tbuckley/cabot-search huggingface dataset:
Laryngeal involvement as a presenting symptom of systemic lupus erythematosus.
Authors: A Kraus, G Guerra-Bautista
Journal: Annals of the Rheumatic Diseases (1990)

Laryngeal involvement as a presenting symptom of systemic lupus erythematosus Sir: The actual prevalence of laryngeal in- volvement in systemic lupus erythematosus (SLE) is unclear, but it seems to be very uncommon.'Furthermore, laryngeal vasculitis in SLE is even more rare and has been scarcely reported.2In fact, in the lupus erythematosus textbook of Wallace and Dubois no mention is made of the actual prevalence and type of damage of the larynx.3We have recently seen a young man with SLE, who developed hoarseness as the first symptom.A 33 year old white man was admitted in December 1988 with a five week history of hoarseness.Three weeks later he noticed anorexia, weight loss, oral ulcers, arthritis, palpable purpura, and paraesthesia in the legs.Before admission the patient had only received non-steroidal anti-inflammatory drugs, without improvement.His medical history was uneventful.Initial examination showed a normal blood pressure, a temperature of 37°C, and a pulse of 90 beats a minute.Polyarthritis, oral ulcers, and palpable purpura in the legs were noticed.An indirect laryngoscopy showed complete paralysis of the right vocal cord without masses and with no evidence of external compression.
Anterior Cingulate Cortex Activity and Impaired Self-Monitoring of Performance in Patients With Schizophrenia: An Event-Related fMRI Study
Authors: C S Carter, A W MacDonald, L L Ross, V A Stenger
Journal: American Journal of Psychiatry (2001)

OBJECTIVE: The authors examined brain activity associated with the internal monitoring of performance to test the hypothesis that error-related activity in the anterior cingulate cortex is impaired in patients with schizophrenia. METHOD: Seventeen patients with schizophrenia and 16 healthy comparison subjects underwent event-related functional magnetic resonance imaging during a continuous performance task; stimulus degradation was used to increase error rates. RESULTS: Comparison subjects, but not schizophrenic patients, showed error-related activity in the anterior cingulate cortex, and this difference in brain activity was significantly different across the two groups. Patients also showed less slowing of reaction time after error commission. CONCLUSIONS: Lower error-related activity in the anterior cingulate cortex and less performance adjustment after error commission are consistent with the hypothesis that disturbances in anterior cingulate cortex function are related to a specific alteration in an evaluative component of executive functioning—the internal monitoring of performance.
Outcome of Hospital Care of Liver Disease Associated With Hepatitis C in the United States
Authors: Ray W. Kim, John B. Gross, John J. Poterucha, Richard G. Locke, Rolland E. Dickson
Journal: Hepatology (2001)

We describe mortality and resource utilization for inpatient care of hepatitis C (HCV) in comparison to alcohol-induced liver disease (ALD) in the United States and identify factors that affect outcomes. The Healthcare Cost and Utilization Project database, a national inpatient sample was used to identify hospitalization records with diagnoses related to liver disease from HCV and ALD. Outcome of hospitalizations was analyzed in terms of in-hospital deaths and health care resource utilization. For 1995, we estimate that there were 26,700 hospitalizations and 2,600 deaths in acute, nonfederal hospitals in the United States for liver diseases caused by HCV. Total charges for these hospitalizations were $514 million. In comparison, ALD was associated with 101,200 hospitalizations, 13,400 deaths, and $1.8 billion in charges. Simultaneous HCV and alcohol abuse was associated with younger ages at the time of hospitalization and death compared with HCV or ALD alone. In a logistic regression analysis, alcohol abuse (odds ratio [OR], 1.4; 95% confidence interval [CI], 1.2-1.5) and human immunodeficiency virus (HIV) infection (OR, 4.5; 95% CI, 4.0-4.9) were associated with an increased risk of death among those with HCV. Liver transplantation and patient death were associated with the largest increase in hospitalization charges. Major complications of cirrhosis, such as variceal bleeding, encephalopathy, and hepatorenal syndrome, and sociodemographic factors, such as race and health insurance, were also significantly associated with the risk of death and hospitalization charges, which were similar in HCV and ALD. This study provides new estimates regarding the public health impact of HCV, for use in health policy decisions and cost-effectiveness analyses of preventive and therapeutic interventions.
MUCOPOLYSACCHARIDES IN MAST CELLS.
Authors: G. I. HORSFIEID, ROY SUMMERLY
Journal: British Journal of Dermatology (1966)

Journal Article MUCOPOLYSACCHARIDES IN MAST CELLS. Get access G. I. HORSFIEID, G. I. HORSFIEID Medical Research Council, Unit for Research on the Experimental Pathology of the Skin, Medical School, Birmingham 15 Search for other works by this author on: Oxford Academic Google Scholar ROY SUMMERLY ROY SUMMERLY Medical Research Council, Unit for Research on the Experimental Pathology of the Skin, Medical School, Birmingham 15 Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 78, Issue 8-9, 1 August 1966, Pages 476–484, https://doi.org/10.1111/j.1365-2133.1966.tb12253.x Published: 01 August 1966
FATAL THROMBO-ARTERITIS OF THE RIGHT MIDDLE CEREBRAL ARTERY OF UNCERTAIN CAUSATION
Authors: F. P. Weber
Journal: BMJ (1923)

CEREBRAL ARTERY.TrEDCAL J0I puncture: fluid under high pressure but clear.No organisms found.Culture sterile.Temperature for the past five days 97.80 to 99.60.All drowsiness has disappeared; appetite and well-
Memory Type 2 Helper T Cells Induce Long-Lasting Antitumor Immunity by Activating Natural Killer Cells
Authors: Masayuki Kitajima, Toshihiro Ito, Damon J. Tumes, Yusuke Endo, Atsushi Onodera, Kahoko Hashimoto, Shinichiro Motohashi, Masakatsu Yamashita, Takashi Nishimura, Steven F. Ziegler, Toshinori Nakayama
Journal: Cancer Research (2011)

Functionally polarized helper T cells (Th cells) play crucial roles in the induction of tumor immunity. There is considerable knowledge about the contributions of IFN-producing Th1 cells that supports the role of cytotoxic cluster of differentiation (CD8) T cells and natural killer (NK) cells, but much less is known about how IL-4-producing Th2 cells contribute to tumor immunity. In this study, we investigated the cellular and molecular mechanisms employed by memory Th2 cells in sustaining tumor immunity by using a mouse model system wherein ovalbumin (OVA) is used as a specific tumor antigen. In this model, we found that OVA-specific memory Th2 cells exerted potent and long-lasting antitumor effects against NK-sensitive OVA-expressing tumor cells, wherein antitumor effects were mediated by NK cells. Specifically, NK cell cytotoxic activity and expression of perforin and granzyme B were dramatically enhanced by the activation of memory Th2 cells. Interleukin 4 (IL-4) produced by memory Th2 cells in vivo was critical for the antitumor effects of the NK cells, which IL-4 directly stimulated to induce their perforin- and granzyme-B-dependent cytotoxic activity. Our findings show that memory Th2 cells can induce potent antitumor immunity through IL-4-induced activation of NK cells, suggesting potential applications in cellular therapy for cancer patients.
Autoimmunity Correlates With Tumor Regression in Patients With Metastatic Melanoma Treated With Anti–Cytotoxic T-Lymphocyte Antigen-4
Authors: Peter Attia, Giao Q. Phan, Ajay V. Maker, Michael R. Robinson, Martha M. Quezado, James C. Yang, Richard M. Sherry, Suzanne L. Topalian, Udai S. Kammula, Richard E. Royal, Nicholas P. Restifo, Leah R. Haworth, Catherine Levy, Sharon A. Mavroukakis, Geoff Nichol, Michael J. Yellin, Steven A. Rosenberg
Journal: Journal of Clinical Oncology (2005)

Previously, we reported our experience treating 14 patients with metastatic melanoma using a fully human antibody to cytotoxic T-lymphocyte antigen-4 (anti-CTLA-4) in conjunction with peptide vaccination. We have now treated 56 patients to evaluate two different dose schedules of anti-CTLA-4 and to explore the relationship between autoimmunity and tumor regression.A total of 56 patients with progressive stage IV melanoma were enrolled onto the study. All had Karnofsky performance status > or = 60% with no prior history of autoimmunity. Twenty-nine patients received 3 mg/kg anti-CTLA-4 every 3 weeks, whereas 27 received 3 mg/kg as their initial dose with subsequent doses reduced to 1 mg/kg every 3 weeks. In both cohorts patients received concomitant vaccination with two modified HLA-A*0201-restricted peptides from the gp100 melanoma-associated antigen, gp100:209-217(210M) and gp100:280-288(288V).Two patients achieved a complete response (ongoing at 30 and 31 months, respectively) and five patients achieved a partial response (durations of 4, 6, 25+, 26+, and 34+ months, respectively), for an overall objective response rate of 13%. Tumor regression was seen in lung, liver, brain, lymph nodes, and subcutaneous sites. Of 14 patients with grade 3/4 autoimmune toxicity, five (36%) experienced a clinical response compared with only two responses in the 42 patients (5%) with no autoimmune toxicity (P = .008). There were no significant differences in response rate or toxicity between the two dose schedules.Administration of anti-CTLA-4 monoclonal antibody plus peptide vaccination can cause durable objective responses, which correlate with the induction of autoimmunity, in patients with metastatic melanoma.
The Chemopreventive Agent Resveratrol Stimulates Cyclic AMP–Dependent Chloride Secretion<i>In vitro</i>
Authors: Irina Blumenstein, Benjamin Keserü, Freya Wolter, Jürgen Stein
Journal: Clinical Cancer Research (2005)

Abstract Resveratrol and its analogs are promising cancer chemoprevention agents, currently under investigation in clinical trials. However, patients administered other plant polyphenols experienced severe diarrhea, likely due to an increase in intracellular cyclic AMP (cAMP). Resveratrol itself raises intracellular cAMP levels in breast cancer cells in vitro. Its future use as a cancer chemopreventive agent could therefore be compromised by its severe side effects. The aim of the study was (a) to define the influence of resveratrol on intestinal Cl− secretion and (b) to elucidate possible intracellular transduction pathways involved. Resveratrol caused a dose- and time-dependent increase in ΔIsc in T84 cells. The specificity of resveratrol was confirmed by using piceatannol 100 μmol/L, the hydroxylated resveratrol analog, which did not alter ΔIsc. A significant elevation of [cAMP]i by resveratrol was assessed in T84 cells. In mouse jejunum, resveratrol induced a time- and dose-dependent increase in ΔIsc as well. In bilateral Cl−-free medium, as well as after inhibition of protein kinase A, resveratrol-induced ΔIsc was reduced significantly. Preincubation of T84 cells with butyrate 2 mmol/L (24 and 48 hours) significantly inhibited resveratrol as well as forskolin-induced Cl− secretion. In summary, the main mechanism of action of resveratrol in intestinal epithelia is cAMP-induced chloride secretion which can be suppressed by butyrate. It can therefore be suggested that in cancer chemoprevention, both agents should be combined to reduce an undesired side effect such as diarrhea and to benefit from the known agonistic effect of both agents on differentiation of colon cancer cells.
NORTHWICK PARK ECT TRIAL
Authors: RobertH. Lenox, LelonA. Weaver, B.N. Gangadhar, S. Kalyanasundaram, R.L. Kapur, Ronald Maggs, EveC. Johnstone, T.J. Crow, C.D. Frith, P.G. Lawler, J.F.W. Deakin, K. Mcpherson, Marilyn Stevens
Journal: The Lancet (1981)
Expression of the MRP2 Gene-Encoded Conjugate Export Pump in Human Kidney Proximal Tubules and in Renal Cell Carcinoma
Authors: THOMAS P. SCHAUB, JÜRGEN KARTENBECK, JÖRG KÖNIG, HERBERT SPRING, JOACHIM DÖRSAM, GERD STAEHLER, STEPHAN STÖRKEL, WALTER F. THON, DIETRICH KEPPLER
Journal: Journal of the American Society of Nephrology (1999)

Human kidney proximal tubule epithelia express the ATP-dependent export pump for anionic conjugates encoded by the MRP2 (cMRP/cMOAT) gene (symbol ABCC2). MRP2, the apical isoform of the multidrug resistance protein, is an integral membrane glycoprotein with a molecular mass of approximately 190 kD that was originally cloned from liver and localized to the canalicular (apical) membrane domain of hepatocytes. In this study, MRP2 was detected in human kidney cortex by reverse transcription-PCR followed by sequencing of a 826-bp cDNA fragment and by immunoblotting using two different antibodies. Human MRP2 was localized to the apical brush-border membrane domain of proximal tubules by double and triple immunofluorescence microscopy including laser scanning microscopy. The expression of MRP2 in renal cell carcinoma was studied by reverse transcription-PCR and immunoblotting in samples from patients undergoing tumor-nephrectomy without prior chemotherapy. Clear-cell carcinomas, originating from the proximal tubule epithelium, expressed MRP2 in 95% (18 of 19) of cases. Immunofluorescence microscopy of MRP2 in clear-cell carcinoma showed a lack of a distinct apical-to-basolateral tumor cell polarity and an additional localization of MRP2 on intracellular membranes. MRP2, the first cloned ATP-dependent export pump for anionic conjugates detected in human kidney, may be involved in renal excretion of various anionic endogenous substances, xenobiotics, and cytotoxic drugs. This conjugate-transporting ATPase encoded by the MRP2 gene has a similar substrate specificity as the multidrug resistance protein MRP1, and may contribute to the multidrug resistance of renal clear-cell carcinomas.
A2.17 Synoviocytes Change Phenotype and Function after Treg-Depletion in Arthritic Mice
Authors: M Böttcher, I Irmler, C Wunrau, A Korb-Pap, G Schett, T Pap, T Kamradt
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Purpose/Objective</h3> Immunizstion with Glucose-6-phosphate isomerase (G6PI) induces arthritis in susceptible strains of mice. Depletion of regulatory T cells (Tregs) prior to immunisation switches the usually acute, self-limiting course to a non-remitting, destructive arthritis. This provides a possibility to study molecular switches for the transition from acute, self-limiting to chronic, destructive arthritis within one mouse model. To examine the role of fibroblast-like synoviocytes (FLS), which are known to modulate immune responses via the production of pro- and anti-inflammatory mediators, the phenotype and function of FLS from mice with either acute, self-limiting or non-remitting, destructive arthritis was studied. <h3>Materials and Methods</h3> FLS from DBA/1 mice that developed either the acute or the chronic form of arthritis were isolated from joints over a time course of 56 days. To investigate the phenotype of FLS ELISA studies as well as zymography have been performed. For the functional clarification of those cells the matrix-associated transepithelial resistance invasion (MATRIN) assay and a cartilage attachment assay have been used. Furthermore, FLS have been transferred in vivo into the knee joints of immunodeficient mice and the joints have been scored histologically. <h3>Results</h3> FLS from Treg-depleted mice produced significantly more cytokines (e.g. Interleukin 6 (IL-6)) upon stimulation with other cytokines, growth factors and TLR ligands. This increased susceptibility to cytokine stimulation in chronic animals compared to acute ones is observable throughout the disease course (56 days). Furthermore, the secretion and activity of matrix metalloproteases (MMPs) was enhanced in the FLS from chronic mice compared to samples from acute ones. Additional functional differences include the collagen-destructive potential and the potential to attach and eventually invade wild type cartilage. Here, FLS from Treg-depleted chronic arthritic mice showed a higher invasive and destructive potential. Ultimately, FLS from Treg-depleted mice were able to destroy cartilage in immunodeficient mice. <h3>Conclusions</h3> Our results are compatible with the hypothesis that uninhibited inflammation in the early phase of Treg-depleted mice causes the acquisition of an autonomously aggressive phenotype of synoviocytes which contribute to the switch from acute to chronic arthritis even in the absence of late support from T and B lymphocytes.
Combination cediranib and olaparib versus olaparib alone for women with recurrent platinum-sensitive ovarian cancer: a randomised phase 2 study
Authors: Joyce F Liu, William T Barry, Michael Birrer, Jung-Min Lee, Ronald J Buckanovich, Gini F Fleming, BJ Rimel, Mary K Buss, Sreenivasa Nattam, Jean Hurteau, Weixiu Luo, Philippa Quy, Christin Whalen, Lisa Obermayer, Hang Lee, Eric P Winer, Elise C Kohn, S Percy Ivy, Ursula A Matulonis
Journal: The Lancet Oncology (2014)
Renal Cells from Spermatogonial Germline Stem Cells Protect against Kidney Injury
Authors: Letizia De Chiara, Sharmila Fagoonee, Andrea Ranghino, Stefania Bruno, Giovanni Camussi, Emanuela Tolosano, Lorenzo Silengo, Fiorella Altruda
Journal: Journal of the American Society of Nephrology (2013)

Spermatogonial stem cells reside in specific niches within seminiferous tubules and continuously generate differentiating daughter cells for production of spermatozoa. Although spermatogonial stem cells are unipotent, these cells are able to spontaneously convert to germline cell-derived pluripotent stem cells (GPSCs) in vitro. GPSCs have many properties of embryonic stem cells and are highly plastic, but their therapeutic potential in tissue regeneration has not been fully explored. Using a novel renal epithelial differentiation protocol, we obtained GPSC-derived tubular-like cells (GTCs) that were functional in vitro, as demonstrated through transepithelial electrical resistance analysis. In mice, GTCs injected after ischemic renal injury homed to the renal parenchyma, and GTC-treated mice showed reduced renal oxidative stress, tubular apoptosis, and cortical damage and upregulated tubular expression of the antioxidant enzyme hemeoxygenase-1. Six weeks after ischemic injury, kidneys of GTC-treated mice had less fibrosis and inflammatory infiltrate than kidneys of vehicle-treated mice. In conclusion, we show that GPSCs can be differentiated into functionally active renal tubular-like cells that therapeutically prevent chronic ischemic damage in vivo, introducing the potential utility of GPSCs in regenerative cell therapy.
Chronic Kidney Disease Awareness, Prevalence, and Trends among U.S. Adults, 1999 to 2000
Authors: Josef Coresh, Danita Byrd-Holt, Brad C Astor, Josephine P Briggs, Paul W Eggers, David A Lacher, Thomas H Hostetter
Journal: Journal of the American Society of Nephrology (2004)

The incidence of kidney failure treatment in the United States increased 57% from 1991 to 2000. Chronic kidney disease (CKD) prevalence was 11% among U.S. adults surveyed in 1988 to 1994. The objective of this study was to estimate awareness of CKD in the U.S. population during 1999 to 2000 and to determine whether the prevalence of CKD in the United States increased compared with 1988 to 1994. Analysis was conducted of nationally representative samples of noninstitutionalized adults, aged 20 yr and older, in two National Health and Nutrition Examination Surveys conducted in 1988 to 1994 (n = 15,488) and 1999 to 2000 (n = 4101) for prevalence +/- SE. Awareness of CKD is self-reported. Kidney function (GFR), kidney damage (microalbuminuria or greater), and stages of CKD (GFR and albuminuria) were estimated from calibrated serum creatinine, spot urine albumin to creatinine ratio (ACR), age, gender, and race. GFR was estimated using the simplified Modification of Diet in Renal Disease Study equation. Self-reported awareness of weak or failing kidneys in 1999 to 2000 was strongly associated with decreased kidney function and albuminuria but was low even in the presence of both conditions. Only 24.3 +/- 6.4% of patients at GFR 15 to 59 ml/min per 1.73 m(2) and albuminuria were aware of CKD compared with 1.1 +/- 0.3% at GFR of 90 ml/min per 1.73 m(2) or greater and no microalbuminuria. At moderately decreased kidney function (GFR 30 to 59 ml/min per 1.73 m(2)), awareness was much lower among women than men (2.9 +/- 1.6 versus 17.9 +/- 5.9%; P = 0.008). The prevalence of moderately or severely decreased kidney function (GFR 15 to 59 ml/min per 1.73 m(2)) remained stable over the past decade (4.4 +/- 0.3% in 1988 to 1994 and 3.8 +/- 0.4% in 1999 to 2000; P = 0.23). At the same time, the prevalence of albuminuria (ACR >/= 30 mg/g) in single spot urine increased from 8.2 +/- 0.4% to 10.1 +/- 0.7% (P = 0.01). Overall CKD prevalence was similar in both surveys (9% using ACR > 30 mg/g for persistent microalbuminuria; 11% in 1988 to 1994 and 12% in 1999 to 2000 using gender-specific ACR cutoffs). Despite a high prevalence, CKD awareness in the U.S. population is low. In contrast to the dramatic increase in treated kidney failure, overall CKD prevalence in the U.S. population has been relatively stable.
Myeloperoxidase Is a Key Regulator of Oxidative Stress–Mediated Apoptosis in Myeloid Leukemic Cells
Authors: Tomonori Nakazato, Morihiko Sagawa, Kenji Yamato, Mingji Xian, Takehiro Yamamoto, Makoto Suematsu, Yasuo Ikeda, Masahiro Kizaki
Journal: Clinical Cancer Research (2007)

Abstract Purpose: We reported previously that reactive oxygen species (ROS) are key mediators of apoptosis induced by a polyphenol, (−)-epigallocatechin-3-gallate (EGCG), in myeloid leukemic cells. This study aimed to further examine the mechanism of ROS-mediated apoptosis induced by EGCG and its relationship to the heme enzyme myeloperoxidase (MPO). Experimental Design: We established stably transfected K562 cells expressing wild-type and mutant MPO. Then, sensitivity against EGCG and other ROS-inducing agent was examined and further investigated the detailed molecular mechanism of ROS-inducing apoptosis in MPO-positive leukemic cells. Results: EGCG rapidly induced apoptosis in MPO-positive leukemia cells. Preincubation of myeloid leukemic cells with the MPO-specific inhibitor, 4-aminobenzoic acid hydrazide, and the heme biosynthesis inhibitor, succinylacetone, resulted in inhibition of the intracellular MPO activity, ROS production, and induction of apoptosis following addition of EGCG. Overexpression of MPO sensitized EGCG-resistant K562 cells to apoptosis induced by EGCG. In contrast, an enzymatically inactive MPO mutant–expressing K562 cell could not respond to EGCG, suggesting that MPO is important for determining the sensitivity to EGCG-induced oxidative stress. Hypochlorous acid scavengers and the hydroxyl radical (·OH) scavenger inhibited EGCG-induced apoptosis in myeloid leukemic cells. The fluorescence intensity of both aminophenyl fluorescein– and hydroxyphenyl fluorescein–loaded myeloid leukemic cells significantly increased on stimulation with EGCG, indicating that EGCG generated highly toxic ROS in myeloid leukemic cells. Conclusions: These results indicated that highly toxic ROS such as ·OH generated via the hydrogen peroxide/MPO/halide system induce apoptosis and that ROS may be the direct mediators of EGCG-induced apoptosis in MPO-positive leukemic cells.