tbuckley/cabot-search huggingface dataset:
The Effects of Polyunsaturated Fat vs Monounsaturated Fat on Plasma Lipoproteins: The Power of a Study
Authors: Mark M. Passey
Journal: JAMA (1990)

<h3>To the Editor.—</h3> It is amazing that despite all the attempts over the past few years to increase the appropriate use of statistics in the general medical literature, you have once again published an interventional trial with negative results with no discussion whatever of the power of the study to detect a difference in the study groups.<sup>1</sup> The following statement by Dreon et al<sup>1</sup>is simply false: "The present results in free-living men and women demonstrated that exchanging unsaturated fats within current guidelines in reduced- fat diets does not affect plasma total cholesterol or LDL [low-density lipoprotein] cholesterol levels." What is true is that the study failed to demonstrate an effect of exchanging unsaturated fats, but the authors do not discuss what the chance is that this was simply because the study groups were too small. I grant you that they did make one insufficient allusion to wide
Chronic hypocalcemia of vitamin D deficiency leads to lower intracellular calcium concentrations in rat hepatocytes.
Authors: M Gascon-Barré, P Haddad, S J Provencher, S Bilodeau, F Pecker, S Lotersztajn, S Vallières
Journal: Journal of Clinical Investigation (1994)

Several lines of evidence indicate that calcium deficiency is associated with cellular defects in many tissues and organs. Owing to the large in vivo gradient between ionized extra- and intracellular Ca2+ concentrations ([Ca2+]i), it is generally recognized that the prevailing circulating Ca2+ does not significantly affect resting cytosolic Ca2+. To probe the consequences of hypocalcemia on [Ca2+]i, a model of chronic hypocalcemia secondary to vitamin D (D) deficiency was used. Hepatocytes were isolated from livers of hypocalcemic D-deficient, of normocalcemic D3-repleted, or of normal control rats presenting serum Ca2+ of 0.78 +/- 0.02, 1.24 +/- 0.03, or 1.25 +/- 0.01 mM, respectively (P < 0.0001). [Ca2+]i was measured in cell couplets using the fluorescent probe Fura-2. Hepatocytes of normocalcemic D3-repleted and of normal controls exhibited similar [Ca2+]i of 227 +/- 10 and 242 +/- 9 nM, respectively (NS), whereas those of hypocalcemic rats had significantly lower resting [Ca2+]i (172 +/- 10 nM; P < 0.0003). Stimulation of hepatocytes with the alpha 1-adrenoreceptor agonist phenylephrine illicited increases in cytosolic Ca2+ leading to similar [Ca2+]i and phosphorylase a (a Ca(2+)-dependent enzyme) activity in all groups but in contrast to normocalcemia, low extracellular Ca2+ was often accompanied by a rapid decay in the sustained phase of the [Ca2+]i response. When stimulated with the powerful hepatic mitogen epidermal growth factor (EGF), hepatocytes isolated from hypocalcemic rat livers responded with a blunted maximal [Ca2+]i of 237.6 +/- 18.7 compared with 605.2 +/- 89.9 nM (P < 0.0001) for their normal counterparts, while the EGF-mediated DNA synthesis response was reduced by 50% by the hypocalcemic condition (P < 0.03). Further studies on the possible mechanisms involved in the perturbed [Ca2+]i homeostasis associated with chronic hypocalcemia revealed the presence of an unchanged plasma membrane Ca2+ ATPase but of a significant decrease in agonist-stimulated Ca2+ entry as indicated using Mn2+ as surrogate ion (P < 0.03). Our data, thus indicate that, in rat hepatocytes, the in vivo calcium status significantly affects resting [Ca2+]i, and from this we raise the hypothesis that this lower than normal [Ca2+]i may be linked, in calcium disorders, to inappropriate cell responses mediated through the calcium signaling pathway as illustrated by the response to phenylephrine and EGF.
Correlative Radionuclide and Magnetic Resonance Imaging in Evaluation of the Spine
Authors: DOMINIQUE DELBEKE, THOMAS A. POWERS, MARTIN P. SANDLER
Journal: Clinical Nuclear Medicine (1989)

The authors retrospectively compared magnetic resonance images and bone scintigraphy obtained from 144 patients. Fifty-six patients having a known primary malignancy were evaluated for metastases (Group 1), and 88 patients were evaluated for back pain (Group 2). Interpretation was normal in 36/144 patients (11 in Group 1 and 25 in Group 2), and similar abnormal foci were visualized in the osseous spine in 54/144 patients (32 in Group 1 and 22 in Group 2). Magnetic resonance imaging showed abnormalities in the osseous spine that were not visualized on bone scintigraphy in 43/144 patients (10 in Group 1 and 33 in Group 2); these included bone metastasis, benign neoplasm (hemangioma), Schmorl's node, intervertebral disk disease, and bone disease (osteophyte, spondylolisthesis, facet hypertrophy). In addition, magnetic resonance imaging showed epidural or paravertebral extension of the tumor or infection in 37/144 patients (30 in Group 1 and 7 in Group 2). Bone scintigraphy demonstrated abnormalities not visualized on magnetic resonance imaging in 11/144 patients (3 in Group 1 and 8 in Group 2). Bone scintigraphy showed abnormalities in locations not evaluated by magnetic resonance imaging but relevant to the symptomatology or disease in 42/144 patients (37 in Group 1 and 5 in Group 2). These data indicate that magnetic resonance imaging and bone scintigraphy are complementary. Bone scintigraphy remains the best screening procedure to show the location of abnormal areas in the spine and elsewhere in the skeleton. Magnetic resonance imaging is useful in differentiating neoplasm, infection, intervertebral disk disease, and, in some instances, degenerative bone disease.
The junctional adhesion molecule JAM-C regulates polarized transendothelial migration of neutrophils in vivo
Authors: Abigail Woodfin, Mathieu-Benoit Voisin, Martina Beyrau, Bartomeu Colom, Dorothée Caille, Frantzeska-Maria Diapouli, Gerard B Nash, Triantafyllos Chavakis, Steven M Albelda, G Ed Rainger, Paolo Meda, Beat A Imhof, Sussan Nourshargh
Journal: Nature Immunology (2011)
BUBONIC PLAGUE IN MANILA
Authors: A. P. GOFF
Journal: JAMA (1913)

After an absence of six years plague again appeared in Manila in June, 1912. Between that date and the present—March, 1913—there have been fifty-five cases, twenty-two of them having occurred in October. The way in which the disease entered Manila is not known certainly, but as there had been a good deal of plague in China for some time before June, 1912, it is presumed that an infected rat came ashore from some boat from the mainland. It is impossible to guard against this danger absolutely. In the rat-poisoning and rat-catching operations which have been carried on, remarkably few infected animals have been found, which of course accounts for the comparatively few human cases reported, and leads to the belief that no serious epidemic will occur in Manila.  All of the cases, except two in the Walled City (Intramuros), have been on the north side of the Pasig River, which
Clinical trial with Ambilhar in Schistosoma mansoni infections in Tanzania.
Authors: J. E. McMahon, C. P. Kilala
Journal: BMJ (1966)

Pathogens in Acrylic Resin-Towers MEDICALJOSHRNAL 1047 of this organism was possible up to 14 days with a two-minute daily shake of the monomer/test-culture mixture.These results confirmed those made by one of the makers (private com- munication).It is probable that the watery film acts as a protective layer round the micro-organisms, as the broth culture and monomer are immiscible liquids.Neither monomer dried on filter paper or applied directly in a ditch nor resin discs had any direct inhibitory action towards any of the test organisms when tested routinely.This is at variance with the findings of Sokolowski et al. (1955), who reported "remarkable bacteriostatic activity" with the Czech product Spofacryl.An 18-hour culture of coagulase-positive staphylococcus scraped from an agar plate direct into monomer resulted in the formation of a brittle residue which was incubated in the monomer for 24 hours at 370 C.This residue, plated out, gave no growth after 18 hours' incubation, but the residue appeared to be more friable and then spread easily.The test organism was recovered after reincubation for a further period of 18 hours.None of the other test organisms survived in this test.B. cereus was not used, as it had shown prolonged survival in broth culture and monomer.
Molecular phylogenetic evidence of cytotoxic T lymphocyte (CTL) selection on human immunodeficiency virus type 1 (HIV-1)
Authors: J. da Silva, A. L. Hughes
Journal: Molecular Biology and Evolution (1999)

The interactions between cells of the vertebrate immune system and pathogens offer exceptional opportunities to study natural selection at the molecular genetic level.In the case of cell-mediated immunity, infected host cells are detected and killed by the host's cytotoxic T lymphocytes (CTLs).CTLs detect infection when they recognize specific intracellularly processed foreign peptides (epitopes) presented on a cell's surface by the protein products of class I major histocompatibility complex (MHC) loci.These peptides are typically 8-10 residues long and may be derived from the proteins of an infecting intracellular pathogen.Which peptides are presented is determined by the host's class I MHC genotype, since different alleles at different loci encode molecules that bind (restrict) different peptides.Whether a CTL recognizes a foreign peptide that is presented depends on whether the CTL is descended from a lineage of lymphocytes whose production was stimulated in response to the peptide, or perhaps a very similar peptide.Therefore, CTLs are a potential source of selection of amino acid replacements in epitope regions that interfere with either MHC binding or CTL recognition.The view that CTLs are an important source of selection on human immunodeficiency virus type 1 (HIV-1), the causative agent of acquired immunodeficiency syndrome (AIDS), is controversial.However, this view is supported by observations of HIV-1 epitope variants increasing in frequency in a patient when the epitopes are not recognized by the patient's CTLs (reviewed by McMichael and Phillips 1997).Clearly, the resolution of the role of CTLs is important for a basic understanding of host-virus interactions and for the development of vaccines.Here, we present molecular phylogenetic evidence of CTL selection on the major proteins of HIV-1 strain C18MBC.This was possible because the class I human leukocyte antigen (HLA) (i.e., human MHC) genotype of the patient in our study was known and because HIV-1 peptides restricted by the common class I HLA molecules have been described.C18MBC was isolated from a patient who showed no symptoms of AIDS for more than 10 years after infection.The complete genome shows large deletions in the functionally important nef gene, but the other eight genes, including the major structural and enzymatic
Hematin-derived anticoagulant. Generation in vitro and in vivo.
Authors: R L Jones
Journal: The Journal of Experimental Medicine (1986)

Prolongation of clotting times produced by hematin was investigated both in vitro and in vivo. Hematin-derived anticoagulant (HDA) was found to be due to a degradative product or derivative of hematin, and was generated in vitro in standing (aging) aqueous solutions of the parent compound. Generation of HDA in vitro was inhibited by antioxidants. The anticoagulant effect of HDA was inhibited by freshly prepared hematin, fresh Sn-protoporphyrin, imidazole, or the iron chelator desferrioxamine. Ferrioxamine did not inhibit HDA, and inhibition by imidazole was reversed with ferric citrate, suggesting a role for iron in the mechanism of HDA activity. HDA activity was dissociated from hematin in plasma by clotting with thrombin. HDA segregated into the clot fraction, whereas hematin remained largely in the serum fraction, suggesting that HDA may preferentially bind to fibrinogen. TLC and HPLC showed a single peak of HDA activity that was not associated with the parent compound. Evidence for HDA generation in vivo was found when rats were injected with fresh (no HDA) hematin. Prolongation of clotting times appeared after hematin appeared in the plasma, and anticoagulant activity persisted after a fall in plasma hematin concentration. Thus, there was a temporal dissociation between hematin and HDA, suggesting that a modification of hematin must occur in vivo before an anticoagulant effect is produced. Generation of HDA in vitro has implications for hematin preparation and administration. Generation of HDA in vivo suggests that similar modifications of endogenous heme or other porphyrins may occur to produce HDA under physiologic or pathophysiologic conditions.
Assessment of pre- and postnatal exposure to polychlorinated biphenyls: lessons from the Inuit Cohort Study.
Authors: Pierre Ayotte, Gina Muckle, Joseph L Jacobson, Sandra W Jacobson, Eric Dewailly
Journal: Environmental Health Perspectives (2003)

Polychlorinated biphenyls (PCBs) are food-chain contaminants that have been shown to induce adverse developmental effects in humans. In the course of an epidemiologic study established to investigate neurodevelopmental deficits induced by environmental PCB exposure in the Inuit population of northern Québec (Nunavik, Canada), we compared three biomarkers of prenatal exposure and models to predict PCB plasma concentration at 6 months postpartum. Concentrations of 14 PCB congeners were measured by high-resolution gas chromatography with electron capture detection in lipids extracted from maternal plasma, cord plasma, breast milk (collected at approximately 1 month postpartum), and 6-month-old infant plasma samples. Similar congener profiles were observed in all biologic samples, and PCB-153, the most abundant and persistent PCB congener, was strongly correlated with other frequently detected PCB congeners in all biologic media. When expressed on a lipid basis, maternal plasma, cord plasma, and milk concentrations of this congener were strongly intercorrelated, indicating that PCB concentration in any of these biologic media is a good indicator of prenatal exposure to PCBs. A multivariate model that included maternal PCB-153 plasma lipid concentration, breast-feeding duration, and the sum of two skin-fold thicknesses (an index of infant body fat mass) explained 72% of PCB-153 plasma concentration variance at 6 months postpartum (p < 0.001). By contrast, based on the product of breast-feeding duration times the concentration of PCBs in plasma lipids, which was used as an index of postnatal PCB exposure in several studies, only 36% of infant plasma concentration was explained.
Case-control study of prescribed fenoterol and death from asthma in New Zealand, 1977-81.
Authors: N Pearce, J Grainger, M Atkinson, J Crane, C Burgess, C Culling, H Windom, R Beasley
Journal: Thorax (1990)

A previous New Zealand case-control study of asthma deaths in the 5-45 year age group during 1981-3 found that prescription of fenoterol (by metered dose inhaler) was associated with an increased risk of death in patients with severe asthma. One major criticism of this study was that drug data for the cases and controls came from different sources. A new case-control design has been used to evaluate the same hypothesis, with a different set of asthma deaths, the same source for drug information being used for both cases and controls. This depended on identifying deaths from asthma during 1977-81 from national mortality records, and ascertaining which patients from those who died had been admitted to a major hospital for asthma during the 12 months before death. The study was confined to this subgroup, which accounted for about 20% of all asthma deaths in the areas served by a major hospital. For each of the eligible patients who died four age matched controls were selected from patients admitted to hospital for asthma during the year that the death occurred who had also had an admission for asthma in the previous 12 months. For the 58 cases and 227 control subjects information on prescribed drugs was collected from the hospital records relating to the previous admission. The odds ratio of asthma death in patients prescribed inhaled fenoterol was 1.99 (95% confidence interval 1.12-3.55, p = 0.02). As in the previous study, subgroups defined by markers of chronic asthma severity were also considered. The inhaled fenoterol odds ratio was 2.98 (95% CI 1.15-7.70, p = 0.02) in patients prescribed three or more categories of asthma drugs, 3.91 (95% CI 1.79-8.54, p less than 0.01) in patients with a previous admission for asthma in the past 12 months, and 5.83 (95% CI 1.62-21.0, p = 0.01) in patients prescribed oral corticosteroids at the time of admission. In patients with the most severe asthma (defined by a previous admission for asthma during the past 12 months and prescribed oral corticosteroids at time of admission) the inhaled fenoterol odds ratio was 9.82 (95% CI 2.23-43.4, p less than 0.01). These findings add further support to the hypothesis that inhaled fenoterol increases the risk of death in patients with severe asthma.
Cancer Cell Profiling by Barcoding Allows Multiplexed Protein Analysis in Fine-Needle Aspirates
Authors: Adeeti V. Ullal, Vanessa Peterson, Sarit S. Agasti, Suan Tuang, Dejan Juric, Cesar M. Castro, Ralph Weissleder
Journal: Science Translational Medicine (2014)

Barcoding technology enabled measurement of hundreds of cellular proteins from cancer patients with single-cell resolution.
Chemotherapy-induced hepatitis B reactivation in lymphoma patients with resolved HBV infection: A prospective study
Authors: Chiun Hsu, Hsiao-Hui Tsou, Shyh-Jer Lin, Ming-Chung Wang, Ming Yao, Wen-Li Hwang, Woei-Yau Kao, Chang-Fang Chiu, Sheng-Fung Lin, Johnson Lin, Cheng-Shyong Chang, Hwei-Fang Tien, Tsang-Wu Liu, Pei-Jer Chen, Ann-Lii Cheng
Journal: Hepatology (2013)

Fatal hepatitis B virus (HBV) reactivation in lymphoma patients with "resolved" HBV infection (hepatitis B surface antigen [HBsAg] negative and hepatitis B core antibody [anti-HBc] positive) can occur, but the true incidence and severity remain unclear. From June 2009 to December 2011, 150 newly diagnosed lymphoma patients with resolved HBV infection who were to receive rituximab-CHOP (cyclophosphamide, doxorubicin, vincristine, prednisolone)-based chemotherapy were prospectively followed. HBV DNA was checked at baseline, at the start of each cycle of chemotherapy, and every 4 weeks for 1 year after completion of rituximab-CHOP chemotherapy. Patients with documented HBV reactivation were treated with entecavir at a dosage of 0.5 mg/day for 48 weeks. HBV reactivation was defined as a greater than 10-fold increase in HBV DNA, compared with previous nadir levels, and hepatitis flare was defined as a greater than 3-fold increase in alanine aminotransferase (ALT) that exceeded 100 IU/L. Incidence of HBV reactivation and HBV-related hepatitis flares was 10.4 and 6.4 per 100 person-year, respectively. Severe HBV-related hepatitis (ALT >10-fold of upper limit of normal) occurred in 4 patients, despite entecavir treatment. Patients with hepatitis flare exhibited significantly higher incidence of reappearance of HBsAg after HBV reactivation (100% vs. 28.5%; P=0.003). In lymphoma patients with resolved HBV infections, chemotherapy-induced HBV reactivation is not uncommon, but can be managed with regular monitoring of HBV DNA and prompt antiviral therapy. Serological breakthrough (i.e., reappearance of HBsAg) is the most important predictor of HBV-related hepatitis flare. (Hepatology 2014;59:2092-2100).
Insulin Response in Relation to Insulin Sensitivity: An Appropriate β-Cell Response in Black South African Women
Authors: Julia H. Goedecke, Estelle V. Lambert, Naomi S. Levitt, Tommy Olsson, Jonathan R. Seckl, Brian R. Walker, Steven E. Kahn
Journal: Diabetes Care (2009)

e are in agreement with Joffe and Distiller (1) that the pathogenesis of type 2 diabetes in black South Africans cannot be inferred from limited studies of insulin responses in small cross-sectional studies.In our cross-sectional study, we only examined black and white premenopausal normoglycemic South African women to determine whether there were differences in insulin sensitivity and ␤-cell function in the absence of the potential confounding effects of hyperglycemia.We thus did not extrapolate our findings to diabetic individuals, but rather recommended "longitudinal studies to determine whether the ␤-cell will continue to compensate in the black women with increasing age or whether it will fail over time leading to disturbances in glucose tolerance" (2).
Aerosol derived airway morphometry in healthy subjects
Authors: P Brand, C Rieger, T Beinert, J Heyder
Journal: European Respiratory Journal (1995)

Monodisperse aerosol particles can be used to non-invasively probe intrapulmonary airspace dimensions. In this study, the aerosol-derived airway morphometry technique was used to study airspace dimensions in 79 healthy subjects, in order to assess reference data for the future clinical application of aerosol-derived airway morphometry, and to investigate the effect of lung inflation, anthropometric, and lung function parameters on aerosol-derived airway morphometry. Intrapulmonary airspace dimensions were assessed by measuring the deposition of monodisperse, hydrophobic submicron aerosol particles during breathholding. Additionally, measurements of spirometric and body plethysmographic lung function were performed. Airspace dimensions were in good agreement with morphometric lung data. Airspace dimensions increased with increasing lung inflation. Interindividual variation of airspace dimensions was lowest in the lung periphery, at high levels of lung inflation, and when the volumetric lung depth was normalized to the end-inspiratory lung volume. Analysis of variance showed an increase of airspace dimensions with age. The results of this study indicate that aerosol-derived airway morphometry is dependent on the level of lung inflation and the age of the subject. These results suggest that in contrast to conventional lung function techniques, aerosol-derived airway morphometry might be a powerful tool for the detection of small changes in peripheral airway geometry.
Trends in cerebral palsy in Western Australia.
Authors: I. MacGillivray
Journal: BMJ (1992)

I have knowledge of 50 deaths (this includes unpublished cases from personal communica- tions).The problem is sporadic and rare; because the consequences are so devastating for the patient, however, the medical and nursing staff managing patients with central venous catheters must prevent air gaining access to the venous circulation.4"
TEMPORARY LOSS OF VOICE FOLLOWING THYROIDECTOMY
Authors: DONALD GUTHRIE
Journal: JAMA (1918)

The temporary loss of voice following thyroidectomy is a complication that gives the surgeon in his early thyroid work an untold amount of anxiety and worry. There are several distinct causes of this complication, which if appreciated by the operator will greatly lessen the liability of its occurrence; but in spite of this, the experienced surgeon will occasionally be greatly disturbed by one of his patients who loses her voice after operation, and who is husky or speechless for months following. The causes of temporary loss of voice may be put under four headings: (1) trauma to the inferior recurrent laryngeal nerves; (2) trauma to the larynx and trachea; (3) syphilis, and (4) hysteria. Trauma to the nerve should be prevented whenever possible—trauma that is caused by pinching with clamps; including the nerve by suture in tying off vessels or catching it in suturing; and stretching the nerve in its