tbuckley/cabot-search huggingface dataset:
Liver failure induced by paracetamol.
Authors: J Spooner
Journal: BMJ (1993)

Hypokalaemia may increase the predisposition to lethal cardiac arrhythmias' and convulsions, especially in hypoxic patients with airways obstruction; serum potassium concentrations should therefore be monitored in every patient with established or suspected theophylline toxicity, and hypokalaemia should be corrected.
The Memphis State University Rubella Outbreak
Authors: Bernard Guyer, James W. Giandelia, Alan L. Bisno, William Schaffner, R. Beverly Ray, Robert C. Rendtorff, Robert H. Hutcheson
Journal: JAMA (1974)

During the spring of 1973, ninety-six cases of rubella occurred at Memphis State University. The epidemic remained confined to the University and did not involve elementary school children, who are the traditional source of infection for young adults. The epidemic occurred despite immunity levels of more than 80% in both the elementary school and college students. This outbreak and others recently reported in high schools and colleges suggest that rubella in these age groups may be a source of exposure for pregnant women.
Sorafenib Inhibits Imatinib-Resistant KIT and Platelet-Derived Growth Factor Receptor β Gatekeeper Mutants
Authors: Teresa Guida, Suresh Anaganti, Livia Provitera, Richard Gedrich, Elizabeth Sullivan, Scott M. Wilhelm, Massimo Santoro, Francesca Carlomagno
Journal: Clinical Cancer Research (2007)

Abstract Purpose: Targeting of KIT and platelet-derived growth factor receptor (PDGFR) tyrosine kinases by imatinib is an effective anticancer strategy. However, mutations of the gatekeeper residue (T670 in KIT and T681 in PDGFRβ) render the two kinases resistant to imatinib. The aim of this study was to evaluate whether sorafenib (BAY 43-9006), a multitargeted ATP-competitive inhibitor of KIT and PDGFR, was active against imatinib-resistant KIT and PDGFRβ kinases. Experimental Design: We used in vitro kinase assays and immunoblot with phosphospecific antibodies to determine the activity of sorafenib on KIT and PDGFRβ kinases. We also exploited reporter luciferase assays to measure the effects of sorafenib on KIT and PDGFRβ downstream signaling events. The activity of sorafenib on interleukin-3–independent proliferation of Ba/F3 cells expressing oncogenic KIT or its imatinib-resistant T670I mutant was also tested. Results: Sorafenib efficiently inhibited gatekeeper mutants of KIT and PDGFRβ (IC50 for KIT T670I, 60 nmol/L; IC50 for PDGFRβ T681I, 110 nmol/L). Instead, it was less active against activation loop mutants of the two receptors (IC50 for KIT D816V, 3.8 μmol/L; IC50 for PDGFRβ D850V, 1.17 μmol/L) that are also imatinib-resistant. Sorafenib blocked receptor autophosphorylation and signaling of KIT and PDGFRβ gatekeeper mutants in intact cells as well as activation of AP1-responsive and cyclin D1 gene promoters, respectively. Finally, the compound inhibited KIT-dependent proliferation of Ba/F3 cells expressing the oncogenic KIT mutant carrying the T670I mutation. Conclusions: Sorafenib might be a promising anticancer agent for patients carrying KIT and PDGFRβ gatekeeper mutations.
Protease inhibition and absorption enhancement by functional nanoparticles for effective oral insulin delivery
Authors: Fang-Yi Su, Kun-Ju Lin, Kiran Sonaje, Shiaw-Pyng Wey, Tzu-Chen Yen, Yi-Cheng Ho, Nilendu Panda, Er-Yuan Chuang, Barnali Maiti, Hsing-Wen Sung
Journal: Biomaterials (2012)
Hemoglobin — From F to A, and Back
Authors: John W. Adamson
Journal: New England Journal of Medicine (1984)

Worldwide, millions of peoples' lives are affected directly or indirectly by inherited abnormalities of the beta-globin chain. Most prominent among these abnormalities are sickle-cell anemia and beta-thalassemia (in which production of the beta-globin chain is vastly reduced or absent). Homozygous persons suffer from ineffective red-cell production and accelerated hemolysis. The markedly increased rate of erythropoiesis results in abnormalities of bone and extension of marrow into both bony and extramedullary sites that are not normally involved in hematopoiesis; in beta-thalassemia, there is massive hepatosplenomegaly.Although a great deal is known about these diseases at the molecular level and improvements in antenatal . . .
The immunological and cytochemical characterization of T‐cell lymphoproliferative diseases
Authors: T. J. Spira, E. W. Ades, D. S. Gordon
Journal: American Journal of Hematology (1981)

Abstract Surface markers, terminal transferase, cytochemical staining, and function of peripheral blood lymphocytes were examined in nine patients with T‐cell lymphoproliferative disease. Anti‐T‐cell antiserum proved useful in characterizing the phenotype of the abnormal cells when only a minority of the abnormal cells formed E‐rosettes. Anti‐B‐cell antiserum was consistently unreactive with the abnormal cells. Terminal transferase was elevated in T‐cell ALL but low in T‐cell CLL, lymphoma‐leukemia, or Sézary syndrome. Lymphocyte proliferative response to nonspecific mitogens was generally depressed as was the response to allogeneic cells. The cells also failed to stimulate in mixed lymphocyte culture, implying a lack of Ia antigens on their surface. Acid phosphatase stain was positive in the three patients tested. Peroxidase and esterase stains were negative, whereas PAS was positive in five of eight patients tested. Prognosis in general, regardless of the clinical picture, (ie, acute, chronic, or lymphoma‐leukemia), was poor with seven of the nine patients dying within 14 months of diagnosis. Therefore, the use of anti‐T‐cell antisera and the E‐rosette surface marker should be used to characterize the phenotype of the malignant cells in lymphoproliferative disease to enable more vigorous treatment of those that are of T‐cell origin and that therefore carry a poor prognosis.
Accelerated Sinus Rhythm Prevents Catecholaminergic Polymorphic Ventricular Tachycardia in Mice and in Patients
Authors: Michela Faggioni, Hyun Seok Hwang, Christian van der Werf, Ineke Nederend, Prince J. Kannankeril, Arthur A.M. Wilde, Björn C. Knollmann
Journal: Circulation Research (2013)

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is caused by mutations in cardiac ryanodine receptor (RyR2) or calsequestrin (Casq2) genes. Sinoatrial node dysfunction associated with CPVT may increase the risk for ventricular arrhythmia (VA).To test the hypothesis that CPVT is suppressed by supraventricular overdrive stimulation.Using CPVT mouse models (Casq2(-/-) and RyR2(R4496C/+) mice), the effect of increasing sinus heart rate was tested by pretreatment with atropine and by atrial overdrive pacing. Increasing intrinsic sinus rate with atropine before catecholamine challenge suppressed ventricular tachycardia in 86% of Casq2(-/-) mice (6/7) and significantly reduced the VA score (atropine: 0.6±0.2 versus vehicle: 1.7±0.3; P<0.05). Atrial overdrive pacing completely prevented VA in 16 of 19 (84%) Casq2(-/-) and in 7 of 8 (88%) RyR2(R4496C/+) mice and significantly reduced ventricular premature beats in both CPVT models (P<0.05). Rapid pacing also prevented spontaneous calcium waves and triggered beats in isolated CPVT myocytes. In humans, heart rate dependence of CPVT was evaluated by screening a CPVT patient registry for antiarrhythmic drug-naïve individuals that reached >85% of their maximum-predicted heart rate during exercise testing. All 18 CPVT patients who fulfilled the inclusion criteria exhibited VA before reaching 87% of maximum heart rate. In 6 CPVT patients (33%), VA were paradoxically suppressed as sinus heart rates increased further with continued exercise.Accelerated supraventricular rates suppress VAs in 2 CPVT mouse models and in a subset of CPVT patients. Hypothetically, atrial overdrive pacing may be a therapy for preventing exercise-induced ventricular tachycardia in treatment-refractory CPVT patients.
Ex vivo characterization of polyclonal memory CD8+ T-cell responses to PRAME-specific peptides in patients with acute lymphoblastic leukemia and acute and chronic myeloid leukemia
Authors: Katayoun Rezvani, Agnes S. M. Yong, Abdul Tawab, Behnam Jafarpour, Rhoda Eniafe, Stephan Mielke, Bipin N. Savani, Keyvan Keyvanfar, Yixin Li, Roger Kurlander, A. John Barrett
Journal: Blood (2008)
Association Between Insulin Sensitivity and Post-Glucose Challenge Plasma Insulin Values in Overweight Latino Youth
Authors: Marc J. Weigensberg, Martha L. Cruz, Michael I. Goran
Journal: Diabetes Care (2003)

OBJECTIVE—To determine associations between directly measured insulin sensitivity (SI) and oral glucose tolerance test (OGTT)-derived plasma insulin values, or calculated SI indices, in overweight peripubertal Latino children at risk for type 2 diabetes. RESEARCH DESIGN AND METHODS—Thirty overweight Latino children with a family history of type 2 diabetes, aged 8–13 years, Tanner stages 1–2, underwent an OGTT. Fasting and 2-h plasma insulin values and OGTT-derived SI indices were compared with SI derived from a frequently sampled intravenous glucose tolerance test (FSIGTT) with minimal model analysis, before and after adjustment for total body fat and lean tissue mass, or BMI. RESULTS—FSIGTT-derived SI for all subjects was 1.62 ± 0.78 × 10−4 min −1 · (μU/ml), with no sex differences. SI correlated (all P values &amp;lt; 0.001) with fasting (r = −0.57) and 2-h (r = −0.58) plasma insulin and all SI indices (r = −0.57 to 0.67). After adjusting for total body fat and lean tissue mass, or BMI, the associations between SI and either fasting insulin or fasting SI indices were no longer significant. However, the 2-h insulin and post-glucose challenge SI indices maintained significant independent associations with SI, even after adjustment for body composition. CONCLUSIONS—In overweight, peripubertal Latino children at risk for type 2 diabetes, the 2-h plasma insulin value and postchallenge SI indices are better independent correlates of SI than fasting values, after accounting for body composition. The 2-h insulin may therefore be superior to fasting insulin as a single blood sample value for clinical or epidemiological estimates of SI, especially when combined with assessment of body composition.
TAL deficiency, all roads lead to oxidative stress?
Authors: Maximilian Hatting, Christian Trautwein, Francisco Javier Cubero, Kris Kowdley, Geoffrey McCaughan
Journal: Hepatology (2009)

Although oxidative stress has been implicated in acute acetaminophen-induced liver failure and in chronic liver cirrhosis and hepatocellular carcinoma (HCC), no common underlying metabolic pathway has been identified. Recent case reports suggest a link between the pentose phosphate pathway (PPP) enzyme transaldolase (TAL; encoded by TALDO1) and liver failure in children. Here, we show that Taldo1–/– and Taldo1+/– mice spontaneously developed HCC, and Taldo1–/– mice had increased susceptibility to acetaminophen-induced liver failure. Oxidative stress in Taldo1–/– livers was characterized by the accumulation of sedoheptulose 7-phosphate, failure to recycle ribose 5-phosphate for the oxidative PPP, depleted NADPH and glutathione levels, and increased production of lipid hydroperoxides. Furthermore, we found evidence of hepatic mitochondrial dysfunction, as indicated by loss of transmembrane potential, diminished mitochondrial mass, and reduced ATP/ADP ratio. Reduced β-catenin phosphorylation and enhanced c-Jun expression in Taldo1–/– livers reflected adaptation to oxidative stress. Taldo1–/– hepatocytes were resistant to CD95/Fas-mediated apoptosis in vitro and in vivo. Remarkably, lifelong administration of the potent antioxidant N-acetylcysteine (NAC) prevented acetaminophen-induced liver failure, restored Fas-dependent hepatocyte apoptosis, and blocked hepatocarcinogenesis in Taldo1–/– mice. These data reveal a protective role for the TAL-mediated branch of the PPP against hepatocarcinogenesis and identify NAC as a promising treatment for liver disease in TAL deficiency. (HEPATOLOGY 2009;50:)
In vitro acetaldehyde formation by human colonic bacteria.
Authors: K Jokelainen, R P Roine, H Vaananen, M Farkkila, M Salaspuro
Journal: Gut (1994)

Incubation of human colonic contents with various ethanol concentrations (2.75-44 mM) in vitro at 37 degrees C resulted in significant accumulation of acetaldehyde--a toxic and highly reactive compound. At pH 9.6, all samples produced notable acetaldehyde concentrations (58 (13) microM; mean (SEM)) even from the lowest (2.75 mM) ethanol concentration, and the production of acetaldehyde increased lin-early with rising ethanol concentration (r = 0.97; p &lt; 0.005), reaching a peak concentration of 238 (37) microM at 44 mM ethanol. The formation of acetaldehyde took place rapidly, as almost 50% of acetaldehyde formed during the total eight hour incubation was detectable after one hour, and 75% of the total after four hours. Maximal acetaldehyde production from 22 mM ethanol occurred at pH 9.6 (160 (35) microM) but appreciable concentrations were also seen at pH 7.4 (110 (38) microM) and pH 6.0 (63 (19) microM). At pH 4.0, by contrast, acetaldehyde formation was negligible (17 (5) microM). 4-Methylpyrazole, a potent inhibitor of alcohol dehydrogenase, showed a decreasing effect on acetaldehyde production in vitro but first at a concentration of 100 mM. Considerable acetaldehyde production by human colonic bacteria--if it occurs also in vivo--could constitute a risk factor for rectal cancer in heavy drinkers and also provide a pathogenetic mechanism for alcohol induced diarrhoea.
Reply to K. Shimada et al
Authors: Won Seog Kim, Seok Jin Kim, Sin-Ho Jung
Journal: Journal of Clinical Oncology (2010)

We thank Drs Shimada and Suzuki for their thoughtful comments 1 on our recent published results. 2 To clarify analytic issues they raised, we reviewed and reanalyzed accordingly.Thus, we reply as follows.First of all, we want to clarify that the primary end point of our study was complete response (CR) as the best response during the treatment (concurrent chemoradiotherapy [CCRT] and VIPD [etoposide, ifosfamide, cisplatin, and dexamethasone]) period, not as the response at the end of treatment.By this criterion, 27 of 30 patients achieved CR including 22 patients with CR during CCRT and five additional CRs during VIPD as described in Figure 2. The statistical hypotheses for a phase II trial usually are one sided (ie, we want to show that the experimental therapy is more efficacious than a historical control therapy.A study with two-sided hypotheses shows that the efficacy of the experimental therapy is different from that of a historical control).Therefore, the rejection rule of the statistical testing specified by the study design coincides with that by the left limit of the exact (not approximate) 90% CI (not 95% as Shimada and Suzuki claim), or equivalently that by the limit of the exact 95% left confidence limit.For a phase II trial with a two-stage design by Simon, 3 the CI matching with the two-stage testing rule should be calculated by Jennison and Turnbull method, 4 refer to Jung and Kim.
Inhaled Corticosteroids in Lung Diseases
Authors: Hengameh H. Raissy, H. William Kelly, Michelle Harkins, Stanley J. Szefler
Journal: American Journal of Respiratory and Critical Care Medicine (2013)

Inhaled corticosteroids (ICSs) are used extensively in the treatment of asthma and chronic obstructive pulmonary disease (COPD) due to their broad antiinflammatory effects. They improve lung function, symptoms, and quality of life and reduce exacerbations in both conditions but do not alter the progression of disease. They decrease mortality in asthma but not COPD. The available ICSs vary in their therapeutic index and potency. Although ICSs are used in all age groups, younger and smaller children may be at a greater risk for adverse systemic effects because they can receive higher mg/kg doses of ICSs compared with older children. Most of the benefit from ICSs occurs in the low to medium dose range. Minimal additional improvement is seen with higher doses, although some patients may benefit from higher doses. Although ICSs are the preferred agents for managing persistent asthma in all ages, their benefit in COPD is more controversial. When used appropriately, ICSs have few adverse events at low to medium doses, but risk increases with high-dose ICSs. Although several new drugs are being developed and evaluated, it is unlikely that any of these new medications will replace ICSs as the preferred initial long-term controller therapy for asthma, but more effective initial controller therapy could be developed for COPD.
Pathology of Tumors
Authors: Milton G. Bohrod
Journal: JAMA (1968)

Willis' book on tumors has been a standard work for 20 years. It is known for its clear statements of the author's opinions, a refreshing quality in any book. The new edition is printed on smoother, whiter paper which makes the type clearer and has improved the quality of most of the pictures. A page-by-page comparison with the third edition would seem to indicate that there is very little new in the field of neoplasia. Minor changes are found in most chapters; deletions are about as numerous as additions. The largest addition and the greatest rewriting are in the chapter on the "Nature of Neoplasia." The bibliography shows only slight changes. Significantly, the references in bold type which the author has "found particularly useful, as marking important discoveries, or as good reviews," are practically entirely unchanged. If you do not own a Willis, you will want to get this new
Witchcraft and Lupus
Authors: Richard A. Kirkpatrick
Journal: JAMA (1982)

<h3>To the Editor.—</h3> Readers might be interested in some follow-up information on my article entitled "Witchcraft and Lupus" (1981;245:1937). The patient who was cured by the Philippine witch doctor returned to our office recently (for the first time in 2 1/2 years) when a small nodule appeared between her buttocks. Although she declined biopsy of the lesion, she did allow testing of blood and urine. A urinalysis disclosed grade 1 albuminuria, and a chemistry screening battery showed normal BUN and serum creatinine levels. The patient was energetic and even asked for a reprint.
Evaluation of effect of changes is essential in policymaking
Authors: S. Dixon
Journal: BMJ (2000)

EDITOR—Dixon and Preker summarise the recent broad trends in reform of international health systems, arguing that the current NHS reforms represent an addition to the debate about public versus private provision.1 In this regard, they see the NHS as an important test bed. We think that two points should be made.

Firstly, entire health systems should not …
Letter to the editor: Intravenous high dose methylprednisolone for thrombotic thrombocytopenic purpura
Authors: Şinasi Özsoylu
Journal: American Journal of Hematology (1988)

A recent article of Jokela et al. [ 11 gives me an opportunity to mention our successful result in the treatment of a patient with thrombotic thrombocytic purpura with intravenous high dose methylprednisolone administration.
INCIDENCE, PREDICTORS AND OUTCOMES OF ACUTE KIDNEY INJURY FOLLOWING TRANSCATHETER AORTIC VALVE REPLACEMENT
Authors: Venkatesan Dyanesh Vidi, Zia Rab, Dan Inder Sraow, Effe A. Mihelis, S. Jacob Scheinerman, Robert Palazzo, Barry M. Kaplan, Rajiv Jauhar, Perwaiz Meraj
Journal: Journal of the American College of Cardiology (2014)
Mechanical ventilation and high-efficiency vacuum cleaning: A combined strategy of mite and mite allergen reduction in the control of mite-sensitive asthma
Authors: Jill A. Warner, Jeanette M. Frederick, Trevor N. Bryant, Christine Weich, Gary J. Raw, Colin Hunter, Frank R. Stephend, Donald A. McIntyre, John O. Warner
Journal: Journal of Allergy and Clinical Immunology (2000)
Clinical Scores to Predict Streptococcal Pharyngitis: Believers and Nonbelievers
Authors: Jan Matthys, Marc De Meyere
Journal: JAMA Internal Medicine (2013)

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Subcutaneous hyalohyphomycosis due to <i>Cephalotheca foveolata</i> in an immunocompetent host
Authors: M.K. Suh, J.W. Lim, Y.H. Lee, G.Y. Ha, H. Kim, J.R. Kim, T. Yaguchi, K. Nishimura
Journal: British Journal of Dermatology (2006)

We report the first case of subcutaneous hyalohyphomycosis caused by the genus Cephalotheca, which has not been reported to cause human infection. A 67‐year‐old immunocompetent farmer presented with a 10‐year history of verrucous erythematous plaques on the right foot dorsum, great toe, heel and sole. Histopathology of the lesions revealed chronic granulomatous inflammation with numerous nonpigmented fungal spores in the dermis. Cultures of biopsy specimens on Sabouraud's dextrose agar for 2 weeks developed into yellowish brown, velvety colonies that subsequently turned black after 8 weeks because of the production of black cleistothecia indicating the teleomorph. On the basis of mycological features, scanning electron microscopic morphology and molecular analysis data, a new species of Cephalotheca was identified and designated Cephalotheca foveolata. Because there was no response to the antifungal agents administered, the patient was successfully treated by surgical excision with skin graft.
Abstract 1134: Slug promotes survival during metastasis through suppression of Puma-mediated apoptosis
Authors: Rachel Hazan
Journal: Cancer Research (2014)

Abstract Tumor cells must overcome apoptosis to survive throughout metastatic dissemination and distal organ colonization. Here we show in the Polyoma Middle T mammary tumor model that N-cadherin causes Slug upregulation, which promotes carcinoma cell survival. Slug was dramatically upregulated in distant metastases relative to primary tumors. Consistent with a role in metastasis, Slug knockdown in metastatic carcinoma cells suppressed pulmonary colonization, due to reducing cell survival, but had no effect on tumor cell invasion or extravasation. In support of a role in cell survival, Slug inhibition by shRNA, sensitized tumor cells to apoptosis by genotoxic stress, resulting in caspase-3 activation and PARP cleavage. Furthermore, the effects of Slug on cell survival were due to direct repression of the pro-apoptotic gene, Puma. Importantly, the survival function of the SLUG-PUMA axis was confirmed in human breast cancer cells, where Slug knockdown increased Puma expression and inhibited lung colonization. Thus, our study demonstrates a pivotal role for Slug in cell survival, which is beyond its role in epithelial-to-mesenchymal transition, implying that disruption of the SLUG-PUMA axis may impinge on the survival of metastatic cancer cells. Citation Format: Rachel Hazan. Slug promotes survival during metastasis through suppression of Puma-mediated apoptosis. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 1134. doi:10.1158/1538-7445.AM2014-1134