tbuckley/cabot-search huggingface dataset:
Survey of human immunodeficiency virus (HIV)-seropositive patients with mycobacterial infection in Japan
Authors: Yayoi Otsuka, Tomoko Fujino, Namiko Mori, Jun-ichiro Sekiguchi, Emiko Toyota, Katsutoshi Saruta, Yoshihiro Kikuchi, Yuka Sasaki, Atsushi Ajisawa, Yoshito Otsuka, Hideaki Nagai, Makoto Takahara, Hideo Saka, Takuma Shirasaka, Yasuki Yamashita, Makiko Kiyosuke, Hideyuki Koga, Shinichi Oka, Satoshi Kimura, Toru Mori, Tadatoshi Kuratsuji, Teruo Kirikae
Journal: Journal of Infection (2005)
Endothelial dysfunction in sleep-disordered breathing seems to be more severe in women
Authors: P Bhatia
Journal: Thorax (2004)

▴ Faulx MD, Larkin EK, Hoit BD, et al . Sex influences endothelial function in sleep-disordered breathing. Sleep2004;27:1113–20 [OpenUrl][1][PubMed][2][Web of Science][3] Sleep disordered breathing (SDB) is associated with an increased prevalence of hypertension and cardiovascular disease independent of age, sex, and body mass index. The adverse cardiovascular effects are thought to be due to combinations of overnight hypoxaemia, hypercapnia, and sympathetic nervous system overactivity. There is limited research that has addressed the influence of these … [1]: {openurl}?query=rft.jtitle%253DSleep%26rft.stitle%253DSleep%26rft.aulast%253DFaulx%26rft.auinit1%253DM.%2BD.%26rft.volume%253D27%26rft.issue%253D6%26rft.spage%253D1113%26rft.epage%253D1120%26rft.atitle%253DSex%2Binfluences%2Bendothelial%2Bfunction%2Bin%2Bsleep-disordered%2Bbreathing.%26rft_id%253Dinfo%253Apmid%252F15532205%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [2]: /lookup/external-ref?access_num=15532205&link_type=MED&atom=%2Fthoraxjnl%2F60%2F1%2F75.atom [3]: /lookup/external-ref?access_num=000224445600011&link_type=ISI
Role of Ca2+ and protein kinase C in shear stress-induced actin depolymerization and endothelin 1 gene expression.
Authors: T Morita, H Kurihara, K Maemura, M Yoshizumi, R Nagai, Y Yazaki
Journal: Circulation Research (1994)

Vascular endothelial cells adapt to changes in blood flow by altering the cell architecture and by producing various substances. We have previously reported that low shear stress induces endothelin 1 (ET-1) expression in endothelial cells and that this induction is mediated by depolymerization of actin fiber. In the present study, we examined the role of Ca2+ and protein kinase C (PKC) in shear stress-induced actin depolymerization and subsequent ET-1 gene expression. Exposure of cultured porcine aortic endothelial cells to low shear stress (5 dyne/cm2) for 3 hours increased the ratio of G-actin to total actin from 54 +/- 0.8% to 80 +/- 1.0%. This shear stress-induced actin depolymerization was completely blocked by chelation of extracellular Ca2+ with EGTA and partially inhibited by intracellular Ca2+ chelation with the tetraacetoxymethyl ester of BAPTA (BAPTA/AM). Pretreatment with staurosporine, a PKC inhibitor, or desensitization of PKC by treatment with 12-O-tetradecanoylphorbol 13-acetate (TPA) for 24 hours also resulted in partial inhibition of shear stress-induced actin depolymerization. Although PKC activation by TPA mildly increased G-actin content, the effect of TPA and shear stress on actin depolymerization was not additive. Moreover, shear stress-induced ET-1 gene expression was inhibited by EGTA, BAPTA/AM, and staurosporine to a degree similar to the inhibition of actin depolymerization. In contrast, ET-1 gene expression induced by cytochalasin B, an actin-disrupting agent, was not affected by staurosporine.(ABSTRACT TRUNCATED AT 250 WORDS)
Chronic cyclosporine therapy impairs endothelium-dependent relaxation in the renal artery of the rat.
Authors: D Diederich, Z Yang, T F Lüscher
Journal: Journal of the American Society of Nephrology (1992)

Cyclosporine is an immunosuppressive substance that causes structural and functional alterations in endothelial cells. To examine the effects of chronic cyclosporine therapy on endothelial function, Wistar Kyoto rats received daily s.c. injections of saline, cyclosporine solvent, or cyclosporine (15, 30, or 50 mg/kg) for up to 2 wk. Blood pressure remained unchanged in all groups. Segments of the renal artery were suspended in organ chambers filled with physiological salt solution, and isometric tension was recorded. In rats treated with 30 or 50 mg/kg/day of cyclosporine, endothelium-dependent relaxations to acetylcholine of the renal artery were significantly impaired when compared with vessels obtained from rats injected with saline or solvent. The reduced acetylcholine-induced relaxation of cyclosporine-treated vessels was improved by preincubation of the preparations with the cyclooxygenase inhibitor indomethacin. Endothelium-independent relaxations in response to sodium nitroprusside were unimpaired in renal artery rings after 1 wk of cyclosporine but were reduced after 2 wk of treatment with 30 mg/kg/day. Contractions of the renal artery in response to norepinephrine and serotonin were not altered by cyclosporine. Thus, (1) high-dose cyclosporine therapy impairs endothelium-dependent relaxations in the renal artery of the rat; (2) an endothelium-derived cyclooxygenase product reduces the effects of endothelium-derived relaxing factor in cyclosporine-treated rats; and (3) chronic cyclosporine treatment slightly impairs vascular smooth muscle relaxation, whereas vascular contractility remains unaltered.
Mitochondrial Membrane Potential and Apoptosis Peripheral Blood Monocytes in Severe Human Sepsis
Authors: CHRISTOPHE ADRIE, MARIA BACHELET, MURIEL VAYSSIER-TAUSSAT, FRANÇOISE RUSSO-MARIE, ISABELLE BOUCHAERT, MINOU ADIB-CONQUY, JEAN-MARC CAVAILLON, MICHAEL R. PINSKY, JEAN-FRANÇOIS DHAINAUT, BARBARA S. POLLA
Journal: American Journal of Respiratory and Critical Care Medicine (2001)

Reduced mitochondrial membrane potential ( ΔΨ m), which is considered as an initial and irreversible step towards apoptosis, as well as cell death regulating proteins, such as Fas, Hsp70, or Bcl-2, may play an important role in sepsis. We studied the relationship between sepsis severity and peripheral blood monocyte ΔΨ m, cell death (necrosis and apoptosis), soluble Fas ligand, Hsp70, and Bcl-2 expression over time in 18 patients with sepsis, and compared these data with those of a group of 17 healthy control subjects. All measurements were performed within 3 d of the onset of severe sepsis (T1), then 7 to 10 d later (T2), and finally at hospital discharge (T3). ΔΨ m was expressed as the percent monocytes with altered ΔΨ m (% ΔΨ m). Patients with sepsis had greater % ΔΨ m at T1 and T2 but not at T3 (14.6 ± 2.6% and 15.9 ± 2%, respectively, versus control 6.6 ± 0.2%, p < 0.01). Septic patients exhibited greater cell death in their monocytes and had greater Hsp70 expression only at T1. Bcl-2 levels were similar in septic and control subjects. Comparing survivors with non-survivors of sepsis, nonsurvivors had a greater % ΔΨ m at T1 (26.4 ± 5.3% versus 10.1 ± 2.7%, p < 0.01) and a significant decrease in Bcl-2 expression, whereas no difference was found in Hsp70 levels. These results indicate that mitochondrial dysfunction and subsequent cell death occur in severe sepsis and suggest that % ΔΨ m is a marker of severity in human sepsis.Keywords: mitochondria; apoptosis; sepsis; heat-shock protein 70; proto-oncogene protein c-Bcl-2
Heterogeneous mutations in the human lipoprotein lipase gene in patients with familial lipoprotein lipase deficiency.
Authors: T Gotoda, N Yamada, M Kawamura, K Kozaki, N Mori, S Ishibashi, H Shimano, F Takaku, Y Yazaki, Y Furuichi
Journal: Journal of Clinical Investigation (1991)

The DNA sequences were determined for the lipoprotein lipase (LPL) gene from five unrelated Japanese patients with familial LPL deficiency. The results demonstrated that all five patients are homozygotes for distinct point mutations dispersed throughout the LPL gene. Patient 1 has a G-to-A transition at the first nucleotide of intron 2, which abolishes normal splicing. Patient 2 has a nonsense mutation in exon 3 (Tyr61----Stop) and patient 3 in exon 8 (Trp382----Stop). The latter mutation emphasizes the importance of the carboxy-terminal portion of the enzyme in the expression of LPL activity. Missense mutations were identified in patient 4 (Asp204----Glu) and patient 5 (Arg243----His) in the strictly conserved amino acids. Expression study of both mutant genes in COS-1 cells produced inactive enzymes, establishing the functional significance of the two mis-sense mutations. In these patients, postheparin plasma LPL mass was either virtually absent (patients 1 and 2) or significantly decreased (patients 3-5). To detect these mutations more easily, we developed a rapid diagnostic test for each mutation. We also determined the DNA haplotypes for patients and confirmed the occurrence of multiple mutations on the chromosomes with an identical haplotype. These results demonstrate that familial LPL deficiency is a heterogeneous genetic disease caused by a wide variety of gene mutations.
PROGNOSTIC CRITERIA IN DEMENTIA PARALYTICA
Authors: MAURICE H. GREENHILL, MORRIS YORSHIS
Journal: American Journal of Psychiatry (1940)

1. One hundred cases of dementia paralytica treated at the Worcester State Hospital between the years 1925-1938 were studied to determine criteria useful in the prognosis. An inquiry into the cause of failure of one-half to two-thirds of paretics to undergo remission under pyretotherapy was also undertaken. 2. These patients were treated by one of four methods: malaria, standard diathermy, modified diathermy and tryparsamide. Thirty-three per cent of the total group underwent remission. 3. The following criteria are found to be of value in the determination of the prognosis: age of the patient, duration of the paretic process, previous therapy, extent of neurological dysfunction, history of epileptiform seizures, degree of defects in sensorium, tendency toward spontaneous remission, type of psychopathology exhibited, and degree of adjustment of the preparetic personality. 4. Most important prognostic criterion is the degree of adjustment in the preparetic personality. All of the patients with well- integrated personalities prior to the onset of dementia paralytica underwent remission no matter what type of therapy they were given. Only three out of 63 patients with poorly adjusted personalities experienced remission. 5. Of the other criteria, the most significant are the extent of neurological dysfunction, degree of defect in sensorium and type of psychopathology. Patients in the delirious, apathetic and agitated groups had the best prognosis, those in the demented and schizophreniform the worst. 6. There is found to be a strong correlation between the degree of adjustment in the preparetic personality and the other prognostic criteria. Well-integrated individuals tended to have milder neurological and sensorium defects, slower progress of symptomatology before therapy, and a tendency to spontaneous remission as well as a better prognosis. 7. Three cases of dementia paralytica are cited to show how a relatively accurate prognosis can be formulated. 8. Causes for the greater resistance to the progress of the paretic process and the better response to therapy in the previously well- integrated individual are discussed.
Partitioning of the elastic work of inspiration in patients with COPD during exercise
Authors: P Sliwinski, D Kaminski, J Zielinski, S Yan
Journal: European Respiratory Journal (1998)

During exercise, dynamic hyperinflation-induced intrinsic positive end-expiratory pressure (PEEPi) and decreased dynamic lung compliance (CL,dyn) of patients with chronic obstructive pulmonary disease (COPD) increase the elastic work of inspiration (Wi) more than would be predicted from the increase in tidal volume (VT). This contributes significantly to their exertional breathlessness. In 10 stable patients with COPD, the dynamic Wi was measured during incremental bicycle exercise to exhaustion. The total Wi was then partitioned into the portion required to overcome PEEPi (Wi,PEEPi) and nonPEEPi elastic load (Wi,nonPEEPi). The latter is used to overcome the increase in the total respiratory system elastance during inflation. From resting breathing to peak exercise, Wi more than doubled (p&lt;0.001). This increase was largely due to Wi,PEEPi, which significantly rose from 1.7+/-0.3 to 5.3+/-0.8 L x cm H2O(-1) (p&lt;0.001). In comparison, Wi,nonPEEPi increased from only 3.0+/-0.4 to 5.1+/-0.5 L x cm H2O(-1) (p&lt;0.01). Consequently, Wi,PEEPi as a fraction of total Wi increased from 35.5+/-5.6 to 51.0+/-3.3% (p&lt;0.02). In addition, the measured Wi,nonPEEPi at peak exercise, when expressed as a percentage of its value during resting breathing, was 25% more than that predicted from the increase in VT alone. Assuming a constant chest wall compliance, this can be attributed to the exercise-induced decrease in CL,dyn, which was 0.27+/-0.04 and 0.17+/-0.02 L x cm H2O(-1) (p&lt;0.01), respectively, during resting breathing and peak exercise. In conclusion, the dynamic hyperinflation-induced intrinsic positive end-expiratory pressure is more important than the increase in tidal volume in raising the work of inspiration during exercise in patients with chronic obstructive pulmonary disease; the decrease in dynamic lung compliance plays a definite but less important role.
Original article: Chemotherapy with MACOP-B and VACOP-B for intermediate- and high-grade non-Hodgkin's lymphoma: Clinical results and analysis of prognostic factors
Authors: G. Pichert, J. Peters, R.A. Stahel, C. Dommann, R. Joss, J.O. Gebbers, T. Kroner, H. Sulser, H.P. Honegger, R. Maurer, S. Pampallona
Journal: Annals of Oncology (1992)
Treatment of Human Epidermal Growth Factor Receptor 2-Overexpressing Breast Cancer Xenografts With Multiagent HER-Targeted Therapy
Authors: G. Arpino, C. Gutierrez, H. Weiss, M. Rimawi, S. Massarweh, L. Bharwani, S. De Placido, C. K. Osborne, R. Schiff
Journal: JNCI Journal of the National Cancer Institute (2007)

Human epidermal growth factor receptor 2 (HER2) is a member of the HER signaling pathway. HER inhibitors partially block HER signaling and tumor growth in preclinical breast cancer models. We investigated whether blockade of all HER homo- and heterodimer pairs by combined treatment with several inhibitors could more effectively inhibit tumor growth in such models.Mice carrying xenograft tumors of HER2-overexpressing MCF7/HER2-18 (HER2-transfected) or BT474 (HER2-amplified) cells were treated with estrogen supplementation or estrogen withdrawal, alone or combined with tamoxifen. One to three HER inhibitors (pertuzumab, trastuzumab, or gefitinib) could also be added (n > or = 8 mice per group). Tumor volumes, HER signaling, and tumor cell proliferation and apoptosis were assessed. Results were analyzed with the t test or Wilcoxon rank sum test and survival analysis methods. All statistical tests were two-sided.Median time to tumor progression was 21 days for mice receiving estrogen and 28 days for mice receiving estrogen and pertuzumab (difference = 7 days; P = .001; hazard ratio [HR] of progression in mice receiving estrogen and pertuzumab versus mice receiving estrogen = 0.27, 95% confidence interval [CI] = 0.09 to 0.77). Addition of gefitinib and trastuzumab to estrogen and pertuzumab increased this time to 49 days (difference = 21 days; P = .004; HR of progression = 0.28, 95% CI = 0.10 to 0.76). MCF7/HER2-18 tumors disappeared completely and did not progress (for > or = 189 days) after combination treatment with pertuzumab, trastuzumab, and gefitinib plus tamoxifen (19 of 20 mice) or plus estrogen withdrawal (14 of 15 mice). Both combination treatments induced apoptosis and blocked HER signaling and proliferation in tumor cells better than any single agent or dual combination. All BT474 tumors treated with pertuzumab, trastuzumab, and gefitinib disappeared rapidly, regardless of endocrine therapy, and no tumor progression was observed for 232 days.Combined treatment with gefitinib, trastuzumab, and pertuzumab to block signals from all HER homo- and heterodimers inhibited growth of HER2-overexpressing xenografts statistically significantly better than single agents and dual combinations.
Trastuzumab plus Adjuvant Chemotherapy for Operable HER2-Positive Breast Cancer
Authors: Edward H. Romond, Edith A. Perez, John Bryant, Vera J. Suman, Charles E. Geyer, Nancy E. Davidson, Elizabeth Tan-Chiu, Silvana Martino, Soonmyung Paik, Peter A. Kaufman, Sandra M. Swain, Thomas M. Pisansky, Louis Fehrenbacher, Leila A. Kutteh, Victor G. Vogel, Daniel W. Visscher, Greg Yothers, Robert B. Jenkins, Ann M. Brown, Shaker R. Dakhil, Eleftherios P. Mamounas, Wilma L. Lingle, Pamela M. Klein, James N. Ingle, Norman Wolmark
Journal: New England Journal of Medicine (2005)

We present the combined results of two trials that compared adjuvant chemotherapy with or without concurrent trastuzumab in women with surgically removed HER2-positive breast cancer.
Basophil allergen threshold sensitivity: a useful approach to anti‐IgE treatment efficacy evaluation
Authors: A. Nopp, S. G. O. Johansson, J. Ankerst, G. Bylin, L. O. Cardell, R. Grönneberg, K. Irander, M. Palmqvist, H. Öman
Journal: Allergy (2006)

Monitoring of the allergen sensitivity of a patient is most important for optimal patient care and a basic prerequisite for immunomodulating treatment. The objective of this study was to investigate how basophil allergen sensitivity can be applied in the monitoring of anti-immunoglobulin E (IgE) treatment.Basophils from timothy grass pollen allergic patients were, by flow cytometry, analysed for allergen threshold sensitivity (CD-sens) by measuring CD63 up-regulation on CD203c-identified basophils. The results were compared with maximal percentage CD63 up-regulation at one allergen dose (CD-max), skin prick test end-point allergen titration, (SPT-sens), nasal provocation titration tests (nasal provocation titre) and serum IgE and IgE antibody concentrations.There was a significant correlation (r = 0.50, P = 0.01) between CD-sens and SPT-sens, CD-sens and the IgE antibody concentration in percentage of 'total IgE' (relative IgE antibody concentration) (r = 0.72, P < 0.001) as well as between CD-sens and nasal provocation titre (r = 0.54, P < 0.05) but, in contrast, CD-max did not correlate with any of the sensitization parameters, i.e. SPT-sens, nasal provocation titre, absolute and relative IgE antibody concentration or CD-sens. CD-sens could be used to monitor omalizumab treatment efficacy while, based on CD-max, four of seven symptom-free patients on omalizumab would have been classified as having ongoing allergy.CD-sens seems to be very useful for the determination of a patient's allergen sensitivity and should be evaluated for the measurement and monitoring of anti-IgE treatment efficacy. CD-max, the conventional approach to basophil allergen challenge, which mirrors cell reactivity, gives incorrect information.
Ca <sup>2+</sup> Elevation Evoked by Membrane Depolarization Regulates G Protein Cycle via RGS Proteins in the Heart
Authors: Masaru Ishii, Atsushi Inanobe, Satoru Fujita, Yasunaka Makino, Yukio Hosoya, Yoshihisa Kurachi
Journal: Circulation Research (2001)

Regulators of G protein signaling (RGS), which act as GTPase activators, are a family of cytosolic proteins emerging rapidly as an important means of controlling G protein-mediated cell signals. The importance of RGS action has been verified in vitro for various kinds of cell function. Their in situ modes of action in intact cells are, however, poorly understood. Here we show that an increase in intracellular Ca(2+) evoked by membrane depolarization controls the RGS action on G protein activation of muscarinic K(+) (K(G)) channel in the heart. Acetylcholine-induced K(G) current exhibits a slow time-dependent increase during hyperpolarizing voltage steps, referred to as "relaxation." This reflects the relief from the decrease in available K(G) channel number induced by cell depolarization. This phenomenon is abolished when an increase in intracellular Ca(2+) is prevented. It is also abolished when a calmodulin inhibitor or a mutant RGS4 is applied that can bind to calmodulin but that does not accelerate GTPase activity. Therefore, an increase in intracellular Ca(2+) and the resultant formation of Ca(2+)/calmodulin facilitate GTPase activity of RGS and thus decrease the available channel number on depolarization. These results indicate a novel and probably general pathway that Ca(2+)-dependent signaling regulates the G protein cycle via RGS proteins.
Two-Year Carcinogenicity Study of Sodium Fluoride in Rats
Authors: J. K. Maurer, M. C. Cheng, B. G. Boysen, R. L. Anderson
Journal: JNCI Journal of the National Cancer Institute (1990)

To determine the carcinogenic potential of sodium fluoride (NaF), we fed Sprague-Dawley rats a diet containing NaF for up to 99 weeks. Rats receiving NaF at a dose of 4, 10, or 25 mg/kg per day added to a low-fluoride diet were compared with controls receiving either a low-fluoride diet or laboratory chow. Each treatment group consisted of 70 rats of each sex. A 30% decrement in weight gain occurred at an NaF dose of 25 mg/kg per day. Evidence of fluoride toxicity was seen in the teeth, bones, and stomach, and the incidence and severity of these changes were related to the dose of NaF and the duration of exposure. Despite clear evidence of toxicity, NaF did not alter the incidence of preneoplastic and neoplastic lesions at any site in rats of either sex. Results from this study indicate that NaF is not carcinogenic in Sprague-Dawley rats.
Effect of zinc supplementation on mortality in children aged 1–48 months: a community-based randomised placebo-controlled trial
Authors: Sunil Sazawal, Robert E Black, Mahdi Ramsan, Hababu M Chwaya, Arup Dutta, Usha Dhingra, Rebecca J Stoltzfus, Mashavi K Othman, Fatma M Kabole
Journal: The Lancet (2007)
Analog Integrated Circuits Design for Processing Physiological Signals
Authors: Yan Li, Carmen C. Y. Poon, Yuan-Ting Zhang
Journal: IEEE Reviews in Biomedical Engineering (2010)

Analog integrated circuits (ICs) designed for processing physiological signals are important building blocks of wearable and implantable medical devices used for health monitoring or restoring lost body functions. Due to the nature of physiological signals and the corresponding application scenarios, the ICs designed for these applications should have low power consumption, low cutoff frequency, and low input-referred noise. In this paper, techniques for designing the analog front-end circuits with these three characteristics will be reviewed, including subthreshold circuits, bulk-driven MOSFETs, floating gate MOSFETs, and log-domain circuits to reduce power consumption; methods for designing fully integrated low cutoff frequency circuits; as well as chopper stabilization (CHS) and other techniques that can be used to achieve a high signal-to-noise performance. Novel applications using these techniques will also be discussed.