tbuckley/cabot-search huggingface dataset:
LYMPHANGIOMA OF SKIN.
Authors: R. D. G. PEACHEY, C.-C. LIM, I. W. WHIMSTER
Journal: British Journal of Dermatology (1970)

Sixty-five cases of lymphangiomata involving skin or mucous membrane have been reviewed and found on clinical and histological grounds to fall into 3 groups. "Classical" lesions of lymphangioma circumscriptum were often extensive, had a predilection for certain areas and were usually present at birth or appeared in early life. Small "localized" lesions had no particular sites of predilection and could appear for the first time at any age. A small number of lesions with a characteristic sponge-like histological appearance were found in areas where skin or mucous membrane was interwoven with striated muscle. A review of the results of surgery in these patients showed recurrence to be unusual after excision of "localized" lesions but to be common when an attempt was made to excise lesions of the "classical" type.
National Institutes of Health Pathways to Prevention Workshop: Advancing the Research on Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
Authors: Carmen R. Green, Penney Cowan, Ronit Elk, Kathleen M. O'Neil, Angela L. Rasmussen
Journal: Annals of Internal Medicine (2015)

The National Institutes of Health (NIH) Pathways to Prevention Workshop: Advancing the Research on Myalgic Encephalomyelitis/Chronic Fatigue Syndrome was cosponsored by the NIH Office of Disease Prevention and the Trans-NIH Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Research Working Group. A multidisciplinary working group developed the agenda, and an Evidence-based Practice Center prepared an evidence report through a contract with the Agency for Healthcare Research and Quality to facilitate the discussion. During the 1.5-day workshop, invited experts discussed the body of evidence and attendees had the opportunity to comment during open discussions. After weighing evidence from the evidence report, expert presentations, and public comments, an unbiased, independent panel prepared a draft report that identified research gaps and future research priorities. The report was posted on the NIH Office of Disease Prevention Web site for 4 weeks for public comment.
French's Index of Differential Diagnosis.
Authors: Herbert French
Journal: Annals of Internal Medicine (1986)

Symptoms listed alphabetically eg: A - Abdominal pain, acute, localized Abdominal pain, general Abdominal pulsation Abdominal rigidity Abdominal swellings Alopecia Amenorrhoea Amnesia Angioma and telangiectasia Anorectal pain Anxiety Appetite, disorders of Apraxia Arcus cornealis Arm, pain in Ataxia Athetosis Aura Axillary swelling.
Abstract 834: The microtubule-disrupting drug BNC105 is a potent inducer of acute apoptosis in CLL
Authors: Darcy J.P. Bates, Edmundo J. Feris, Alexey V. Danilov, Alan Eastman
Journal: Cancer Research (2014)

Abstract The cytotoxicity of microtubule-disrupting drugs such as the vinca alkaloids has generally been considered to occur during mitosis. However, we have reported that vinca alkaloids can induce apoptosis rapidly (&amp;lt;6 h) from all phases of the cell cycle, and even in post-mitotic quiescent cells such as peripheral chronic lymphocytic leukemia (CLL). Microtubule disruption still appears to be required as acute apoptosis also occurs with combretastatin A4 (CA4) which targets the colchicine-binding site on tubulin, but not with paclitaxel which stabilizes microtubules. The mechanism of this rapid apoptosis is associated with two different pathways: induction of the pro-apoptotic BCL2 family member NOXA and activation of c-Jun N-terminal kinase (JNK). A proof-of-concept clinical trial revealed that vincristine activated JNK in peripheral lymphocytes of patients with CLL, but failed to induce NOXA or apoptosis, suggesting that this might not be the best microtubule disruptor to use clinically. Further investigation revealed that the vascular disrupting agent BNC105 (provided by Bionomics Ltd), which also targets the colchicine-binding site on tubulin, is a much more potent activator of JNK and inducer of NOXA in various leukemia cell lines and freshly isolated CLL cells. BNC105 induced ATF3, phospho-ATF2 and NOXA proteins and activated JNK at low nM concentrations. As a single agent, BNC105 induced JNK-dependent apoptosis in CLL cells ex vivo at clinically achievable concentrations, and much more potently than either vinblastine or CA4. The combination of BNC105 with the BCL2 inhibitor ABT-199 increased apoptosis levels in CLL cells and various leukemia cell lines. Furthermore, the addition of BNC105 partially overcame stroma-mediated resistance to ABT-199 in CLL cells suggesting potential efficacy of this combination in the lymph node microenvironment. Survival of normal lymphocytes was not affected by BNC alone or in combination, even though JNK was activated. These results suggest BNC105 is an excellent candidate for clinical trials to induce acute apoptosis in hematopoietic malignancies. Citation Format: Darcy J.P. Bates, Edmundo J. Feris, Alexey V. Danilov, Alan Eastman. The microtubule-disrupting drug BNC105 is a potent inducer of acute apoptosis in CLL. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 834. doi:10.1158/1538-7445.AM2014-834
Changes in cerebral cortex size are governed by fibroblast growth factor during embryogenesis
Authors: Flora M. Vaccarino, Michael L. Schwartz, Rossana Raballo, Jon Nilsen, Julianne Rhee, Ming Zhou, Thomas Doetschman, J. Douglas Coffin, Jason J. Wyland, Yu-Ting E. Hung
Journal: Nature Neuroscience (1999)
Abstract 4422: A Hippo-independent pathway modulates YAP-induced resistance of cancer cells to antitubulin drugs
Authors: Yulei Zhao, Prem Khanal, Xiaolong Yang
Journal: Cancer Research (2014)

Abstract Antitubulin drugs have been widely used for the treatment of various human cancers including breast and lung cancer, etc. Although these drugs are effective as first-line treatment of cancers, many cancer patients are either intrinsically resistant or later develop resistant to drugs, which is one of the major obstacles for successful cancer treatment. Therefore, understanding the molecular mechanism underlying antitubulin drug resistance is critical for future prognosis of cancer treatment and development of novel therapeutic drugs for cancer treatment. The Hippo pathway is an emerging signaling pathway that plays important roles in various biological processes including organ size control, tumorigenesis, stem cell differentiation and renewal, etc. Although tremendous progress has been made toward our understanding of the roles of the Hippo pathway in cancer development, if and how is its role in drug resistance remains largely unknown. Recently, we and others have provided convincing evidence that some core components of the Hippo pathway are involved in the resistance of cancer cells to antitubulin drug Taxol. However, the signaling pathways or genes mediating their effects in chemotherapeutic drug response remain to be identified. In this study, we have discovered that Hippo core component YAP oncoprotein and transcriptional co-activitor is specifically phosphorylated only after treatment of cancer cells with antitubulin drugs. Most significantly, we have identified a Hippo-independent pathway in which activated Cdk1 can directly phosphorylate YAP, which subsequently inactivates YAP function in transactivation and anti-apoptosis during antitubulin drug treatment. These findings have significant implication not only in future use of YAP as a prognostic marker in predicting antitubulin drug response in patients but also provide a novel approach for future targeting and inactivating YAP by activating its phosphorylation for treatment of antitublin drug resistant cancer patients caused by YAP activation. Citation Format: Yulei Zhao, Prem Khanal, Xiaolong Yang. A Hippo-independent pathway modulates YAP-induced resistance of cancer cells to antitubulin drugs. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4422. doi:10.1158/1538-7445.AM2014-4422
Purification and characterization of two new allergens from the salivary glands of the horsefly, Tabanusyao
Authors: D. Ma, Y. Li, J. Dong, S. An, Y. Wang, C. Liu, X. Yang, H. Yang, X. Xu, D. Lin, R. Lai
Journal: Allergy (2010)

Horsefly bite can cause allergic reactions in humans. There is no information about allergenic horsefly proteins.The current work aims to purify and characterize IgE-binding proteins from horsefly salivary glands.Two IgE-binding proteins, Tab a 1 and Tab a 2 with molecular weight of 26 and 35 kd, respectively, were purified and characterized from 60,000 pairs of horsefly salivary glands of Tabanus yao, respectively. Their primary sequences were determined by Edman degradation and cDNA cloning. Their allergenicity was examined using enzyme-linked immunosorbent assay (ELISA), ELISA inhibition tests, and immunoblots.Immunoblotting demonstrated IgE binding by 32 and 34 of 37 (86.5% and 91.8%) subjects' sera to Tab a 1 and Tab a 2, respectively. They were identified as an antigen 5-related (Ag 5) protein and hyaluronidase, respectively. ELISA inhibitions of serum IgE reactivity to the horsefly salivary gland extract (SGE) using purified Tab a 1 and Tab a 2 were significant (about 45%). In addition, these proteins showed some IgE-binding capacity to sera of subjects with wasp sting allergy.We have first identified and characterized two IgE-binding proteins, Tab a 1, an Ag 5-like protein and Tab a 2, a hyaluronidase, from the horsefly salivary glands. They appear to be of importance for the allergic reactions induced by horsefly bite. These allergens are thus not only found in stinging but also found in hematophagous insects. These results also provided support for the presence of the so-called wasp-horsefly syndrome (WHS).
355. Specific Lysis of Multiple Myeloma Cells by T-Cells Engineered To Express a Chimeric Immune Receptor Targeting WUE-Antigen
Authors: Max S. Topp, Horst D. Hummel, Gabriele Kuntz, Christina Neff, Hermann Einsele
Journal: Molecular Therapy (2004)

Multiple myeloma (MM) is the second most common hematological malignancies with an incidence of 4.1/100.000 per year. Disease control can be achieved by high-dose chemotherapy followed by autologous stem transplantation but relapse occurs in over 90% of all patients. Thus the development of novel concepts for eradication of minimal residual disease are highly warranted. Adoptive immunotherapy represent an attractive approach for augmenting tumor immunity and may be achieved by genetically modifying T-cells with an MM-specific chimeric immunoreceptor targeting the cell-surface antigen Wue-1. In contrast to healthy plasma cells Wue-1 is homogenously over expressed by primary MM cells and is not detected in other hematopoietic and nonhematopoietic tissues. An antibody-derived single-chain variable domains (scFvs) was fused with the CD3-ζ intracellular signaling domain. Primary CD4+ and CD8+ T-cells were genetically modified by retroviral-mediated gene-transfer with the constructed receptor and T-cell clones established from both genetically modified CD4+ and CD8+ T-cells. Cr-release assays performed with the generated CD8+ T-cells utilizing Wue-antigen (Wue-Ag) expressing MM cell lines as targets resulted into 72% specific lysis of the MM cells (E/T 5:1). In contrast non-Wue-Ag expressing targets were not recognized. Both CD4+ and CD8+ T-cells modified T-cells produced cytokines in responses to Wue-Ag expressing MM cell lines. Cytokine production could be blocked by preincubating target cell with the anti-Wue antibody, demonstrating the specific stimulation of modified T-cell by the interaction of the expressed chimeric receptor and Wue-Ag. Furthermore utilizing freshly isolated CD138+ cells from MM patients as stimulators resulted in specific production of cytokines and specific lysis by the modified T-cells, demonstrating that primary MM cells despite escape mechanism can be eradicated. In summary, CD4+ and CD8+ T-cells can be render to be highly specific for MM cells by expression of a chimeric immunoreceptors targeting Wue-surface Ag and therefore represents an attractive approach targeting relapsed multiple myeloma.
Topical administration of the pan-Src kinase inhibitors, dasatinib and LCB 03-0110, prevents allergic contact dermatitis in mice
Authors: S.H. Jung, X. Sun, W.-S. Ryu, B.-S. Yang
Journal: British Journal of Dermatology (2012)

Allergic contact dermatitis (ACD) is a delayed type of T cell-mediated cutaneous inflammatory response, in which multiple cell types are involved. Dasatinib and LCB 03-0110 are small molecule multityrosine kinase inhibitors, and they share remarkably similar target kinases such as the c-Src family, Btk and Syk, which play key roles in the cell signalling of T cells and other inflammatory cells. To test the anti-ACD activity of dasatinib and LCB 03-0110 and compare it with that of tacrolimus (FK506) and triamcinolone acetonide (a glucocorticoid), which are widely used for topical treatment of ACD, and to examine the two compounds for their capacity to induce skin atrophy, a side-effect. ACD was induced on the ears of mice by repeated topical application of oxazolone. Each test compound was then topically applied on the ear. Ear swelling, epidermal thickness and levels of inflammatory cytokines were measured. The skin atrophy induced by the compounds was tested during prolonged application on the dorsal skin of hairless mice, followed by haematoxylin and eosin staining. Dasatinib and LCB 03-0110 suppressed the symptoms of ACD such as ear swelling, increase in epidermal thickness and synthesis of inflammatory cytokines (i.e. interleukin-1β, tumour necrosis factor-α and interferon-γ) in a dose-dependent manner. The two compounds showed near-equal potency to tacrolimus; however, their potency was lower than that of triamcinolone acetonide. Prolonged treatment with the two compounds did not induce any skin atrophy, whereas use of steroidal agents induced severe atrophy. Dasatinib and LCB 03-0110 could be used as effective agents for the treatment of ACD without the adverse side-effect of skin atrophy.
Tuberculosis screening among intravenous drug users (IDU) in Georgia
Authors: Nana Kiria, Medea Gegia, Iagor Kalandadze
Journal: European Respiratory Journal (2011)

Background:  IDU is widespread in Georgia and regardless of HIV status it is at increased risk of developing active TB. It is necessary to identify the screening and effectively address the TB cases among IDUs.   Aim:  To assess the prevalence of TB among IDUs.   Methodology:  Using the data of prospective cohort study: from April 2008 to January 2011 IDUs at harm reduction and VCT sites were screened for TB symptoms using the questionnaire.  TB suspect cases were referred to TB units for further investigation and diagnosis.   Results:  4985 IDUs were screened for TB symptoms, 79 (2%) from them were female and 4906 (98%) –male. Mean age was 33. 81 (1.6%) from the screened IDU-s were HIV-positive and 2304 (46%) were diagnosed to have Hepatitis B or C.  436 (8.7%) were defined as TB suspects. They were presented at TB unites for further examinations. TB was confirmed in 175 cases, 109 (62%) had pulmonary TB and 66 (38%) – extrapulmonary. The prevalence of TB among IDU-s was 3510 per 100.000 which is 26 times greater as compared to TB prevalence in general population.   Conclusions:  Given the high risk for TB among IDUs, interventions such as active case finding, is urgently needed to detect TB cases as early as possible and treat them adequately.
Oyster Sloop, Cos Cob
Authors: M. Therese Southgate
Journal: JAMA (2000)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Incorporation of bevacizumab (B) and erlotinib (Er) with induction (Ind) and concurrent (Conc) carboplatin (Cb)/paclitaxel (P) and 74 Gy of thoracic radiotherapy in stage III non-small cell lung cancer (NSCLC)
Authors: M. A. Socinski, T. E. Stinchcombe, J. S. Halle, D. T. Moore, W. J. Petty, A. W. Blackstock, S. N. Gettinger, R. H. Decker, A. H. Khandani, D. E. Morris
Journal: Journal of Clinical Oncology (2009)

7528 Background: Therapies directed at both the epidermal growth factor receptor (EGFR) and the vascular endothelial growth factor (VEGF) pathways have been shown to improve survival in NSCLC and also have radiosensitizing properties. Methods: Pts receive Ind Cb (AUC 6), P (225 mg/m 2 ) and B (15 mg/kg) on d1 and 22. PET scans are done pre- and post-I. On day 43, pts receive weekly Cb (AUC 2 x 7) and P (45 mg/m 2 x 7) with 74 Gy (2 Gy/d) of thoracic conformal radiotherapy (TCRT). Cohort I (n=5) received B at 10 mg/kg q2wks during C therapy. Cohorts II and III (both n=5) received the same dose of B as in cohort I but also received Er at 100 mg and 150 mg po Tuesday - Friday of each week of C therapy, respectively. The primary endpoint is PFS at 1 year. All histologies are allowed including squamous (SQ) (an early stopping rule is in place for pulmonary hemorrhagic (PH) complications in SQ pts). Results: Thus far, 31 eligible PS 0–1 pts have been accrued (med age 62 yrs, range 41–74, 19 non- squamous, 12 SQ, 63% IIIA, 37% IIIB). Ind CbP + B has been well tolerated (1 gr 3 hypertension). No PH during Ind has been seen (including the 12 SQ cell pts). Response after Ind, 37% PR, 59% SD, 4% PD. Tumor volumes and PET SUVs have significantly decreased comparing pre- and post-Ind studies (p=0.0001 and p=0.0002, respectively). Cohort II has been expanded as the phase II regimen. To date, 25 of 26 (96%) pts have achieved the dose of 74 Gy (1 pt stopped at 60 Gy due to ILD). During Conc therapy, the principal toxicity has been esophagitis (53.8% gr 2, 19.2% gr 3). One grade 3 PH occurred in 1 SQ pt. One gr 5 late (&gt; 2 mos after treatment) PH occurred in a SQ pt. Overall response rate following treatment - 68.2% (95% CI, 45–86%). The PFS at 1 year is 58% (95% CI, 34–76%) with an estmated 1-year overall survival rate of 79% (95% CI, 53–92%) which compares favorably to our historical experience. Conclusions: Preliminarily, we conclude that 1) Incorporation of B and E into this treatment paradigm appears feasible, 2) Esophagitis remains the primary toxicity, 3) Phase II accrual continues but early analysis of survival appears promising. Further details regarding the TCRT parameters and toxicity will be presented. [Table: see text]
HIV Vaccine Strategies Use Broadly Neutralizing Antibody Approach
Authors: Tracy Hampton
Journal: JAMA (2015)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
1012. Ad Interactions with the Complement Systems of Humans and Mice
Authors: Haixiang Jiang, Ruth Everett, Anne Kiang, Zhaoxia Wang, Huame Zhang, Delila Serra, Michael M. Frank, Andrea Amalfitano
Journal: Molecular Therapy (2004)

Advanced generation Ad vectors can allow for long term persistence by avoiding activation of the adaptive arm of the immune response. Unfortunately, significant acute toxicities can be incurred after i.v. injection of Ads. Precious little is known about Ad interactions with the acellular defense systems present in the blood, including the complement system. The complement system has evolved to rapidly sequester invading pathogens, while rapidly initiating multiple downstream immune functions. However, inappropriate or excessive complement activation is also known to be associated with a number of serious clinical consequences. Intriguingly, many of these are known to also occur after high dose Ad injections, suggesting that Ads may be directly activating the complement cascade. We therefore set out to test this hypothesis. The exposure of Ad5 capsids to Ad-seropositive or sero-negative human serum resulted in activation of the complement cascade, suggesting that the presence of anti-Ad antibodies was not required for Ad induced complement activation. We found that complement consumption occurred despite specific blockade of the classical complement pathway (using the AP50 assay) implicating the alternative complement pathway as being directly activated by Ads. Ads also activated the alternative pathway when C1q depleted human serum (C1q is typically required for classical complement pathway activation) was utilized in the AP50 assay. Supporting these observations, we did not detect consumption of human C4 activity in either of these experiments. In vitro analyses confirmed that the human C3 protein could bind to immobilized Ad5 particles in the presence of EGTA (blocks classical pathway) but not EDTA (blocks both the classical and alternative complement pathways). This result was also achieved when Ad5 particles were incubated with C1q depleted serum. Again, the human C4 protein was not found to bind Ad particles under any of these assay conditions. We also found that 125-I labeled C3 bound to immobilized Ad particles, and this binding was significantly enhanced in the presence of purified Factor B and Factor D (members of the alternative pathway). Our results demonstrate that high titer Ads directly interact with proteins of the alternative complement pathway, leading to C3 binding of the virus particles. Most recently, we have found that human Ads activate the murine complement system, and blockade of the murine complement system prevented a typical Ad induced toxicity, namely thrombocytopenia.