tbuckley/cabot-search huggingface dataset:
Bupropion for Smoking Cessation in African American Light Smokers: A Randomized Controlled Trial
Authors: L. S. Cox, N. L. Nollen, M. S. Mayo, W. S. Choi, B. Faseru, N. L. Benowitz, R. F. Tyndale, K. S. Okuyemi, J. S. Ahluwalia
Journal: JNCI Journal of the National Cancer Institute (2012)

Previous research demonstrated the efficacy of sustained release bupropion (bupropion SR) for smoking cessation in whites as well as moderate to heavy (≥10 cigarettes per day [CPD]) African American smokers. We evaluated whether bupropion SR was effective for smoking cessation among African American light smokers (≤10 CPD). A randomized, double-blind placebo-controlled trial was conducted from December 27, 2007, to May 13, 2010. All participants were African American light smokers (≤10 CPD), aged 18 years or older. Participants were randomly assigned to receive 300 mg bupropion SR (150 mg once daily for 3 days and then 150 mg twice daily) (n = 270 participants) or placebo (n = 270 participants) for 7 weeks, and up to six sessions of health education counseling. Serum cotinine was measured at baseline (week 0). The primary outcome was salivary cotinine–verified 7-day point prevalence smoking abstinence at week 26; a cut point of 15 ng/mL differentiated smokers from nonsmokers. Salivary cotinine–verified smoking abstinence at end of medication treatment at week 7 was also examined. Odds ratios (OR) for smoking abstinence and 95% confidence intervals (CIs) were calculated using logistic regression models. All statistical tests were two-sided. Participants at baseline visit (week 0) smoked an average of 8.0 CPD and had a mean serum cotinine level of 275.8 ng/mL (SD = 155.8 ng/mL); most used menthol cigarettes (83.7%) and smoked within 30 minutes of waking (72.2%). After imputing those lost to follow-up as smokers, no statistically significant difference in long-term smoking abstinence rates at week 26 was observed between bupropion SR and placebo groups (13.3% vs 10.0%, OR = 1.39, 95% CI = 0.82 to 2.35, P = .23). Cotinine-verified smoking abstinence rate at end of medication week 7 was higher in the bupropion SR vs placebo group (23.7% vs 9.6%, OR = 2.92, 95% CI = 1.78 to 4.77, P < .001). Bupropion SR was effective in promoting smoking cessation during the medication phase of treatment but showed no effect on long-term smoking cessation among African American light smokers. More research is needed to identify strategies for sustaining abstinence among African American light smokers.
Long-term control of disseminated pleomorphic xanthoastrocytoma with anaplastic features by means of stereotactic irradiation
Authors: Tomoyuki Koga, Akio Morita, Keisuke Maruyama, Minoru Tanaka, Yasushi Ino, Junji Shibahara, David N. Louis, Guido Reifenberger, Jun Itami, Ryusuke Hara, Nobuhito Saito, Tomoki Todo
Journal: Neuro-Oncology (2009)

Pleomorphic xanthoastrocytoma (PXA) is a rare astrocytic neoplasm of the brain. Some PXAs are accompanied by anaplastic features and are difficult to manage because of frequent recurrences that lead to early death. No previous reports have demonstrated consistent efficacy of adjuvant radiotherapy or chemotherapy for this disease. We report a case of PXA with anaplastic features treated with stereotactic irradiation (STI) that resulted in long-term control of repeatedly recurring nodules throughout the neuraxis. A 47-year-old woman presented with an epileptic seizure due to a large tumor in the right frontal lobe. The tumor was resected and diagnosed as PXA with anaplastic features. Sixteen months later, a relapse at the primary site was noted and treated with stereotactic radiosurgery using Gamma Knife. Two years later, the patient developed a tumor nodule in the cervical spinal cord that histologically corresponded to a small-cell glioma with high cellularity and prominent MIB-1 (mindbomb homolog 1) labeling. In the following months, multiple nodular lesions appeared throughout the CNS, and STI was performed six times for eight intracranial lesions using Gamma Knife and twice using a linear accelerator, for three spinal cord lesions in total. All lesions treated with STI were well controlled, and the patient was free from symptomatic progression for 50 months. However, diffuse dissemination along the craniospinal axis eventually progressed, and she died 66 months after initial diagnosis. Autopsy showed that the nodules remained well demarcated from the surrounding nervous system tissue. STI may be an effective therapeutic tool for controlling nodular dissemination of PXA with anaplastic features.
STUDIES IN THE BLOOD CYTOLOGY OF THE RABBIT
Authors: Louise Pearce, Albert E. Casey
Journal: The Journal of Experimental Medicine (1931)

Successive blood counts at weekly intervals were made on rabbits inoculated with a transplantable malignant neoplasm of epithelial origin. There were 78 animals distributed in 9 groups; the period of observation after inoculation was 2 months. The results have been considered with respect to the character of the tumor process as determined by postmortem examination, the animals being classified as deaths, probable deaths, probable recoveries, and recoveries. The blood findings have been analyzed on the basis of the values derived from normal rabbits. A comparison has also been made with the results of preinoculation counts. In rabbits in which the tumor process was of pronounced or well marked severity, the numbers of monocytes became greatly increased; the neutrophiles and the total white blood cells were also increased; the eosinophiles, and to a less extent, the basophiles and lymphocytes were decreased; the red cell count was decreased and the hemoglobin content was lowered. In rabbits which recovered from the tumor inoculation, there were no outstanding changes in the blood picture when the findings for the entire observation period were considered. In the group of probable recoveries, the results were variable; there was, however, a definite although moderate increase of monocytes, and in general, the findings reflected the mildness of the disease when compared with those of the fatal cases and the group of probable deaths.
Household Net Worth, Racial Disparities, and Hormonal Therapy Adherence Among Women With Early-Stage Breast Cancer
Authors: Dawn L. Hershman, Jennifer Tsui, Jason D. Wright, Ellie J. Coromilas, Wei Yann Tsai, Alfred I. Neugut
Journal: Journal of Clinical Oncology (2015)

Purpose Nonadherence to adjuvant hormonal therapy is common and is associated with increased prescription copayment amount and black race. Studies suggest that household wealth may partly explain racial disparities. We investigated the impact of net worth on disparities in adherence and discontinuation. Patients and Methods We used the OptumInsight insurance claims database to identify women older than age 50 years diagnosed with early breast cancer, from January 1, 2007, to December 31, 2011, who were using hormonal therapy. Nonadherence was defined as a medication possession ratio of ≤ 80% of eligible days over a 2-year period. We evaluated the association of demographic and clinical characteristics, annual household income, household net worth (&lt; $250,000, $250,000 to $750,000, or &gt; $750,000), insurance type, and copayments (&lt; $10, $10 to $20, or &gt; $20) with adherence to hormonal therapy. Logistic regression analyses were conducted by sequentially adding sociodemographic and financial variables to race. Results We identified 10,302 patients; 2,473 (24%) were nonadherent. In the unadjusted analyses, adherence was negatively associated with black race (odds ratio [OR], 0.76; P &lt; .001), advanced age, comorbidity, and Medicare insurance. Adherence was positively associated with medium (OR, 1.33; P &lt; .001) and high (OR, 1.66; P &lt; .001) compared with low net worth. The negative association of black race with adherence (OR, 0.76) was reduced by adding net worth to the model (OR, 0.84; P &lt; .05). Correcting for other variables had a minimal impact on the association between race and adherence (OR, 0.87; P = .08). The interaction between net worth and race was significant (P &lt; .01). Conclusion We found that net worth partially explains racial disparities in hormonal therapy adherence. These results suggest that economic factors may contribute to disparities in the quality of care.
Expression Level of Valosin-Containing Protein (p97) Is Associated with Prognosis of Esophageal Carcinoma
Authors: Shinji Yamamoto, Yasuhiko Tomita, Yoshihiko Hoshida, Norishige Iizuka, Shinya Kidogami, Hiroshi Miyata, Shuji Takiguchi, Yoshiyuki Fujiwara, Takushi Yasuda, Masahiko Yano, Shoji Nakamori, Masato Sakon, Morito Monden, Katsuyuki Aozasa
Journal: Clinical Cancer Research (2004)

Esophageal squamous cell carcinoma (ESCC) frequently shows a poor prognosis because of the occurrence of systemic metastasis, mainly via lymphatic vessels. Valosin-containing protein (VCP) has been shown to be associated with antiapoptotic function and metastasis via activation of the nuclear factor-kappaB signaling pathway. In the present study, we examined the association of VCP with the recurrence and prognosis of ESCC.VCP expression in 156 ESCC patients [139 males and 17 females; age range, 38-82 (median, 60) years] was analyzed by immunohistochemistry. Staining intensity in tumor cells was categorized as weaker (level 1) or equal to or stronger (level 2) than that in endothelial cells. The correlation of VCP expression between the mRNA and protein levels was examined in 12 patients.Fifty-seven (37.3%) cases showed level 1 and 96 (62.7%) level 2 VCP expression. Quantitative reverse transcription-PCR analysis revealed greater VCP mRNA expression in level 2 (n = 6) than level 1 cases (n = 6; P < 0.05). ESCC with level 2 expression showed higher rates of lymph node metastasis (P < 0.01) and deep tumor invasion (P < 0.01), and poorer disease-free and overall survival rates (P < 0.001 for both analyses) than ESCC with level 1 expression. Multivariate analysis revealed that VCP expression level is an independent prognosticator for disease-free and overall survival. Furthermore, VCP level was an indicator for disease-free survival in the early (pT1) and the advanced (pT2-pT4) stage groups.This study demonstrated the prognostic significance of VCP expression in ESCC.
Effective Adjunctive Therapy by an Innate Defense Regulatory Peptide in a Preclinical Model of Severe Malaria
Authors: Ariel H. Achtman, Sandra Pilat, Charity W. Law, David J. Lynn, Laure Janot, Matt L. Mayer, Shuhua Ma, Jason Kindrachuk, B. Brett Finlay, Fiona S. L. Brinkman, Gordon K. Smyth, Robert E. W. Hancock, Louis Schofield
Journal: Science Translational Medicine (2012)

Case fatality rates for severe malaria remain high even in the best clinical settings because antimalarial drugs act against the parasite without alleviating life-threatening inflammation. We assessed the potential for host-directed therapy of severe malaria of a new class of anti-inflammatory drugs, the innate defense regulator (IDR) peptides, based on host defense peptides. The Plasmodium berghei ANKA model of experimental cerebral malaria was adapted to use as a preclinical screen by combining late-stage intervention in established infections with advanced bioinformatic analysis of early transcriptional changes in co-regulated gene sets. Coadministration of IDR-1018 with standard first-line antimalarials increased survival of infected mice while down-regulating key inflammatory networks associated with fatality. Thus, IDR peptides provided host-directed adjunctive therapy for severe disease in combination with antimalarial treatment.
Phenazopyridine and Aseptic Meningitis
Authors: TIMOTHY E. HERLIHY
Journal: Annals of Internal Medicine (1987)

Letters and Corrections1 January 1987Phenazopyridine and Aseptic MeningitisTIMOTHY E. HERLIHY, M.D.TIMOTHY E. HERLIHY, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-106-1-172_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: We write to report the case of a patient who developed aseptic meningitis after taking phenazopyridine hydrochloride.A 56-year-old white man was hospitalized with acute onset of fever and confusion. His past history was significant for prostate cancer, stage B2, and mild hypertension. At admission, he was taking two medications: triamterine-hydrochlorothiazide (50 mg/25 mg; Dyazide, SmithKline & French, Philadelphia, Pennsylvania), one tablet a day; and phenazopyridine hydrochloride (200 mg; Pyridium, Parke-Davis, Morris Plains, New Jersey), one tablet three times a day. The phenazopyridine treatment was started approximately 10 days before admission because of symptoms of dysuria after...References1. WIDENERLITTMAN HG. Ibuprofen-induced meningitis in systemic lupus erythmatosus. JAMA. 1978;329:1062-4. CrossrefGoogle Scholar2. RUPPERTBARTH GW. Tolmetin-induced aseptic meningitis. JAMA. 1981;243:67-8. CrossrefGoogle Scholar3. VON REYN D. Recurrent aseptic meningitis due to sulindac. Ann Intern Med. 1983;99:343-4. LinkGoogle Scholar4. GARAGUSINEEFEMANN VLO. Acute meningoencephalitis, associated with isoniazid and administration. JAMA. 1976;235:1141-2. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByDrug-Induced Aseptic Meningitis and Other MimicsPhenazopyridineDrug-Induced Aseptic Meningitis and Other MimicsDrug-induced aseptic meningitisDrug-Induced Aseptic MeningitisTrimethoprim-Sulfamethoxazole-Induced Meningitis in Patients With HIV InfectionDrug-induced meningitisDrug- and Chemical-Induced Aseptic Meningitis: A Review of the LiteratureThe Acute Aseptic Meningitis SyndromeNoninfectious Causes of Acute CNS InflammationTrimethoprim-sulfamethoxazole-associated aseptic meningitis: Case reports and review of the literatureAnti-inflammatory analgesics and drugs used in rheumatoid arthritis and gout 1 January 1987Volume 106, Issue 1Page: 172-173KeywordsFeversHypertensionMeningitisProstate cancer Issue Published: 1 January 1987 PDF DownloadLoading ...
Purified cardiomyocytes from bone marrow mesenchymal stem cells produce stable intracardiac grafts in mice
Authors: N HATTAN, H KAWAGUCHI, K ANDO, E KUWABARA, J FUJITA, M MURATA, M SUEMATSU, H MORI, K FUKUDA
Journal: Cardiovascular Research (2004)

We have previously isolated cardiomyogenic cells from murine bone marrow (CMG cells). Regenerated cardiomyocytes are important candidates for cell transplantation, but as they are stem cell derived, they can be contaminated with various cell types, thereby requiring characterization and purification. Our objectives were to increase the efficiency of cell transplantation and to protect the recipients from possible adverse effects using an efficient and effective purification process as well as to characterize regenerated cardiomyocytes.Noncardiomyocytes were eliminated from a mixture of stem-cell-derived cells using a fluorescence-activated cell sorter to specifically isolate CMG cells transfected with a recombinant plasmid containing enhanced green fluorescent protein (EGFP) cDNA under the control of the myosin light chain-2v (MLC-2v) promoter. Gene expression and the action potential were investigated, and purified cells were transplanted into the heart of adult mice.Six percent to 24% of transfected CMG cells expressed EGFP after differentiation was induced, and a strong EGFP-positive fraction was selected. All the sorted cells began spontaneous beating after 3 weeks. These cells expressed cardiomyocyte-specific genes such as alpha-skeletal actin, beta-myosin heavy chain, MLC-2v, and CaV1.2 and incorporated bromodeoxyuridine for 5 days. The isolated EGFP-positive cells were expanded for 5 days and then transplanted into the left ventricle of adult mouse hearts. The transplanted cells survived for at least 3 months and were oriented in parallel to the cardiomyocytes of the recipient heart.The purification and transplantation of differentiated cardiomyocytes from adult stem cells provides a viable model of tissue engineering for the treatment of heart failure.
Adrenergic receptor blocker reverses cardiac metabolic remodeling and improves right ventricular function in experimental pulmonary hypertension
Authors: Jose Gomez-Arroyo, Shiro Mizuno, Laszlo Farkas, Donatas Kraskauskas, Daniela Farkas, Ayser Husseini, Antonio Abbate, Herman Bogaard, Norbert Voelkel
Journal: European Respiratory Journal (2011)

Albeit right ventricular failure (RVF) is a major complication in patients with pulmonary arterial hypertension, the knowledge on the pathobiology of RVF is still incomplete and RV-targeted therapies are practically non-existent. Since a metabolic switch has been reported for left heart failure, we sought to describe any potential changes in cardiac fuel metabolism and mitochondrial function in RVF.  PAH was induced in S-D rats by a combination of a VEGF-receptor blocker followed by 4 weeks of 10% hypoxia (SuHx).Gene expression was evaluated by RT-PCR and confirmed by western blot. Rats were treated with vehicle/carvedilol for 4 weeks after hypoxia exposure.RV function was measured by echocardiogram and reported as TAPSE.  As an initial step, we evaluated the expression of PGC1α, a master regulator of cardiac energetics and mitochondrial biogenesis.SuHx RV tissue had a 60% downregulation of PGC1α when compared to controls (p 2 =0.77,p  Our data suggests a switch in cardiac substrate utilization and mitochondrial dysfunction during RVF. We propose carvedilol as a potential treatment to reverse this metabolic switch.
MicroRNA-155 Functions as an OncomiR in Breast Cancer by Targeting the<i>Suppressor of Cytokine Signaling 1</i>Gene
Authors: Shuai Jiang, Hong-Wei Zhang, Ming-Hua Lu, Xiao-Hong He, Yong Li, Hua Gu, Mo-Fang Liu, En-Duo Wang
Journal: Cancer Research (2010)

Abstract MicroRNA-155 (miR-155) is overexpressed in many human cancers; however, the mechanisms by which miR-155 functions as a putative oncomiR are largely unknown. Here, we report that the tumor suppressor gene suppressor of cytokine signaling 1 (socs1) is an evolutionarily conserved target of miR-155 in breast cancer cells. We found that mir-155 expression is inversely correlated with socs1 expression in breast cancer cell lines as well as in a subset of primary breast tumors. We also identified a 24A→G mutation in the miR-155 binding site of the SOCS1 3′ untranslated region in a breast tumor that reduced miR-155 repression, implicating a mechanism for miRNA targets to avoid repression. Ectopic expression of miR-155 significantly promoted the proliferation of breast cancer cells, the formation of soft agar foci in vitro, and the development of tumors in nude mice. In breast cancer cells, RNA interference silencing of socs1 recapitulates the oncogenic effects of miR-155, whereas restoration of socs1 expression attenuates the protumorigenesis function of miR-155, suggesting that miR-155 exerts its oncogenic role by negatively regulating socs1. Overexpression of miR-155 in breast cancer cells leads to constitutive activation of signal transducer and activator of transcription 3 (STAT3) through the Janus-activated kinase (JAK) pathway, and stimulation of breast cancer cells by the inflammatory cytokines IFN-γ and interleukin-6 (IL-6), lipopolysaccharide (LPS), and polyriboinosinic:polyribocytidylic acid [poly(I:C)] significantly upregulates mir-155 expression, suggesting that miR-155 may serve as a bridge between inflammation and cancer. Taken together, our study reveals that miR-155 is an oncomiR in breast cancer and that miR-155 may be a potential target in breast cancer therapy. Cancer Res; 70(8); 3119–27. ©2010 AACR.
Renal structure and function in insulin-dependent diabetes mellitus and type I membranoproliferative glomerulonephritis in humans.
Authors: S M Mauer, P Lane, M Hattori, P Fioretto, M W Steffes
Journal: Journal of the American Society of Nephrology (1992)

Renal pathological changes of diabetes include thickening of all renal extracellular basement membranes and the mesangial matrix and, to a lesser extent, mesangial cell expansion. Two renal lesions appear critical in diabetic nephropathy. Mesangial expansion out of proportion to the size of the glomerulus is related to proteinuria, hypertension, and declining GFR. Arteriolar hyalinosis is related to global glomerulosclerosis, and both are correlated with the clinical features of nephropathy. By the time renal dysfunction is clinically detectable, these lesions tend to be advanced. Interstitial volume may be increased in insulin-dependent diabetes mellitus, particularly in areas containing sclerotic glomeruli or marked tubular atrophy. Parallel findings were documented for type I membranoproliferative glomerulonephritis in which the increased mesangial volume fraction was related to decreased GFR, increased glomerular permeability to protein, and hypertension. As in diabetes, the cortical interstitial volume fraction is correlated with functional abnormalities in type I membranoproliferative glomerulonephritis. Thus, in both of these chronic glomerular disorders, mesangial expansion and interstitial expansion are associated with disordered renal function. Thus, it is not true that glomerular structural changes correlate poorly with glomerular function. Whether it is the glomerular or interstitial pathology or both that is causally responsible for the dysfunction requires further study.
Human mast cells and type 2 innate lymphoid cells activate gene expression and mucus composition in human bronchial epithelial cells via IL-13
Authors: Deepti Nagarkar, Vladimir Ramirez-Carrozzi, David Choy, Kevin Lee, Robert Soriano, Alexander Abbas, Zora Modrusan, Rajita Pappu, Joe Arron
Journal: European Respiratory Journal (2014)

Background: Mechanisms driving asthma exacerbations are not well understood. Epithelial cells are primary responders to invading pathogens. Type 2 cytokine producing cells including mast cells are found in airway epithelium of asthmatics; innate type 2 lymphoid cells (ILC2s) contribute to type 2 inflammation in mouse asthma models and have been found in adult human lungs.  Objectives: Understanding mechanisms by which effector cells including mast cells and ILC2s may act on bronchial epithelium to exacerbate airway pathology.  Methods: Normal human bronchial epithelial cells (NHBE) were cultured at air-liquid interface. Peripheral blood CD34+ cell derived human mast cells or lineage-CRTH2+ CD161+CD127+ ILC2s were added basolaterally, and stimulated with either IL-33 or control media, alone or in combination with anti-IL-13 for 72 hours. Effects on NHBE were assessed via gene expression.  Results: IL-33 significantly enhanced IL-13 production in mast cells. Expression of CCL26, MUC5AC, and periostin was significantly upregulated in IL-13 treated NHBE and in NHBE co-cultured with IL-33 stimulated mast cells, compared to control. NHBE responses were significantly attenuated with addition of anti-IL-13 to the IL-33 treated mast cells. Co-culture of ILC2s with NHBE strongly upregulated CCL26, MUC5AC, and periostin expression in NHBE, and responses were suppressed by the addition of anti-IL-13. Similar patterns were observed via microarray analysis.  Conclusions: IL-13 from activated mast cells and ILC2s may amplify airway inflammation in asthmatics by increasing cytokine expression and mucus secretion, contributing to increased airway obstruction.
Preoperative PET/CT in early-stage breast cancer
Authors: M. Bernsdorf, A.K. Berthelsen, V.T. Wielenga, N. Kroman, D. Teilum, T. Binderup, U.B. Tange, M. Andersson, A. Kjær, A. Loft, J. Graff
Journal: Annals of Oncology (2012)