tbuckley/cabot-search huggingface dataset:
AB0231 Rheumatoid arthritis (ra) patients present relevant and diverse alterations in lipid and lipoprotein metabolism associated to cardiovascular (cv) risk: preliminary results
Authors: J. Calvo Alén, C. Baamonde, E. Aurrecoechea, V. M. Martínez-Taboada, J. Gómez-Gerique
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> The causal mechanisms of the elevated cardiovascular (CV) risk in RA have not been totally clarified. In fact, usual standard tests to assess lipid metabolism are not usually different between patients and general population. <h3>Objectives</h3> Our objective was to perform a more in depth study of this latter issue using novel and more specific markers. We show here preliminary results <h3>Methods</h3> RA patients and matched healthy controls were cross-sectionally evaluated including inflammatory markers (ESR, hsCRP, Pentraxina 3 and SAA), disease activity, by joints counts and DAS28, disability, by MHAQ questionnaire (only for RA patients) and specifically a comprehensive lipid and lipoprotein assessment which in addition of conventional tests included the following determinations: Lipoprotein, and apolipoprotein A1 (ApoA1) and B (ApoB) levels (total and lipoprotein specific), levels of paroxonase 1 (PON1), HDL, LDL, VLDL and total cholesterol, triglycerides and phospholipids levels as well as number of molecules of these lipids (mc, mt and mf respectively) in each lipoprotein, total mass (M) and number of particles (np) of the afore mentioned lipoproteins, and levels of PCSK9 receptor. Standard statistical tests were used for comparing patients and controls. <h3>Results</h3> One-hundred twenty-seven RA patients (mean age±: 59.9±12.2 years; 81% women and 63% seropositive) and 29 healthy controls (56.14±9.8; p=NS; 81% women) were evaluated. As expected, patients showed significant higher acute phase reactants levels. Standard lipid determinations including total and HDL, LDL and VLDL cholesterol, triglycerides and others as lipoproteins, phospholipids or Apo-B were comparable in both subsets. However, RA patients presented several risk markers as lower levels of Apo-A1 HDL (p=0.032) and higher of mc LDL and VLDL (p=0.023 and 0.002 respectively), mt LDL and VLDL (p=0.042 and =0.001) and np VLDL (p=0.007). Unexpectedly, paroxonase levels were higher among RA patients (p=0.0001) <h3>Conclusions</h3> RA patients present diverse alterations of lipid and lipoprotein metabolism, which may confer them a CV risk profile. The higher levels of paroxonase are against this idea; the reason of this finding might be due to the competitive action for HDL of the inflammatory molecules, such as SAA, which could render functionally inactive the most part of this enzyme. <h3>Disclosure of Interest</h3> None Declared
SAT0284 In Early PSA, the Ultrasonography of Hands and Wrists Synovitis and Digital soft Tissue Involvement Is More Sensitive Than Traditional Clinical Examination
Authors: F. Bandinelli, V. Denaro, F. Prignano, L. Collaku, M. Matucci Cerinic
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Clinical measures are widely used in established psoriatic arthritis (PsA) but in early phase of disease, often fail to identify the joint and tendons involvement. <h3>Objectives</h3> To investigate the ultrasonography (US) abnormalities in hands and wrists of early PsA patients and to compare them with clinical evaluation <h3>Methods</h3> We performed a retrospective study on 112 early PsA (onset of inflammatory symptoms lower than one year) in the period 2008-2010, diagnosed with CASPAR criteria(1). Data were carried out by the analysis of medical records of all patients, completed of demographic data, historical information, clinical (swollen joints and dactylitis count) and MyLab70 Xview (linear probe 15 MHz and PRF 1 Mhz) and US (Power doppler [PD] positive synovitis, erosions, tenosynovitis and PD in soft tissue around flexor finger tendons) hands and wrists assessment. <h3>Results</h3> Out of 224 wrists and 1120 MCP, 1120 PIP and 1120 DIP totally observed, synovitis was more frequently found on wrist (50/224; 22,3%) and US resulted more sensitive than clinical evaluation (swollen joints): in wrists 50/224 (22,3%) vs 42/224 (18,7%), in MCP 28/1220 (2,5%) vs 11/1120 (1%), in IPP 24/1120 (2,1%) vs 15/1120 (1,3%), in IPD 3/1120 (0,3%) vs 1/1120 (0,09%). Also erosions were present only in MCP (mostly II e III MCP) in 10/1120 joints (0,9%). At US, PD signal in soft tissue around tendons (68/1120, 6,1%) was more frequent than tenosynovitis of flexors (29/1120, 2,6%) and were both found also in patients without clinical dactilitis (55/68 PD [80,8] of soft tissue and 18/29 [62%] of tenosynovitis). <h3>Conclusions</h3> In early PsA, US detected synovitis (more frequently at wrists), erosions and PD signals in soft tissue are present in early phase of PsA. In all cases, US is more sensitive than clinical evaluation to detect synovitis and dactilytis. <h3>References</h3> Taylor W, Gladman D, Helliwell P, Marchesoni A, Mease P, Mielants H; CASPAR Study Group. Classification criteria for psoriatic arthritis: development of new criteria from a large international study. Arthritis Rheum. 2006 Aug;54(8):2665-73. <h3>Disclosure of Interest</h3> None Declared
A large impacted pancreatic duct stone causing acute cholangitis
Authors: Piyapan Prueksapanich, Phonthep Angsuwatcharakon, Rungsun Rerknimitr, Pinit Kullavanijaya
Journal: Endoscopy (2013)

A 67-year-old woman with diabetes presented with persistent pain in the right upper quadrant radiating through to her back. Later, she developed a high fever and jaundice. On examination, her epigastrium was soft with mild tenderness but no signs of peritonitis. Abdominal ultrasonography showed a 1.3-cm round hyperechoic lesion with an acoustic shadow at the distal end of the common bile duct, which was dilated, but no evidence of stones in the gallbladder. Endoscopic retrograde cholangiopancreatography (ERCP) was carried out and duodenoscopy revealed a bulging ampulla with whitish material at the opening ([Fig. 1 a]). The initial impression was of an impacted biliary stone causing cholangitis.
Planners should focus on retaining staff to fill European workforce shortages
Authors: R. Watson
Journal: BMJ (2011)

The European Commission is financing the development of an action plan to help tackle serious staff shortages in the European Union. 

Isabel de la Mata, a commission representative, said that the actions needed to be cross cutting, going beyond health policy to take into account human resources, education and training strategies, employment, and social and cohesion policies. She urged a large number of EU member states to participate so that data on the current state of the health workforce could be as comprehensive as possible. She was speaking at an international conference in Brussels on 7-9 December on …
Case 62-1963
Authors: John H. Knowles, Benjamin Castleman
Journal: New England Journal of Medicine (1963)

Presentation of CaseA fifty-six-year-old plumber was admitted to the hospital because of pain in the chest.The patient had been in good health until twenty-one months previously, when he began to experience right-sided chest pain. Six months later he was told that an x-ray film of the chest was abnormal. Twelve months before admission he entered another hospital because of persistent chest pain accompanied by dyspnea and a cough productive of white sputum. There had been no chills, fever, weight loss or fatigue. A tuberculin skin test (second-strength PPD) was reported as strongly positive, but studies of the sputum . . .
Activity and expression of the multidrug resistance proteins P-glycoprotein, MRP1, MRP2, MRP3 and MRP5 in de novo and relapsed acute myeloid leukemia
Authors: DM van der Kolk, EGE de Vries, L Noordhoek, E van den Berg, MA van der Pol, M Müller, E Vellenga
Journal: Leukemia (2001)
PMO-260 Bone protection is under used in IBD patients: data from the 3rd round UK IBD audit
Authors: G Walker, I Arnott, C Probert
Journal: Gut (2012)

<h3>Introduction</h3> BSG guidelines recommend that supplementation of calcium and vitamin D is given when systemic steroid use is necessary and that co-administration of bisphosphonates with steroids is given for patients aged over 65 years or with known osteoporosis/osteopenia.<sup>1</sup> Data collected in the 3rd Round UK IBD audit were used to determine whether these guidelines were followed. <h3>Methods</h3> Retrospective patient data from 198 sites of up to 40 patients per site were collected using an online form. Inclusion criteria were age &gt;17 years at the date of admission with a discharge diagnosis of IBD from September 2010 to August 2011. A list of relevant ICD10 and OPCS codes was provided to aid patient identification. Data items collected in UC and CD included the number of patients discharged taking corticosteroids (CS) and bone protective agents. In CD only data were collected on CS and bone protective agent use in the outpatient setting. Statistical analysis used Fishers exact test to generate two-tailed p values. <h3>Results</h3> Bone protective agents are underused. Bone protective agents were more likely to be used in UC patients discharged on steroids than in CD (UC: 66.2%, 1443/2181; CD: 58.7%, 1022/1742, p=0.021). Among 600 CD outpatients prescribed steroids for &gt;3 months in the previous year 404 (67.3%) also received bone protection; this was not significantly different to inpatient care of CD patients (p=0.07). Of 600 outpatients who had received steroids for over 3 months in the last year 132 (22.2%) had a DEXA scan. <h3>Conclusion</h3> Compliance with BSG guidelines regarding the use of bone protection for patients taking steroids is poor. Only 2/3 of IBD inpatients discharged on steroids were given bone protective agents. This figure is similar to patients treated in the outpatient setting. Approximately 1/5 CD patients who received a course of steroids in the outpatient setting also had a DEXA scan. Unfortunately further information was not available in order evaluate whether these patients were risk stratified for fragility fractures. It remains unclear why bone protection was significantly better prescribed in UC patients than CD. Further analysis of this data with logistic regression is needed in order to see whether other factors are influencing these results. Clinicians are further encouraged to prescribe bone protection for these patients. Bone protective measures must be promoted and hopefully the culture of prescribing can be changed for the better. <h3>Competing interests</h3> None declared. <h3>Reference</h3> 1. <b>Mowat C</b>, Cole A, Windsor A, <i>et al.</i> Guidelines for the management of inflammatory bowel disease in adults. <i>Gut</i> 2011. doi:10.1136/gut.2010.224154.
P344Osteoclasts activation contributes to remodeling of the stem cell niche in diabetes
Authors: C Reni, G Mangialardi, M Meloni, C Emanueli, P Madeddu
Journal: Cardiovascular Research (2014)

We have previously shown that mice and human patients with diabetes mellitus develop microangiopathy in bone marrow (BM) resulting in depletion of stem cells (SCs). Since the endosteal niche was the most pauperised, we decided to investigate if activation of osteoclasts (OCLs) may participate in this process through detachment of SC from the endosteal niche leading to inappropriate mobilization. The study was performed in streptozotocin-induced type 1 diabetic (T1D) mice at 5, 11 and 20 weeks from induction of diabetes and in age-matched non-diabetic controls (C). Histochemical analysis of femoral bones at late stages of DM (20 weeks) showed a profound BM remodeling characterized by reduction of the hematopoietic component, fat accumulation and bone rarefaction. The activation of osteoclastogenesis was already seen at 5 weeks as assessed by counting the number of tartrate resistant acid phosphatase (TRAP) positive OCLs in the trabecular bone (2.9±0.3 vs. 1.6±0.7 cells/mm of endosteal length in C, p<0.01). Osteoclast activation was associated with a marked increase in peripheral blood lineage- Sca1+ cKit+ (LSK) cells (0.7±0.4 vs. 0.2±0.1% of total MNCs in C, p<0.05). Unexpectedly, mRNA and protein expression of Receptor Activator of NF-κB Ligand (RANKL), an inducer of OCL differentiation and activation, was reduced in total BM at 20 and 11 weeks (mRNA: 0.3±0.01 vs. 1.2±0.3 ddCT in C; Protein: 11.8±2 vs. 28.7±5 pg/ml, p<0.05 for both comparisons) thus implying that OCL activation occurs through a non-canonical mechanism. Interestingly, we found T1D induces acidosis in BM (pH: 6.9±0.02 vs. 7.0±0.03 in C, p<0.05). Moreover, similar pH changes in culturing media increased the number of BM-derived OCL-like cells in vitro (2.0±0.3 fold increase relative to C, p<0.05) suggesting a crucial role of acidosis in OCLs activation.
Cancer of the Uterine Cervix
Authors: Stephen A. Cannistra, Jonathan M. Niloff
Journal: New England Journal of Medicine (1996)

Invasive cervical cancer is uncommon in the United States, with an incidence of 15,800 cases and 4800 deaths in 1995.1 This relatively low incidence is largely due to the effectiveness of screening programs that assess cervical cytology by Pap smear. On a global scale, however, cancer of the cervix is a major cause of death, especially in Third World countries, where such screening is often not routinely performed. Pap-smear screening is designed to detect precursor lesions in cervical epithelium, which may antedate the development of invasive cancer by several years. In contrast to other screening strategies, such as mammography, which . . .
Duodenal diverticulitis: a rare cause of abnormal liver function tests
Authors: P. Deepak, R. Devi, P. Mohan
Journal: Endoscopy (2012)

A 52-year-old woman presented with a 2-week history of pain in her right upper abdomen radiating to the ipsilateral shoulder, associated with pale colored stools, dark colored urine, and a poor appetite, without febrile episodes. Physical examination revealed right upper quadrant tenderness with a positive Murphy's sign. Initial tests revealed leukocytosis with aspartate transaminase at 245 IU/L (up to 42 IU/L), alanine transaminase 283 IU/L (up to 40 IU/L), alkaline phosphatase 257 IU/L (up to 92 IU/L), total bilirubin 1.5 mg/dL (up to 1.2 mg/dL), and direct bilirubin 0.6 mg/dL (up to 0.4 mg/dL).
THE MECHANISM OF BLOOD PRESSURE-LOWERING EFFECT OF SODIUM-GLUCOSE COTRANSPORTER 2 INHIBITORS IN PATIENTS WITH OBESE TYPE 2 DIABETES MELLITUS
Authors: Mariko Kawasoe, Shin Kawasoe, Yukiko Maruguchi, Hitoshi Uenomachi, Shoko Kajiya, Takuro Kubozono, Masaaki Miyata, Mitsuru Ohishi
Journal: Journal of the American College of Cardiology (2016)
CS-23 * DEFINING THE NETWORKS AND INTERSECTION OF EGFR AMPLIFICATION AND NFKBIA DELETION IN HUMAN GLIOMA
Authors: A. Mishra, J. Kong, D. Brat
Journal: Neuro-Oncology (2014)

Nuclear factor KappaB (NF-κB) is a critical transcriptional regulator in glioblastoma (GBM) and is normally inhibited by IKBα, the product of NFKBIA. The relative mutual exclusivity of EGFR amplification and NFKBIA deletion suggested a redundancy of fundamental signaling pathways mediated by EGFR and NF-κB. Our bioinformatics analysis of TCGA GBM data showed that only 11.2% cases with EGFR amplification had hemizygous deletion for NFKBIA gene and only 0.2% had homozygous deletion, whereas non-amplified tumors had 18.5% hemizygous deletion and 0.4% homozygous deletion. Using TCGA GBM data, we identified common genes that were upregulated or downregulated in a similar fashion in both EGFR amplified and NFKBIA deleted GBM samples. Ingenuity Pathway Analysis (IPA) of common genes implicated TNF, p53, NF-κB and c-MYC as shared signaling pathways, suggesting they could be final common pathways downstream of EGFR amplification and NFKBIA deletion and explain relative exclusivity. Therefore, we examined the relationship of EGFR status on NFKBIA expression and the impact of aberrant NFKBIA expression on glioma viability. We found that stable over-expression of wt-EGFR in U87MG cells is associated with reduced NFKBIA compared to cells expressing basal levels of EGFR. When we transiently silenced NFKBIA in these cells, we noted increased level of PARP mediated apoptosis, suggesting that complete loss of NFKBIA in EGFR amplified cells is less compatible with viability. Additionally, overexpression of NFKBIA led induction of apoptosis in stably transformed human astrocytes as determined by FACS analysis of AnnexinV. Therefore our results demonstrate a complex interplay of EGFR and NFKBIA expression, which ultimately dictates downstream NF-κB signaling. These findings are consistent with our insilico analysis of TCGA GBMs, which demonstrate relative exclusivity of NFKBIA loss and EGFR amplification, yet aberrant NF-κB signaling across all GBM subclasses, independent of EGFR status. Our ultimate goal is to therapeutically manipulate NFKBIA downstream signaling networks.
Differentiation and cell-type-restricted expression of HOXC4, HOXC5 and HOXC6 in myeloid leukemias and normal myeloid cells
Authors: JJ Bijl, JW van Oostveen, JMM Walboomers, ATP Brink, W Vos, GJ Ossenkoppele, CJLM Meijer
Journal: Leukemia (1998)
The Intensity of Hemodialysis and the Response to Erythropoietin in Patients with End-Stage Renal Disease
Authors: Onyekachi Ifudu, Joseph Feldman, Eli A. Friedman
Journal: New England Journal of Medicine (1996)

Anemia (characterized by a hematocrit of 30 percent or lower) persists in 40 to 60 percent of patients treated for end-stage renal disease with maintenance hemodialysis, despite concomitant erythropoietin (epoetin) therapy. We tested the hypothesis that inadequate dialysis is a key reason for the insufficient response to erythropoietin in patients with end-stage renal disease who are receiving hemodialysis.We prospectively studied 135 randomly selected patients undergoing hemodialysis who had been receiving intravenous erythropoietin for at least four months. The adequacy of dialysis was assessed by measuring the percent reduction in the blood urea nitrogen concentration and the serum albumin concentration. The hematocrit was measured weekly for four weeks, transferrin saturation was measured, and coexisting illnesses were documented. To determine the effect of an increased level of dialysis on the hematocrit, the thrice-weekly schedule of dialysis was increased to raise the mean urea-reduction value from 60.7 to 72 percent for six weeks in 20 consecutive patients whose base-line urea-reduction value was less than 65 percent. The change in the hematocrit in these patients was compared with that observed in the next 20 patients who had an equivalent base-line urea-reduction value but whose level of dialysis was not altered.The mean hematocrit of the entire group was 29.2 +/- 4 percent, and the mean thrice-weekly dose of erythropoietin was 59 +/- 29 U per kilogram of body weight. The mean serum albumin concentration was 3.8 +/- 0.4 g per deciliter, the mean urea-reduction value was 62 +/- 4.8 percent, and the mean transferrin saturation was 20 +/- 9 percent. Multiple regression analysis revealed direct correlations between the hematocrit and the serum albumin concentration (P = 0.009) and between the hematocrit and the urea-reduction value (P = 0.012) after adjustment for other factors. A logistic-regression analysis indicated that an 11 percent increase in the urea-reduction value doubled the odds that a patient would have a hematocrit above 30 percent. After six weeks of increased intensity of dialysis in 20 patients with base-line urea-reduction values of less than 65 percent, the mean (+/- SE) hematocrit rose from 28.4 +/- 0.78 percent to 32.3 +/- 0.71 percent (P = 0.002); there was no significant change in a control group of 20 patients with equivalent base-line urea-reduction values in whom the dialysis level was not altered (28.2 +/- 0.84 percent to 26.3 +/- 0.85 percent; P = 0.175).In patients with end-stage renal disease, inadequate hemodialysis is associated with a suboptimal response to erythropoietin therapy. Increasing the intensity of dialysis in patients with anemia who are receiving inadequate dialysis results in a significant increase in the hematocrit.
THE ALANINE AMINOTRANSFERASE/ ASPARTATE AMINOTRANSFERASE RATIO PREDICTS FUTURE CARDIOVASCULAR EVENTS IN PATIENTS WITH ESTABLISHED CORONARY ARTERY DISEASE AND HOMA INSULIN RESISTANCE
Authors: Alexander Vonbank, Christoph Saely, Philipp Rein, Daniela Zanolin, Andreas Leiherer, Heinz Drexel
Journal: Journal of the American College of Cardiology (2016)
Chronic Lung Injury in Preterm Lambs
Authors: KURT H. ALBERTINE, GREGORY P. JONES, BARRY C. STARCHER, JOHN F. BOHNSACK, PENNY L. DAVIS, SOO-CHUL CHO, DAVID P. CARLTON, RICHARD D. BLAND
Journal: American Journal of Respiratory and Critical Care Medicine (1999)

The cause of chronic lung disease of early infancy, often called bronchopulmonary dysplasia (BPD), remains unclear, partly because large-animal models that reliably reproduce BPD have not been available. We developed a model of BPD in lambs that are delivered prematurely and ventilated for 3 to 4 wk after birth to determine whether the histopathology of chronic lung injury in premature lambs mimics that which occurs in preterm infants who die with BPD, and to compare two ventilation strategies to test the hypothesis that differences in tidal volume (Vt) influence histopathologic outcome. The two ventilation strategies were slow, deep ventilation (20 breaths/min, 15 ± 2 ml/kg body weight Vt; n = 5) or rapid, shallow ventilation (60 breaths/min, 6 ± 1 ml/kg body weight Vt; n = 5). Lambs were delivered at 125 ± 4 d gestation (term = 147 d), treated with surfactant, and mechanically ventilated with sufficient supplemental oxygen to maintain normal arterial oxygenation (60 to 90 mm Hg). Quantitative histologic analysis revealed lung structural abnormalities for both groups of experimental lambs compared with lungs of control term lambs that were < 1 d old (matched for developmental age; n = 5) or 3 to 4 wk old (matched for postnatal age; n = 5). Compared with control lambs, chronically ventilated preterm lambs had pulmonary histopathology characterized by nonuniform inflation patterns, impaired alveolar formation, abnormal abundance of elastin, increased muscularization of terminal bronchioles, and inflammation and edema. Slow, deep ventilation was associated with less atelectasis, less alveolar formation, and more elastin when compared with rapid, shallow ventilation. We conclude that prolonged mechanical ventilation of preterm lambs disrupts lung development and produces pulmonary histopathologic changes that are very similar to those that are seen in the lungs of preterm infants who die with BPD. This chronic lung disease is not prevented by surfactant replacement at birth, does not appear to require arterial hyperoxia, and is influenced by Vt.