tbuckley/cabot-search huggingface dataset:
Diagnosing Encephalitis, Not Otherwise Specified
Authors: Zhi-li Wang, Eric Lancaster, Li Yang
Journal: JAMA Neurology (2015)

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Phase II Study of Capecitabine and Oxaliplatin in First- and Second-Line Treatment of Advanced or Metastatic Colorectal Cancer
Authors: Markus M. Borner, Daniel Dietrich, Roger Stupp, Rudolf Morant, Hanspeter Honegger, Martin Wernli, Richard Herrmann, Bernhard C. Pestalozzi, Piercarlo Saletti, Silvia Hanselmann, Samuel Müller, Peter Brauchli, Monica Castiglione-Gertsch, Aron Goldhirsch, Arnaud D. Roth
Journal: Journal of Clinical Oncology (2002)

PURPOSE: To determine the efficacy and tolerability of combining oxaliplatin with capecitabine in the treatment of advanced nonpretreated and pretreated colorectal cancer. PATIENTS AND METHODS: Forty-three nonpretreated patients and 26 patients who had experienced one fluoropyrimidine-containing regimen for advanced colorectal cancer were treated with oxaliplatin 130 mg/m 2 on day 1 and capecitabine 1,250 mg/m 2 bid on days 1 to 14 every 3 weeks. Patients with good performance status (World Health Organization grade 0 to 1) were accrued onto two nonrandomized parallel arms of a phase II study. RESULTS: The objective response rate was 49% (95% confidence interval [CI], 33% to 65%) for nonpretreated and 15% (95% CI, 4% to 35%) for pretreated patients. The main toxicity of this combination was diarrhea, which occurred at grade 3 or 4 in 35% of the nonpretreated and 50% of the pretreated patients. Grade 3 or 4 sensory neuropathy, including laryngopharyngeal dysesthesia, occurred in 16% of patients on both cohorts. Capecitabine dose reductions were necessary in 26% of the nonpretreated and 45% of the pretreated patients in the second treatment cycle. The median overall survival was 17.1 months and 11.5 months, respectively. CONCLUSION: Combining capecitabine and oxaliplatin yields promising activity in advanced colorectal cancer. The main toxicity is diarrhea, which is manageable with appropriate dose reductions. On the basis of our toxicity experience, we recommend use of capecitabine in combination with oxaliplatin 130 mg/m 2 at an initial dose of 1,250 mg/m 2 bid in nonpretreated patients and at a dose of 1,000 mg/m 2 bid in pretreated patients.
Effect of multiple actuations, delayed inhalation and antistatic treatment on the lung bioavailability of salbutamol via a spacer device.
Authors: D. J. Clark, B. J. Lipworth
Journal: Thorax (1996)

BACKGROUND: The aim of this study was to extend previous in vitro observations regarding the effects of multiple actuations of aerosols into spacer devices, delayed inhalation, and antistatic treatment of spacer devices on the amount of drug delivered for inhalation. An in vivo study of lung bioavailability of salbutamol from a large volume (Volumatic) spacer was conducted. METHODS: Ten healthy volunteers of mean age 20.5 years with a mean forced expiratory volume in one second of 112.1% predicted were studied in a randomised single blind (investigator blind) crossover study. 1200 micrograms of salbutamol was given with mouth rinsing (100 micrograms/puff) on four study days: single puffs via spacer, multiple puffs via spacer (3 x 4 puffs), single puffs with 20 second delay before inhalation via spacer, and single puffs via an antistatic treated spacer. All spacers, including those treated with antistatic, were prewashed prior to each study day. Measurements of lung bioavailability were made at five, 10, and 20 minutes after inhalation to determine peak (Cmax) and average (Cav) plasma salbutamol levels. Systemic beta 2 responses including finger tremor, heart rate, and plasma potassium levels were also evaluated. RESULTS: Single puffs from the spacer produced higher plasma salbutamol levels and greater systemic beta 2 responses than either multiple puffs or single puffs with delayed inhalation for a 1200 micrograms dose. For Cmax this amounted to a 1.93-fold (95% CI 1.68 to 2.19) greater lung bioavailability for single puffs than for multiple puffs and a 1.80-fold (95% CI 1.59 to 2.00) greater lung bioavailability for single puffs than for single puffs with a 20 second delay. Comparison of the normal and antistatic treated spacers (both prewashed) revealed differences for Cmax with levels 1.23-fold (95% CI 1.04 to 1.41) greater for the normal spacer. CONCLUSIONS: Delayed inhalation from a Volumatic spacer and the use of multiple puffs results in a considerable decrease in the delivery of salbutamol to the lungs with an approximate twofold reduction in lung bioavailability. Washing a Volumatic spacer is as effective as an antistatic lining in reducing the effects of static charge on salbutamol delivery in vivo.
Effect of nedocromil sodium on sulphur dioxide induced bronchoconstriction.
Authors: C M Dixon, R W Fuller, P J Barnes
Journal: Thorax (1987)

Nedocromil sodium is a pyranoquinoline derivative that has been developed for the treatment of asthma. We report the results of a double blind randomised study of the effect of two doses of nedocromil sodium (2 and 4 mg) and matched placebo, delivered by metered dose pressurised aerosol, on bronchoconstriction induced by sulphur dioxide in six asthmatic subjects. Nedocromil sodium had no effect on baseline lung function. The magnitude of sulphur dioxide induced bronchoconstriction monitored by partial forced expiratory flow at 30% of reference vital capacity was significantly inhibited by nedocromil sodium 4 mg (p less than 0.05) but not by 2 mg. The maximum changes after placebo and after nedocromil 2 mg and 4 mg were -44.7, -32.7, and -11.8 l min-1. The area under the curve monitoring the effect over 6 minutes was significantly inhibited by both doses to the same extent, the mean changes after placebo and after nedocromil 2 mg and 4 mg being -349.3, -31.2, and 44.6 l. Dyspnoea was monitored by visual analogue scale and showed a significant reduction over 6 minutes with both doses of nedocromil. After placebo and after nedocromil 2 mg and 4 mg the mean maximum changes were 31.5, 13.7, and 15.7 mm, and the mean changes in area under the visual analogue scale-time curve were 289, 194, and 151 mm.min respectively.
Effect of Canarypox Virus (ALVAC)-Mediated Cytokine Expression on Murine Prostate Tumor Growth
Authors: M. Kawakita, G. S. Rao, J. K. Ritchey, D. K. Ornstein, M. A. Hudson, T. J. Harmon, T. L. Ratliff, P. A. Humphrey, J. Tartaglia, E. Paoletti
Journal: JNCI Journal of the National Cancer Institute (1997)

Background: Canarypox virus, ALVAC, does not replicate in infected mammalian cells and has potential as a vector for gene therapy in the treatment of cancer. Purpose: Recombinant viruses carrying DNA sequences encoding interleukin 2 (ALVAC—IL-2), interferon gamma (ALVAC—IFN γ), tumor necrosis factor-α (ALVAC—TNF-α), or the co-stimulatory molecule B7-1 (ALVAC—B7-1) were investigated as agents for the treatment of a newly defined mouse prostate tumor model. Methods: RM-1 mouse prostate cancer cells, which are syngeneic (i.e., same genetic background) to C57BL/6 mice, were used. The expression of foreign gene products in vitro in infected RM-1 cells was measured by immunoprecipitation, bioassay, or flow cytometry. The effects of foreign gene product expression on RM-1 tumor cell growth in C57BL/6 mice were measured after subcutaneous injection (in the back) of 5 × 10 5 uninfected or infected cells; measurements included determinations of time to a measurable tumor size, tumor size as a function of time, and survival. The induction of protective immunity by uninfected and infected RM-1 cells was tested by injection of lethally irradiated (70 Gy) cells and subsequent challenge with uninfected cells. The generation of cytotoxic T cells was monitored by use of a 51 Cr release assay. Severe combined immunodeficient (SCID) mice were used to determine whether T or B lymphocytes were involved in ALVAC vector-mediated antitumor responses. Data were analyzed by use of Pearson's modification of the chi-squared test and Kaplan—Meier survival methods. Reported P values are two-sided. Results: The level of foreign gene product expression in ALVAC-infected RM-1 cells was dependent on the multiplicity of virus infection used; a multiplicity of five viruses per infected cell was chosen for subsequent experiments. RM-1 tumor growth in C57BL/6 mice was not affected by tumor cell expression of IL-2 alone, IFN γ alone, or B7-1 alone; however, expression of TNF-α alone significantly delayed tumor growth at early time points (compared with parental ALVAC-infected tumors, P = .0001 at day 21 and P = .037 at day 28). Tumor cell expression of both TN6F-α and IL-2 completely inhibited tumor growth in 60%–100% of treated mice. No protection against subsequent tumor challenge was detected in mice previously exposed to RM-1 cells expressing both TNF-α and IL-2. Cytotoxic T-lymphocyte activity toward RM-1 cells was not observed in C57BL/6 mice that rejected tumors. Tumor cell expression of TNF-α and IL-2 also resulted in tumor growth inhibition in SCID mice. Conclusions: RM-1 mouse prostate cancer cells are readily infected by ALVAC vectors, and foreign gene products are efficiently expressed. Inhibition of RM-1 tumor growth by tumor cell expression of TNF-α and IL-2 appears to involve nonspecific antitumor activity.
Clinical cross-reactivity between amoxicillin and cephadroxil in patients allergic to amoxicillin and with good tolerance of penicillin
Authors: J. Sastre, L.-D. Quijano, A. Novalbos, G. Hernandez, J. Cuesta, M. Heras, M. Lluch, M. Fernandez
Journal: Allergy (1996)

In recent years, patients allergic to amoxicillin (AX) but with good tolerance of penicillin G (PG) have been described. It has been suggested that the epitope implicated in this type of sensitization might be located on the side-chain of the AX molecule. Thus, cross-reactivity between AX and cephadroxil (CEPH), a cephalosporin which shares an identical side-chain with AX, is suspected. This study aimed to demonstrate clinical cross-reactivity between AX and CEPH in patients allergic to AX and showing good tolerance of PG. In 76 of 576 subjects with suspected allergic reaction to PG and/or AX, the diagnosis of allergy was confirmed. All of these had specific IgE to PG, penicillin V, or AX, and/or positive skin tests to PPL (penicilloyl-polylysine), or MDM (minor determinant mixture), or PG, or AX, and/or positive challenge tests with PG and/or AX. Sixteen subjects (21%) allergic to AX (11 with positive skin test and five with positive challenge test to AX) and good tolerance of PG (all with negative parenteral challenge test) were selected. These 16 patients were subsequently challenged with CEPH (up to 500 mg). Fourteen patients tolerated CEPH, and two (12%) had an immediate allergic reaction. Our study indicates that allergy to the side-chain of aminopenicillins seems to have little clinical relevance in patients with allergic reactions to aminopenicillins but with good tolerance of PG, as 88% of patients with this clinical characteristic tolerate a cephalosporin which shares an identical side-chain. It seems that IgE from most of these patients recognizes an epitope different from the side-chain and the beta-lactam ring.
Insulin-induced hypoglycemia stimulates corticotropin-releasing factor and arginine vasopressin secretion into hypophysial portal blood of conscious, unrestrained rams.
Authors: A Caraty, M Grino, A Locatelli, V Guillaume, F Boudouresque, B Conte-Devolx, C Oliver
Journal: Journal of Clinical Investigation (1990)

Insulin-induced hypoglycemia (IIH) is a strong stimulator of pituitary ACTH secretion. The mechanisms by which IIH activates the corticotrophs are still controversial. Indeed, in rats the variations of corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) secretion in hypophysial portal blood (HPB) during IIH have been diversely appreciated. This may be due to the stressful conditions required for portal blood collection in rats. We studied the effects of IIH on the secretion of CRF and AVP in HPB and on the release of ACTH and cortisol in peripheral plasma in conscious, unrestrained, castrated rams. After the injection of a low (0.2 IU/kg) or high dose (2 IU/kg) of insulin, ACTH and cortisol levels in peripheral plasma increased in a dose-related manner. After injection of the low dose of insulin, CRF and AVP secretion in HPB were equally stimulated. After injection of the high dose of insulin, CRF secretion was further stimulated, while AVP release was dramatically increased. These results suggest that when the hypoglycemia is moderate, CRF is the main factor triggering ACTH release, and that the increased AVP secretion potentiates the stimulatory effect of CRF. When hypoglycemia is deeper, AVP secretion becomes predominant and may by itself stimulate ACTH release.
Intermediate phenotypes in patients with autosomal dominant hyper-IgE syndrome caused by somatic mosaicism
Authors: Amy P. Hsu, Kathryn J. Sowerwine, Monica G. Lawrence, Joie Davis, Carolyn J. Henderson, Kol A. Zarember, Mary Garofalo, John I. Gallin, Douglas B. Kuhns, Theo Heller, Joshua D. Milner, Jennifer M. Puck, Alexandra F. Freeman, Steven M. Holland
Journal: Journal of Allergy and Clinical Immunology (2013)
GENETICS OF A NEW IgVH (T15 IDIOTYPE) MARKER IN THE MOUSE REGULATING NATURAL ANTIBODY TO PHOSPHORYLCHOLINE
Authors: R. Lieberman, M. Potter, E. B. Mushinski, W. Humphrey, S. Rudikoff
Journal: The Journal of Experimental Medicine (1974)

The idiotype present on the Fab of a phosphorylcholine-binding IgA myeloma protein TEPC 15 (T15) of BALB/c origin was found in normal serum of BALB/c mice. Molecules carrying the T15 idiotype in normal serum could be adsorbed with Sepharose phosphorylcholine beads and R36A pneumococci. The T15 idiotype is absent in germ-free BALB/c but appears when the mice are conventionalized. A survey of normal sera of inbred strains for the T15 idiotype showed it to be present in BALB/c, 129, C57L, C58, and ST and absent or in low levels in CBA, C3H, C57BL/6, C57BL/Ka, C57BL/10, SJL, B10.D2, DBA/2, RIII, A, AL, AKR, NZB, and NH inbred strains of mice. The T15 idiotype is associated with some but not all strains carrying the IgC(H) allotypes found in BALB/c. Linkage of genes controlling the T15 idiotype in normal serum to the IgC(H) locus of BALB/c was demonstrated in F(2) progeny of a BALB/c and C57BL cross, Bailey's recombinant inbred strains, C x BD, C x BE, C x BG, C x BH, C x BI, C x BJ, C x BK, and CB20 congenic strains. Among these strains, only those possessing the IgC(H) locus of BALB/c including the F(2) progeny consisting of BALB/c homozygotes and BALB/c/C57BL heterozygotes and C x BG and C x BJ recombinants showed the T15 idiotype.
Risk of Second Malignant Neoplasm Among Patients With Lymphoma
Authors: Vincenzo Pitini, Carmela Arrigo, Maria Grazia Sauta, Giuseppe Altavilla
Journal: Journal of Clinical Oncology (2011)

TO THE EDITOR: The recently published article, “Long-Term Complications of Lymphoma and Its Treatment,” by Ng et al 1 provides a much needed overview of its topic. Unfortunately, however, the article fails to emphasize two key concepts: first, the necessity of investigating the impact of associated rituximab treatment in nonHodgkin’s lymphoma on long-term complications, and second, the differences in risk of a new, second malignancy caused by a lymphoma subtype. Briefly, the monoclonal antibody rituximab has increased disease-free survival for many lymphoid malignant diseases and seems not to have a significant influence on secondary myelodysplastic syndromes/acute myeloid leukemia, whereas it has emerged as an independent risk factor for solid tumor development. 2 In addition, even if the precise role played by B cells in cancer biology remains to be defined, recent reports stress antitumor B-cell— derived immunity. 3,4 In other words, it seems conceivable that the profound immunosuppression that is secondary to B-cell deletion by rituximab may contribute to the expansion of tumor cells. Given that the occurrences of lung cancer and melanoma are limited to more indolent lymphomas, it is plausible that long-term immune dysfunction from the underlying disease or repeated treatments is responsible. Furthermore, the heightened risks immediately after chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL) and follicular lymphoma (FL) diagnoses suggest an intrinsic mechanism, possibly involving prediagnostic immune alterations or defects in a cell cycle and apoptosis, which are more characteristic of indolent rather than aggressive lymphomas. Recent findings demonstrate substantial heterogeneity in the occurrence of a second malignancy by a lymphoma subtype, which suggests differences in etiology. Specifically, significantly different patterns of second malignancy after CLL/SLL, diffuse large B-cell lymphoma (DLBCL), and FL among patients without HIV/AIDS-related lymphoma have been reported. 5 Most notable were the elevated risks for lung cancer and melanoma after the more indolent lymphomas, but not after the more aggressive DLBCL. Furthermore, survivors of CLL/SLL and FL have demonstrated a greater risk of developing other nonhematologic malignancies (ie, salivary gland, colon, anus, and thyroid), whereas, in contrast, no evidence has been reported, to our
A universal method for automated gene mapping.
Authors: Peder Zipperlen, Knud Nairz, Ivo Rimann, Konrad Basler, Ernst Hafen, Michael Hengartner, Alex Hajnal
Journal: Genome biology (2005)

Abstract Small insertions or deletions (InDels) constitute a ubiquituous class of sequence polymorphisms found in eukaryotic genomes. Here, we present an automated high-throughput genotyping method that relies on the detection of fragment-length polymorphisms (FLPs) caused by InDels. The protocol utilizes standard sequencers and genotyping software. We have established genome-wide FLP maps for both Caenorhabditis elegans and Drosophila melanogaster that facilitate genetic mapping with a minimum of manual input and at comparatively low cost.
VISUAL MOTOR COMPUTATIONS IN INSECTS
Authors: Mandyam V. Srinivasan, Shaowu Zhang
Journal: Annual Review of Neuroscience (2004)

With their relatively simple nervous systems and purpose-designed behaviors and reflexes, insects are an excellent organism in which to investigate how visual information is acquired and processed to guide locomotion and navigation. Flies maintain a straight course and monitor their motion through the environment by sensing the patterns of optic flow induced in the eyes. Bees negotiate narrow gaps by balancing the speeds of the images in their two eyes, and they control flight speed by holding constant the average image velocity as seen with their two eyes. Bees achieve a smooth landing on a horizontal surface by holding the image velocity of the surface constant during approach, thus ensuring that flight speed is automatically close to zero at touchdown. Foraging bees estimate the distance that they have traveled to reach a food source by integrating the optic flow experienced en route; this integration gives them a visually driven "odometer." Insects have also evolved sophisticated visuomotor mechanisms for pursuing prey or mates and possibly for concealing their own motion while shadowing objects of interest.
Extranuclear Coactivator Signaling Confers Insensitivity to Tamoxifen
Authors: Rakesh Kumar, Hao Zhang, Caroline Holm, Ratna K. Vadlamudi, Goran Landberg, Suresh K. Rayala
Journal: Clinical Cancer Research (2009)

Abstract Purpose: Tamoxifen is one of many standard therapeutic options currently available for estrogen receptor-α–positive breast cancer patients. Emerging data have suggested that levels of estrogen receptor coregulatory proteins play a significant role in acquiring resistance to antiestrogen action. It has been suggested that high levels of estrogen receptor coactivators and its mislocalization may enhance the estrogen agonist activity of tamoxifen and contribute to tamoxifen resistance. Experimental Design: In an effort to understand the impact of nongenomic signaling and its contribution to hormone resistance in a whole-animal setting, we generated a transgenic mouse expressing a cytoplasmic version of proline-, glutamic acid–, and leucine-rich protein–1 (PELP1) mutant defective in its nuclear translocation (PELP1-cyto) and implanted these mice with tamoxifen pellets to assess its responsiveness. Results: We show that mammary glands from these mice developed widespread hyperplasia with increased cell proliferation and enhanced activation of mitogen-activated protein kinase and AKT as early as 12 weeks of age. Treatment with tamoxifen did not inhibit this hyperplasia; instead, such treatment exaggerated hyperplasia with an enhanced degree of alteration, indicative of hypersensitivity to tamoxifen. Analysis of molecular markers in the transgenic mammary glands from the tamoxifen-treated transgenic mice showed higher levels of proliferation markers proliferating cell nuclear antigen and activated mitogen-activated protein kinase than in untreated PELP1-cyto cell-derived mice. We also found that nude mice with MCF-7/PELP1-cyto cell-derived tumor xenografts did not respond to tamoxifen. Using immunohistochemical analysis, we found that 43% of human breast tumor samples had high levels of cytoplasmic PELP1, which shows a positive correlation between tumor grade and proliferation. Patients whose tumors had high levels of cytoplasmic PELP1 exhibited a tendency to respond poorly to tamoxifen compared with patients whose tumors had low levels of cytoplasmic PELP1. Conclusions: These findings suggest that PELP1 localization could be used as a determinant of hormone sensitivity or vulnerability. The establishment of the PELP1-cyto transgenic mouse model is expected to facilitate the development of preclinical approaches for effective intervention of breast tumors using cytoplasmic coregulators and active nongenomic signaling.