tbuckley/cabot-search huggingface dataset:
Xanthocillin Cream for Local Treatment
Authors: F.R. Bettley
Journal: BMJ (1959)

BREAST ABSCESS B Ihm remain opposed to breast-feeding despite full propaganda should be allowed to bottle-feed their babies and receive instruction in the correct technique for doing this. (3)If breast-feeding is stopped, lactation should be vigorously suppressed under medical supervision.We would suggest that stilboestrol be given in a dosage of 45 mg.three times a day.The breast should be emptied regularly by manual expression and lumpy collections dispersed by gentle centripetal massage. ( 4 An antibiotic should be given if infection is suspected.If there is no local response after 48 hours the antibiotic should be stopped.Prolonging antibiotic treatment in the absence of a response leads to excessive fibrosis and protraction of the disease.( 5) The antibiotic of choice in this series was chloramphenicol.Summary One hundred consecutive cases of puerperal breast abscess requiring hospital treatment were studied.It was shown that the duration of the disease has increased compared with earlier reports from the same hospital (Macpherson, 1943).This increase seems to be due to the widespread use of antibiotics.Very high resistance rates to antibiotics were shown.The failure of antibiotic treatment was largely due to this resistance.The modification of the pathology of the disease when treated with antibiotics to which the organism is not fully sensitive is discussed.The importance of adequate suppression of lactation and of avoidance of breast engorgement in the prevention of infection in those who stop breast-feeding is stressed.Recommendations to reduce the incidence and duration of the disease are made.This work was made possible by the help and co-operation of Sister Gordon and the medical and nursing staff of the surgical out-patient department of the
A randomized phase III adjuvant study in high-risk cervical cancer: simultaneous radiochemotherapy with cisplatin (S-RC) versus systemic paclitaxel and carboplatin followed by percutaneous radiation (PC-R): a NOGGO-AGO Intergroup Study
Authors: J. Sehouli, I.B. Runnebaum, C. Fotopoulou, U. Blohmer, A. Belau, H. Leber, L.C. Hanker, W. Hartmann, R. Richter, M.D. Keyver-Paik, C. Oberhoff, G. Heinrich, A. du Bois, C. Olbrich, E. Simon, K. Friese, R. Kimmig, D. Boehmer, W. Lichtenegger, S. Kuemmel
Journal: Annals of Oncology (2012)
Inhibition of E-Selectin Gene Expression by Transforming Growth Factor β in Endothelial Cells Involves Coactivator Integration of Smad and Nuclear Factor κB–Mediated Signals
Authors: Maria R. DiChiara, Jeanne Marie Kiely, Michael A. Gimbrone, Mu-En Lee, Mark A. Perrella, James N. Topper
Journal: The Journal of Experimental Medicine (2000)

Transforming growth factor (TGF)-β1 is a pleiotropic cytokine/growth factor that is thought to play a critical role in the modulation of inflammatory events. We demonstrate that exogenous TGF-β1 can inhibit the expression of the proinflammatory adhesion molecule, E-selectin, in vascular endothelium exposed to inflammatory stimuli both in vitro and in vivo. This inhibitory effect occurs at the level of transcription of the E-selectin gene and is dependent on the action of Smad proteins, a class of intracellular signaling proteins involved in mediating the cellular effects of TGF-β1. Furthermore, we demonstrate that these Smad-mediated effects in endothelial cells result from a novel competitive interaction between Smad proteins activated by TGF-β1 and nuclear factor κB (NFκB) proteins activated by inflammatory stimuli (such as cytokines or bacterial lipopolysaccharide) that is mediated by the transcriptional coactivator cyclic AMP response element–binding protein (CREB)-binding protein (CBP). Augmentation of the limited amount of CBP present in endothelial cells (via overexpression) or selective disruption of Smad–CBP interactions (via a dominant negative strategy) effectively antagonizes the ability of TGF-β1 to block proinflammatory E-selectin expression. These data thus demonstrate a novel mechanism of interaction between TGF-β1–regulated Smad proteins and NFκB proteins regulated by inflammatory stimuli in vascular endothelial cells. This type of signaling mechanism may play an important role in the immunomodulatory actions of this cytokine/growth factor in the cardiovascular system.
Coexistence of Minicircular and a Highly Rearranged mtDNA Molecule Suggests That Recombination Shapes Mitochondrial Genome Organization
Authors: Meng Mao, Andrew D. Austin, Norman F. Johnson, Mark Dowton
Journal: Molecular Biology and Evolution (2013)

Recombination has been proposed as a possible mechanism to explain mitochondrial (mt) gene rearrangements, although the issue of whether mtDNA recombination occurs in animals has been controversial. In this study, we sequenced the entire mt genome of the megaspilid wasp Conostigmus sp., which possessed a highly rearranged mt genome. The sequence of the A+T-rich region contained a number of different types of repeats, similar to those reported previously in the nematode Meloidogyne javanica, in which recombination was discovered. In Conostigmus, we detected the end products of recombination: a range of minicircles. However, using isolated (cloned) fragments of the A+T-rich region, we established that some of these minicircles were found to be polymerase chain reaction (PCR) artifacts. It appears that regions with repeats are prone to PCR template switching or PCR jumping. Nevertheless, there is strong evidence that one minicircle is real, as amplification primers that straddle the putative breakpoint junction produce a single strong amplicon from genomic DNA but not from the cloned A+T-rich region. The results provide support for the direct link between recombination and mt gene rearrangement. Furthermore, we developed a model of recombination which is important for our understanding of mtDNA evolution.
Screening for Hepatitis B Virus Infection in Pregnant Women: Evidence for the U.S. Preventive Services Task Force Reaffirmation Recommendation Statement
Authors: Kenneth Lin, John Vickery
Journal: Annals of Internal Medicine (2009)

Background: Screening for hepatitis B virus (HBV) infection in pregnant women to identify newborns who will require prophylaxis against perinatal infection is a well-established, evidence-based standard of current medical practice. In 2004, the U.S. Preventive Services Task Force (USPSTF) recommended universal screening of pregnant women for HBV infection at the first prenatal visit. Purpose: To search for large, high-quality studies related to hepatitis B screening in pregnancy that have been published since the 2004 USPSTF recommendation. Data Sources: English-language studies indexed in PubMed and the Cochrane Database of Systematic Reviews and published between 1 January 2001 and 5 March 2008. Study Selection: For benefits of screening and newborn prophylaxis, we included systematic reviews; meta-analyses; and randomized, controlled trials. For harms of screening, we included systematic reviews; meta-analyses; randomized, controlled trials; cohort studies; case–control studies; and case series of large, multisite databases. Abstracts and full articles were independently reviewed for inclusion by both reviewers. Data Extraction: Data on the benefits of screening, including benefits of hepatitis B immune globulin and hepatitis B vaccine prophylaxis of newborns of hepatitis B surface antigen–positive mothers, were extracted by 1 reviewer. Data Synthesis: No new studies met inclusion criteria. A 2006 systematic review of randomized, controlled trials found that newborn prophylaxis reduced perinatal transmission of HBV infection; all relevant trials were published in 1996 or earlier. Limitation: The focused search strategy, which was restricted to English-language articles, may have missed some smaller studies or new research published in languages other than English. Conclusion: No new evidence was found on the benefits or harms of screening for HBV infection in pregnant women. Previously published randomized trials support the 2004 USPSTF recommendation for screening.
Imaging growth and isocitrate dehydrogenase 1 mutation are independent predictors for diffuse low-grade gliomas
Authors: C. Goze, M. Blonski, G. Le Maistre, L. Bauchet, E. Dezamis, P. Page, P. Varlet, L. Capelle, B. Devaux, L. Taillandier, H. Duffau, J. Pallud
Journal: Neuro-Oncology (2014)

We explored whether spontaneous imaging tumor growth (estimated by the velocity of diametric expansion) and isocitrate dehydrogenase 1 (IDH1) mutation (estimated by IDH1 immunoexpression) were independent predictors of long-term outcomes of diffuse low-grade gliomas in adults.
Contributory Factors to Unsteadiness During Walking Up and Down Stairs in Patients With Diabetic Peripheral Neuropathy
Authors: Joseph C. Handsaker, Steven J. Brown, Frank L. Bowling, Glen Cooper, Constantinos N. Maganaris, Andrew J.M. Boulton, Neil D. Reeves
Journal: Diabetes Care (2014)

OBJECTIVE Although patients with diabetic peripheral neuropathy (DPN) are more likely to fall than age-matched controls, the underlying causative factors are not yet fully understood. This study examines the effects of diabetes and neuropathy on strength generation and muscle activation patterns during walking up and down stairs, with implications for fall risk. RESEARCH DESIGN AND METHODS Sixty-three participants (21 patients with DPN, 21 diabetic controls, and 21 healthy controls) were examined while walking up and down a custom-built staircase. The speed of strength generation at the ankle and knee and muscle activation patterns of the ankle and knee extensor muscles were analyzed. RESULTS Patients with neuropathy displayed significantly slower ankle and knee strength generation than healthy controls during stair ascent and descent (P &amp;lt; 0.05). During ascent, the ankle and knee extensor muscles were activated significantly later by patients with neuropathy and took longer to reach peak activation (P &amp;lt; 0.05). During descent, neuropathic patients activated the ankle extensors significantly earlier, and the ankle and knee extensors took significantly longer to reach peak activation (P &amp;lt; 0.05). CONCLUSIONS Patients with DPN are slower at generating strength at the ankle and knee than control participants during walking up and down stairs. These changes, which are likely caused by altered activations of the extensor muscles, increase the likelihood of instability and may be important contributory factors for the increased risk of falling. Resistance exercise training may be a potential clinical intervention for improving these aspects and thereby potentially reducing fall risk.
Thrombotic obstruction of the Bjork-Shiley valve: the Glasgow experience.
Authors: S J Ryder, H Bradley, J J Brannan, M A Turner, W H Bain
Journal: Thorax (1984)

Thrombotic obstruction is the most feared complication of the Björk-Shiley tilting disc prosthesis. From 1971 to 1982 1186 Björk-Shiley valves were implanted in 900 patients. There were 93 deaths in hospital. Eight hundred and seven patients have been followed for a total of 4146 patient years; 14 patients were lost to follow up. Nineteen cases of thrombotic obstruction were identified at necropsy or at a repeat operation in the study group. The mitral prosthesis was thrombosed in 16 patients, the aortic in two, and the tricuspid in one. The incidence for this complication has been calculated to be 0.46 per 100 patient years for all valve positions, 0.79 for single mitral valve replacements, 0.18 for aortic replacements, and 0.63/100 for the tricuspid position. The maximum possible incidence of this complication in this population has been calculated to be 1.4 per 100 patient years. The mortality rate was 41.7% for reoperation and 63% for the development of the complication. Risk factors that have been identified are inadequate anticoagulant control, poor preoperative exercise capacity, and possibly also the implantation of small prostheses.
Doxorubicin and etoposide sensitize small cell lung carcinoma cells expressing caspase-8 to TRAIL
Authors: Alena Vaculova, Vitaliy Kaminskyy, Elham Jalalvand, Olga Surova, Boris Zhivotovsky
Journal: Molecular Cancer (2010)

Abstract Background TRAIL is considered as a promising anti-cancer agent, because of its ability to induce apoptosis in cancer but not in most normal cells. However, growing evidence exist that many cancer cells are resistant to its apoptotic effects. SCLC is a typical example of tumor entity where TRAIL monotherapy is not efficient. Results We demonstrated that doxorubicin and etoposide markedly sensitized SCLC cells expressing caspase-8 to apoptotic effects of TRAIL. The drug-mediated sensitization of these cells was associated with increase of surface and total DR5 protein level, specific cleavage of cFLIP L , decrease of cFLIP S level, and a strong activation of caspase-8. The involvement of mitochondria-mediated pathway was demonstrated by enhanced Bid cleavage, Bax activation, and cytochrome c release. Activation of caspase-8 induced by combined treatment was shown to occur upstream of mitochondria and effector caspases. Conclusions Our results highlight significant applicability of doxorubicin and etoposide in sensitization of SCLC cells expressing caspase-8 to treatment with TRAIL.
Chronic Graft-versus-Host Autoimmune Disease in Fc Receptor γ chain-deficient Mice Results in Lipoprotein Glomerulopathy
Authors: Yutaka Kanamaru, Atsuhito Nakao, Isao Shirato, Ko Okumura, Hideoki Ogawa, Yasuhiko Tomino, Chisei Ra
Journal: Journal of the American Society of Nephrology (2002)

ABSTRACT. Lipoprotein glomerulopathy (LPG) is a unique renal disease characterized by intraglomerular lipoprotein thrombi associated with severe proteinuria and frequent progression to renal failure. The histologic hallmark of LPG is the presence of laminated thrombi, consisting of lipid droplet, within the lumina of dilated glomerular capillaries. The findings of thrombi consisting of lipoproteins raised the possibilities that LPG might be related to a primary abnormality in lipid metabolism. However, the precise pathogenic basis of LPG remains unresolved. It was herein found that chronic graft-<i>versus</i>-host disease (GVHD) induced by the transfer of Ia-incompatible spleen cells from B6.C-H2<sup>bm12</sup> into coisogenic C57BL/6 mice with deficiency of Fc receptor γ chain (FcRγ) resulted in glomerulopathy that resembled LPG. The uptake of acetylated LDL was partially decreased in peritoneal macrophages isolated from FcRγ-deficient mice compared with wild-type mice, suggesting that partial impairment of modified LDL uptake might contribute to the development of LPG associated with chronic GVHD in FcRγ-deficient mice. LPG has been suggested to be a disorder of primary abnormality in lipid metabolism; these findings would therefore provide novel insight into the disease process.
REMISSION INDUCTION WITH ADENOSINE-DEAMINASE INHIBITOR 2'-DEOXYCOFORMYCIN IN THY-LYMPHOBLASTIC LEUKÆMIA
Authors: H.Grant Prentice, K. Ganeshaguru, KennethF. Bradstock, AnthonyH. Goldstone, JohnF. Smyth, Beatrix Wonke, George Janossy, A.Victor Hoffbrand
Journal: The Lancet (1980)
Thymomodulin increases release of granulocyte-macrophage colony stimulating factor and of tumour necrosis factor in vitro
Authors: B Balbi, MT Valle, S Oddera, E Balleari, F Manca, GA Rossi, L Allegra
Journal: European Respiratory Journal (1992)

To evaluate the effects of thymomodulin (TMD), a thymic biological response modifier derived from calf thymus, on the release of various cytokines involved in the lung immune reactions, human alveolar macrophages (AM) and peripheral blood lymphocytes (PBL) were cultured either alone or in co-cultures. In co-cultures of AM with PBL, TMD did not induce any change in gamma-interferon (gamma-IFN) and interleukin-1 (IL-1) secretion, while it was able to increase the level, of tumour necrosis factor (TNF) (TMD 100 micrograms.m-1, p < 0.05 vs control cultures), and of granulocyte macrophage colony-stimulating factor (GM-CSF) (TMD 1, 10 and 100 micrograms.ml-1 p < 0.05, < 0.05 and < 0.01, respectively, vs control cultures). In cultures of AM alone, TMD did not induce changes in the levels of any of the tested cytokines, whilst in supernatants from PBL lymphocyte cultures, TMD at 1, 10 and 100 micrograms.ml-1 increased the amounts of GM-CSF (p < 0.01 each comparison vs control cultures). Thus, TMD seems to directly stimulate lymphocytes to secrete GM-CSF and to modulate macrophage-lymphocyte interactions, resulting in the release of TNF and GM-CSF.
Down-regulation of the P2Y12 purinergic receptor expression on human bronchial epithelial cells by transforming growth factor-β
Authors: Siiri Altraja, Alan Altraja
Journal: European Respiratory Journal (2013)

We have demonstrated presence of the P2Y12 purinergic receptor on human bronchial epithelial cells (HBEC). Apart from acting as an alternative receptor for leukotriene E4, neither its function nor regulation on HBEC is known, not to mention its role in airway remodelling. In this context, we hypothesized that transforming growth factor-β (TGF-β) could affect expression of the P2Y12 receptor on HBEC.

To test the hypothesis, cultured HBEC were exposed to TGF-β1 (0-10 ng/mL) for 1-24 h. The expression of P2Y12 mRNA was evaluated with use of RT-qPCR.

A slight decrease in the expression of P2Y12 not reaching significance was observed at 1-3 h. TGF-β1 significantly suppressed the expression of P2Y12 in HBEC at 12 h (3.5–5.9-fold decrease from control; p=0.001 and p=0.001 at 2 ng/mL and 10 ng/mL, respectively). This decrease persisted by 24 h (3.2–4.0-fold decrease from baseline; p=0.013 and p<0.001 with concentrations of 2 ng/mL and 10 ng/mL, respectively). The decrease was clearly concentration-dependent (p=0.001 and p<0.001 at 12 and 24 h, respectively). The time-dependence in down-regulation of the expression of P2Y12 in HBEC was observed only at higher concentrations of TGF-β1 (p=0.01 at 10 ng/mL).

Our results indicate that TGF-β1 down-regulate the P2Y12 in HBEC providing a novel insight into mechanisms by which TGF-β1 may execute its anti-inflammatory properties. However, the impact of this mechanism both independently and in the light of the summary effects of TGF-β1, known as a pro-remodelling factor, remains to be tested.

Supported by the Estonian Science Foundation grants No. 9103 and 9043.
A new concept of a multidisciplinary lymphoedema centre: established in connection to a department of dermatology and the Copenhagen Wound Healing Center
Authors: S. Birkballe, T. Karlsmark, S. Noerregaard, F. Gottrup
Journal: British Journal of Dermatology (2012)

Lymphoedema is increasingly recognized as a significant problem in healthcare. The number of patients is growing, posing a future challenge to healthcare systems and economics. Over the past decade, specialized lymphoedema management has been established around the world to accommodate the growing demands. However, information on organization, experiences and outcome are scarce.To conduct a clinical perspective analysis describing the establishment, organization, function and results of a new, multidisciplinary lymphoedema centre functioning as a university hospital unit in connection to a department of dermatology and the Copenhagen Wound Healing Center and integrated as a national expert function in the public healthcare organization of Denmark.Data were collected following the establishment of a lymphoedema centre based on the structured, multidisciplinary organization of lymphoedema management.During the first 4·5 years a total of 8058 patient consultations were performed. The mean duration of symptoms at the first visit was 19 years (range 1-67) and 31% of patients had never received any diagnosis or treatment prior to referral. Complications were found in 48% of referred patients. All patients received appropriate diagnostic investigations and treatment according to best practice. Multidisciplinary assessment involving four or more different healthcare professions was needed in 86% of cases. Research opportunities and expert education of staff were enhanced.A multidisciplinary lymphoedema centre improves management, knowledge and awareness of lymphoedema. This model, with minor adjustments, may be applicable for other regions and countries.
Intraperitoneal Injection of a Hairpin RNA–Expressing Plasmid Targeting Urokinase-Type Plasminogen Activator (uPA) Receptor and uPA Retards Angiogenesis and Inhibits Intracranial Tumor Growth in Nude Mice
Authors: Christopher S. Gondi, Sajani S. Lakka, Dzung H. Dinh, William C. Olivero, Meena Gujrati, Jasti S. Rao
Journal: Clinical Cancer Research (2007)

Abstract Purpose: The purpose of this study was to evaluate the therapeutic potential of using plasmid-expressed RNA interference (RNAi) targeting urokinase-type plasminogen activator (uPA) receptor (uPAR) and uPA to treat human glioma. Experimental Design: In the present study, we have used plasmid-based RNAi to simultaneously down-regulate the expression of uPAR and uPA in SNB19 glioma cell lines and epidermal growth factor receptor (EGFR)–overexpressing 4910 human glioma xenografts in vitro and in vivo, and evaluate the i.p. route for RNAi-expressing plasmid administered to target intracranial glioma. Results: Plasmid-mediated RNAi targeting uPAR and uPA did not induce OAS1 expression as seen from reverse transcription-PCR analysis. In 4910 EGFR-overexpressing cells, down-regulation of uPAR and uPA induced the down-regulation of EGFR and vascular endothelial growth factor and inhibited angiogenesis in both in vitro and in vivo angiogenic assays. In addition, invasion and migration were inhibited as indicated by in vitro spheroid cell migration, Matrigel invasion, and spheroid invasion assays. We did not observe OAS1 expression in mice with preestablished intracranial tumors, which were given i.p. injections of plasmid-expressing small interfering RNA–targeting uPAR and uPA. Furthermore, the small interfering RNA plasmid targeting uPAR and uPA caused regression of preestablished intracranial tumors when compared with the control mice. Conclusion: In conclusion, the plasmid-expressed RNAi targeting uPAR and uPA via the i.p. route has potential clinical applications for the treatment of glioma.