tbuckley/cabot-search huggingface dataset:
Functional 3D Neural Mini‐Tissues from Printed Gel‐Based Bioink and Human Neural Stem Cells
Authors: Qi Gu, Eva Tomaskovic‐Crook, Rodrigo Lozano, Yu Chen, Robert M. Kapsa, Qi Zhou, Gordon G. Wallace, Jeremy M. Crook
Journal: Advanced Healthcare Materials (2016)

Direct‐write printing of stem cells within biomaterials presents an opportunity to engineer tissue for in vitro modeling and regenerative medicine. Here, a first example of constructing neural tissue by printing human neural stem cells that are differentiated in situ to functional neurons and supporting neuroglia is reported. The supporting biomaterial incorporates a novel clinically relevant polysaccharide‐based bioink comprising alginate, carboxymethyl‐chitosan, and agarose. The printed bioink rapidly gels by stable cross‐linking to form a porous 3D scaffold encapsulating stem cells for in situ expansion and differentiation. Differentiated neurons form synaptic contacts, establish networks, are spontaneously active, show a bicuculline‐induced increased calcium response, and are predominantly gamma‐aminobutyric acid expressing. The 3D tissues will facilitate investigation of human neural development, function, and disease, and may be adaptable for engineering other 3D tissues from different stem cell types.
Abstract 4636: Increased expression of CSE1L/hCAS in colorectal cancer: Correlation with tumor progression
Authors: Steven C. Shivers, Domenico Coppola, Steven A. Eschrich, Dung-Tsa Chen, David Shibata, Timothy J. Yeatman, Mokenge P. Malafa
Journal: Cancer Research (2010)

Abstract Introduction. The chromosome segregation and human cellular apoptosis susceptibility gene (CSE1L/hCAS) has been implicated in cancer and has been shown to be amplified in several human maligancies, including colorectal cancer. In this work, we sought to evaluate the gene expression of CSE1L/hCAS in colorectal cancer cell lines and tumor tissue and to examine CSE1L/hCAS expression in colorectal cancer progression. Methods. In order to examine CSE1L/hCAS at the gene expression level, we surveyed three different datasets from studies in which Affymetrix U133+ gene chips had been performed on tissue samples from patients with colorectal cancer, as well as patients with adenomas and normal individuals. We examined relative gene expression levels for 3 probe sets on the U133+ gene chip that closely align to the RefSeq for the CSE1L/hCAS gene. In order to examine CSE1L/hCAS at the level of protein expression, we utilized a tissue microarray (TMA) that had been previously created at the Moffitt Cancer Center from primary colorectal tumors of various stages, adenomas and normal tissues and performed immunohistochemical (IHC) staining for the CSE1L/hCAS protein. Results. CSE1L/hCAS showed increased gene expression in all of the adenoma and colorectal cancer patient samples tested by microarray, compared to tissue samples from normal individuals. However, there was not a significant difference in CSE1L/hCAS mRNA levels between patients with adenoma and those with invasive cancer, nor between patients compared by cancer stage, grade, vascular invasion, sex or age. IHC staining also demonstrated intense nuclear and/or cytoplasmic staining for the CSE1L/hCAS gene product in adenomas and invasive colorectal cancers. Furthermore, later stage specimens showed more intense nuclear staining, while early stage lesions, and even fibroblasts in nearby normal tissue, showed predominately cytoplasmic staining for CSE1L/hCAS. Conclusions. These results demonstrate that increased expression of the CSE1L/hCAS gene, while not specific for invasive cancer cells, might be a good marker for early detection of colorectal cancer. This gene appears to be expressed early and across all stages of cancer development. Because of its early expression and potential involvement in a variety of important cellular processes, we believe that this gene product might represent a potential target for prevention and/or treatment of early colorectal cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4636.
NCI Strengthens Commitment to Prostate Cancer
Authors: N. Volkers
Journal: JNCI Journal of the National Cancer Institute (1992)

Journal Article NCI Strengthens Commitment to Prostate Cancer Get access Nancy Volkers Nancy Volkers Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 84, Issue 7, April 1992, Pages 478–479, https://doi.org/10.1093/jnci/84.7.478 Published: 01 April 1992
Disparity between serum and nipple aspirate fluid (NAF) estradiol concentrations during the menstrual cycle.
Authors: RT Chatterton, RE Heinz, M Habe-Evans, SA Khan
Journal: Cancer Research (2009)

Abstract Abstract #4077 Background: NAF, elicited from healthy women, may provide information about the hormonal environment of the breast and the potential risk for breast cancer. We have studied NAF sex hormone changes across the menstrual cycle and after menopause to determine the relationship to serum concentrations.&amp;#x2028; Methods: Subjects were women attending the Lynn Sage Breast Center at Northwestern Memorial Hospital. Samples of NAF from 20 premenopausal and 23 postmenopausal women were evaluated. Premenopausal women were divided into groups 1 through 4, backdating from the day of menstruation, -28 through -19, -18 through -13, -12 through -6 and -5 through 0, respectively. NAF and venous blood were collected using standard methods. Total protein was measured by a fluorometric procedure. Unconjugated steroids, estradiol (E2), estrone, progesterone (P), and testosterone (T), were extracted into ethyl acetate-hexane (3:2) and were separated by HPLC on a C-18 column with gradient elution before assay. DHEA sulfate, estrone sulfate, and cathepsin D were measured in the aqueous fraction. All analytes were measured by immunoassays. Transformation of the data of all analytes to their natural logarithms normalized the data. Data were analyzed by ANOVA.&amp;#x2028; Results: The protein concentration in the samples was similar among all groups, mean = 128 mg/ml (P=0.904). In NAF only E2 and P differed during the menstrual cycle, P = 0.064 and 0.007, respectively, but the pattern of NAF E2 followed that of NAF P and not serum E2. The figure shows the geometric mean values at each phase of the menstrual cycle. Ovulation should occur in group 2 (-18 through -13 days from menstruation). With the exception of P and DHEA sulfate, which were lower, analytes in samples from postmenopausal women were not significantly different from those from premenopausal women.&amp;#x2028; &amp;#x2028; Comment: The most significant finding is that NAF E2 does not parallel serum levels but follows closely NAF P levels. NAF E2 was actually lowest when serum E2 was highest. Changes in other analytes during the menstrual cycle were minimal. Estradiol, its direct precursors, and the E2-related protein, cathepsin D, were not decreased in NAF after menopause. (Supported by NIH R01 CA 120555-01). Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 4077.
Cytokine Release in an Ovarian Carcinoma Patient Following Intravenous Administration of Bispecific Antibody OC/TR F(ab')2
Authors: J. G. TIBBEN, O. C. BOERMAN, R. A. M. J. CLAESSENS, F. H. M. CORSTENS, M. VAN DEUREN, P. H. M. D. MULDER, J. W. M. VAN DER MEER, K. G. G. KEIJSER, L. F. A. G. MASSUGER
Journal: JNCI Journal of the National Cancer Institute (1993)
Abstract 4204: <i>Essential role of odontoblastic Smad4 in suppressing multiple keratocystic odontogenic tumors in mice</i>
Authors: Yuanrong Gao, Guan Yang, Tujun Weng, Juan Du, Xuejiu Wang, Jian Zhou, Songlin Wang, Xiao Yang
Journal: Cancer Research (2010)

Abstract Keratocystic odontogenic tumors (KCOT) are cystic epithelial neoplasias with a high recurrence rate. However, the molecular mechanisms underlying the initiation and progression of KCOTs are still largely unknown. Here, we show that specific ablation of Smad4 in odontoblasts unexpectedly resulted in spontaneous KCOTs in mice. The mutant mice exhibited malformed teeth characterized by fractured incisors and truncated molar roots. These abnormalities were mainly caused by disrupted odontoblast differentiation that led to irregular dentin formation. The cystic tumors arising from the reactivation of epithelial rests of Malassez (ERM), in which Smad4 remained intact, proliferated and formed stratified and differentiated squamous epithelia which exhibited a dramatic up-regulation of Hedgehog signaling. Odontoblasts which are responsive to TGF-β/BMP signals may produce signal molecules to inhibit the activation of ERM. Indeed, we observed a down-regulation of BMP signals from Smad4 mutant odontoblasts to adjacent Hertwig's epithelial root sheath (HERS). Intriguingly, KCOTs frequently emerged from Smad4-deficient ERMs in the keratinocyte specific Smad4 knockout mice, suggesting a novel mechanism that reciprocal TGF-β/BMP signaling between odontoblasts and HERS were required for tooth root development and suppression of KCOT formation. These findings provide insight into the genetic basis underlying KCOTs and important implications for new directions in KCOT treatments. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4204.
Abstract 5526: Mass-action law algorithm-based computer simulation for efficient and econo-green cancer drug discovery and development.
Authors: Ting-Chao Chou
Journal: Cancer Research (2013)

Abstract Physico-chemical principle of the mass-action law algorithm (MALA) is the basis for systematic pharmacodynamics (PD) that leads to general median-effect equation (MEE) for single entity effect and the combination index equation (CIE) for multiple entity interactions (Chou TC, Pharmacol. Rev. 58: 621-681, 2006; Free web access: http://pharmrev.aspetjournals.org/content/58/3/621). “Median” is the common-link and universal reference point for single and multiple entities and for 1st-order and higher-order dynamics. Median is also the harmonic mean of kinetic constants where the harmony is the state of pure non-competitiveness [Chou, Nature Precedings (npre.2008.2064-2). Available free at http://precedings.nature.com/documents/2064/version/2]. Based on MEE, all dose-effect curves whether hyperbolic or sigmoidal, weak or strong, 1st-order or higher-order, in vitro or in vivo, can be linearlized by the median-effect plot with small number of data points in small size experiments (Chou, J. Theor. Biol. 59: 253-276, 1976; Pharmacol. Rev. .ibid). Based on CIE, CI&amp;lt;1, =1, and &amp;gt;1 quantitatively indicates synergism, additive effect, and antagonism, respectively (Chou &amp; Talalay, Adv. Enz. Regul. 22: 27-55, 1984; Cancer Res. 70: 440-446, 2011). Thus. MEE is the common denominator for simple and complex bio-systems in vitro, in animal and in clinics. Computerized simulation of MEE or CIE can take &amp;lt;1 second, and the graphics can be drawn automatically (CompuSyn, www.combosyn.com, Free download). Applying this theory in this author's laboratory (personnel &amp;lt; 5 for decades) has published 253 articles that have been cited 13,749 times in over 523 different biomedical journals with h-index of 55 (Thomson Reuters Web of Science, www.researcherid.com/rid/B-4111-2009) along with 30 US patents. Thus, MALA-PD theory is the common denominator for integrating complex bio-systems and its computerized simulation have proven to lead to efficient, quantitative and econo-green bio-research and new drug discovery and development as illustrated in Chou, Integr. Biol. 3: 548-559, 2011; DOI: 10.1039/c0ib00130a and in Am. J. Cancer Res. 1(7): 925-954, 2011, Free web access: www.ajcr.us. Citation Format: Ting-Chao Chou. Mass-action law algorithm-based computer simulation for efficient and econo-green cancer drug discovery and development. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 5526. doi:10.1158/1538-7445.AM2013-5526 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
Abstract 4191: HECT-type ubiquitin ligase ITCH targets lysosomal-associated protein multispanning transmembrane 5 (LAPTM5) and prevents LAPTM5-mediated cell death
Authors: Jun Inoue, Takaya Ishihara, Ken-ichi Kozaki, Issei Imoto, Johji Inazawa
Journal: Cancer Research (2012)

Abstract Lysosomal-associated protein multispanning transmembrane 5 (LAPTM5) is a membrane protein on the intracellular vesicles. We have previously demonstrated that the accumulation of LAPTM5-positive vesicles was closely associated with the programmed cell death occurring during the spontaneous regression of neuroblastomas. While the accumulation of LAPTM5 protein might occur at the post-translational level, the molecular mechanism has been unclear. Here, we found that the level of LAPTM5 protein is negatively regulated by the degradation through ubiquitination by ITCH, an E3 ubiquitin ligase. ITCH directly binds to the PPxY motif of LAPTM5 via its WW domains and promotes ubiquitination through a HECT-type ligase domain. Overexpression of ITCH led to the degradation of LAPTM5 protein, and conversely, knockdown of ITCH by siRNA resulted in the stabilization of LAPTM5 protein. In addition, the inhibition of ITCH enhanced the cell death occurred by accumulation of LAPTM5 in neuroblastoma cells. These findings suggest that LAPTM5 is a novel substrate in terms of degradation by the ubiquitin ligase ITCH, and this system might act as a negative regulator in the spontaneous regression of neuroblastomas by preventing LAPTM5-mediated cell death. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4191. doi:1538-7445.AM2012-4191
Case 2-1984
Authors: Richard C. Cabot, Robert E. Scully, Eugene J. Mark, Betty U. McNeely, David M. Dawson, Douglas C. Miller
Journal: New England Journal of Medicine (1984)

Presentation of CaseA 47-year-old man was admitted to the hospital because of right hemiplegia.He was well until 19 years earlier, when diplopia developed. During the next two years the diplopia waxed and waned, and he complained on several occasions of vertigo accompanied by vomiting. Physical examination showed a Grade 2 apical systolic murmur. Several neurologic consultants observed diplopia and varying visual-field abnormalities, enlargement of the left pupil although both pupils were reactive, weakness of the right medial rectus muscle, variable nystagmus, dysmetria and dysdiadochokinesis, inconstant sensory abnormalities in the lower extremities, and intermittently present Babinski signs. Repeated lumbar . . .
The ‘clip-band closure' technique: a new endoscopic traction method for closure of a large ulcer
Authors: G. Curcio, A. Granata, N. Azzopardi, D. Pagano, L. Barresi, I. Tarantino, M. Spada, M. Traina
Journal: Endoscopy (2013)

We present the case of a 69-year-old man with a rectal granular-type laterally spreading tumor (LST) of about 50 mm in diameter who underwent endoscopic submucosal dissection (ESD) using a Hybrid knife I-type (Erbe, Tübingen, Germany) at our institute ([Fig. 1]).
A Clinical Study of the Effects of Hydrochlorothiazide on the Renal Excretion of Electrolytes and Free Water
Authors: Wlodzimierz Januszewicz, Henry O. Heinemann, Felix E. Demartini, John H. Laragh
Journal: New England Journal of Medicine (1959)

HYDROCHLOROTHIAZIDE (6-chloro-7-sulfamyl-3,4,dihydro-l,2,4, benzothiadiazine-1,1,-dioxide) is the 3,4,dihydro derivative of chlorothiazide wherein the 3,4 double bond is saturated by two hydrogen atoms (Fig. 1). In animals the compound has been shown to produce an increased renal excretion of sodium, potassium and chloride.1 However, in its effects on electrolyte excretion, dihydrochlorothiazide appeared to be five times more potent than chlorothiazide when given intravenously to dogs and some ten times more potent than chlorothiazide when given orally.Previous studies have characterized the effect of chlorothiazide on electrolyte transport in normal subjects and in patients with heart failure, cirrhosis and nephrosis.2 , 3 The intravenous administration of . . .
The Impact of HLA Mismatches on the Survival of First Cadaveric Kidney Transplants
Authors: Philip J. Held, Barry D. Kahan, Lawrence G. Hunsicker, David Liska, Robert A. Wolfe, Friedrich K. Port, Daniel S. Gaylin, Jose R. Garcia, Lawrence Agodoa, Henry Krakauer
Journal: New England Journal of Medicine (1994)

The benefits of HLA-A, B, and DR matching of cadaveric kidney grafts and recipients remain controversial when viewed from the perspective of social equity and graft survival.
THU0565 Effectiveness of Collective Educational Intervention in the Management of Subcutaneous Biological Agents in Patients with Inflammatory Rheumatism
Authors: L. Berard, J.-F. Menard, J. Benichou, T. Lequerre, O. Vittecoq, S. Pouplin
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Educational programs are key-part of inflammatory rheumatism management. Nevertheless, few studies have assessed practical skills and safety use of subcutaneous biological agents. <h3>Objectives</h3> To evaluate the impact of collective educational intervention (CEI) on good clinical practices and safety skills in patients with inflammatory rheumatism treated with subcutaneous biological agents. <h3>Methods</h3> A self-questionnaire was developed to assess expected behaviours (injection skills, clinical items supervision, attitudes in front of different practical situations), knowledge of vaccinal status, required medical follow-up and need for information of patients with inflammatory rheumatism requiring subcutaneous biological agents. First administration was made in the hospital where every single patients receive individual education. Our interventional group was composed by voluntary patients at the first administration, who participate at one CEI performed 3 to 6 months later. The CEI lasted 2 hours by small groups including from 6 to 12 patients. Baseline self-questionnaire was filled by patients before the CEI, then good technical and clinical pratices were reminded by the educational team. This self-questionnaire was also filled at a one-year follow-up visit by control group and intervention group. We compared the one-year questionnaires for each arm. <h3>Results</h3> From July 2009 to July 2012 : 64 and 305 patients, respectively included in the CEI and control groups, completed the one-year follow-up visit. At 12 months, the educational group showed significant better technical injection skills and better infectious risk management : pulmonary, urinary, cutaneous, Ear-Nose-Throat (ENT) (p&lt;0,001), digestive (p= 0,008), surgical (p=0,009) and dental (p=0,015). The CEI group had significantly better knowledges of their vaccinal status compared to the control group. Additionnally, the CEI group improved significatively its required attitudes (pulmonary, cutaneous, urinary and ENT infectious risk management) at 12 months compared to baseline assessment. <h3>Conclusions</h3> In this study, the collective educational intervention improvedsafety skills acquisition in biological treatments management, persisting at one-year follow-up compared to control group. <h3>References</h3> Albano MG, et al. Characteristics and development of therapeutic pateint education in rheumatoid arthritis : analysis of the 2003-2008 literature. Joint Bone Spine 2010;77:405-10 Riemsma R, et al. Patient education for adults with rheumatoid arthritis. Cochrane Database Syst Rev 2003;(2):CD003688 <h3>Disclosure of Interest</h3> None Declared
Abstract 549: MAGI3-Akt3, a novel fusion protein in the PI 3-K pathway in cancer.
Authors: Kristin Brown, Alex Toker
Journal: Cancer Research (2013)

Abstract Aberrant activation of the PI3-K/Akt pathway is found in approximately 70% of breast cancers. We recently identified a recurrent rearrangement that produces an in-frame fusion protein containing Akt3 and the scaffolding protein MAGI3 (1). MAGI3-Akt3 is the first fusion protein that has been identified in the PI 3-K pathway. We propose that MAGI3-Akt3 is a novel oncogene in breast cancer and that the oncogenic activity of the fusion protein results from disruption of the PI 3-K/Akt pathway. Within the fusion, Akt3 has a disrupted PH domain prior to glutamate 17 (E17). As a result the fusion protein is constitutively phosphorylated in the Akt3 kinase domain and expression of MAGI3-Akt3 in breast cancer cells enhances Akt substrate phosphorylation. Constitutive MAGI3-Akt3 kinase activity can be inhibited by ATP-competitive small molecule Akt inhibitors but is resistant to the allosteric Akt inhibitor MK2206 which is currently in phase II clinical trials. Our results indicate that ATP competitive Akt inhibitors should be evaluated in clinical trials for the treatment of fusion-positive breast cancers. The fusion protein also contains a severely truncated portion of the scaffolding protein MAGI3. In particular, the fusion lacks the second PDZ domain of MAGI3 that has been reported to bind to PTEN and be required for the inhibitory effect of PTEN on PI 3-K pathway activity. We have demonstrated that disruption of MAGI3 in breast cancer cell lines does indeed promote PI 3-K pathway hyperactivity in a PTEN-dependent manner. In addition, the fusion lacks the fifth PDZ domain of MAGI3 and our studies indicate that this disrupts the interaction of MAGI3 with PHLPP2, a phosphatase that directly dephosphorylates Akt at pS473. Our studies therefore demonstrate that the MAGI3-Akt3 translocation significantly perturbs PI 3-K pathway activity via activation of an oncogene (Akt3) and dysregulation of two tumor suppressors (PTEN and PHLPP2). We are currently continuing studies to elucidate the oncogenic mechanism(s) of MAGI3-Akt3 in breast cancer. Citation Format: Kristin Brown, Alex Toker. MAGI3-Akt3, a novel fusion protein in the PI 3-K pathway in cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 549. doi:10.1158/1538-7445.AM2013-549
PARATHYROID HORMONE LEVELS AND HIGH-RESIDUAL PLATELET REACTIVITY IN PATIENTS RECEIVING DUAL ANTIPLATELET THERAPY WITH ACETYLSALICYLIC ACID AND CLOPIDOGREL OR TICAGRELOR
Authors: Monica Verdoia, Matteo Nardin, Lucia Barbieri, Alon Schaffer, Paolo Marino, Harry Suryapranata, Giuseppe De Luca
Journal: Journal of the American College of Cardiology (2016)