tbuckley/cabot-search huggingface dataset:
<i>Fibroblast Growth Factor Receptor 3</i> Mutation Analysis on Voided Urine for Surveillance of Patients with Low-Grade Non-Muscle–Invasive Bladder Cancer
Authors: Tahlita C.M. Zuiverloon, Madelon N.M. van der Aa, Theo H. van der Kwast, Ewout W. Steyerberg, Hester F. Lingsma, Chris H. Bangma, Ellen C. Zwarthoff
Journal: Clinical Cancer Research (2010)

Mutations in the fibroblast growth factor receptor 3 (FGFR3) have been found in 70% of the low-grade non-muscle-invasive bladder cancer (NMI-BC) tumors. We aim to determine the potential of FGFR3 mutation analysis on voided urine to detect recurrences during surveillance of patients with low-grade NMI-BC.FGFR3 mutation status of the study inclusion tumor was determined from 200 low-grade NMI-BC patients. Patients with an FGFR3-mutant inclusion tumor were selected for analysis and monitored by cystoscopy, and voided urine samples were collected. FGFR3 mutation analysis was done on 463 prospectively collected urines. Sensitivity and predictive value of the assay were determined for detection of concomitant recurrences. Longitudinal and Cox time-to-event analyses were done to determine the predictive value for detection of future recurrences.Median follow-up was 3.5 years. The sensitivity of the assay for detection of concomitant recurrences was 26 of 45 (58%). Of the 105 positive urine samples, 85 (81%) were associated with a concomitant or a future recurrence. An FGFR3-positive urine was associated with a 3.8-fold (P < 0.0001) higher risk of having a recurrence in the Cox analysis. In contrast, only 41 of 358 (11%) FGFR3-negative urine samples were associated with a recurrence. Positive predictive value increased from 25% to 90% in patients having consecutive FGFR3-positive urine tests.FGFR3 mutation analysis on voided urine is a simple and noninvasive diagnostic method for detection of recurrences during surveillance of patients presenting with a low-grade FGFR3-mutant NMI-BC tumor.
Protection of mice from experimental infection with type III group B Streptococcus using monoclonal antibodies.
Authors: M L Egan, D G Pritchard, H C Dillon, B M Gray
Journal: The Journal of Experimental Medicine (1983)

Mouse hybridoma antibodies of several major classes against group B streptococcus type III have been produced. Mice were immunized with either whole heat-killed or acid-treated organisms to obtain antibodies against both the complete (sialated) or incomplete (nonsialated) forms of the type III polysaccharide. Resulting monoclonal antibodies showed exclusive specificity for either the complete or incomplete antigen. The ability of these antibodies to protect mice from a lethal challenge of live type III organisms was tested with a mucin model that permitted use of very small inocula given intraperitoneally with antibody and mucin. Antibodies specific for the nonsialated antigen were not protective, whether of IgM, IgG2a, or IgG3 isotypes. Antibodies specific for the complete antigen were, however, highly protective, including monoclonals of IgM, IgG2a, and IgA isotypes. These mouse monoclonal antibodies against group B streptococci that are directed against either complete or incomplete antigenic determinants, and include isotypes other than IgM, should be particularly useful for studying the mechanism of protection against experimental infection.
Fatigue is not a necessary stimulus for strength gains during resistance training
Authors: J P Folland, C S Irish, J C Roberts, J E Tarr, D A Jones
Journal: British Journal of Sports Medicine (2002)

High resistance training enhances muscular strength, and recent work has suggested an important role for metabolite accumulation in this process.To investigate the role of fatigue and metabolite accumulation in strength gains by comparing highly fatiguing and non-fatiguing isotonic training protocols.Twenty three healthy adults (18-29 years of age; eight women) were assigned to either a high fatigue protocol (HF: four sets of 10 repetitions with 30 seconds rest between sets) to maximise metabolic stress or a low fatigue protocol (LF: 40 repetitions with 30 seconds between each repetition) to minimise changes. Subjects lifted on average 73% of their 1 repetition maximum through the full range of knee extension with both legs, three times a week. Quadriceps isometric strength of each leg was measured at a knee joint angle of 1.57 rad (90 degrees ), and a Cybex 340 isokinetic dynamometer was used to measure the angle-torque and torque-velocity relations of the non-dominant leg.At the mid-point of the training, the HF group had 50% greater gains in isometric strength, although this was not significant (4.5 weeks: HF, 13.3 (4.4)%; LF, 8.9 (3.6)%). This rate of increase was not sustained by the HF group, and after nine weeks of training all the strength measurements showed similar improvements for both groups (isometric strength: HF, 18.2 (3.9)%; LF, 14.5 (4.0)%). The strength gains were limited to the longer muscle lengths despite training over the full range of movement.Fatigue and metabolite accumulation do not appear to be critical stimuli for strength gain, and resistance training can be effective without the severe discomfort and acute physical effort associated with fatiguing contractions.
Three-dimensional reconstruction of coronary arteriole plexus image by contrast echocardiography using high frequency transducer
Authors: Fuminobu Ishikura, Syunichi Ose, Yasushi Kashiwagi, Sachiko Yagura, Kenntaro Ohtani, Jyuri Okazaki, Hideo Hirayama, Toshihiko Asanuma, Akiko Iwata, Tsutomu Toshida, Tetsuya Kawagishi, Yoshitaka Mine, Shintaro Beppu
Journal: Journal of the American College of Cardiology (2002)
Effect of Acid, Alkali, and Meals on Blood Level and Excretion of Sulphapyridine in Children
Authors: H. E. C. Wilson
Journal: BMJ (1943)

The effect of the sulphonamide drugs on the acid-base metabolism has received a certain amount of attention without, however, any clear-cut conception as to the nature or cause of the upset having been.obtained.Beckmann et al. (1940) have shown in adults that with doses of about 6 g. a day there is a proportionate fall in the sodium and bicarbonate, with a rise in the chloride of the blood.These changes were associated with a temporary increase in the sodium excretion and a smaller one in the chloride ex- cretion which shortly fell to the normal rate of output.They state that the electrolytic pattern of the blood resembles that observed after the administration of acid salts such as ammonium chloride and ammonium sulphate, except that the increase in the blood chloride is bound to sodium in the case of the acid salts, while after sulphanilamide they assume that the extra chloride.must pre- sumably be bound to the serum proteins.
Videothoracoscopic treatment of oesophageal leiomyoma
Authors: G C Roviaro, M Maciocco, F Varoli, C Rebuffat, C Vergani, A Scarduelli
Journal: Thorax (1998)

<h3>BACKGROUND</h3> Oesophageal leiomyomas are usually so easily removed that thoracotomy seems out of proportion and thoracoscopic removal is therefore highly desirable. <h3>METHODS</h3> Out of a total of 1003 thoracoscopic operations undertaken between July 1991 and December 1996, seven patients underwent thoracoscopic removal of oesophageal leiomyoma. All of them had been preoperatively studied by oesophagogastroscopy and computed tomographic scanning of the chest which had confirmed the presence of a lesion with benign features. The surgical technique required intubation with a double lumen tube. Operative access was gained through the right chest via three ports and a small utility thoracotomy in the inframammary sulcus. The mean operating time was 120 minutes. <h3>RESULTS</h3> Conversion to open thoracotomy was necessary in one case with a very large horseshoe-shaped leiomyoma which was firmly adherent. The mean postoperative hospital stay was seven days. No intraoperative deaths or postoperative complications occurred. <h3>CONCLUSIONS</h3> The simplicity and safety of the thoracoscopic approach, combined with reduced surgical trauma and postoperative pain and functional and cosmetic advantages, make this technique the approach of choice for the removal of oesophageal leiomyomas.
EXPERIMENTS ON THE RÔLE OF THE CHICKEN MITE, DERMANYSSUS GALLINAE, AND THE MOSQUITO IN THE EPIDEMIOLOGY OF ST. LOUIS ENCEPHALITIS
Authors: Margaret G. Smith, Russell J. Blattner, Florence M. Heys, Albert Miller
Journal: The Journal of Experimental Medicine (1948)

The present experimental results concern primarily the question, whether or not mosquitoes feeding on chickens having viremia, as a result of the bite of infected mites, can acquire the virus of St. Louis encephalitis and whether or not mosquitoes thus infected, can transmit the virus to chickens and hamsters. During the course of the investigation, 7 species of mosquitoes of 3 genera were infected with the virus in one or two or all of three ways: by feeding on a suspension of infected mouse brain tissue, by feeding on chickens in which viremia had been produced by subcutaneous inoculation of virus, and by feeding on chickens having viremia as a result of the bite of infected mites. These mosquitoes transmitted the virus to chickens at periods varying from 5 to 33 days after the infective meal. The virus of St. Louis encephalitis was transmitted to hamsters by Culex pipiens at periods varying from 4 to 27 days after feeding on chickens having viremia as a result of the bite of infected mites. While viremia was demonstrated readily in hamsters, signs of encephalitis did not develop. In all transmission experiments the method of chorioallantoic passage proved necessary for the demonstration of viremia. A concept of the epidemiology of St. Louis encephalitis is presented: two blood-sucking vectors may be involved, one an arachnid, the mite, maintaining the virus in nature by transovarial passage, and the other, an insect, the mosquito, which carries the infection from birds to other vertebrates including man.
Mismatch repair deficiencies transforming stem cells into cancer stem cells and therapeutic implications
Authors: Minal Vaish
Journal: Molecular Cancer (2007)

For the exceptional self-renewal capacity, regulated cell proliferation and differential potential to a wide variety of cell types, the stem cells must maintain the intact genome. The cells under continuous exogenous and endogenous genotoxic stress accumulate DNA errors, drive proliferative expansion and transform into cancer stem cells with a heterogeneous population of tumor cells. These cells are a common phenomenon for the hematological malignancies and solid tumors. In response to DNA damage, the complex cellular mechanisms including cell cycle arrest, transcription induction and DNA repair are activated. The cells when exposed to cytotoxic agents, the apoptosis lead to cell death. However, the absence of repair machinery makes the cells resistant to tumor sensitizing agents and result in malignant transformation. Mismatch repair gene defects are recently identified in hematopoietic malignancies, leukemia and lymphoma cell lines. This review emphasizes the importance of MMR systems in maintaining the stem cell functioning and its therapeutic implications in the eradication of cancer stem cells and differentiated tumor cells as well. The understanding of the biological functions of mismatch repair in the stem cells and its malignant counterparts could help in developing an effective novel therapies leaving residual non-tumorigenic population of cells resulting in potential cancer cures.
Selective Natrexone-Derived Opioid Receptor Antagonists
Authors: A E Takemori, P S Portoghese
Journal: The Annual Review of Pharmacology and Toxicology (1992)

Due to the massive data sets available for drug candidates, modern drug discovery has advanced to the big data era. Central to this shift is the development of artificial intelligence approaches to implementing innovative modeling based on the dynamic, ...Read More
Bacterial Cellulose Nanofibrillar Patch as a Wound Healing Platform of Tympanic Membrane Perforation
Authors: Jangho Kim, Seung Won Kim, Subeom Park, Ki Taek Lim, Hoon Seonwoo, Yeonju Kim, Byung Hee Hong, Yun‐Hoon Choung, Jong Hoon Chung
Journal: Advanced Healthcare Materials (2013)

Abstract Bacterial cellulose (BC)‐based biomaterials on medical device platforms have gained significant interest for tissue‐engineered scaffolds or engraftment materials in regenerative medicine. In particular, BC has an ultrafine and highly pure nanofibril network structure and can be used as an efficient wound‐healing platform since cell migration into a wound site is strongly meditated by the structural properties of the extracellular matrix. Here, the fabrication of a nanofibrillar patch by using BC and its application as a new wound‐healing platform for traumatic tympanic membrane (TM) perforation is reported. TM perforation is a very common clinical problem worldwide and presents as conductive hearing loss and chronic perforations. The BC nanofibrillar patch can be synthesized from Gluconacetobacter xylinus ; it is found that the patch contained a network of nanofibrils and is transparent. The thickness of the BC nanofibrillar patch is found to be approximately 10.33 ± 0.58 μm, and the tensile strength and Young's modulus of the BC nanofibrillar patch are 11.85 ± 2.43 and 11.90 ± 0.48 MPa, respectively, satisfying the requirements of an ideal wound‐healing platform for TM regeneration. In vitro studies involving TM cells show that TM cell proliferation and migration are stimulated under the guidance of the BC nanofibrillar patch. In vivo animal studies demonstrate that the BC nanofibrillar patch promotes the rate of TM healing as well as aids in the recovery of TM function. These data demonstrate that the BC nanofibrillar patch is a useful wound‐healing platform for TM perforation.
Expression Cloning of an Immunodominant Family of <i>Mycobacterium tuberculosis</i> Antigens Using Human Cd4+ T Cells
Authors: Mark R. Alderson, Teresa Bement, Craig H. Day, Liqing Zhu, David Molesh, Yasir A. W. Skeiky, Rhea Coler, David M. Lewinsohn, Steven G. Reed, Davin C. Dillon
Journal: The Journal of Experimental Medicine (2000)

Development of a subunit vaccine for Mycobacterium tuberculosis (Mtb) is likely to be dependent on the identification of T cell antigens that induce strong proliferation and interferon gamma production from healthy purified protein derivative (PPD)(+) donors. We have developed a sensitive and rapid technique for screening an Mtb genomic library expressed in Escherichia coli using Mtb-specific CD4(+) T cells. Using this technique, we identified a family of highly related Mtb antigens. The gene of one family member encodes a 9.9-kD antigen, termed Mtb9.9A. Recombinant Mtb9.9A protein, expressed and purified from E. coli, elicited strong T cell proliferation and IFN-gamma production by peripheral blood mononuclear cells from PPD(+) but not PPD(-) individuals. Southern blot analysis and examination of the Mtb genome sequence revealed a family of highly related genes. A T cell line from a PPD(+) donor that failed to react with recombinant Mtb9.9A recognized one of the other family members, Mtb9.9C. Synthetic peptides were used to map the T cell epitope recognized by this line, and revealed a single amino acid substitution in this region when compared with Mtb9.9A. The direct identification of antigens using T cells from immune donors will undoubtedly be critical for the development of vaccines to several intracellular pathogens.
Activin A: an autocrine inhibitor of initiation of DNA synthesis in rat hepatocytes.
Authors: H Yasuda, T Mine, H Shibata, Y Eto, Y Hasegawa, T Takeuchi, S Asano, I Kojima
Journal: Journal of Clinical Investigation (1993)

The present study was conducted to examine the effect of activin A on growth of rat hepatocytes. EGF induced a 10-fold increase in DNA synthesis as assessed by [3H]thymidine incorporation in cultured hepatocytes. When activin A was added together with EGF, DNA synthesis induced by EGF was markedly inhibited. Inhibition was detected at a concentration of 10(-10) M, and 5 x 10(-9) M activin A almost completely blocked EGF-mediated DNA synthesis. Similarly, activin A completely blocked DNA synthesis induced by hepatocyte growth factor/scatter factor. Activin A was capable of inhibiting EGF-mediated DNA synthesis, even when added 36 h after the addition of EGF. With the same time interval, TGF-beta also blocked EGF-induced DNA synthesis. Although both activin A and TGF-beta inhibited growth of hepatocytes in a similar manner, either activin A or TGF-beta did not compete with each other in their binding when assessed by competitive binding using an iodinated ligand. When hepatocytes were incubated with EGF, release of bioactivity of activin A into culture medium was detected after 48 h or later. Activity of activin A was released from parenchymal cells but not from nonparenchymal cells. mRNA for beta A subunit of activin was detected only slightly in unstimulated hepatocytes, but markedly increased at 48 h after the addition of EGF. To determine whether endogenously produced activin A affects DNA synthesis, we examined the effect of follistatin, an activin-binding protein that blocks the action of activin A. An addition of follistatin significantly enhanced EGF-induced DNA synthesis. Finally, in partial hepatectomized rat, expression of mRNA for beta A subunit in liver was markedly increased 24 h after the partial hepatectomy. These results indicate that activin A inhibits initiation of DNA synthesis in hepatocytes by acting on its own receptor and that activin A acts as an autocrine inhibitor of DNA synthesis in rat hepatocytes.
The inhibition of anaplastic lymphoma kinase in non-small cell lung tumours with the ALK rearrangement may result in tumour shrinkage
Authors: L. Hancock
Journal: Thorax (2011)

In this study, the therapeutic efficacy of inhibiting anaplastic lymphoma kinase (ALK) in oncogenic fusion genes consisting of EML4 and ALK was explored in an early-phase clinical trail of crizotinib. Tumour samples from 1500 patients with non-small cell lung cancer (NSCLC) …
Redox-Dependent Transcriptional Regulation
Authors: Hongjun Liu, Renata Colavitti, Ilsa I. Rovira, Toren Finkel
Journal: Circulation Research (2005)

Reactive oxygen species contribute to the pathogenesis of a number of disparate disorders including tissue inflammation, heart failure, hypertension, and atherosclerosis. In response to oxidative stress, cells activate expression of a number of genes, including those required for the detoxification of reactive molecules as well as for the repair and maintenance of cellular homeostasis. In many cases, these induced genes are regulated by transcription factors whose structure, subcellular localization, or affinity for DNA is directly or indirectly regulated by the level of oxidative stress. This review summarizes the recent progress on how cellular redox status can regulate transcription-factor activity and the implications of this regulation for cardiovascular disease.
Comparison of Biologic Behavior and Histology of Transplanted Mammary Tumors in GR Mice&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;&lt;xref ref-type="fn" rid="FN3"&gt;3&lt;/xref&gt;
Authors: D H Percy, V L Morris, J I Macinnes
Journal: JNCI Journal of the National Cancer Institute (1982)

Mammary tumors that arose spontaneously in inbred GR mice were transplanted into syngeneic castrated males. The hormone responsiveness of the transplants was studied in mice treated with estrone and progesterone and was compared with the hormone responsiveness in mice that received no hormone treatment. Microscopic examination of hormone-responsive and hormone-independent tumors revealed similar histologic patterns in both groups. It was evident that pale cells, which are classically associated with hormone-responsive tumors, may also be present in transplanted hormone-independent tumors in this strain. No correlation was found between the histologic pattern of these transplanted tumors and the biologic behavior, hormonal status, or presence of a specific murine mammary tumor virus (MuMTV) proviral fragment. Mammary tumors also appeared capable of undergoing differentiation into more than one morphologic type. Two cotransplanted tumors (derived from the same parental tumor) had markedly different histologic patterns; however, analysis of MuMTV proviral fragments indicated that the MuMTV-infected cells were of the same parentage.
Tryptophan Catabolism in Cancer: Beyond IDO and Tryptophan Depletion
Authors: Michael Platten, Wolfgang Wick, Benoît J. Van den Eynde
Journal: Cancer Research (2012)

Tryptophan catabolism in cancer is increasingly being recognized as an important microenvironmental factor that suppresses antitumor immune responses. It has been proposed that the essential amino acid tryptophan is catabolized in the tumor tissue by the rate-limiting enzyme indoleamine-2,3-dioxygenase (IDO) expressed in tumor cells or antigen-presenting cells. This metabolic pathway creates an immunosuppressive milieu in tumors and in tumor-draining lymph nodes by inducing T-cell anergy and apoptosis through depletion of tryptophan and accumulation of immunosuppressive tryptophan catabolites. Competitive inhibitors of IDO are currently being tested in clinical trials in patients with solid cancer, with the aim of enhancing the efficacy of conventional chemotherapy. There are, however, certain tumor types that are capable of catabolizing tryptophan but are largely IDO-negative. Recent evidence from studies in malignant gliomas and other types of cancers points to alternative enzymatic pathways of tryptophan catabolism involving tryptophan-2,3-dioxygenase (TDO). TDO, which is considered responsible for regulating systemic tryptophan levels in the liver, is constitutively expressed in some cancers and is equally capable of suppressing antitumor immune responses. Depletion of tryptophan induces signaling events in T cells, leading to anergy and apoptosis; however, active immunomodulation by accumulating tryptophan catabolites, most notably kynurenine, appears to play an equally important role. These immunomodulatory effects of kynurenine are mediated by the aryl hydrocarbon receptor. This intracellular transcription factor has classically been viewed as a receptor for environmental toxins, such as dioxin, and its important role in influencing immune responses, especially in epithelial barriers, is only beginning to emerge. This review summarizes the exciting developments in our understanding of tryptophan catabolism as a key factor in the immunobiology of cancer.
A Randomized Comparison of Sirolimus- Versus Paclitaxel-Eluting Stent Implantation in Patients With Diabetes Mellitus
Authors: Seung-Whan Lee, Seong-Wook Park, Young-Hak Kim, Sung-Cheol Yun, Duk-Woo Park, Cheol Whan Lee, Myeong-Ki Hong, Kyoung-Suk Rhee, Jei Keon Chae, Jae-Ki Ko, Jae-Hyeong Park, Jae-Hwan Lee, Si Wan Choi, Jin-Ok Jeong, In-Whan Seong, Yoon Haeng Cho, Nae-Hee Lee, June Hong Kim, Kook-Jin Chun, Hyun-Sook Kim, Seung-Jung Park
Journal: Journal of the American College of Cardiology (2008)
Leukemia-associated minor histocompatibility antigen discovery using T-cell clones isolated by in vitro stimulation of naive CD8+ T cells
Authors: Marie Bleakley, Brith E. Otterud, Julia L. Richardt, Audrey D. Mollerup, Michael Hudecek, Tetsuya Nishida, Colette N. Chaney, Edus H. Warren, Mark F. Leppert, Stanley R. Riddell
Journal: Blood (2010)