’ to put a plan in place, “given the fact that all precursors for an outbreak …
NICE recommends cancer tests for unexplained blood clots
Authors: J. Wise
Journal: BMJ (2012)

Investigations for cancer should be carried out in patients aged over 40 who have a deep vein thrombosis or pulmonary embolism without an obvious cause, guidelines from the National Institute for Health and Clinical Excellence (NICE) recommend for the first time.

The recommendation has been made because the risk of blood clots is about four times greater in people with cancer than in those without. Cancer and thrombophilia are major risk factors for blood clots. Other risk factors include a history of deep venous thrombosis, age over 60 years, recent surgery or injury, obesity, prolonged travel, acute medical illness, immobility, and pregnancy.

Roshan Agarwal, a member of the Guideline Development Group and consultant medical oncologist at the Hammersmith Hospital, London, said: “One in 10 of all patients diagnosed with a blood clot has an underlying cancer. One in five cancer patients will …
A TNF- and c-Cbl-dependent FLIPS-degradation pathway and its function in Mycobacterium tuberculosis–induced macrophage apoptosis
Authors: Manikuntala Kundu, Sushil Kumar Pathak, Kuldeep Kumawat, Sanchita Basu, Gargi Chatterjee, Shresh Pathak, Takuya Noguchi, Kohsuke Takeda, Hidenori Ichijo, Christine B F Thien, Wallace Y Langdon, Joyoti Basu
Journal: Nature Immunology (2009)
Histological features 3 to 320 days after stenting of human saphenous vein bypass grafts
Authors: H.M.M. van Beusekom, P.W. Serruys, W.J. van der Giessen, B.H. Strauss, P.J. de Feyter, H. van Loon, R.J. van Suylen, H. Suryapranata, M.J. van den Brand
Journal: Journal of the American College of Cardiology (1991)
Assessment of Peripheral Vascular Disease in Diabetes: Report and Recommendations of an International Workshop Sponsored by the American Heart Association and the American Diabetes Association
Authors: Trevor J Orchard, D Eugene Strandness
Journal: Diabetes Care (1993)

Recognizing the considerable excess burden of both cerebrovascular disease and LEAD suffered by individuals with IDDM or NIDDM (1,2), a workshop was convened to 1) provide a current review of the knowledge pertaining to the prevalence, incidence, and risk factor associations of cerebrovascular disease and PVD in diabetes, and 2) review and make recommendations about the methodology for identifying and quantifying LEAD in both clinical and research settings.
Developmental toxicology: status of the field and contribution of the National Toxicology Program.
Authors: B A Schwetz, M W Harris
Journal: Environmental Health Perspectives (1993)

The NTP has conducted developmental toxicity studies on more than 50 chemicals, often in multiple species. Several chemicals caused developmental toxicity in the absence of any toxicity to the mother. Although hazard to humans is determined by the level of exposure to the chemical and its inherent toxicity, those agents that selectively disturb the development of the conceptus are of particular concern because other manifestations of toxicity would not warn the mother of overexposure. Whether the LOAEL (lowest-observed adverse effect level) for maternal toxicity was high or low did not correlate with the potential of chemicals to cause developmental toxicity. The form of developmental toxicity that determined the LOAEL most frequently was decreased body weight in mice and rats, but not rabbits, where the LOAEL was determined more often by an increase in resorptions. Several in vitro and short-term tests appear promising as screens to predict the outcome of developmental toxicity studies in mammals. However, the only screens that have undergone formal validation studies are those evaluated by the NTP. Improvements in our ability to predict risk to humans have been limited by our knowledge of the mechanisms by which agents cause developmental toxicity. Thus, future growth is dependent on a better understanding of the biological processes that regulate normal development, therein providing the necessary framework for understanding mechanisms of abnormal development.
Liver cell models in in vitro toxicology.
Authors: A Guillouzo
Journal: Environmental Health Perspectives (1998)

In vitro liver preparations are increasingly used for the study of hepatotoxicity of chemicals. In recent years their actual advantages and limitations have been better defined. The cell models, slices, and mainly primary hepatocyte cultures, appear to be the most powerful in vitro systems, as liver-specific functions and responsiveness to inducers are retained either for a few days or several weeks depending on culture conditions. Maintenance of phase I and phase II xenobiotic metabolizing enzyme activities allows various chemical investigations to be performed, including determination of kinetic parameters, metabolic profile, interspecies comparison, inhibition and induction effects, and drug-drug interactions. In vitro liver cell models also have various applications in toxicology: screening of cytotoxic and genotoxic compounds, evaluation of chemoprotective agents, and determination of characteristic liver lesions and associated biochemical mechanisms induced by toxic compounds. Extrapolation of the results to the in vivo situation remains a matter of debate. Presently, the most convincing applications of liver cell models are the studies on different aspects of metabolism and mechanisms of toxicity. For the future, there is a need for better culture conditions and differentiated hepatocyte cell lines to overcome the limited availability of human liver tissues. In addition, strategies for in vitro analysis of potentially toxic chemicals must be better defined.
Both increased and decreased platelet adhesion to thermally injured subendothelium is caused by denaturation of von Willebrand factor.
Authors: A N Bos, M J Post, P G de Groot, J J Sixma, C Borst
Journal: Circulation (1993)

Thermal angioplasty methods heat the arterial wall. We related platelet adhesion to the temperature to which subendothelium and purified adhesive proteins had been exposed.Cultured subendothelium, purified von Willebrand factor, collagen types I and III, or fibronectin was applied to glass coverslips. Coverslips were mounted on a heating device that applied a temperature gradient from 30 to 100 degrees C. De-endothelialized umbilical arteries were heated by immersion in phosphate-buffered saline. After cooling to room temperature, the surfaces were perfused with blood at 37 degrees C (shear rate, 1600 sec-1). Compared with 37 degrees C, platelet adhesion to endothelial cell matrix was significantly reduced by 25%, 50% or 75% after heating to 69 +/- 1 degree C (mean +/- SEM, P < .05), 72 +/- 1 degree C, or 75 +/- 1 degree C, respectively. Platelet coverage to umbilical artery subendothelium was in the same way significantly reduced after heating to 71 +/- 1 degree C, or 77 +/- 1 degree C, respectively. In contrast to endothelial cell matrix, however, heating to about 55 degrees C increased platelet coverage from 30 +/- 5% to 54 +/- 6% (P < .05). Both platelet adhesion to von Willebrand factor and monoclonal antibody binding against the GpIb binding site of von Willebrand factor showed a comparable temperature dependence as platelet adhesion to subendothelium, provided the proper von Willebrand factor concentration was used. Platelet adhesion to heated collagen types I and III was increased and maximal at 57 +/- 2 degrees C and 62 +/- 2 degrees C, respectively. Preincubation of collagen III with proteins resulted in decreased platelet adhesion with increasing temperatures. Heating did not affect the reactivity of fibronectin.In vitro platelet adhesion to human subendothelium is reduced by more than 50% after heating it briefly to more than 74 degrees C. Temperatures in excess of 80 degrees C reduce platelet adhesion by at least 85%. Thermal denaturation of von Willebrand factor is responsible not only for the decreased thrombogenicity above 71 degrees C but also for the increased thrombogenicity near 55 degrees C, provided that the von Willebrand factor concentration is low.
Identification of the lymphokine soluble immune response suppressor in urine of nephrotic children.
Authors: H W Schnaper, T M Aune
Journal: Journal of Clinical Investigation (1985)

Patients with minimal change nephrotic syndrome (MCNS) frequently have suppressed in vivo and in vitro immune responsiveness of uncertain etiology. Because increased suppressor cell activity has been associated with this disease, urines from MCNS patients were screened for activity of the lymphokine soluble immune response suppressor (SIRS), a product of concanavalin A- or interferon-activated suppressor T cells. Urines from untreated MCNS patients suppressed polyclonal plaque-forming cell responses of cultured splenocytes. This suppressive activity was identified as human SIRS by the following functional and physical criteria: molecular weight estimated by gel filtration; kinetics of suppression; inhibition of suppression by catalase, levamisole, and 2-mercaptoethanol; abrogation of activity by acid or protease treatment; elution pattern on high performance liquid chromatography; and cross-reactivity with monoclonal antimurine SIRS antibodies. Suppressive activity disappeared from urine after initiation of treatment but before remission of symptoms. Urines were tested from 11 patients with MCNS, all of whom excreted SIRS. In addition, two nephrotic patients with acute glomerulonephritis and three nephrotic patients with membranoproliferative disease excreted SIRS, but other nephrotics and all nonnephrotic patients did not. These results indicate that excretion of SIRS occurs in certain cases of nephrotic syndrome and that the presence of SIRS in the urine is not accounted for solely by the presence of proteinuria or nephrosis. Serum from four nephrotic patients also contained SIRS, whereas neither serum nor urine from six normal subjects contained SIRS activity. The systemic presence of SIRS in these four patients, and the identification of SIRS in urines from a larger group of patients, suggest a possible role for SIRS in the suppressed immune responses often found in nephrotic syndrome.
The orthopaedic approach to managing osteoarthritis of the knee
Authors: Sam Gidwani, Adrian Fairbank
Journal: BMJ (2004)

<b>Objectives:</b> To ascertain whether detailed isokinetic knee muscle testing reflects the results of other functional measurements in footballers and to look for any correlations between quadriceps tendon thickness and knee strength. <b>Methods:</b> Ultrasonographic evaluation of the quadriceps tendon (Hitachi EUB-405), isokinetic knee testing (Biodex System 3), and sprint measurements using telemetric photoelectric cells (Chronometre Prosport ESC TX02) were carried out on 29 elite footballers. Jumping capacity was evaluated using Bosco’s jumping mat (Ergojump). Anaerobic fitness was assessed by auricular capillary blood lactate measurements (YSI Model 1500 Sport Lactate Analyzer). <b>Results:</b> Quadriceps tendon thickness correlated positively with jumping and sprint measurements and negatively with extensor and flexor strength. However, these correlations did not reach statistical significance. There were significant correlations between knee extensor strength at 60 °/s and jumping or sprint measurements and between the extension acceleration values of both knees during isokinetic tests at 240 °/s and the sprint measurements. No significant correlation was found between the fatigue ratio values of both knees at 240 °/s and the calculated fatigue ratios from the sprint measurements. <b>Conclusions:</b> Apart from a few variables which correlated with the performance tests, the isokinetic studies did not fully predict the various functional measurements. Neither was there any relation between the quadriceps tendon measurements and the knee strength values nor with the functional performance.
Molecular and functional characterisation of hepatic slam CD229 and ITS implication in the development of hepatocellular carcinoma
Authors: H. Bouhlal, R. Nyga, F. Cartier, C. Ossart, L. Lamotte, D. Chatelain, J. P. Marolleau, K. Lassoued, H. Bouhlal
Journal: Gut (2011)

<h3>Introduction</h3> Hepatocarcinoma (HCC) is a cancer whose molecular mechanisms are still widely unknown. In this study, the authors show that the signalling lymphocyte activation molecule (SLAM) CD229 initially known to be expressed at the surface of certain immune cells, as well as its adaptor proteins SAP and EAT-2, are expressed in hepatocytes. A comparative analysis of the expression level of these proteins between normal and tumorous hepatocytes, together with an analysis of the function of the receptor, points to its potential role in the oncogenesis of hepatocarcinoma. <h3>Methods</h3> The expression of CD229 (mRNA and protein) in the samples (n=10) of normal liver and HCC collected on patients in the Digestive Surgery and Pathological Anatomy Units (Amiens Teaching Hospital) or in Huh-7 and Hep-G2 cell lines was assessed through flow cytometry, western blotting, confocal microscopy and real time PCR. The molecular interactions between CD229 and its protein partners have been analysed by co-immunoprecipitation. To end with, the study of the proliferation of the cells which do or do not express CD229 has been carried out through CFSE. <h3>Results</h3> The authors show for the first time the expression of the CD229 molecule in the hepatocytes, whose sequence is similar to that initially described in immune cells. The expression levels of CD229 are one fourth as high in Huh-7 and Hep-G2 cell lines as in normal hepatocytes. Similarly, the expression rate of CD229 decreases in tumorous cells compared to peri-tumorous cells in the same subject (n=10, p&lt;0.05). The authors also show the expression of SAP and EAT-2 proteins which play the role of adaptor molecule to initiate a signal transduction triggered by the activation of CD229. Hepatic CD229 also recruits tyrosine kinase Lyn – and not Fyn as previously shown in lymphocytes. Moreover, this receptor is functional because its stimulation divides the proliferation of Huh-7 cells by three at the utmost. <h3>Conclusion</h3> Our results highlight the specific expression as well as the functionality of SLAM CD229 receptor in hepatocytes. The low expression level of this receptor in HCC compared to normal hepatocytes, combined to its inhibiting effects on the proliferation of hepatocytes following its stimulation or over expression, points to its implication in the hepatic carcinogenesis process.
REPORT CXIV. TWO CASES OF JEJUNAL ULCER FOLLOWING GASTRO-JEJUNOSTOMY, IN ONE OF WHICH GASTRIC ANALYSIS WERE MADE BEFORE AND AFTER OPERATION FOR JEJUNAL ULCER
Authors: H. J. Paterson
Journal: BMJ (1909)

NOTWITHSTANDING all that has been written in recent years on the subject of gastro-jejunostomy, there remains at least one problem in connexion therewith in need of further investigation and elucidation.The fear of the possible occurrence of a jejunal ulcer still casts a shadow, faint, it is true, over the otherwise admirable results which follow this operation when performed in appro- priate cases.It is of the utmost importance that all instances of this condition should be published, in order that we may have all the available material from which to draw conclusions as to the etiology of this condition, as to the best methods of preventing it, and of treatment should it occur.The notes of the following case which has been under my care are of interest, as it is, so far as I can gather, the first case in which an attempt has been made to obtain an accurate analysis of the gastric contents, and of the fluid escaping from a jejunal fistula before and after operation for ulcer of the jejunum.CASE I.-Anterior Gastro-jejtnostomny for Pyloric Stenosis: Per- foration of a Jejunal Ulcer Fire Years later: Resection of Affected Portions of Jejuinuin, and Anterior Gastro-jejunostomy 11en Y."H. I., married, aged 47, was admitted into the London Temperance Hospital on August 21st, 1902, under the care of my colleague, Dr. Soltau Fenwick, suffering from pain after food, vomiting, and loss of flesh.The patient stated that she had always been healthy until two years previously, when she began to suffer from pain after food, which gradually increased in severity, and she had lost 3 st. in weight.For one year she had suffered from vomiting, usually two or three times weekly, large quantities of undigested food being brought up.On admission the patient was much wasted
Treatment with a Luteinizing Hormone–Releasing Hormone Agonist in Adolescents with Short Stature
Authors: Jack A. Yanovski, Susan R. Rose, Giovanna Municchi, Ora H. Pescovitz, Suvimol C. Hill, Fernando G. Cassorla, Gordon B. Cutler
Journal: New England Journal of Medicine (2003)

Treatment with a luteinizing hormone-releasing hormone (LHRH) agonist increases adult height in children with LHRH-dependent precocious puberty and is prescribed by some practitioners to augment height in short adolescents. We performed a randomized clinical trial to determine whether treatment with an LHRH agonist increases adult height in short adolescents with normally timed puberty.Fifty short adolescents (18 boys and 32 girls) with low predicted adult height (mean [+/-SD], 3.3+/-1.2 SD below the population mean) received either placebo (24 subjects) or an LHRH agonist (26 subjects). The mean (+/-SD) duration of treatment was 3.5+/-0.9 years in the LHRH-agonist group and 2.1+/-1.2 years in the placebo group (P<0.001). Adult height was measured when bone age exceeded 16 years in girls and 17 years in boys and when the rate of growth was less than 1.5 cm per year.Forty-seven adolescents (94 percent) were followed until they attained adult height. At the time adult height was achieved, the subjects who had been treated with an LHRH agonist were older than those who had received placebo (20.5+/-2.1 years vs. 18.0+/-2.5 years, P=0.01) and were taller (standard-deviation score, -2.2+/-1.1 vs. -3.0+/-1.2; P=0.01). Analysis of covariance showed that LHRH-agonist treatment resulted in an increase of 0.6 (95 percent confidence interval, 0.2 to 0.9) in the standard-deviation score for height, or an increase of 4.2 cm (95 percent confidence interval, 1.7 to 6.7), over the initially predicted adult height (P=0.01). Treatment with an LHRH agonist resulted in significantly greater adult height than did placebo in boys and girls, in adolescents with idiopathic short stature, and in those who had a growth-limiting syndrome. The principal adverse event in the LHRH-agonist group was decreased accretion of bone mineral density (mean lumbar vertebral bone mineral density at the time adult height was achieved, 1.6+/-1.2 SD below the population mean, vs. 0.3+/-1.2 SD below the population mean in the placebo group; P<0.001).Treatment with an LHRH agonist for 3.5 years increases adult height by 0.6 SD in adolescents with very short stature but substantially decreases bone mineral density. Such treatment cannot be routinely recommended to augment height in adolescents with normally timed puberty.
Re: Cellular Telephones and Cancer--a Nationwide Cohort Study in Denmark
Authors: B. Hocking
Journal: JNCI Journal of the National Cancer Institute (2001)

Re: Cellular Telephones and Cancer-a Nationwide Cohort Study in DenmarkJohansen et al. (1) have assessed the risk of cancer in Danish cellular telephone users.They conducted a retrospective cohort study of cancer incidence in 420 095 residential subscribers compared with national cancer data and found no excess of brain cancer or other cancers of primary interest.
478 Enotypes and viremia of hepatitis B and D viruses are associated with outcomes of chronic hepatitis D patients
Authors: C.W. Su, Y.H. Huang, T.I. Huo, H.H. Shih, I.J. Sheen, S.W. Chen, E.C. Lee, S.D. Lee, J.C. Wu
Journal: Journal of Hepatology (2006)