Ultra-fast track extubation protocol following cardiovascular surgery: Predictors of failure and outcomes.

OBJECTIVES: Identifying independent predictor factors of failure of ultra-fast track (UFT) extubation and to compare in-hospital outcomes with UFT extubation versus fast track (FT) extubation after cardiovascular surgery in adults. MATERIAL AND METHODS: Retrospective analysis of 1498 consecutive patients aged over 18 years-old undergoing cardiovascular surgery at a single institution. Between December 2014 and December 2016, FT extubation was used (N = 713) while, between December 2016 and December 2018, all patients were preoperatively considered suitable for UFT extubation (N = 785). In this instance, a standardized anaesthetic protocol was applied in all cases. The decision to not extubate in the operating room (OR) was based on intraoperative haemodynamic and ventilation. RESULTS: Extubation in the OR was possible in 699 (89%) patients. Significant independent predictors factors of UFT extubation failure were: preoperative NYHA class III-IV, myocardial infarction within two days prior to surgery, preoperative intra-aortic balloon counterpulsation, urgent/emergent surgery, intraoperative transfusion of platelets and intraoperative inotropic and vasopressor support. UFT extubation was associated with lower rates of cardiovascular complications such as congestive cardiac insufficiency (OR: 1,57; 95% CI: 1,13-2,19; p = 0,008) and new-onset postoperatory atrial fibrillation (OR: 1,40; 95% CI: 1,06-1,86; p = 0,020). Patient extubated in the OR presented lower risk of overall complications, shorter intensive care unit stay and higher short-term survival, although, no statistically significance was found when performing the multivariate adjustment. CONCLUSIONS: A routine immediate extubation in the OR following adult cardiovascular surgery is a feasible and safe practice, associated with low cardiovascular morbidity.

Postoperative arterial hypotension: the unnoticed enemy.

Postoperative hypotension is a frequently underestimated health problem associated with high morbidity and mortality and increased use of health care resources. It also poses significant clinical, technological, and human challenges for healthcare. As it is a modifiable and avoidable risk factor, this document aims to increase its visibility, defining its clinical impact and the technological challenges involved in optimizing its management, taking clinical-technological, humanistic, and economic aspects into account.

Obesity and female sexual dysfunctions: A systematic review of prevalence with meta-analysis.

Obesity represents a major global health challenge. Female sexual dysfunctions have a negative impact on quality of life and overall health balance. A higher rate of female sexual dysfunctions in obese women has been suggested. This systematic review summarized the literature on female sexual dysfunction prevalence in obese women. The review was registered (Open Science Framework OSF.IO/7CG95) and a literature search without language restrictions was conducted in PubMed, Embase and Web of Science, from January 1990 to December 2021. Cross-sectional and intervention studies were included, the latter if they provided female sexual dysfunction rate data in obese women prior to the intervention. For inclusion, studies should have used the female sexual function index or its simplified version. Study quality was assessed to evaluate if female sexual function index was properly applied using six items. Rates of female sexual dysfunctions examining for differences between obese vs class III obese and high vs low quality subgroups were summarized. Random effects meta-analysis was performed, calculating 95% confidence intervals (CI) and examining heterogeneity with I2 statistic. Publication bias was evaluated with funnel plot. There were 15 relevant studies (1720 women participants in total with 153 obese and 1567 class III obese women). Of these, 8 (53.3%) studies complied with >4 quality items. Overall prevalence of female sexual dysfunctions was 62% (95% CI 55-68%; I2 85.5%). Among obese women the prevalence was 69% (95% CI 55-80%; I2 73.8%) vs 59% (95% CI 52-66%; I2 87.5%) among those class III obese (subgroup difference p=0.15). Among high quality studies the prevalence was 54% (95% CI 50-60%; I2 46.8%) vs 72% (95% CI 61-81%; I2 88.0%) among low quality studies (subgroup difference p=0.002). There was no funnel asymmetry. We interpreted that the rate of sexual dysfunctions is high in obese and class III obese women. Obesity should be regarded as a risk factor for female sexual dysfunctions.

Weight loss induced by 6-month lifestyle intervention improves early endothelial activation and fibrinolysis in obese adolescents.

BACKGROUND: Adolescent obesity is associated with an increased risk of adult obesity and subsequent cardiovascular diseases. The present study aimed to assess the effect of weight loss after 6-month lifestyle intervention in obese adolescents on biomarkers of endothelial activation and fibrinolytic system. METHODS: Eighty-five obese adolescents aged 10 to 16 years were assigned to a 6-month lifestyle intervention and 61 completed the programme. We examined the effect of the intervention on adhesion molecules (selectin E, soluble intercellular adhesion molecule 1 and soluble vascular adhesion molecule 1) and fibrinolytic parameters [plasminogen activator inhibitor-1 (PAI-1) and fibrinogen]. Thirty-six lean adolescents were studied only at baseline as a comparison group. RESULTS: Compared with lean participants, obese adolescents at baseline demonstrated significantly higher levels of triglycerides, glucose, insulin, homeostasis model assessment, soluble intercellular adhesion molecule 1, PAI-1 and fibrinogen. After 6-month lifestyle intervention, those obese adolescents with decreased standard deviation score-body mass index (SDS-BMI) displayed significant decreases in insulin (19.2 ± 11.2 vs. 26.8 ± 13.2 mU/L, P≤ 0.01), homeostasis model assessment (4.24 ± 3.19 vs. 6.58 ± 4.08, P≤ 0.01), selectin E (100.2 ± 60.9 vs. 116.0 ± 69.0 ng/mL, P≤ 0.01) and PAI-1 (39.6 ± 38.0 vs. 51.8 ± 25.6 ng/mL, P≤ 0.05) with respect to the baseline levels. No changes in these parameters were observed in the obese adolescents with stable or increased SDS-BMI. The changes of triglycerides after intervention in subgroup with decreased SDS-BMI were significantly greater than those in subgroup with stable SDS-BMI. CONCLUSIONS: The present study demonstrated increased endothelial activation and impairment of the fibrinolytic system in early life, which is in part reversible by a 6-month lifestyle intervention.

Guidelines for enhanced recovery after cardiac surgery. Consensus document of Spanish Societies of Anesthesia (SEDAR), Cardiovascular Surgery (SECCE) and Perfusionists (AEP). / Vía clínica de recuperación intensificada en cirugía cardiaca. Documento de consenso de la Sociedad Española de Anestesiología, Reanimación y Terapéutica del Dolor (SEDAR), la Sociedad Española de Cirugía Cardiovascular y Endovascular (SECCE) y la Asociación Española de Perfusionistas (AEP).

The ERAS guidelines are intended to identify, disseminate and promote the implementation of the best, scientific evidence-based actions to decrease variability in clinical practice. The implementation of these practices in the global clinical process will promote better outcomes and the shortening of hospital and critical care unit stays, thereby resulting in a reduction in costs and in greater efficiency. After completing a systematic review at each of the points of the perioperative process in cardiac surgery, recommendations have been developed based on the best scientific evidence currently available with the consensus of the scientific societies involved.

[Design and validation of the second edition of the Women's Sexual Function Questionnaire, FSM-2]. / Diseño y validación de la segunda edición del Cuestionario de Función Sexual de la Mujer, FSM-2.

OBJECTIVE: To design and validate the second edition of the Female Sexual Function questionnaire (FSF-2). MATERIAL AND METHODS: A cross-sectional and multicentre study was conducted on 187 women (18-70 years) who completed a test (preliminary questionnaire FSF-2), and then answered a structured anamnesis on female sexual function. Four weeks later they completed a retest, which was equal to the test but with an additional question about possible influence of recent events in their sex life. RESULTS: The mean age of the women was 43.51 years. Internal consistency of the questionnaire: Cronbach's α of the 0.919 test, of structured anamnesis 0.921, of the 0.920 retest. Test-retest reliability: mean test scores 30.53 ± 8.605, retest 30.05 ± 8.770, without significant differences. Correlation between total test and retest scores (intraclass correlation coefficient) 0.960, significant (P<.01); between total test scores and structured anamnesis 0.977, significant (P<.01). Concordance between test questions and structured anamnesis (kappa index), minimum 0.706, maximum 0.915; between test and retest questions, minimum 0.630, maximum 0.802. Content validity by expert consensus. Criteria validity: specificity of the questionnaire exceeding 90% for all items/domains, sensitivity greater than 80%, except for items 5, 6, 9 (70-80%). Validity of the construct through factor analysis, grouping of items into 2 components (they explain 66.586% of variance). CONCLUSIONS: The FSF-2 questionnaire is reliable and valid. It evaluates the sexual response of women, describing important aspects of their sexual activity as a couple: anticipatory anxiety, initiative, confidence to communicate, preferences and events that may influence. It can detect sexual dysfunction in the couple.

[Design and validation of a Male Sexual Function Questionnaire]. / Diseño y validación del Cuestionario de Función Sexual del Hombre, FSH.

OBJECTIVE: The objective of this work was to design and validate a questionnaire on Male Sexual Function (MSF) in the Spanish language, following the criteria contemplated in the Diagnostic and Statistical Manual of Mental Disorders, DSM-5, for the diagnosis of sexual dysfunctions. MATERIAL AND METHODS: A cross-sectional and multicentre study was conducted on 163 men (18-70 years) who self-completed a test (MSF questionnaire). They then answered questions on the Structured History of Male Sexual Function (AMSF). Four weeks later they completed a re-test, which was the same, but including a supplementary question about the possible influence of recent events. RESULTS: Internal consistency: Cronbach's α test 0.840, AMSF 0.835, retest 0.855. Test-retest reliability: mean test scores 33.13±6.566, retest 33.11±6.791; Student t 0.122, not significant (P=.903); correlation total test-retest scores (intraclass correlation coefficient) 0.979, significant correlation (P<.01); total correlations test-AMSF scores (intraclass correlation coefficient) 0.966, significant correlation (P<.01). Concordance: between questions of the AMSF test (Kappa index) minimum 0.749, maximum 0.934; between test-retest questions: 0.724, 0.844. Content validity using expert consensus. Criteria validity: specificity>90% for all items / domains, sensitivity>80% except item 4 (76%). Content validity: using factor analysis, grouping of items into 4 components (explain 75% variance); high correlation between "sexual desire" and "confidence in erection". CONCLUSIONS: The MSF questionnaire is reliable, stable and valid, with high specificity and sensitivity. It evaluates the sexual response of the male, describing aspects of interest: anticipatory anxiety, initiative, confidence to communicate preferences, events that may influence. Can detect sexual dysfunction in the couple.

TGF-beta induced transdifferentiation of mammary epithelial cells to mesenchymal cells: involvement of type I receptors.

The secreted polypeptide transforming growth factor-beta (TGF-beta) exerts its multiple activities through type I and II cell surface receptors. In epithelial cells, activation of the TGF-beta signal transduction pathways leads to inhibition of cell proliferation and an increase in extracellular matrix production. TGF-beta is widely expressed during development and its biological activity has been implicated in epithelial-mesenchymal interactions, e.g., in branching morphogenesis of the lung, kidney, and mammary gland, and in inductive events between mammary epithelium and stroma. In the present study, we investigated the effects of TGF-beta on mouse mammary epithelial cells in vitro. TGF-beta reversibly induced an alteration in the differentiation of normal mammary epithelial NMuMG cells from epithelial to fibroblastic phenotype. The change in cell morphology correlated with (a) decreased expression of the epithelial markers E-cadherin, ZO-1, and desmoplakin I and II; (b) increased expression of mesenchymal markers, such as fibronectin; and (c) a fibroblast-like reorganization of actin fibers. This phenotypic differentiation displays the hallmarks of an epithelial to mesenchymal transdifferentiation event. Since NMuMG cells make high levels of the type I TGF-beta receptor Tsk7L, yet lack expression of the ALK-5/R4 type I receptor which has been reported to mediate TGF-beta responsiveness, we evaluated the role of the Tsk7L receptor in TGF-beta-mediated transdifferentiation. We generated NMuMG cells that stably overexpress a truncated Tsk7L type I receptor that lacks most of the cytoplasmic kinase domain, thus function as a dominant negative mutant. These transfected cells no longer underwent epithelial to mesenchymal morphological change upon exposure to TGF-beta, yet still displayed some TGF-beta-mediated responses. We conclude that TGF-beta has the ability to modulate E-cadherin expression and induce a reversible epithelial to mesenchymal transdifferentiation in epithelial cells. Unlike other transdifferentiating growth factors, such as bFGF and HGF, these changes are accompanied by growth inhibition. Our results also implicate the Tsk7L type I receptor as mediating the TGF-beta-induced epithelial to mesenchymal transition.

Recombinant Vgr-1/BMP-6-expressing tumors induce fibrosis and endochondral bone formation in vivo.

Members of the TGF-beta superfamily appear to modulate mesenchymal differentiation, including the processes of cartilage and bone formation. Nothing is yet known about the function of the TGF-beta-related factor vgr-1, also called bone morphogenetic protein-6 (BMP-6), and only limited studies have been conducted on the most closely related factors BMP-5, osteogenic protein-1 (OP-1) or BMP-7, and OP-2. Because vgr-1 mRNA has been localized in hypertrophic cartilage, this factor may play a vital role in endochondral bone formation. We developed antibodies to vgr-1, and documented that vgr-1 protein was expressed in hypertrophic cartilage of mice. To further characterize the role of this protein in bone differentiation, we generated CHO cells that overexpressed recombinant murine vgr-1 protein. Western blot analysis documented that recombinant vgr-1 protein was secreted into the media and was proteolytically processed to yield the mature vgr-1 molecule. To assess the biological activity of recombinant vgr-1 in vivo, we introduced the vgr-1-expressing CHO cells directly into the subcutaneous tissue of athymic nude mice. CHO-vgr-1 cells produced localized tumors, and the continuous secretion of vgr-1 resulted in tumors with a strikingly different gross and histological appearance as compared to the parental CHO cells. The tumors of control CHO cells were hemorrhagic, necrotic, and friable, whereas the CHO-vgr-1 tumors were dense, firm, and fibrotic. In contrast with control CHO tumors, the nests of CHO-vgr-1 tumor cells were surrounded by extensive connective tissue, which contained large regions of cartilage and bone. Further analysis indicated that secretion of vgr-1 from the transfected CHO tumor cells induced the surrounding host mesenchymal cells to develop along the endochondral bone pathway. These findings suggest that endochondral bone formation.

Altered metabolic and adhesive properties and increased tumorigenesis associated with increased expression of transforming growth factor beta 1.

Transforming growth factor-beta (TGF-beta) is a potent mediator of cell proliferation and extracellular matrix formation, depending on the cell type and the physiological conditions. TGF-beta is usually secreted in a "latent" complex that needs activation before it can exert its effects. Several observations correlate increased expression of TGF-beta 1 with tumorigenesis. To evaluate the physiological relevance of increased TGF-beta 1 synthesis in tumor cells we established cell clones overexpressing TGF-beta 1 and observed the resulting physiological changes in TGF-beta overproducing cells in vitro and in vivo. As a model system we used the human E1A-transformed 293 tumor cells, which are insensitive to the direct growth modulatory effects of TGF-beta. The selection of this cell line allows an assessment of physiological alterations independent of TGF-beta induced proliferative changes. The use of two TGF-beta 1 expression vectors containing either the natural or a modified TGF-beta 1 precursor cDNA permitted the establishment of separate 293 cell lines overexpressing latent or active TGF-beta. Comparison of the resulting changes in glycolytic rate, adhesiveness and integrin and plasminogen activator expression established that, in vitro, both types of clones behaved similarly, indicating that expression of latent TGF-beta induces autocrine changes in the tumor cells and thus suggesting that some level of cell-associated activation occurs. TGF-beta overexpression resulted in an increased metabolic rate due to enhanced glycolysis, a property long associated with tumor cells. This increased glycolysis was not associated with altered proliferation. Cells overexpressing TGF-beta also displayed enhanced fibronectin mRNA and plasminogen activator synthesis and increased adhesiveness in vitro. They showed enhanced survival when plated sparsely on plastic in the absence of serum, and attached more readily to laminin. In addition, synthesis of several beta 1 integrins, in particular the alpha 1/beta 1, alpha 2/beta 1, and alpha 3/beta 1, all of which recognize laminin, were enhanced. Finally, cells overexpressing active TGF-beta, but not latent TGF-beta, also showed increased tumorigenicity in nude mice. Thus, an increase in endogenous TGF-beta synthesis confers several proliferation-independent phenotypic changes which may be of significance for the survival of the tumor cell inoculum or its subsequent growth, and for tumor formation and development. In the case of cells expressing active TGF-beta, the release of active TGF-beta into the vicinity of the tumor cells may also result in a more hospitable environment for tumor growth.

Cloning of a type I TGF-beta receptor and its effect on TGF-beta binding to the type II receptor.

Transforming growth factor-beta (TGF-beta) affects cellular proliferation, differentiation, and interaction with the extracellular matrix primarily through interaction with the type I and type II TGF-beta receptors. The type II receptors for TGF-beta and activin contain putative serine-threonine kinase domains. A murine serine-threonine kinase receptor, Tsk 7L, was cloned that shared a conserved extracellular domain with the type II TGF-beta receptor. Overexpression of Tsk 7L alone did not increase cell surface binding of TGF-beta, but coexpression with the type II TGF-beta receptor caused TGF-beta to bind to Tsk 7L, which had the size of the type I TGF-beta receptor. Overexpression of Tsk 7L inhibited binding of TGF-beta to the type II receptor in a dominant negative fashion. Combinatorial interactions and stoichiometric ratios between the type I and II receptors may therefore determine the extent of TGF-beta binding and the resulting biological activities.

Dog mastocytoma cells produce transforming growth factor beta 1.

Transforming growth factor-beta (TGF beta) promotes deposition of extracellular matrix and is associated with fibrotic conditions both in experimental animals and in humans. Although a role for mast cells has been suspected in the pathogenesis of fibrosis, no potent mediator capable of stimulating fibroblast growth or extracellular matrix deposition has been identified in mast cell supernatants. We report here the constitutive production of TGF beta 1 by four dog mastocytoma cell lines. TGF beta 1 was identified by characteristic biologic activity, blockade of biologic effect by specific neutralizing antibody, and by recognition of a band with the appropriate migration by western blot. TGF beta 1 mRNA, but not TGF beta 2 or TGF beta 3 mRNA, was also produced constitutively by all four cell lines. Quantitation by bioassay revealed baseline TGF beta secretion of approximately 1 ng/10(6) cells over 48 h. Stimulation of mastocytoma cells with phorbol ester increased the rate of release of TGF beta 1, most markedly in the first 30 min after stimulation, without increasing TGF beta 1 mRNA. Dog mastocytoma cells produced TGF beta 1 primarily in a latent form, inactive until treated with acid. Both pure TGF beta 1 and TGF beta-containing mastocytoma cell-conditioned media inhibited mitogenesis and proliferation in dog mastocytoma cell lines, suggesting that mast cell tumor lines would not grow preferentially based on their ability to produce TGF beta. These studies may make possible further investigation of the mechanism by which mast cells contribute to the induction of fibrosis.

Dominant negative mutants of transforming growth factor-beta 1 inhibit the secretion of different transforming growth factor-beta isoforms.

Transforming growth factor-beta (TGF-beta) is a secreted polypeptide factor that is thought to play a major role in the regulation of proliferation of many cell types and various differentiation processes. Several related isoforms have been structurally characterized, three of which, TGF-beta 1, -beta 2, and -beta 3, have been detected in mammalian cells and tissues. Each TGF-beta form is a homodimer of a 112-amino-acid polypeptide which is encoded as a larger polypeptide precursor. We have introduced several mutations in the TGF-beta 1 precursor domain, resulting in an inhibition of TGF-beta 1 secretion. Coexpression of these mutants with wild-type TGF-beta 1, -beta 2, and -beta 3 results in a competitive and specific inhibition of the secretion of different TFG-beta forms, indicating that these mutated versions act as dominant negative mutants for TGF-beta secretion. Overexpression of dominant negative mutants can thus be used to abolish endogenous secretion of TGF-beta and structurally related family members, both in vitro and in vivo, and to probe in this way the physiological functions of the members of the TGF-beta superfamily.

Increased transforming growth factor beta expression inhibits cell proliferation in vitro, yet increases tumorigenicity and tumor growth of Meth A sarcoma cells.

Several observations correlate increased expression of transforming growth factor (TGF) beta 1 with tumorigenesis, suggesting that expression of this multifunctional growth factor may provide an advantage in tumor formation. However, many tumor cells are inhibited in their proliferation by TGF-beta in vitro, thus suggesting that TGF-beta synthesis could exert an antiproliferative effect on tumor formation. To evaluate the physiological relevance of increased TGF-beta 1 synthesis in such tumor cells which are strongly inhibited in their proliferation by TGF-beta, we chose Meth A sarcoma cells as a model system. We established cell clones overexpressing TGF-beta 1 and determined its effect on tumor formation in mice that are not immunocompromised. Increased expression of biologically active TGF-beta 1 resulted in a profound growth inhibition in the transfected clones and increased adhesiveness in vitro. However, these cells were much more tumorigenic than Meth A cells that did not overexpress TGF-beta 1, as assessed by both tumor incidence and tumor growth. In addition, parental Meth A cells were inhibited in their tumor formation by neutralizing TGF-beta antibodies and stimulated by exogenous TGF-beta. Our results thus provide evidence that increased TGF-beta synthesis provides a major advantage for tumorigenesis, even if the cells are growth inhibited by their endogenous TGF-beta synthesis in culture. These results suggest that, in vivo, direct effects of TGF-beta on the tumor environment, such as increased extracellular matrix formation and cell-matrix interactions, and local suppression of the immune surveillance may provide a growth advantage which overrules any direct antiproliferative effects of TGF-beta, as suggested by the effects in culture.

Differential regulation of p21waf-1/cip-1 and Mdm2 by etoposide: etoposide inhibits the p53-Mdm2 autoregulatory feedback loop.

The Mdm2 protein is frequently overexpressed in human non-seminomatous germ cell tumours and transitional carcinoma of the bladder where it may contribute to tolerance of wtp53. Mdm2 forms an autoregulatory feedback loop with p53; the Mdm2 gene is responsive to transactivation by p53 and once synthesized the Mdm2 protein terminates the p53 response. We show here that the topoisomerase poison etoposide, like ultra violet irradiation, inhibits Mdm2 synthesis. Cytotoxic concentrations of etoposide (IC90 for > 3 h) result in inhibition of Mdm2 induction at both the RNA and protein level. Rapid apoptosis ensues. Global transcription is not inhibited: p21waf-1/cip1 and GADD45 expression increase in a dose dependent manner. Inhibition of Mdm2 synthesis depends on the continuous presence of etoposide, suggesting the DNA damage may prevent transcription. Downregulation of Mdm2 transcript occurs in cells expressing HPV16-E6 suggesting that inhibition of Mdm2 transcription is p53-independent. When cells are -treated with a pulse (1 h) of etoposide and reincubated in drug free medium, Mdm2 synthesis commences immediately after damage is repaired (3 h) and the p53 response is attenuated. Induction of apoptosis and loss of clonogenicity are 3-5-fold lower under pulse treatment conditions. This is the first observation of inhibition of Mdm2 transcription following treatment with topoisomerase (topo II) poisons, a feature that may be useful in tumour types where p53 is tolerated by overexpression of Mdm2.

Stage- and lineage-specific expression of the HOXA10 homeobox gene in normal and leukemic hematopoietic cells.

There is growing evidence that the HOX homeobox-containing transcription factors are differentially expressed during hematopoiesis. We have previously demonstrated that the HOXA10 gene is expressed in unfractionated normal marrow and in immortalized leukemic cell lines with myelomonocytic features, but not in cell lines with lymphoid or erythroid features. To gain insights into the patterns of activation of this gene during hematopoietic differentiation, we have examined HOXA10 expression in CD34+ and CD34- subfractions of normal marrow and normal peripheral blood, as well as samples from patients with a variety of acute and chronic leukemias. HOXA10 is strongly expressed in CD34+ normal marrow cells, markedly downregulated in CD34- marrow cells, and inactive in mature neutrophils, monocytes, and lymphocytes. HOXA10 is expressed in all types of acute myelogenous leukemia (AML) with the notable exception of acute promyelocytic leukemia (AML-M3). HOXA10 message is observed in chronic myelogenous leukemia (CML) but appears to be reduced in accelerated phase and blast crisis, particularly lymphoid blast crisis. With rare exception, HOXA10 expression is not observed in samples of acute or chronic lymphoid leukemias. Normal marrow and patient samples appear to contain a single transcript which encodes a full-length homeobox-containing protein, while immortalized cell lines contain an additional alternatively spliced transcript. These studies indicate that HOXA10 expression is restricted to early stages of myeloid differentiation.

Relevance of training in transbronchial fine-needle aspiration technique.

Transbronchial fine-needle aspiration (TBFNA) is a valuable and low-risk procedure that provides access to mediastinal nodes. To learn if increased experience improved TBFNA performance, we compared overtime TBFNA diagnostic yields between a skilled bronchoscopist and another without experience on TBFNA technique. We found higher TBFNA yields in the experienced bronchoscopist (p < 0.001); however, after some experience, the TBFNA reliability improved (p < 0.02) and the use of the procedure increased (p < 0.0001). Thus, to achieve acceptable TBFNA results, a training period is required that we estimate in about 50 procedures.

New biomorphic SiC ceramics coated with bioactive glass for biomedical applications.

A new generation of light, tough and high-strength material for medical implants for bone substitutions with a good biological response is presented. The innovative product that fulfills all these requirements is based on biomorphic silicon carbide ceramics coated with a bioactive glass layer. The combination of the excellent mechanical properties and low density of the biomorphic SiC ceramics, used as a base material for implants, with the osteoconducting properties of the bioactive glass materials opens new possibilities for the development of alternative dental and orthopedic implants with enhanced mechanical and biochemical properties that ensures optimum fixation to living tissue. Biomorphic SiC is fabricated by molten-Si infiltration of carbon templates obtained by controlled pyrolysis of wood. Through this process, the microstructure of the final SiC product mimics that of the starting wood, which has been perfected by natural evolution. The basic features of such microstructure are its porosity (ranging from 30% to 70%) and its anisotropy, which resembles the cellular microstructure and the mechanical characteristics of the bone. The SiC ceramics have been successfully coated with a uniform and adherent bioactive glass film by pulsed laser ablation using an excimer ArF laser. The excellent coverage of the SiC rough surface without film spallation or detachment is demonstrated. In order to assess the coating bioactivity, in vitro tests by soaking the samples in simulated body fluid have been carried out. After 72 h, the formation of a dense apatite layer has been observed even in interconnecting pores by SEM and energy dispersive X-ray spectroscopy analysis demonstrating the bioactive response of this product.