tbuckley/cabot-search huggingface dataset:
AB1227 The comparative efficacy of physiotherapy, injection and pharmacotherapy in patients with temporomandibular joint dysfunction
Authors: M. Okumus, O. Elcim, O. Surmelioglu, E. Ceceli, F. Tuncay, P. Borman
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Temporomandibular joint disorders are common and lead to functional disability not only in temporomandibular joint but also in teeth, soft tissues and components of mastication. Patients with temporomandibular joint (TMJ) disorders report symptoms which include jaw and neck pain, headache and clicking or grating within the joint. Pharmacotherapy, physical therapy modalities, injection and exercise are all used for the treatment of TMJ disorders however no therapies have been shown to be uniquely superior for the treatment of pain or oral dysfunction in this chronic syndrome. <h3>Objectives</h3> The aim of this study was to evaluate the comparative effects of physical therapy and injection therapy along with the exercises in a group of patients with TMJ disorders. <h3>Methods</h3> Fourty nine patients with a mean age 37.57±15.14 years were recruited to the study. Patients were evaluated for complaints and clinical findings and then randomly allocated to three treatment groups. All patients got education and learned TMJ exercises to perform as home exercise program. The patients in the first group (n=17) received pharmacotherapy (non-steroidal anti-inflammatory drugs for a duration of 10 days with anti-inflammatory doses), the second group (n=15) received physical therapy comprising superficial local heat and TENS for 10 sessions; the third group (n=17) received hyaluronic acid injection to TMJ. The main outcome measures were pain at rest and movement of jaw assessed by VAS; and mouth opening distance. Oral health impact profile (OHIP-14) was used in all patients to assess people's perceptions of the social impact of oral disorders on their well-being. All the measurements were performed at baseline, at the end of therapies, one month and three months after therapies. <h3>Results</h3> Fourteen men and 35 women were completed the study. All patients reported to perform their home exercise program twice a day. Pain by VAS in rest and movement of jaw decreased in all patient groups (5.9±1.4 vs 5.6±1.9 vs 6.2±2.2; 1.1±0.9 vs 1.4±1.1 vs 2.5±1.6 respectively) but the most significant improvement was observed in the injection group than in other groups at first and third months (p&lt;0.05). The improvement in mouth opening distances and well being scores were similar between the groups after first and third months (p&gt;0.05). <h3>Conclusions</h3> Our results indicated that all of the treatments including pharmacotherapy, physiotherapy, hyaluronic acid injection therapy improved the patients' pain and functional status at the end of the therapies but hyaluronic acid injection treatment to TMJ were found to be more efficacious and long lasting in regard to pain, than in other therapies. Further studies are needed to confirm our results in larger groups of patients suffering from TMJ disorders. <h3>Disclosure of Interest</h3> None Declared
A Child with Gross Hematuria
Authors: Lakshmi Ganapathi, Michael Somers
Journal: New England Journal of Medicine (2015)

A previously healthy 8-year-old boy presented with recurrent terminal gross hematuria. Two years earlier, after he had been swimming near a dam in Ghana, hematuria had developed, which subsequently resolved. Urine microscopy revealed oval eggs and free-swimming larvae, shown in a video.
Abstract 2180: Antagonistic relationship between the tumor suppressor ING4 and estrogen signaling in breast cancer
Authors: Timothy G. Whitsett, Suwon Kim
Journal: Cancer Research (2011)

Abstract ING4 is a tumor suppressor that plays a role in many cancer-related cellular processes, including cell proliferation, apoptosis, contact inhibition and cell migration. Our lab found ING4 is deleted in 15% of estrogen receptor (ER)-positive breast cancers, implicating a role for ING4 as a tumor suppressor in estrogen-driven breast cancer. Estrogen is a tumor promoter in breast cancer, causing cell proliferation, cell survival and cell migration. We hypothesize that estradiol (E2) exposure suppresses ING4, and conversely that the expression of ING4 modulates estrogen-induced phenotypes in breast cancer cells. We employed qPCR to test whether E2 suppressed ING4 in a time-, dose- and ER-dependent manner. By over-expressing or knocking down the expression of ING4 in MCF-7 breast cancer cells, we determined whether ING4 affected E2-induced cell proliferation. Physiological levels of E2 (100pM-10nM) suppressed the expression of ING4 in MCF-7 cells by more than 50% at early time points (6-24 hours). The suppression of ING4 by E2 was dependent on ER, as blocking ER with a pure anti-estrogen completely abrogated the suppression of ING4 by E2. Having shown that E2 suppressed ING4, we next tested whether the expression level of ING4 could affect E2-induced cell proliferation in breast cancer cells. The knockdown of ING4 by shRNA in MCF-7 cells resulted in a hyper-proliferation in response to E2 exposure. Conversely, the over-expression of ING4 in MCF-7 cells completely abolished the proliferative response to E2 seen in MCF-7 pMIG (vector alone) cells. In hormone-depleted media, MCF-7 cells over-expressing ING4 underwent apoptosis as demonstrated by the cleavage of caspase-7 and PARP. Estradiol exposure did not rescue the apoptotic phenotype. The over-expression of ING4 in MCF-7 cells suppressed the protein expression of Bcl-2, facilitating cell death. The suppression of Bcl-2 was necessary for cell death as the ectopic expression of Bcl-2 rescued the apoptotic phenotype induced by ING4 over-expression in hormone-depleted media. This work demonstrates an antagonistic relationship between E2 signaling and the tumor suppressor ING4 in breast cancer cells. The suppression of ING4 by E2 may indicate a novel mechanism of E2 action in breast cancer. This work also suggests that the expression of ING4 in estrogen-driven breast cancer may determine the magnitude of response to estrogen and anti-estrogen therapeutics. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2180. doi:10.1158/1538-7445.AM2011-2180
PTU-043 Capsule Endoscopy Retention; Is Prediction Without A Patency Pre-study Possible?
Authors: R Makins, R Hopkins
Journal: Gut (2014)

<h3>Introduction</h3> Small intestinal capsule endoscopy (CE) is used to investigate occult gastrointestinal bleeding, iron deficiency anaemia, to evaluate the small intestine for Crohn’s disease (CD), polyposis syndromes or complications of NSAID use. The only significant complication is capsule retention, either long term or transient, potentially leading to luminal obstruction. The Patency Capsule can be used prior to CE to confirm the likelihood of safe passage however is only for use in conjunction with the system by Given Imaging (Diagmed UK, Personal communication). We use Mirocam CE equipment (Intromedic). Consequently reliance must be placed on radiological studies along with clinical evaluation when assessing the risk of retention. The aim of this study was to determine, in patients where capsule retention had occurred in the setting of a previously reported normal radiological study, whether retrospective review of the radiology could identify stricturing disease and therefore determine whether retention could have been predicted with prior radiological imaging alone. <h3>Methods</h3> We reviewed records of all patients who had undergone CE in Gloucestershire since the inception of the local service in 2008. Identified all patients in whom capsule retention occurred. Defined capsule retention as occuring in patients where a stricturing lesion was seen, the capsule appeared not to pass the lesion and colonic mucosa was not positively identified. We retrospectively reviewed any relevant radiological studies performed prior to the CE to determine whether, with hindsight, abnormalities could be identified that would have significantly increased the risk of capsule retention. <h3>Results</h3> 465 CE performed locally in Gloucestershire since 2008. CE retention occured above a stricture in 6 (4 male, mean age 45, range 27–61). Indications for CE abdominal pain +/- anaemia. In 5 the strictures were thought to be secondary to CD (past history of CD in 2 only), in 1 due to NSAID use. No stricturing lesions had been identified previously on either barium follow through (2) or cross sectional (CT) imaging (4). 4 studies had been performed locally, 2 by other providers, reported by non-specialist radiologists. On retrospective review significant stricturing lesions were seen on all studies, findings contraindicating CE. <h3>Conclusion</h3> CE is a safe and widely used tool. The risk of capsule retention increases in the setting of Crohn’s disease. We have shown that in cases where capsule retention occurred in our institution, where prior radiology was reported as normal, stricturing lesions could be positively identified when reviewed retrospectively by a specialist radiologist. We conclude that thorough radiological assessment is adequate to predict capsule retention and patency studies prior to CE are therefore unnecessary. <h3>Disclosure of Interest</h3> None Declared.
SP0023 Recommendations for Reporting in Clinical Studies of the Earliest Phases of RA: The Eular Study Group for Risk Factors for RA
Authors: K. Raza
Journal: Annals of the Rheumatic Diseases (2013)

<h3></h3> The Study Group for Risk Factors for Rheumatoid Arthritis (RA) was established by the EULAR Standing Committee on Investigative Rheumatology to facilitate research into the pre-clinical and earliest clinically apparent phases of RA. Key initial aims were to develop recommendation for [1] terminologies to be used to define specific phases up to the development of RA; [2] approaches to dating “onset” in patients with clinically apparent disease; [3] urgent research priorities. The Study Group has recommended that, in prospective studies, individuals without RA are described as having: (a) genetic risk factors for RA; (b) environmental risk factors for RA; (c) systemic autoimmunity associated with RA; (d) symptoms without clinical evidence of arthritis; (e) unclassified arthritis; where (a) to (e) may be used in a combinatorial manner. It was recommended that the prefix ‘pre-RA with:’ could be used before any/any combination of (a) to (e) but only to describe retrospectively a phase that an individual had progressed through once it was known that they had developed RA. An approach to quantifying disease duration was recommended which involved providing durations since the onset of symptoms, since onset of joint swelling as well as from the time of fulfilment of classification criteria. These recommendations should facilitate communication between researchers and comparisons between studies focussed on the earliest phases of RA. <h3>Disclosure of Interest</h3> None Declared
Abstract 2814: Potent and selective small molecule inhibitors of polo-like kinase 1: Biological characterization
Authors: Sheelagh Frame, Claire Aspinall, Robert O'Neil, Jonathan Hollick, Stephen Taylor, Ted Hupp, David Blake, Daniella I. Zheleva
Journal: Cancer Research (2012)

Abstract Polo-like kinase 1 (Plk1) is one of the emerging new generation of anti-mitotic targets. Plks are a family of serine-threonine kinases involved in the regulation of mitosis and maintenance of DNA integrity. Plk1 is required for almost every step of mitosis: promotes mitotic entry, contributes to centrosome maturation, regulates kinetochore assembly, contributes to spindle assemble checkpoint and initiates mitotic exit. Besides promoting proliferation, Plk1 overexpression contributes to oncogenesis by promoting chromosome instability and aneuploidy. Overexpression of Plk1 is associated with tumor development and many cancers have elevated Plk1 levels compared to surrounding normal tissues. Numerous studies have shown that Plk1 expression levels correlate with disease progression, invasiveness and poor patient prognosis. Furthermore, pre-clinical studies have demonstrated that cancer cell proliferation is blocked in vitro and in vivo via inhibition of Plk1 using siRNA or small molecule inhibitors. Collectively, these observations support the selection of Plk1 as an attractive target for cell cycle-directed cancer therapy and several small molecule inhibitors are currently being investigated in clinical trials. Using a de novo ligand design approach we have identified pyrimidodiazepinone small molecules, which are ATP-competitive, highly selective and potent Plk1 inhibitors. These molecules have good drug-like properties, oral bioavailability and efficacy in mouse xenograft models. To characterize the cell sensitivity toward the Plk1 inhibitors we have used washout and outgrowth assays in a panel of oesophageal, lung and colon cancer cell lines. The anti-proliferative activity of Plk1 inhibitors was correlated with the Plk1 expression level, p53 and Ras mutational status. Generally, we found that cell lines harbouring p53 mutations are more sensitive towards these inhibitors. Time-lapse microscopy and flow cytometry studies of RKO cell line (WT p53) treated with Plk1 inhibitors demonstrated that a proportion of cells arrested just before the G2-/-M transition and were able to resume normal proliferation upon compound removal. These results suggest that Plk1 inhibitors should have better therapeutic window when used for treatment of tumors with mutant p53, p53 mutational status could be used as a patient stratification marker, and tumor types with high frequency of p53 mutations, such as oesophageal cancer, could be suitable therapeutic indications for Plk1 inhibitors. 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 2814. doi:1538-7445.AM2012-2814
Abstract 505: Jagged 2 knockdown inhibits invasion in colorectal cancer cell lines
Authors: Wan He, SC Cesar Wong, Charles ML Chan, WS Ho, Thomas CC Au, Money YY Lam, Anthony TC Chan
Journal: Cancer Research (2012)

Abstract Background: The notch pathway is involved in control of cell differentiation in various tissues including pancreas, muscle and bone marrow. Jagged 2 (JAG2) is a ligand for the notch pathway and was found to be overexpressed in malignant plasma cells from patients with multiple myeloma, causing the secretion and release of IL-6, VEGF, and IGF-1 in the microenvironment supporting myeloma cell growth. In breast cancers, it was found to be overexpressed at the hypoxic invasive front and was significantly correlated with metastasis free survival. Furthermore, up-regulation of JAG2 expression in mouse lung adenocarcinoma cells promoted its metastasis in mice. However, the expression pattern and function of JAG2 in colorectal cancer (CRC) is not clear. Therefore in this study, we examined the expression of JAG2 in CRC cell lines and determined the effect(s) of JAG2 knockdown by RNA interference in CRC cell lines. Materials and Methods: The expression of JAG2 protein was examined in four CRC cell lines (SW480, SW620, HCT116, DLD-1) and also in 1 normal colon epithelial cell line (CCD18co) using the western blot. To investigate the effects JAG2 knockdown in CRC cell lines, a pool of 4 siRNAs against JAG2 was transfected into the 4 CRC cell lines listed above. The effects on cell growth was then determined by the CellTiter 96® AQueous One Solution Cell Proliferation Assay (the MTS assay) and the Matrigel invasion assay was performed to assess its effects on invasive capability. Results: Western blot results showed that JAG2 protein was expressed in all 4 colorectal cancer cell lines including SW480, SW620, HCT116 and DLD-1 but not in the CCD18co normal colon epithelial cell line. The MTS assay showed that cell growth was not affected by JAG2 knockdown in the CRC cell lines. Interestingly, the invasive capability of HCT116 and DLD-1cells was reduced after JAG2 knockdown. Conclusions: Results from this study suggest that JAG2 may play a role in the invasiveness of CRC cell lines but not in cell proliferation. JAG2 may be a promising therapeutic target for inhibition of metastasis in colorectal cancer. 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 505. doi:1538-7445.AM2012-505
Novel thermal tumor ablation for breast cancer in mice using magnetic nanoparticles.
Authors: K Motomura, M Ishitobi, Y Komoike, H Koyama, H Inaji, M Inoue, H Nagae, I Nagano
Journal: Cancer Research (2009)

Abstract Abstract #2158 Background: Thermal ablation therapy using lasers, ultrasound and microwaves is being investigated as a less invasive alternative to surgery for breast cancer. This study examined the efficacy of magnetic nanoparticles, which produce heat when exposed to an alternating magnetic field, for the destruction of breast cancer in mice.&amp;#x2028; Material and Methods: Tumors were induced on both sides of the back of BALB/C mice by subcutaneous injection of MDA-MB-231 breast cancer cells. Magnetic nanoparticles were injected in and around one of the tumors in a mouse, while saline were injected in another tumor (control). Mice were exposed to an alternating magnetic field for 40 min. The temperature of the tumor injected with nanoparticles reached 45°C and was maintained at that temperature by adjusting the magnetic field intensity. Histopathological response was evaluated one to two months after thermal ablation therapy.&amp;#x2028; Results: In 8 (67%) of 12 mice, complete tumor regression was observed in tumors treated with nanoparticle injection, while there was no regression in control tumors in any of the mice. There was no irreversible damage seen in normal tissue surrounding the nanoparticle injected tumors.&amp;#x2028; Discussion: Since this procedure can destroy cancer cells specifically without injuring normal tissue, it may be applicable to the treatment of human breast cancer. Moreover, it may be possible to develop this procedure into a systemic therapy for tumor-specific targeting. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 2158.
TWO INCISION VERSUS THREE INCISION PROCEDURE TIMES FOR IMPLANTATION OF SUBCUTANEOUS IMPLANTABLE CARDIOVERTER DEFIBRILLATORS: A TWO CENTER EXPERIENCE
Authors: Christina Dookhan, Abhijit Ghatak, Santosh Padala, Rizwan Alimohammad, David Steckman, Henry Tan, James O'Brien, Mandeep Sidhu, Assaf Tzur, Ivan Mendoza
Journal: Journal of the American College of Cardiology (2016)
Abstract 616: A cumulative molecular model for the mechanisms of green tea catechins in the chemoprevention of prostate cancer
Authors: Shahnjayla K. Connors, Nagi B. Kumar
Journal: Cancer Research (2012)

Abstract Background: Prostate cancer (CaP) is the most commonly diagnosed cancer in men. It's long latency, slow progression, and high incidence rates make it ideal for targeting chemoprevention therapies. Studies suggest that green tea may be suitable candidate for CaP chemoprevention. The green tea catechin (GTC) chemopreventive mechanisms against CaP cells, however, are not completely clear. Understanding and refining models of the fundamental molecular pathways by which GTCs modulate prostate carcinogenesis is essential to most appropriately utilize green tea for CaP prevention in clinical settings. Objective: The objective of the study was to review the current literature and develop a model that attempts to recreate the molecular mechanisms and pathways by which GTCs modulate prostate carcinogenesis. Methods: Laboratory studies, clinical studies, and clinical trials focused on GTC chemoprevention of CaP were critically analyzed and reviewed for mechanisms of GTC chemoprevention. The most prevalent mechanisms were combined into a multi-mechanistic model that attempts to recreate the cumulative events that occur as GTCs exert anti-cancer activity on prostate cancer cells and tissues. Results: GTCs exert anti-cancer actions on CaP cells and tissue through six major mechanisms: proteasome inhibition, cell cycle arrest, inhibition of cell proliferation, induction of apoptosis, suppression of carcinogenesis/progression, and inhibition of metastasis. We have proposed a novel model in which GTCs exert chemopreventive effects on CaP though these six major mechanisms that work simultaneously and dependently, largely driven by proteasome inhibition-induced regulation of the NFκB pathway. The cumulative effect of these mechanisms ultimately leads to the inhibition of CaP cell growth, progression, and metastasis. Conclusions: Several mechanisms of GTC chemopreventive activity on CaP cells and tissues have been identified in laboratory and clinical studies. Although GTCs act through distinct cell cycle regulative pathways, the cumulative chemopreventative effect appears to be attributed to their well-coordinated ensemble, rather than a single pathway. Additionally, transitioning to the use of standardized GTC preparations may more accurately reflect human tea consumption, deliver the maximum amount of GTCs, and allow for more generalizable results in epidemiological, laboratory, and clinical studies. We are currently testing and refining our novel cumulative model to fully elucidate the complex mechanism of GTC chemoprevention of prostate cancer in its entirety. 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 616. doi:1538-7445.AM2012-616