Influencia de la premedicación con esteroides sistémicos en el sangrado y visualización del campo quirúrgico durante la cirugía endoscópica nasosinusal

IntroductionChronic rhinosinusitis (CRS) is the inflammation of the nasal and paranasal sinus mucosa persisting for at least 12 weeks. The success of endoscopic sinus surgery (ESS) depends on minimising oedema and intraoperative bleeding. For this purpose, some surgeons advocate the use of preoperative systemic steroids (SS).Our aim was to assess if the administration of preoperative SS in patients with CRS with or without nasal polyps (NP) facilitates the surgical procedure.MethodsNon-randomized clinical trial in CRS patients with or without NP. Patients in the ESS group received oral meprednisone preoperatively, whereas the control group did not. The visibility of the surgical field, intraoperative bleeding and surgery duration were recorded.ResultsEach group (SS group and control group) included 27 patients. The administration of SS reduced the values of all the parameters in patients without NP, with no significant differences. In patients with NP, only operative bleeding was reduced significantly.ConclusionsEven though all the parameters decreased with the preoperative administration of SS, only operative bleeding was significantly reduced in patients with CRS with NP.     

Involvement of autophagy in ovarian cancer: a working hypothesis

ABSTRACT: Autophagy is a lysosomal-driven catabolic process that contributes to preserve cell and tissue homeostases through the regular elimination of damaged, aged and redundant self-constituents. In normal cells, autophagy protects from DNA mutation and carcinogenesis by preventive elimination of pro-oxidative mitochondria and protein aggregates. Mutations in oncogenes and oncosuppressor genes dysregulate autophagy. Up-regulated autophagy may confer chemo- and radio-resistance to cancer cells, and also a pro-survival advantage in cancer cells experiencing oxygen and nutrient shortage. This fact is the rationale for using autophagy inhibitors along with anti-neoplastic therapies. Yet, aberrant hyper-induction of autophagy can lead to cell death, and this phenomenon could also be exploited for cancer therapy. The actual level of autophagy in the cancer cell is greatly affected by vascularization, inflammation, and stromal cell infiltration. In addition, small non-coding microRNAs have recently emerged as important epigenetic modulators of autophagy. The present review focuses on the potential involvement of macroautophagy, and on its genetic and epigenetic regulation, in ovarian cancer pathogenesis and progression.     

Mechanical Properties and Durability of CNT Cement Composites

In the present paper, changes in mechanical properties of Portland cement-based mortars due to the addition of carbon nanotubes (CNT) and corrosion of embedded steel rebars in CNT cement pastes are reported. Bending strength, compression strength, porosity and density of mortars were determined and related to the CNT dosages. CNT cement paste specimens were exposed to carbonation and chloride attacks, and results on steel corrosion rate tests were related to CNT dosages. The increase in CNT content implies no significant variations of mechanical properties but higher steel corrosion intensities were observed.     

The Basic Pharmacology of Ticlopidine and Clopidogrel

This review summarises some of the key developments that have taken place in our understanding of platelet-collagen interactions within the last 18 months. Within this time, the major activatory collagen receptor glycoprotein VI (GPVI) has been sequenced and shown to reconstitute collagen responses in a megakaryocytic cell line. It is a member of the Ig superfamily of proteins, with two extracellular Ig domains, and is constitutively associated with the Fc receptor n -chain (FcR n -chain). GPVI signals through a pathway that shares many features with those of immune receptors, with critical roles for Syk and the adapters LAT and SLP-76 in the activation of PLC n 2. Significant developments have also taken place in regard to the role of the major adhesion receptor for collagen, the integrin f 2 g 1 (also known as GPIa-IIa). An f 2 g 1-selective collagen-based peptide has been developed and co-crystalisalised with the I-domain of the f 2 subunit. Polymorphisms in f 2 have been shown to cause wide variation in expression of f 2 g 1, with the f 2 allele T 807 /A 873 leading to a high level of the integrin and increased risk of stroke in young people. Activation of platelets by a wide range of agonists has been shown to increase the affinity of f 2 g 1 to intermediate or high affinity states. This has important implications for the two-site, two-state model of collagen-platelet interactions. A new model is proposed in which collagen binds initially to either f 2 g 1 or GPVI, leading to subsequent binding to the other receptor and conversion of the integrin to a high affinity state. In this model, both receptors generate intracellular signals which support platelet activation.     

Patterns and Predictors of Multiple Sexual Partnerships Among Newly Arrived Latino Migrant Men

Multiple sexual partnerships (MSP), both concurrent and serial short gap, are thought to increase the risk of HIV and sexually transmitted infection (STI) acquisition and transmission. In this study we evaluate potential individual and environmental risk factors for engaging in MSP in a cohort of newly arrived Latino migrant men (LMM) in New Orleans, LA, USA. Participants were surveyed at three time points over a nine-month period to examine factors associated with MSP. Of the 113 men, 32.5 % reported ever MSP. In 290 observations, 19.5 % of men had concurrent, and 15.0 % had serial short gap partnerships in at least one interviews. Substance was associated with MSP, OR (95 % CI) 2.00 (1.16, 3.45) whereas belonging to a community organization was found to be protective, OR 0.32 (0.17, 0.59). Interventions to reduce substance use and promote social connection are needed to prevent a potential HIV/STI epidemic in this population.     

Human C3 mutation reveals a mechanism of dense deposit disease pathogenesis and provides insights into complement activation and regulation

Dense deposit disease (DDD) is a severe renal disease characterized by accumulation of electron-dense material in the mesangium and glomerular basement membrane. Previously, DDD has been associated with deficiency of factor H (fH), a plasma regulator of the alternative pathway (AP) of complement activation, and studies in animal models have linked pathogenesis to the massive complement factor 3 (C3) activation caused by this deficiency. Here, we identified a unique DDD pedigree that associates disease with a mutation in the C3 gene. Mutant C3_923ΔDG, which lacks 2 amino acids, could not be cleaved to C3b by the AP C3-convertase and was therefore the predominant circulating C3 protein in the patients. However, upon activation to C3b by proteases, or to C3(H₂O) by spontaneous thioester hydrolysis, C3_923ΔDG generated an active AP C3-convertase that was regulated normally by decay accelerating factor (DAF) but was resistant to decay by fH. Moreover, activated C3b_923ΔDG and C3(H₂O)_923ΔDG were resistant to proteolysis by factor I (fI) in the presence of fH, but were efficiently inactivated in the presence of membrane cofactor protein (MCP). These characteristics cause a fluid phase–restricted AP dysregulation in the patients that continuously activated and consumed C3 produced by the normal C3 allele. These findings expose structural requirements in C3 that are critical for recognition of the substrate C3 by the AP C3-convertase and for the regulatory activities of fH, DAF, and MCP, all of which have implications for therapeutic developments.