86,667 research outputs found
Reinfusion Drains in primary total hip arthroplasty
No full textIntroduction: Primary total hip replacement can result in a considerable
amount of blood loss. Higher pre-operative and post-operative hemoglobin
(Hb) levels are related to earlier functional recovery, higher patient satisfaction
and shorter hospital length of stay. A number of strategies to reduce
the need for blood transfusion have been employed such as retransfusion
drains.
Objectives: The goal of the study was to evaluate the effects of reinfusion
drains on hematological parameters of patients undergoing total hip arthroplasty
(THA).
Methods: We retrospectively reviewed 103 patients (reinfusion group) who
underwent THA with the use of a postoperative reinfusion drain and 100
patients (no reinfusion group) who underwent THA with no postoperative
reinfusion drain used. Preoperative variables evaluated were: age, sex and
body mass index (BMI); comorbidities; and type of anesthesia. Postoperative
variables evaluated were: Hb, hematocrit (Hct) and platelets (Plt) levels at
the first, second, third, and fourth postoperative days and at discharge. We
also assessed the total blood loss during the postoperative in-hospital stay
and the number of units of blood eventually transfused.
Results: Eighty-four (84%) patients in the reinfusion group and 42 patients
(40.8%) in the no reinfusion group were transfused with at least
one unit of blood postoperatively (1.3 ± 0.9 and 0.5 ± 0.7; p<0.001, respectively).
The need for transfusion was found to be 7 times higher in
the no reinfusion group compared to the reinfusion group. In the first and
second postoperative day, Hb levels were higher in the reinfusion group
(p = 0.002 and p<0.001, respectively). Hct levels were significantly higher
in the reinfusion group at first, second, third and fourth postoperative
days and at discharge. No other statistically significant differences were
detected.
Conclusions: Proper management of patients undergoing THA using reinfusion
drains can reduce or eliminate the need for transfusions
Nitric Oxide/Cyclic GMP-Dependent Calcium Signalling Mediates IL-6- and TNF-α-Induced Expression of Glial Fibrillary Acid Protein
No full textAstrocyte activation is characterized by hypertrophy with increased glial fibrillary acidic protein (GFAP), whose expression may involve pro-inflammatory cytokines. In this study, the effects of pro-inflammatory IL-6 and TNF-α and anti-inflammatory cytokines IL-4 and IL-10 on nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) signalling, intracellular calcium concentration ([Ca2+]i) and GFAP expression were investigated. In human glioblastoma astrocytoma U-373 MG cells, IL-6 and TNF-α, but not IL-4 or IL-10, increased iNOS, cGMP, [Ca2+]i and GFAP expression. The inhibitors of iNOS (1400 W), soluble guanylyl cyclase (ODQ) and IP3 receptors (ryanodine and 2-APB) reversed the increase in cGMP or [Ca2+]i, respectively, and prevented GFAP expression. In rat striatal slices, IL-6 and TNF-α, at variance with IL-4 and IL-10, promoted a concentration-dependent increase in Ca2+ efflux, an effect prevented by 1400 W, ODQ and RY/2APB. These data were confirmed by in vivo studies, where IL-6, TNF-α or the NO donor DETA/NO injected in the striatum of anaesthetised rats increased cGMP levels and increased GFAP expression. The present findings point to NO/cGMP-dependent calcium signalling as part of the mechanism mediating IL-6- and TNF-α-induced GFAP expression. As this process plays a fundamental role in driving neurotoxicity, targeting NO/cGMP-dependent calcium signalling may constitute a new approach for therapeutic interventions in neurological disorders
Left Atrial Function Predicts Cardiovascular Events in Patients With Chronic Heart Failure With Reduced Ejection Fraction
No full textBackground: Heart failure (HF) is known to be the most widespread epidemic of cardiovascular disease. Among several factors with prognostic value for the clinical course of HF, left atrial (LA) function has not yet been fully examined. The aim of this prospective study was to evaluate LA function for the prediction of major cardiovascular outcomes in stable patients with chronic HF with reduced ejection fraction. Additionally, as secondary end points, cardiovascular mortality and atrial fibrillation were analyzed separately. Methods: The predictive value of LA function evaluated by speckle-tracking echocardiography was assessed in a population of 286 outpatients referred to the authors’ institution for routine evaluation of chronic HF. Global peak atrial longitudinal strain was measured at the end of the reservoir phase and calculated by averaging in all LA segments. Results: During a median follow-up period of 48 ± 11 months, major adverse cardiac events occurred in 98 patients (34%). In a multivariate model, global peak atrial longitudinal strain (hazard ratio, 0.95; 95% CI, 0.94–0.96; P =.02), left ventricular ejection fraction (hazard ratio, 0.95; 95% CI, 0.93–0.97; P =.01), and renal failure (hazard ratio, 0.98; 95% CI, 0.97–0.99; P =.01) were independent predictors of an adverse outcome. Sixty-six patients (23%) died of cardiac causes. Fifty-four patients (19%) developed atrial fibrillation. Patients with lower global peak atrial longitudinal strain showed worse event-free survival and developed atrial fibrillation more frequently than those with higher levels. Conclusions: LA function assessed by speckle-tracking echocardiography is an independent prognostic marker in patients with HF with reduced ejection fraction
Variations on the Author
No full text“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Infezioni periprotesiche di ginocchio: revisione in due tempi con spaziatori articolati preformati in cemento antibiotato
No full textRisultati a medio termine dell'artroprotesi inversa di spalla. Comunicazione 5° Congresso Accademia Universitaria di Ortopedia e Traumatologia
No full textThe PDE4 inhibitor CHF6001 prevents keratinocytes proliferation by modulating cellular inflammation pathways
No full textPsoriasis is a skin disease characterized by abnormal keratinocyte proliferation and inflammation. Currently, there are no cures for this disease, so the goal of treatment is to decrease inflammation and slow down the associated rapid cell growth and shedding. Recent advances have led to the usage of phosphodiesterase 4 (PDE4) inhibitors for treatment of this condition. For example, apremilast is an oral, selective PDE4 inhibitor that is able to reduce skin inflammation and is Food and Drug Administration (FDA)-approved to treat adults with moderate to severe psoriasis and/or psoriatic arthritis. However, common target-related adverse events, including diarrhea, nausea, headache, and insomnia limit the usage of this drug. To circumvent these effects, the usage of PDE4 inhibitors specifically designed for topical treatment, such as CHF6001, may combine local anti-inflammatory activity with limited systemic exposure, improving tolerability. In this study, we showed that CHF6001, currently undergoing clinical development for COPD, suppresses human keratinocyte proliferation as assessed via BrdU incorporation. We also observed decreased re-epithelialization in a scratch-wound model after CHF6001 treatment. At the molecular level, CHF6001 inhibited translocation of phosphorylated NF-κB subunit p65, promoting loss of nuclear cyclin D1 accumulation and an increase of cell cycle inhibitor p21. Furthermore, CHF6001 decreased oxidative stress, measured by assessing lipid peroxidation (4-HNE adduct formation), through the inactivation of the NADPH oxidase. These results suggest that CHF6001 has the potential to treat skin disorders associated with hyperproliferative keratinocytes, such as psoriasis by targeting oxidative stress, abnormal re-epithelization, and inflammation
[Newspaper Clipping: Author Claims Evidence of Second JFK Assassin #1]
No full textNewspaper article titled "Author Claims Evidence of Second JFK Assassin." The article states that author Richard J. Whalen concluded "that there is circumstantial evidence to support the theory of a second assassin in the shooting of President John F. Kennedy.
Scavenger Receptor B1 involvement in COPD pathogenesis
No full textChronic obstructive pulmonary disease (COPD) is one of the main causes of morbidity and mortality in the United States. Oxidative stress due to cigarette smoking seems to be one of the major driving mechanisms in COPD pathogenesis. Since the scavenger receptor B1 (SR-B1) appears to play a key role in mediating the uptake for ɑ-tocopherol and other antioxidants in lung tissue, we aimed to investigate its role in COPD pathogenesis.
Methods: Lung tissue biopsies were obtained from 12 subjects; 6 of these had a diagnosis of
COPD in a stable clinical state, the others 6 were current (n = 1) or ex-smokers (n = 5) with
normal lung function (controls). 4-Hydroxynonenal (4-HNE)–SR-B1 adducts were detected
by immunoprecipitation. ɑ-tocopherol concentration was determined by HPLC.
Results: SR-B1 levels were lower in COPD patients and these results parallel with
lower levels of vitamin E in lung tissue found in COPD patients. This effect can be the
consequence of oxidative posttranslational modifications, confirmed by the binding of the
peroxidation product 4-HNE to SR-B1 possibly leading to its degradation.
Conclusions: The loss of SR-B1 may be involved in lung ɑ-tocopherol content decrease
with the consequence of making lung tissue more susceptible to oxidative damage as
suggested by the SR-B1–4-HNE adduct formation, and more prone to COPD development.
Thus, our findings suggest a novel role of SR-B1 in pathomechanisms underlying COPD
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