Bacterial c-di-GMP has a key role in establishing host-microbe symbiosis.

Most microbes evolve faster than their hosts and should therefore drive evolution of host-microbe interactions. However, relatively little is known about the characteristics that define the adaptive path of microbes to host association. Here we identified microbial traits that mediate adaptation to hosts by experimentally evolving the free-living bacterium Pseudomonas lurida with the nematode Caenorhabditis elegans as its host.

A History of Mouse Genetics: From Fancy Mice to Mutations in Every Gene.

The laboratory mouse has become the model organism of choice in numerous areas of biological and biomedical research, including the study of congenital birth defects. The appeal of mice for these experimental studies stems from the similarities between the physiology, anatomy, and reproduction of these small mammals with our own, but it is also based on a number of practical reasons: mice are easy to maintain in a laboratory environment, are incredibly prolific, and have a relatively short reproductive cycle. Another compelling reason for choosing mice as research subjects is the number of tools and resources that have been developed after more than a century of working with these small rodents in laboratory environments.

Secretory pathway calcium ATPase 1 (SPCA1) controls mouse neural tube closure by regulating cytoskeletal dynamics.

Neural tube closure relies on the apical constriction of neuroepithelial cells. Research in frog and fly embryos has found links between the levels of intracellular calcium, actomyosin dynamics and apical constriction. However, genetic evidence for a role of calcium in apical constriction during mammalian neurulation is still lacking.

Pbx loss in cranial neural crest, unlike in epithelium, results in cleft palate only and a broader midface.

Orofacial clefting represents the most common craniofacial birth defect. Cleft lip with or without cleft palate (CL/P) is genetically distinct from cleft palate only (CPO). Numerous transcription factors (TFs) regulate normal development of the midface, comprising the premaxilla, maxilla and palatine bones, through control of basic cellular behaviors.

The Transcriptional Repressive Activity of KRAB Zinc Finger Proteins Does Not Correlate with Their Ability to Recruit TRIM28.

KRAB domain Zinc finger proteins are one of the most abundant families of transcriptional regulators in higher vertebrates. The prevailing view is that KRAB domain proteins function as potent transcriptional repressors by recruiting TRIM28 and promoting heterochromatin spreading. However, the extent to which all KRAB domain proteins are TRIM28-dependent transcriptional repressors is currently unclear.

Hyperbaric index in the primary prevention of hypertensive complications in high-risk pregnancy.

Introduction: Preeclampsia (PE) is a major cause of fetal morbidity and mortality. In the Western World, PE affects 2-7% of pregnancies and is responsible for 50,000 deaths annually. Early detection is a priority as it can change the clinical course, but there are no biomarkers or instrumental methods with high sensitivity and specificity.

Splenic rupture after colorectal cancer screening.

The number of colonoscopies performed in recent years is increasing dramatically, specially those related to colorectal cancer screening programmes. For this reason, there is a direct relationship with the number of exceptional complications such as splenic rupture. We describe a clinical case of a splenic rupture with hemodynamic instability.

TRIM28 Controls Genomic Imprinting through Distinct Mechanisms during and after Early Genome-wide Reprogramming.

Genomic imprinting depends on the establishment and maintenance of DNA methylation at imprinting control regions. However, the mechanisms by which these heritable marks influence allele-specific expression are not fully understood. By analyzing maternal, zygotic, maternal-zygotic, and conditional Trim28 mutants, we found that the transcription factor TRIM28 controls genomic imprinting through distinct mechanisms at different developmental stages.

[Prevalence of malnutrition in not critically ill older inpatients].

Background: Elder people suffer physiological changes and illnes that increase the risk of malnutrition. Nutritional status is a major prognosis factor in older people. This study is aimed at estimating the prevalence of malnutrition among the population of 65 and over inpatients as much at admission as at discharge.

[Prevalence of malnutrition in not critically ill inpatients].

Background: Malnutrition is a frequent issue in our hospitals, and it is associated with an increase in morbi- mortality and financial costs, together with a decline in the patients' quality of life. This study is aimed at establishing the prevalence of malnutrition in our health centre, as much at admission as at discharge.

Methods: Transversal observational study assessing 277 adult patients, who were admitted consecutively, and applying the Nutritional Risk Screening 2002 (NRS-2002) in the first 48 hours from admission and then again at discharge.

[Diagnostic hysteroscopy indications and results in Complexo Hospitalario Universitario De Ourense].

Background: Diagnostic hysteroscopy is an endoscopic technique that allows the evaluation of the endocervical canal and uterine cavity.

Objective: To evaluate indications, complications and referral to operative hysteroscopy. To analyze the correlation between sonographic display, hysteroscopy findings and histological diagnosis.

The ENU-induced cetus mutation reveals an essential role of the DNA helicase DDX11 for mesoderm development during early mouse embryogenesis.

Background: DDX11 is a DNA helicase of the conserved FANCJ/RAD3/XPD family involved in maintaining genome stability. Studies in yeast and humans have shown requirements for DDX11 in sister chromatid cohesion and DNA repair. In mouse, loss of Ddx11 results in embryonic lethality.

Modulation of WNT signaling activity is key to the formation of the embryonic head.

The formation of the embryonic head begins with the assembly of the progenitor tissues of the brain, the head and face primordia and the foregut that are derived from the primary germ layers during gastrulation. Specification of the anterior-posterior polarity of major body parts and the morphogenesis of the head and brain specifically is driven by inductive signals including those mediated by BMP, Nodal, FGF and WNT. A critical role of β-catenin dependent WNT signalling activity for head morphogenesis has been revealed through the analysis of the phenotypic impact of loss of function mutation of an antagonist: DKK1, a transcriptional repressor: GSC; and the outcome of interaction of Dkk1 with genes coding three components of the canonical signalling pathway: the ligand WNT3, the co-receptor LRP6 and the transcriptional co-factor, β-catenin.

TRIM28 is required by the mouse KRAB domain protein ZFP568 to control convergent extension and morphogenesis of extra-embryonic tissues.

TRIM28 is a transcriptional regulator that is essential for embryonic development and is implicated in a variety of human diseases. The roles of TRIM28 in distinct biological processes are thought to depend on its interaction with factors that determine its DNA target specificity. However, functional evidence linking TRIM28 to specific co-factors is scarce.

[Referrals to a gastroenterology outpatient clinic from primary care: evaluation of two programs].

Objectives: To analyze the effect of implementing a high-resolution clinic (HRC) and an increasing resolution capacity program in primary care (IRCPPC) for referrals to a gastroenterology outpatient clinic from primary care and the resources used.

Methods: A retrospective and observational study based on a review of referral sheets and databases was performed. We analyzed the number and reason for referrals, delay times and resource consumption in two periods: before (first 4 months of 2007) and after (first 4 months of 2009) the launch of the IRCPPC and HRC.

Lung cancer in women: a comparison with men and an analysis of cases diagnosed in Ourense (Spain) 1999-2006.

Introduction And Objective: To analyse frequency, characteristics and survival of women with lung cancer (LC), in contrast to male patients.

Patients And Methods: A retrospective study was performed in patients with LC diagnosed by histocytology from 1999 to 2006. Survival was estimated by the Kaplan-Meier method.

The mouse KRAB zinc-finger protein CHATO is required in embryonic-derived tissues to control yolk sac and placenta morphogenesis.

Yolk sac and placenta are required to sustain embryonic development in mammals, yet our understanding of the genes and processes that control morphogenesis of these extraembryonic tissues is still limited. The chato mutation disrupts ZFP568, a Krüppel-Associated-Box (KRAB) domain Zinc finger protein, and causes a unique set of extraembryonic malformations, including ruffling of the yolk sac membrane, defective extraembryonic mesoderm morphogenesis and vasculogenesis, failure to close the ectoplacental cavity, and incomplete placental development. Phenotypic analysis of chato embryos indicated that ZFP568 does not control proliferation or differentiation of extraembryonic lineages but rather regulates the morphogenetic events that shape extraembryonic tissues.

Risk factors associated with the development of ischemic colitis.

Aim: To ascertain the role of cardiovascular risk factors, cardiovascular diseases, standard treatments and other diseases in the development of ischemic colitis (IC).

Methods: A retrospective, case-control study was designed, using matched data and covering 161 incident cases of IC who required admission to our hospital from 1998 through 2003. IC was diagnosed on the basis of endoscopic findings and diagnostic or compatible histology.

Chato, a KRAB zinc-finger protein, regulates convergent extension in the mouse embryo.

In Xenopus and zebrafish embryos, elongation of the anterior-posterior body axis depends on convergent extension, a process that involves polarized cell movements and is regulated by non-canonical Wnt signaling. The mechanisms that control axis elongation of the mouse embryo are much less well understood. Here, we characterize the ENU-induced mouse mutation chato, which causes arrest at midgestation and defects characteristic of convergent extension mutants, including a shortened body axis, mediolaterally extended somites and an open neural tube.

Analysis of mouse embryonic patterning and morphogenesis by forward genetics.

Many aspects of the genetic control of mammalian embryogenesis cannot be extrapolated from other animals. Taking a forward genetic approach, we have induced recessive mutations by treatment of mice with ethylnitrosourea and have identified 43 mutations that affect early morphogenesis and patterning, including 38 genes that have not been studied previously. The molecular lesions responsible for 14 mutations were identified, including mutations in nine genes that had not been characterized previously.

Tcf3: a transcriptional regulator of axis induction in the early embryo.

The roles of Lef/Tcf proteins in determining cell fate characteristics have been described in many contexts during vertebrate embryogenesis, organ and tissue homeostasis, and cancer formation. Although much of the accumulated work on these proteins involves their ability to transactivate target genes when stimulated by beta-catenin, Lef/Tcf proteins can repress target genes in the absence of stabilized beta-catenin. By ablating Tcf3 function, we have uncovered an important requirement for a repressor function of Lef/Tcf proteins during early mouse development.

Essential role of glycosaminoglycans in Fgf signaling during mouse gastrulation.

In vitro studies have suggested that proteoglycans facilitate signaling by mammalian growth factors, but genetic evidence supporting this role has been lacking. Here, we characterize the ENU-induced mutation lazy mesoderm (lzme), which disrupts the single mouse gene encoding UDP-glucose dehydrogenase (Ugdh), an enzyme required for the synthesis of the glycosaminoglycan (GAG) side chains of proteoglycans. lzme mutants arrest during gastrulation with defects in migration of mesoderm and endoderm, a phenotype similar to that of mutants in the fibroblast growth factor (Fgf) pathway.