Análisis de los protocolos de rehabilitación pre y post-cirugía del ligamento cruzado anterior (LCA) de la rodilla. Revisión bibliográfica.

Se realiza una revisión bibliográfica con el objetivo de conocer los protocolos actuales de rehabilitación tras la reconstrucción quirúrgica del ligamento cruzado anterior de la rodilla. Se efectúa una búsqueda de los estudios clínicos experimentales actuales que evalúan los procedimientos y protocolos de fisioterapia utilizados durante la rehabilitación del LCA. La búsqueda se realiza en las bases de datos: Medline, PEDro y Science Direct, entre diciembre de 2013 y enero de 2014. Se incluyen los publicados a partir del 2010, desarrollados en humanos con ruptura parcial o total del ligamento y redactados en español o inglés. Se analizan los 21 estudios que cumplen con los criterios de inclusión y exclusión estipulados y se valora el proceso metodológico empleado, la presencia de sesgos y limitaciones, la aplicabilidad de los resultados y la descripción precisa de los protocolos. Se concluye afirmando que no existe unanimidad en los protocolos y procedimientos de fisioterapia y que éstos no ofrecen diferencias destacables si se comparan con los diseñados 20 años atrás. Por lo que se propone y elaborar un protocolo de rehabilitación propio teniendo en cuenta la información obtenida y usando como referencia las guías clínicas más empleadas en la práctica clínica.

NAD+-dependent post-translational modification of Escherichia coli glyceraldehyde-3-phosphate dehydrogenase

Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is a multifunctional housekeeping protein reported to be a target of several covalent modifications in many organisms. In a previous study we showed that enterohemorragic (EHEC) and enteropathogenic (EPEC) Escherichia coli strains secrete GAPDH and that this protein binds to human plasminogen and fibrinogen. Here we report that GAPDH of these pathogens is ADP-ribosylated either in the cytoplasm or in the extracellular medium. GAPDH catalyzes its own modification which involves Cys149 at the active site. ADP-ribosylation of extracellular GAPDH may play important role in the interaction with the host as it has been proposed in other pathogens.

TGF-β dependent regulation of oxygen radicals during transdifferentiation of activated hepatic stellate cells to myofibroblastoid cells

Background: The activation of hepatic stellate cells (HSCs) plays a pivotal role during liver injury because the resulting myofibroblasts (MFBs) are mainly responsible for connective tissue re-assembly. MFBs represent therefore cellular targets for anti-fibrotic therapy. In this study, we employed activated HSCs, termed M1-4HSCs, whose transdifferentiation to myofibroblastoid cells (named M-HTs) depends on transforming growth factor (TGF)-β. We analyzed the oxidative stress induced by TGF-β and examined cellular defense mechanisms upon transdifferentiation of HSCs to M-HTs. Results: We found reactive oxygen species (ROS) significantly upregulated in M1-4HSCs within 72 hours of TGF-β administration. In contrast, M-HTs harbored lower intracellular ROS content than M1-4HSCs, despite of elevated NADPH oxidase activity. These observations indicated an upregulation of cellular defense mechanisms in order to protect cells from harmful consequences caused by oxidative stress. In line with this hypothesis, superoxide dismutase activation provided the resistance to augmented radical production in M-HTs, and glutathione rather than catalase was responsible for intracellular hydrogen peroxide removal. Finally, the TGF-β/NADPH oxidase mediated ROS production correlated with the upregulation of AP-1 as well as platelet-derived growth factor receptor subunits, which points to important contributions in establishing antioxidant defense. Conclusion: The data provide evidence that TGF-β induces NADPH oxidase activity which causes radical production upon the transdifferentiation of activated HSCs to M-HTs. Myofibroblastoid cells are equipped with high levels of superoxide dismutase activity as well as glutathione to counterbalance NADPH oxidase dependent oxidative stress and to avoid cellular damage.

Common Quail (Coturnix coturnix) post-breeding movements and migration patterns: from knowledge to management.

Hemos investigado los patrones de los movimientos postcría de la codorniz común (Coturnix coturnix) en la península ibérica con el fin de describir su fenología de paso migratorio y algunas características fisiológicas de los individuos. Esta información es necesaria para un ajuste óptimo de los períodos de caza. Hemos trabajado a partir de dos conjuntos de datos: a) capturas efectuadas en una zona que no es de cría (Garraf) de agosto a octubre en 2009 y 2010; b) recuperaciones, posteriores a la presunta época de cría, de individuos anillados en Europa y recapturados en España durante el período 1933-2005. Los resultados obtenidos muestran que los movimientos postcría en Garraf están formados por dos oleadas: una primera, que se produce sobre el 10 VIII, formada principalmente por jóvenes del año inactivos sexualmente que no son fisiológicamente migrantes; y una segunda, mucho más intensa, que se produce sobre el 17 IX, formada principalmente por migrantes jóvenes del año inactivos sexualmente. La época de caza en España tiene lugar principalmente durante la primera oleada, preservando el paso de los migrantes provenientes de España y de otros países europeos. La información de los movimientos postcría en otras regiones españolas y en otros países europeos en los que la codorniz común es una especie cinegética popular, permitiría mejorar el ajuste entre el período de caza y la migración, proporcionando recomendaciones de gestión cinegética más precisas para esta especie.

Mutant huntingtin impairs the post-Golgi trafficking of brain-derived neurotrophic factor but not its Val66Met polymorphism.

Brain-derived neurotrophic factor (BDNF) polymorphism is associated with the pathophysiology of several neurodegenerative disorders, including Huntington"s disease. In view ofthese data andthe involvement of huntingtin in intracellular trafficking, we examined the intracellular transport and release of Val66Val BDNF (Val-BDNF) and Val66Met BDNF (Met-BDNF) in transfected striatal knock-in cells expressing wild-type or mutant full-length huntingtin. Colocalization studies with specific markers for endoplasmic reticulum showed no differences between the Val-BDNF and Met-BDNF and were not modified by mutant huntingtin. However, post-Golgi trafficking was altered by mutant huntingtin dependent on the BDNF form. Thus, fluorescence recovery after photobleaching (FRAP) and inverse FRAP analysis showed retention of Met-BDNF inthe Golgi apparatus with respectto Val-BDNF in wild-type cells. Strikingly, mutant huntingtin diminished post-Golgi trafficking of Val-BDNF, whereas Met-BDNF was not modified. Accordingly, a reduction in the number of transport vesicles was only observed in mutant huntingtin cells transfected with Val-BDNF but not Met-BDNF. Moreover, mutant huntingtin severely affectedthe KCl-evoked release of Val-BDNF, although it had little effect on Met-BDNF regulated release. The constitutive release of Val-BDNF or Met-BDNF in mutant cells was only slightly reduced. Interestingly, mutant huntingtin only perturbed post-Golgi trafficking of proteins that follow the regulated secretory pathway (epidermal growth factor receptor or atrial natriuretic factor), whereas it did not change those that follow the constitutive pathway (p75 NTR ). We conclude that mutant huntingtin differently affects intracellular transport and release of Val-BDNF and Met-BDNF. In addition, our findings reveal a new role for huntingtin in the regulation of the post-Golgi trafficking of the regulated secretory pathway.

Estimación de funciones no lineales en mezclas post-no lineales

This paper proposes a new method for blindly inverting a nonlinear mapping which transforms a sum of random variables. This is the case of post-nonlinear (PNL) source separation mixtures. The importance of the method is based on the fact that it permits to decouple the estimation of the nonlinear part from the estimation of the linear one. Only the nonlinear part is inverted, without considering on the linear part. Hence the initial problem is transformed into a linear one that can then be solved with any convenient linear algorithm. The method is compared with other existing algorithms for blindly approximating nonlinear mappings. Experiments show that the proposed algorithm outperforms the results obtained with other algorithms and give a reasonably good linearized data

Cell fusion reprogramming leads to a specific hepatic expression pattern during mouse bone marrow derived hepatocyte formation In Vivo

The fusion of bone marrow (BM) hematopoietic cells with hepatocytes to generate BM derived hepatocytes (BMDH) is a natural process, which is enhanced in damaged tissues. However, the reprogramming needed to generate BMDH and the identity of the resultant cells is essentially unknown. In a mouse model of chronic liver damage, here we identify a modification in the chromatin structure of the hematopoietic nucleus during BMDH formation, accompanied by the loss of the key hematopoietic transcription factor PU.1/Sfpi1 (SFFV proviral integration 1) and gain of the key hepatic transcriptional regulator HNF-1A homeobox A (HNF-1A/Hnf1a). Through genome-wide expression analysis of laser captured BMDH, a differential gene expression pattern was detected and the chromatin changes observed were confirmed at the level of chromatin regulator genes. Similarly, Tranforming Growth Factor-β1 (TGF-β1) and neurotransmitter (e.g. Prostaglandin E Receptor 4 [Ptger4]) pathway genes were over-expressed. In summary, in vivo BMDH generation is a process in which the hematopoietic cell nucleus changes its identity and acquires hepatic features. These BMDHs have their own cell identity characterized by an expression pattern different from hematopoietic cells or hepatocytes. The role of these BMDHs in the liver requires further investigation.

Paranoia and post-traumatic stress disorder in the months after a physical assault: a longitudinal study examining shared and differential predictors.

Background: Being physically assaulted is known to increase the risk of the occurrence of post-traumatic stress disorder (PTSD) symptoms but it may also skew judgements about the intentions of other people. The objectives of the study were to assess paranoia and PTSD after an assault and to test whether theory-derived cognitive factors predicted the persistence of these problems. Method: At 4 weeks after hospital attendance due to an assault, 106 people were assessed on multiple symptom measures (including virtual reality) and cognitive factors from models of paranoia and PTSD. The symptom measures were repeated 3 and 6 months later. Results: Factor analysis indicated that paranoia and PTSD were distinct experiences, though positively correlated. At 4 weeks, 33% of participants met diagnostic criteria for PTSD, falling to 16% at follow-up. Of the group at the first assessment, 80% reported that since the assault they were excessively fearful of other people, which over time fell to 66%. Almost all the cognitive factors (including information-processing style during the trauma, mental defeat, qualities of unwanted memories, self-blame, negative thoughts about self, worry, safety behaviours, anomalous internal experiences and cognitive inflexibility) predicted later paranoia and PTSD, but there was little evidence of differential prediction. Conclusions: Paranoia after an assault may be common and distinguishable from PTSD but predicted by a strikingly similar range of factors.

Effect of meal ingestion on liver stiffness in patients with cirrhosis and portal hypertension.

BACKGROUND AND AIMS: Liver stiffness is increasingly used in the non-invasive evaluation of chronic liver diseases. Liver stiffness correlates with hepatic venous pressure gradient (HVPG) in patients with cirrhosis and holds prognostic value in this population. Hence, accuracy in its measurement is needed. Several factors independent of fibrosis influence liver stiffness, but there is insufficient information on whether meal ingestion modifies liver stiffness in cirrhosis. We investigated the changes in liver stiffness occurring after the ingestion of a liquid standard test meal in this population. METHODS: In 19 patients with cirrhosis and esophageal varices (9 alcoholic, 9 HCV-related, 1 NASH; Child score 6.9±1.8), liver stiffness (transient elastography), portal blood flow (PBF) and hepatic artery blood flow (HABF) (Doppler-Ultrasound) were measured before and 30 minutes after receiving a standard mixed liquid meal. In 10 the HVPG changes were also measured. RESULTS: Post-prandial hyperemia was accompanied by a marked increase in liver stiffness (+27±33%; p<0.0001). Changes in liver stiffness did not correlate with PBF changes, but directly correlated with HABF changes (r = 0.658; p = 0.002). After the meal, those patients showing a decrease in HABF (n = 13) had a less marked increase of liver stiffness as compared to patients in whom HABF increased (n = 6; +12±21% vs. +62±29%,p<0.0001). As expected, post-prandial hyperemia was associated with an increase in HVPG (n = 10; +26±13%, p = 0.003), but changes in liver stiffness did not correlate with HVPG changes. CONCLUSIONS: Liver stiffness increases markedly after a liquid test meal in patients with cirrhosis, suggesting that its measurement should be performed in standardized fasting conditions. The hepatic artery buffer response appears an important factor modulating postprandial changes of liver stiffness. The post-prandial increase in HVPG cannot be predicted by changes in liver stiffness.

The evolution of post-zygotic isolation barriers by immune-triggered hybrid incompatibilities in Arabidopsis thaliana

A long-standing question in evolutionary biology is what defines a species. The biological species concept considers a species as a population of individuals that interbreeds freely and produces viable offspring. Therefore, reproductive isolation is the essence of species. Hybrid necrosis is one form of post-zygotic reproductive isolation. In this chapter, we summarize what is known to date about this phenomenon and highlight progress made in the understanding of these immune-triggered hybrid incompatibilities through our research in the plant model Arabidopsis thaliana.

The evolution of post-zygotic isolation barriers by immune-triggered hybrid incompatibilities in Arabidopsis thaliana

A long-standing question in evolutionary biology is what defines a species. The biological species concept considers a species as a population of individuals that interbreeds freely and produces viable offspring. Therefore, reproductive isolation is the essence of species. Hybrid necrosis is one form of post-zygotic reproductive isolation. In this chapter, we summarize what is known to date about this phenomenon and highlight progress made in the understanding of these immune-triggered hybrid incompatibilities through our research in the plant model Arabidopsis thaliana.

Predictors of psychiatric hospitalization during 6 months of maintenance treatment with olanzapine long-acting injection: post hoc analysis of a randomized, double-blind study.

BACKGROUND: Hospitalization is a costly and distressing event associated with relapse during schizophrenia treatment. No information is available on the predictors of psychiatric hospitalization during maintenance treatment with olanzapine long-acting injection (olanzapine-LAI) or how the risk of hospitalization differs between olanzapine-LAI and oral olanzapine. This study aimed to identify the predictors of psychiatric hospitalization during maintenance treatment with olanzapine-LAI and assessed four parameters: hospitalization prevalence, incidence rate, duration, and the time to first hospitalization. Olanzapine-LAI was also compared with a sub-therapeutic dose of olanzapine-LAI and with oral olanzapine. METHODS: This was a post hoc exploratory analysis of data from a randomized, double-blind study comparing the safety and efficacy of olanzapine-LAI (pooled active depot groups: 405 mg/4 weeks, 300 mg/2 weeks, and 150 mg/2 weeks) with oral olanzapine and sub-therapeutic olanzapine-LAI (45 mg/4 weeks) during 6 months' maintenance treatment of clinically stable schizophrenia outpatients (n=1064). The four psychiatric hospitalization parameters were analyzed for each treatment group. Within the olanzapine-LAI group, patients with and without hospitalization were compared on baseline characteristics. Logistic regression and Cox's proportional hazards models were used to identify the best predictors of hospitalization. Comparisons between the treatment groups employed descriptive statistics, the Kaplan-Meier estimator and Cox's proportional hazards models. RESULTS: Psychiatric hospitalization was best predicted by suicide threats in the 12 months before baseline and by prior hospitalization. Compared with sub-therapeutic olanzapine-LAI, olanzapine-LAI was associated with a significantly lower hospitalization rate (5.2% versus 11.1%, p < 0.01), a lower mean number of hospitalizations (0.1 versus 0.2, p = 0.01), a shorter mean duration of hospitalization (1.5 days versus 2.9 days, p < 0.01), and a similar median time to first hospitalization (35 versus 60 days, p = 0.48). Olanzapine-LAI did not differ significantly from oral olanzapine on the studied hospitalization parameters. CONCLUSIONS: In clinically stable schizophrenia outpatients receiving olanzapine-LAI maintenance treatment, psychiatric hospitalization was best predicted by a history of suicide threats and prior psychiatric hospitalization. Olanzapine-LAI was associated with a significantly lower incidence of psychiatric hospitalization and shorter duration of hospitalization compared with sub-therapeutic olanzapine-LAI. Olanzapine-LAI did not differ significantly from oral olanzapine on hospitalization parameters.