Antarctic and Southern Ocean (ASO) marine ecosystems have been changing for at least the last 30 years, including in response to increasing ocean temperatures and changes in the extent and seasonality of sea ice; the magnitude and direction of these changes differ between regions around Antarctica that could see populations of the same species changing differently in different regions. This article reviews current and expected changes in ASO physical habitats in response to climate change. It then reviews how these changes may impact the autecology of marine biota of this polar region: microbes, zooplankton, salps, Antarctic krill, fish, cephalopods, marine mammals, seabirds, and benthos. The general prognosis for ASO marine habitats is for an overall warming and freshening, strengthening of westerly winds, with a potential pole-ward movement of those winds and the frontal systems, and an increase in ocean eddy activity. Many habitat parameters will have regionally specific changes, particularly relating to sea ice characteristics and seasonal dynamics. Lower trophic levels are expected to move south as the ocean conditions in which they are currently found move pole-ward. For Antarctic krill and finfish, the latitudinal breadth of their range will depend on their tolerance of warming oceans and changes to productivity. Ocean acidification is a concern not only for calcifying organisms but also for crustaceans such as Antarctic krill; it is also likely to be the most important change in benthic habitats over the coming century. For marine mammals and birds, the expected changes primarily relate to their flexibility in moving to alternative locations for food and the energetic cost of longer or more complex foraging trips for those that are bound to breeding colonies. Few species are sufficiently well studied to make comprehensive species-specific vulnerability assessments possible. Priorities for future work are discussed.

Accumulation of frameshift mutations at genes containing coding mononucleotide repeats is thought to be the major molecular mechanism by which mismatch repair-deficient cells accumulate functional alterations. These mutations resulting from microsatellite instability (MSI) can affect genes involved in pathways with a putative oncogenic role, but may also arise in genes without any expected role in MSI carcinogenesis because of the high mutation background of these tumours. We here screened 39 MSI colorectal tumours for the presence of mutations in 25 genes involved in DNA damage signalling and repair pathways. Using a maximum likelihood statistical method, these genes were divided into two different groups that differed significantly in their mutation frequencies, and likely represent mutations that do or do not provide selective pressure during MSI tumour progression. Interestingly, the so-called real-target mutational events were found to be distributed among genes involved in different functional pathways of the DNA metabolism, for example, DNA damage signalling (DNA-PKcs, ATR), double-strand break (DSB) repair (DNA-PKcs, RAD50), mismatch repair (MSH3, MSH6, MBD4) and replication (POLD3). In particular, mutations in MRE11 and/or RAD50 were observed in the vast majority of the tumours and resulted in the concomitant loss of immunohistochemical expression of both proteins. These data might explain why MSI colorectal cancers (CRC) behave differently in response to a wide variety of chemotherapeutic agents, notably those targeting DNA. More generally, they give further insights into how MSI leads to functional changes with synergistic effects in oncogenic pathways.

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The mammalian CoREST ([co]repressor for element-1-silencing transcription factor) complex was first identified associated with the repressor for element-1 silencing transcription factor (REST)/neuronal restrictive silencing factor. The CoREST complex is a chromatin-modifying corepressor complex that acts with REST to regulate neuronal gene expression and neuronal stem cell fate. Components of a CoREST-like complex have been identified recently in Xenopus laevis, Caenorhabditis elegans, and Drosophila melanogaster. Like the mammalian complex, the Drosophila complex is required to regulate neuronal gene expression, whereas the C. elegans homologs regulate the expression of the hop-1 presenilin gene, suggesting an ancient conserved function of CoREST complexes in regulating neuronal gene expression.

Background: Magnesium deficiency is common in type 2 diabetes and may have a negative impact on glucose homeostasis and insulin resistance, as well as on the evolution of complications such as retinopathy, thrombosis and hypertension. Objective: To assess the dietary magnesium intake of patients with type 2 diabetes in Zurich, Switzerland and to compare the magnesium intake of diabetic and non-diabetic subjects. Design: The magnesium intake of 97 randomly selected patients with type 2 diabetes and 100 healthy, non-diabetic controls matched for age and sex was estimated using a diet history method. During winter and summer periods, mean daily magnesium intakes were calculated from detailed information given by the test subjects about their eating habits over the previous 2 months. The calculations were performed using EBIS, a computer program based on a German nutrient data base (BLS 2.3), with food items specific to Switzerland added or directly analysed when necessary. Results: The mean AE s.d. daily magnesium intake of the male diabetic and male control subjects was 423.2 AE 103.1 and 421.1 AE 111.0 mg, respectively. The mean daily magnesium intake of the female diabetic and female control subjects was 419.1 AE 109.7 and 383.5 AE 109.7 mg, respectively. There were no significant differences in daily magnesium intake between the diabetic and the non-diabetic subjects and mean intakes in both groups exceeded Swiss recommended dietary intakes. Conclusions: Dietary intake of magnesium appears sufficient in Swiss adults with type 2 diabetes and is unlikely to contribute to the aetiology of magnesium deficiency.

These results demonstrate that provided the surgeon is highly skilled in laparoscopy, operative laparoscopy is efficient for the treatment of patients presenting painful symptoms related to deep endometriotic infiltrating the RVS. From the technical point of view the rectum must be freed, leaving the deep endometriotic nodule attached to the posterior wall of the vagina. Resection of the whole lesion requires the posterior wall of the vagina to be resected, whereas ureterolysis is often unnecessary. So for lesions located on the RVS the vagina is opened systematically, unlike the situation when resecting deep endometriotic lesions infiltrating the USL. Deep pelvic endometriosis is not synonymous with endometriosis of the RVS. Lesions truly infiltrating the RVS represent only a small proportion of all deep endometriosis lesions.

BackroundThe transobturator tape procedure (TOT) is an effective surgical treatment of female stress urinary incontinence. However data concerning safety are rare, follow-up is often less than two years, and complications are probably underreported. The aim of this study was to describe early and late complications associated with TOT procedures and identify risk factors for erosions.MethodsIt was a 27 months follow-up of a cohort of 233 women who underwent TOT with three different types of slings (Aris®, Obtape®, TVT-O®). Follow-up information was available for 225 (96.6%) women.ResultsThere were few per operative complications. Forty-eight women (21.3%) reported late complications including de novo or worsening of preexisting urgencies (10.2%), perineal pain (2.2%), de novo dyspareunia (9%), and vaginal erosion (7.6%). The risk of erosion significantly differed between the three types of slings and was 4%, 17% and 0% for Aris®, Obtape® and TVT-O® respectively (P = 0.001). The overall proportion of women satisfied by the procedure was 72.1%. The percentage of women satisfied was significantly lower in women who experienced erosion (29.4%) compared to women who did not (78.4%) (RR 0.14, 95% CI 0.05-0.38, P < 0.001).ConclusionLate post operative complications are relatively frequent after TOT and can impair patient's satisfaction. Women should be informed of these potential complications preoperatively and require careful follow-up after the procedure. Choice of the safest sling material is crucial as it is a risk factor for erosion.

The development of the C. elegans uterus provides a model for understanding the regulatory pathways that control organogenesis. In C. elegans, the ventral uterus develops through coordinated signaling between the uterine anchor cell (AC) and a ventral uterine (VU) cell. The nhr-67 gene encodes the nematode ortholog of the tailless nuclear receptor gene. Fly and vertebrate tailless genes function in neuronal and ectodermal developmental pathways. We show that nhr-67 functions in multiple steps in the development of the C. elegans uterus. First, it functions in the differentiation of the AC. Second, it functions in reciprocal signaling between the AC and an equipotent VU cell. Third, it is required for a later signaling event between the AC and VU descendants. nhr-67 is required for the expression of both the lag-2/Delta signal in the AC and the lin-12/Notch receptor in all three VU cells and their descendants, suggesting that nhr-67 may be a key regulator of Notch-signaling components. We discuss the implications of these findings for proposed developmental regulatory pathways that include the helix-loop-helix regulator hlh-2/daughterless and transcription factor egl-43/Evi1 in the differentiation of ventral uterine cell types.