tbuckley/cabot-search huggingface dataset:
An improved optically imageable metastatic model of human colon cancer orthotopically implanted on the cecum
Authors: Huaiyu Ma, Jin Wei Wang, Xiao-Ming Li, Zhijian Yang, Meng Yang, A. R. Moossa, Robert M. Hoffman
Journal: Cancer Research (2005)

Proc Amer Assoc Cancer Res, Volume 46, 2005

5670 

We report here an improved colon cancer mouse model developed with surgical orthotopic implantation (SOI) of green fluorescent protein (GFP)-expressing HCT-116 human colon cancer. Tumor fragments derived from subcutaneous growth of HCT116- GFP were implanted onto the cecum near the ascending colon. This procedure avoided tumor invasion to the abdominal wall of the implanted animals often seen when the tumor tissue was implanted on the ascending colon. The implantation site on the cecum near the ascending colon also eliminated intestinal obstruction that often occurred when the tumor was implanted on the ascending colon. The average lifespan of HCT116-tumor bearing mice was extended by this new transplantation site by approximately 2 weeks. Tumor growth, progression, and carcinomatosis could be readily visualized in real time in the live animal by use of GFP whole-body fluorescence imaging. The new model had a 100% take rate. The tumors metastasized to the mesentery lymph nodes (32%), liver (26%), and lung (11%). The micrometastatic lesions in the lymph nodes, liver, and lungs could be visualized by fluorescence microscopy. This imageable patient-like model should facilitate discovery and evaluation of novel therapeutics for colon cancer.
Abstract 13025: Deficiency of Interleukin-1 Receptor Antagonist Promotes Angiotensin II-induced Aortic Inflammation and Aneurysm
Authors: Koji Akita, Kikuo Isoda, Sarasa Isobe, Tomiharu Niida, Hiroyuki Daida
Journal: Circulation (2014)

Introduction: Angiotensin II (AngII) increases arterial pressure and induces inflammation. Although interleukin-1 receptor antagonist (IL-1Ra) is one of the most important anti-inflammatory cytokines, the role of IL-1Ra in AngII-induced aortic inflammation and aneurysm remains unknown. Methods and Results: To determine the contrition of IL-1Ra to AngII-induced aortic inflammation, male wild-type (WT) (n=18) and IL-1Ra-deficient (IL-1Ra-/-) (n=18) mice were infused with AngII (3000ng/kg per minute) using subcutaneous osmotic pumps for 28 days. 7 days after infusion, real-time PCR of abdominal aorta in IL-1Ra-/- mice revealed significantly increased mRNA levels of IL-6 (2.1-fold, p&lt;0.01), TNF-α (4.1-fold, p&lt;0.01), and MMP-9 (20.3-fold, p&lt;0.05) compared with WT mice. 14 days after infusion, both systolic blood pressure (178±21 vs 135±21 mmHg, p&lt;0.01)and abdominal aortic width (1.02±0.12 vs 0.82±0.05 mm, p&lt;0.01) in IL-1Ra-/- mice significantly increased compared with WT mice. Moreover, AngII infusion into IL-1Ra-/- mice also led to a significant increased occurrence of fatal aortic rupture (IL-1Ra-/-: 89% vs WT: 6%, p&lt;0.01). Next, WT (n=6) and IL-1Ra-/- (n=6) mice were infuse with AngII for only 14 days, and histological analyses were performed at 28 days after operation. Interestingly, the abdominal aortic width in IL-1Ra-/- mice more significantly increased than those in WT mice (1.57±0.34 vs 0.80±0.04 mm, p&lt;0.01), although IL-1Ra-/- and WT mice did not differ with regard to systolic blood pressure (105±15 vs 109±13 mmHg, p=0.61) at 28 days after operation. Histological analyses revealed there were numerous inflammatory cells around the abdominal aorta in IL-1Ra-/- mice, but not in WT mice. Furthermore, elastin staining showed destruction of the elastic lamina of abdominal aorta in IL-1Ra-/- mice. TNF-α protein expression also increased significantly in IL-1Ra-/- mice compared to WT mice at 28days. Conclusions: The present study shows that IL-1Ra deficiency in mice led to increase inflammation and the development of aortic aneurysm after AngII infusion. Furthermore, our results also showed IL-1Ra deficiency continued the AngII-induced inflammation even though blood pressure was improved after cessation of AngII infusion.
Abstract 9395: The Clinical Role of Atrial Fibrillation in Patients with Arrhythmogenic Right Ventricular Dysplasia
Authors: Ardan M Saguner, Samuel Baldinger, Argelia Medeiros-Domingo, Sabrina Ganahl, Felix C Tanner, Corinna Brunckhorst, Firat Duru
Journal: Circulation (2014)

Introduction: Atrial fibrillation/flutter (Afib/Aflu) in general, and clinical variables predicting Afib/Aflu in particular, are not well defined in patients with arrhythmogenic right ventricular dysplasia (ARVD). Hypothesis: We hypothesized that transthoracic echocardiography (TTE) and ECG could be helpful to predict Afib/Aflu in these patients. Methods and Results: 12-lead ECGs and TTEs of 90 patients from three tertiary-care centers diagnosed with definite or borderline ARVD according to the 2010 Task Force Criteria were analyzed. Data were compared in two patient groups: (1) patients with Afib/Aflu and (2) all other patients. Eighteen (20%) patients experienced Afib/Aflu during a follow-up period of 5.8 years (interquartile range 2.0-10.4 years). Kaplan-Meier analysis (Figure) revealed reduced times to Afib/Aflu among patients with echocardiographic RV fractional area change &lt;27% (p&lt;0.001), left atrial diameter ≥24.4 mm/m2 (p=0.001), and right atrial short axis diameter ≥22.1 mm/m2 (p=0.05). From all ECG variables, P sinistroatriale conferred the highest hazard ratio (3.37, 95% CI 0.92-12.36, p=0.067). Five patients with Afib/Aflu experienced inappropriate ICD shocks compared to four patients without Afib/Aflu (36% vs. 9%, p=0.03). Presence of Afib/Aflu was more prevalent in heart transplanted patients and in those who succumbed to cardiac death compared to the remaining patients (56% vs. 16%, p=0.014). Conclusions: Afib/Aflu are associated with inappropriate ICD shocks, heart transplantation, and cardiac death in patients with ARVD. Echocardiographic evidence of reduced RV function and atrial dilation helps to identify those ARVD patients being at increased risk for Afib/Aflu, which may help to guide individual patient management.
LONG STANDING PRODUCTIVE COUGH AS CHIEF CLINICAL MANIFESTATION IN MITRAL STENOSIS; A CASE COMPLICATED BY THROMBOSIS OF LEFT AURICLE
Authors: Estelle E. Kleiber
Journal: Annals of Internal Medicine (1941)

Excerpt In most cases of mitral stenosis with failure, cough is one of a number of symptoms: in few does it overshadow all others. It may be due to chronic congestive catarrh of the bronchial mucosa, but in the case reported below the mildness of the pulmonary changes offered no explanation of the cough. Indeed in this case the absence of marked pulmonary congestion is a crucial point since it aids in establishing the fact that severe and productive cough in this condition can be due merely to the mechanical pressure of an enlarged auricle on the trachea and bronchi. CASE
Comparison of agar-based media for primary isolation of glycopeptide-resistant enterococci
Authors: P.R. Chadwick, D.F.J. Brown, M.H. Wilcox, T.A. Collyns, E. Walpole, J. Dillon, R. Smith, G. Gopal Rao, B.A. Oppenheim
Journal: Clinical Microbiology and Infection (1997)
Abstract 766: Human ABCB1 and ABCG2 confer acquired resistance to Polo-like kinase 1 inhibitors, BI 2536, volasertib and GSK641364
Authors: Chung-Pu Wu, Hong-May Sim, Suresh V. Ambudkar
Journal: Cancer Research (2014)

Abstract The overexpression of the serine/threonine specific polo-like kinase 1 (Plk1) has been detected in various types of cancer, and thus has fast become an attractive therapeutic target for cancer therapy. Plk1 inhibitors BI 2536, volasertib and GSK461364, were designed to selectively inhibit cancer cell proliferation by promoting G2/M cell cycle arrest at nanomolar concentrations. Unfortunately, alike most chemotherapeutic agents, the development of acquired resistance to Plk1 inhibitors is prone to present a significant therapeutic challenge. One of the most common mechanisms for acquired resistance in cancer chemotherapy is associated with the overexpression of ATP-binding cassette (ABC) transporters ABCB1, ABCC1 and ABCG2. Here, we discovered that in human cancer cells, the overexpression of ABCB1 and/or ABCG2 can lead to acquired resistance to three selective Plk1 inhibitors, BI 2536, volasertib and GSK461364. Moreover, these Plk1 inhibitors stimulate the ATPase activity of ABCB1 and ABCG2, as well as competitively inhibit the drug substrate transport mediated by ABCB1 and ABCG2. More significantly, the reduced chemosensitivity and Plk1 inhibitors-mediated G2/M cell cycle arrest in cancer cells overexpressing either ABCB1 or ABCG2 can be significantly restored in the presence of selective inhibitor of ABCB1 and ABCG2. Taken together, our findings indicate that in order to circumvent ABCB1 or ABCG2-mediated acquired resistance to Plk1 inhibitors, a combined regimen of Plk1 inhibitors and modulators or clinically active drugs that potently inhibit the function of ABC drug transporters, should be considered as a potential treatment strategy in the clinic. Citation Format: Chung-Pu Wu, Hong-May Sim, Suresh V. Ambudkar. Human ABCB1 and ABCG2 confer acquired resistance to Polo-like kinase 1 inhibitors, BI 2536, volasertib and GSK641364. [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 766. doi:10.1158/1538-7445.AM2014-766
心搏骤停的院前急救——初级心肺脑复苏术（上）
Authors: 冯庚
Journal: BMJ (2005)

(上接2005年第7期第438页) 五、人工呼吸 1958年美国的Elam和Safar教授通过对在麻醉状态下呼吸停顿患者的研究,首先创造了口对口人工呼吸法,应用该法每次可向患者肺内吹入800～1 200 ml气体,提供的潮气量可以满足患者需要,逐渐被全世界的医生采纳.人工呼吸不仅可以抢救心搏骤停患者,同样也适用于其他呼吸停止和自主呼吸不能满足自身需要的患者.院前急救时常用的人工呼吸方法大致有吹气人工呼吸、面罩式人工呼吸以及挤胸人工呼吸3种.
Abstract 5116: Inhibition of PI3K/AKT signaling by NVP-BKM120 promotes ABT-737-induced toxicity in established and primary cultured glioblastoma cells
Authors: Esther P. Jane, Daniel R. Premkumar, Alejandro Morales, Kimberly A. Foster, Ian Pollack
Journal: Cancer Research (2014)

Abstract Identification of therapeutic strategies that might enhance the efficacy of Bcl-2 inhibitor ABT-737 is of great interest in many cancers including glioma. Our recent study suggested that Akt is a crucial mediator of apoptosis sensitivity in response to ABT-737 in glioma cell lines. Inhibitors of PI3-K/Akt are currently being assessed clinically in patients with glioma, as PI3K/Akt inhibition would be expected to have many pro-apoptotic effects, we hypothesized that there may be unique synergy between PI3-K inhibitors and BH3-mimetics. We assessed the combination of the PI3K inhibitor BKM120 and the Bcl-2 family inhibitor ABT-737 in established and primary cultured glioma cells. We found that the combined treatment with these agents led to a significant activation of caspase-8, 3, PARP and cell death irrespective of PTEN status. The enhanced lethality observed with the combination also appears dependent upon the loss of mitochondrial membrane potential, release of cytochrome c, smac/DIABLO and apoptosis-inducing factor to the cytosol. Further study revealed that the upregulation of Noxa, truncation of Bid, activation of Bax and Bak caused by these inhibitors was the key factor for the synergy. In addition, we demonstrated the release of proapoptotic proteins Bim and Bak from Mcl-1. We found defects in chromosome segregation leading to multinuclear cells and loss of colony forming ability, suggesting the potential use of BKM120 as a promising agent to improve the anti-cancer activities of ABT-737. Citation Format: Esther P. Jane, Daniel R. Premkumar, Alejandro Morales, Kimberly A. Foster, Ian Pollack. Inhibition of PI3K/AKT signaling by NVP-BKM120 promotes ABT-737-induced toxicity in established and primary cultured glioblastoma cells. [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 5116. doi:10.1158/1538-7445.AM2014-5116
Improve CPR Training
Authors: Rebecca Voelker
Journal: JAMA (2000)

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Encoding a superantigen by <i>Staphylococcus aureus</i> does not affect clinical characteristics of infected atopic dermatitis lesions
Authors: A. Kozman, Y. Yao, P. Bina, C. Saha, W. Yao, M.H. Kaplan, J.B. Travers
Journal: British Journal of Dermatology (2010)

Bacterial infection with Staphylococcus aureus is a known trigger for the worsening of atopic dermatitis (AD). Staphylococcal superantigens have been theorized to make a potential contribution to this worsening of AD seen with infection.We sought to assess whether encoding a superantigen by S. aureus affects the inflammatory characteristics of impetiginized AD skin lesions.Fifty-two children with clinically impetiginized lesions of AD which were positive for S. aureus were enrolled in this study. A lesion was graded clinically using the Eczema Area and Severity Index (EASI), and then wash fluid was obtained from the lesion for quantitative bacterial culture, and measurement of bacterial products lipoteichoic acid and staphylococcal protein A and cytokines. The staphylococcal isolate was tested for antibiotic susceptibilities and the presence of a superantigen.Fifty-four per cent (28 of 52) of the staphylococcal isolates encoded a superantigen. The presence of a superantigen had no significant effect on EASI score, amounts of bacterial products or inflammatory cytokines in the AD lesion.These studies suggest that the expression of a superantigen by S. aureus alone does not play an important role in the increased skin inflammation associated with staphylococcal infection in childhood AD.
Abstract 16308: Vitamin K Epoxide Reductase Complex 1 (vkorc1) a New Insight into the Molecular Design, Operation and Mechanism of Warfarin Inhibition
Authors: Nadeem Wajih
Journal: Circulation (2011)

Gamma-carboxylation of vitamin K dependent proteins are dependent on the formation of reduced vitamin K by VKOR.VKORC1 is believed to be a subunit of a VKOR enzyme complex in the ER membrane and harbors a warfarin sensitive CXXC redox center. Previous kinetic studies proposed that warfarin binds strongly to CXXC center in VKOR when present in its oxidized form. In this work, we presented new model of warfarin inhibition of VKOR. Extracted rat liver microsomes were pre reduced with 5 mM Tris(hydroxypropyl)Phosphine (THP) and VKOR inhibition was measured by warfarin. In some of the experiments, oxidized extracted microsomes were used to determine the VKOR inhibition by warfarin. In both the oxidized and reduced microsomes warfarin was able to completely abolish the VKOR activity regardless of reduced or oxidized state of VKOR CXXC redox center. Our finding of warfarin inhibition does not agree with the previous model of VKOR inhibition by warfarin which suggests that warfarin only inhibits VKOR activity when the CXXC redox center of VKOR is reduced. To further extend our previous finding that Protein disulfide isomerase (PDI) plays an important role in the reduction of VKOR CXXC redox center, we added purified recombinant PDI to rat liver extracted microsomes, which had been washed extensively to completely remove indigenous PDI from the microsomes. To these membranes, we reconstituted the VKOR complex by adding the purified recombinant PDI and VKOR activity was triggered by reduced RNAse. In control experiments, purified PDI was not added to the washed microsomes. Washed and extracted microsomes, when reconstituted with purified PDI, triggered VKOR supported gamma carboxylase activity. Furthermore, we have purified recombinant rat VKOR from sf9 insect cells and assess the role of PDI in VKOR activity in presence of reduced RNase and lipid rich buffer. In our vitro system, reduced RNase triggered VKOR activity in presence of PDI suggests an important role of PDI in modulating VKOR activity. In addition, we co-immunolocalized PDIVKOR complex in ER of HEK293 cells supports our previous finding that PDI interacts with VKOR in the ER. Our new findings presented here modify our current understanding of operation of the posttranslational gamma carboxylation system in the ER.
A memorable patient: Heroic surgery
Authors: Martin Christie
Journal: BMJ (2004)

It is in the nature of surgery that surgeons will sometimes find themselves in a position to rescue people from certain death. In the developed world this tends not to happen to trainees because there is always a senior to call on for advice and assistance, and as a consequence most surgeons will have reached a degree of competence by the time they have to shoulder the responsibility on their own.

In Papua New Guinea in 1974 it was different. Our hospital was the end of the line, with no onward referral. Our surgeon was on leave, and I was standing in, when a pick-up truck deposited a woman who had been flown out from the remote highlands. As I walked into the cubicle where she was squatting on the bed, my heart sank. A broken spear shaft was sticking out of her back, and the tip was just visible where it had pierced the skin overlying her manubrium sternum. It was immediately obvious that the necessary surgery was way beyond my level of training, and equally obvious that she was doomed unless the spear was removed.

A chest x ray showed no pneumothorax, and, after discussing it with Peter, a nurse anaesthetist trained in Port Moresby, we decided to give it a crack. While preparations were being made in the theatre, a hurried glance through Hamilton Bailey's Emergency Surgery did not reveal any similar case, and Grant's Anatomy was frankly frightening.

With the skill of a master, Peter intubated the patient on her side, because the spear sticking out of her back precluded any other possibility. The spear shaft had been snapped off, presumably in order to fit her into the Missionary Aviation Fellowship plane. What remained was the business end, which was of a hardwood carved in a saw tooth fashion, with barbs that prevented it from being pulled out backwards. I gave it a tentative pull anyway, and to our surprise it dislodged and could be extracted without too much difficulty. The tip, however, was still poking out of the front and would need an anterior approach.

Laying the patient on her back, we prepared the area, and as I cut down I tried to shut out visions of the anatomical structures that the spear must have passed through in order to transfix the manubrium. I freed the tip by nibbling the bone, and then it was loose, so I gently teased it out. A gush of blood followed, but settled with direct pressure, and the job was done. A second x ray showed a haemopneumothorax, for which a chest drain was needed, but the patient went on to make a full recovery.

What did I learn from this? Primarily that when the situation looks hopeless don't be afraid to have a go. But remember, the patient and the surgeon both need luck on their side.
Recent progress in the treatment and prevention of cancer‐related lymphedema
Authors: Simona F. Shaitelman, Kate D. Cromwell, John C. Rasmussen, Nicole L. Stout, Jane M. Armer, Bonnie B. Lasinski, Janice N. Cormier
Journal: CA A Cancer Journal for Clinicians (2014)

Abstract Answer questions and earn CME/CNE This article provides an overview of the recent developments in the diagnosis, treatment, and prevention of cancer‐related lymphedema. Lymphedema incidence by tumor site is evaluated. Measurement techniques and trends in patient education and treatment are also summarized to include current trends in therapeutic and surgical treatment options as well as longer‐term management. Finally, an overview of the policies related to insurance coverage and reimbursement will give the clinician an overview of important trends in the diagnosis, treatment, and management of cancer‐related lymphedema. CA Cancer J Clin 2015;65:55–81. © 2014 American Cancer Society.
Characterization of a monoclonal IgMK (IgMGAS) anti-Gd cold agglutinin (CA). Its coexistence with a monoclonal IgG3K (IgGGAS) without CA activity that might be clonally related to IgMGAS
Authors: MA De la Fuente, C Egile, A Pereira, M Juan, F Vivanco, D Roelcke, G Dighiero, T Gallart
Journal: Blood (1994)
Provision of intensive care for children
Authors: J. Ratcliffe
Journal: BMJ (1998)

Paediatric intensive care is a low volume, high cost specialty which depends on the training and skill of staff and availability of specialist equipment. Critically ill children have a changing range of illness and pathophysiology from early infancy to adolescence which is different from that of critically ill adults. In Britain paediatric intensive care has developed in an ad hoc and fragmented way. Now, however, after two decades of effort, Britain may be moving towards a more integrated service.

The Paediatric Intensive Care Society and the British Paediatric Association voiced concerns about paediatric intensive care in the early 1980s. The Paediatric Intensive Care Society has defined standards for paediatric intensive care,1 and these have been an important reference source that has informed many of the subsequent developments. This document defines two levels of paediatric intensive care. Level 2 refers to stable intubated children or unstable non-intubated children with airway problems requiring continuous nursing supervision, and level 3 to children who require complex therapeutic and nursing procedures in addition. (Level 1 is high dependency care.)

In 1993 a multidisciplinary working party on paediatric intensive care highlighted the fragmented configuration of paediatric intensive care provision.2 Its report was based on a retrospective survey of 12 882 children identified as having received intensive …