Multidrug-resistant Pseudomonas aeruginosa is one of the main opportunistic pathogens causing severe infection. One of the mechanisms involved in the resistance to imipenem in clinical isolates is the loss of the OprD porin. Changes like substitutions, deletions, insertions, or mutations in the oprD gene can modify the conformation of OprD porin or inhibit its presence and generate resistance to carbapenems. The aim of this work was to obtain anti-OprD polyclonal antibodies and to determine by both immunofluorescence microscopy (IFI) and Western blot assays, the presence of the OprD porin in resistant-carbapenem P. aeruginosa strains with different changes in the oprD gene. Changes in the gene oprD were identified in clinical isolates of P. aeruginosa. When proteins were translated, several polymorphisms were found; however, these did not affect the presence of OprD porin (PCM25, PCM36, and PCM78). Also it was detected an insertion sequence ISPa1328 (PCM52) and a premature stop codon (PCM91), which inhibited the presence of the OprD porin. This study shows how changes in the oprD gene of P. aeruginosa clinical isolates affect the presence of the OprD porin detected by Western blot and indirect immunofluorescence assays using specific polyclonal anti-OprD antibodies generated in this work.NIN (NODULE INCEPTION) is a transcription factor that plays a key role during root nodule initiation. However, its role in later nodule developmental stages is unclear. Both NIN mRNA and protein accumulated at the highest level in the proximal part of the infection zone in Medicago truncatula nodules. Two nin weak allele mutants, nin-13/16, form a rather normal nodule infection zone, whereas a fixation zone is not formed. Instead, a zone with defence responses and premature senescence occurred and symbiosome development gets arrested. Mutations in nin-13/16 resulted in a truncated NIN lacking the conserved PB1 domain. However, this did not cause the nodule phenotype as nin mutants expressing NINΔPB1 formed wild-type-like nodule. The phenotype is likely to be caused by reduced NIN mRNA levels in the cytoplasm. Transcriptome analyses of nin-16 nodules showed that expression levels of defence/senescence-related genes are markedly increased, whereas the levels of defence suppressing genes are reduced. Although defence/senescence seems well suppressed in the infection zone, the transcriptome is already markedly changed in the proximal part of infection zone. In addition to its function in infection and nodule organogenesis, NIN also plays a major role at the transition from infection to fixation zone in establishing a functional symbiosis.The prevalence of dermatological disease and skin conditions is a significant issue facing refugees and migrants in the WHO European Region. Displaced populations in particular are vulnerable to dermatological diseases, due to the often poor conditions in which they live and transit through at different stages of their journey. Exposure to adverse weather conditions and heightened risk for injuries and violence are also potential causes for skin conditions and abnormalities. Through a review of published literature focusing on refugee and migrant health, this paper outlines the prevalence of skin conditions and dermatological diseases among these populations, and the impact of migration and displacement on susceptibility for them. It then discusses some of the challenges associated with managing skin conditions and highlights key opportunities to strengthen the integration of skin health within health care for migrants and refugees in the WHO European Region.Although breastfeeding is known to improve health, economic and environmental outcomes, breastfeeding initiation and continuation rates are low in the United Kingdom. The global WHO/UNICEF Baby Friendly Hospital Initiative (BFHI) aims to reverse declining rates of breastfeeding by shifting the culture of infant feeding care provision throughout hospital maternity settings. In the United Kingdom, the global BFHI has been adapted by UNICEF UK reflecting a paradigm shift towards the experiences of women and families using maternity services. This research used a critical ethnographic approach to explore the influence of the national UNICEF UK Baby Friendly Initiative (BFI) standards on the culture of one typical maternity service in England, over a period of 8 weeks, across four phases of data collection between 2011 and 2017. Twenty-one staff and 26 service users were recruited and engaged in moderate-level participant observation and/or guided interviews and conversations. Basic, organising and a final global theme emerged through thematic network analysis, describing the influence of the BFI on providing, receiving and leading infant feeding care in a hospital maternity setting. Using Antonovsky’s sense of coherence construct, the findings discussed in this paper highlight how the BFI offers 'informational’ (comprehensible), 'practical’ (manageable) and ’emotional’ (meaningful) support for both staff and service users, strengthened by effective, local leadership and a team approach. This is juxtaposed against the tensions and demands of the busy hospital maternity setting. It is recommended that ongoing infant feeding policy, practice and leadership balance relational and rational approaches for positive infant feeding care and experiences to flourish.Microorganisms or LPS (lipopolysaccharide), an outer membrane component of Gram-negative bacteria, can induce a systemic inflammatory response that leads to sepsis, multiple organ dysfunction, and mortality. Here, we investigated the role of cyclophilin D (CypD)-dependent mitochondrial permeability transition (mPT) in the immunosuppressive phase of LPS-induced endotoxic shock. The liver plays an important role in immunity and organ dysfunction; therefore, we used liver RNA sequencing (RNA-seq) data, Ingenuity® Pathway Analysis (IPA ® ) to investigate the complex role of mPT formation in inflammatory reprogramming and disease progression. LPS induced significant changes in the expression of 2844 genes, affecting 179 pathways related to mitochondrial dysfunction, defective oxidative phosphorylation, nitric oxide (NO) and reactive oxygen species (ROS) accumulation, nuclear factor, erythroid 2 like 2 (Nrf2), Toll-like receptors (TLRs), and tumor necrosis factor α receptor (TNFR)-mediated processes in wild-type mice. The disruption of CypD reduced LPS-induced alterations in gene expression and pathways involving TNFRs and TLRs, in addition to improving survival and attenuating oxidative liver damage and the related NO- and ROS-producing pathways. CypD deficiency diminished the suppressive effect of LPS on mitochondrial function, nuclear- and mitochondrial-encoded genes, and mitochondrial DNA (mtDNA) quantity, which could be critical in improving survival. Our data propose that CypD-dependent mPT is an amplifier in inflammatory reprogramming and promotes disease progression. The mortality in human sepsis and shock is associated with mitochondrial dysfunction. Prevention of mPT by CypD disruption reduces inflammatory reprogramming, mitochondrial dysfunction, and lethality; therefore, CypD can be a novel drug target in endotoxic shock and related inflammatory diseases.

Conventional therapy for canine acral lick dermatitis (ALD) consists of systemic antibiotics and anti-anxiety medications. Low-level laser therapy (LLLT) is a noninvasive therapy used to treat inflammatory and painful conditions.

The primary objective was to determine whether LLLT with conventional therapy would be beneficial as an adjunct treatment for ALD. We hypothesized that LLLT and conventional therapy combined would result in a greater reduction in licking Visual Analog Score (LVAS) compared to conventional therapy alone. Secondary objectives were to assess change in lesion/ulcer size, thickness and hair growth.

Thirteen dogs with a skin lesion consistent with ALD.

Dogs were randomly assigned to two groups. All dogs received systemic antibiotics and trazodone. The treatment group (TG) received LLLT by laser (130mW, 2min) with blue and red light-emitting diodes (LEDs), while the control group (CG) had sham therapy (laser/LEDs off). Treatments were administered three times weekly for two weeks, then twice weekly for two weeks for a total of 10 visits. Descriptive statistics were performed (mean, median); primary and secondary objectives were assessed with nonparametric ANOVA (Kruskal-Wallis test), with significance set at P<0.05.

Thirteen dogs (six CG, seven TG) were enrolled. There were no significant differences in median LVAS, lesion/ulcer size or thickness of the ALD lesion between TG and CG. There was a significantly greater increase (24%) in hair growth in TG (P=0.0081) compared to CG.

Treatment of ALD requires multimodal therapy. Although combining LLLT with conventional therapy did not result in a significantly greater reduction in LVAS, there was a significant increase in hair growth compared to conventional therapy alone.

Treatment of ALD requires multimodal therapy. Although combining LLLT with conventional therapy did not result in a significantly greater reduction in LVAS, there was a significant increase in hair growth compared to conventional therapy alone.In current clinical practice, care of diseased patients is often restricted to separated disciplines. However, such an organ-centered approach is not always suitable. For example, cognitive dysfunction is a severe burden in heart failure patients. Moreover, these patients have an increased risk for age-associated dementias. The underlying molecular mechanisms are presently unknown, and thus, corresponding therapeutic strategies to improve cognition in heart failure patients are missing. Using mice as model organisms, we show that heart failure leads to specific changes in hippocampal gene expression, a brain region intimately linked to cognition. These changes reflect increased cellular stress pathways which eventually lead to loss of neuronal euchromatin and reduced expression of a hippocampal gene cluster essential for cognition. Consequently, mice suffering from heart failure exhibit impaired memory function. These pathological changes are ameliorated via the administration of a drug that promotes neuronal euchromatin formation. Our study provides first insight to the molecular processes by which heart failure contributes to neuronal dysfunction and point to novel therapeutic avenues to treat cognitive defects in heart failure patients.The most appropriate type of diets to maintain or lose body weight over the medium to long term has been a matter of controversy and debates for more than half a century. Both voluntarily and coercive food restriction, resulting in negative energy and macronutrient balance and hence weight loss, have not been designed to be maintained for the long term. By contrast, when a classical and traditional type of alimentation is consumed in ad lib conditions (e.g., the Mediterranean „diet”), it generally provides an appropriate nutritional density of essential macronutrients and micronutrients; it is hence appropriate for long-term use, and it provides several benefits for health if the compliance of the individuals is maintained over time. In this short review, we focus on four specific aspects first, the need to agree on a clear definition of what is „low” versus „high” in terms of total carbohydrate intake and total fat intakes, both generally inversely related, in a representative individual with a certain lifestyle and a certain body morphology; second, the importance of discussing the duration over which it could be prescribed, that is, acute versus chronic conditions, focusing on the comparison between the fashion and often ephemeral low-carbohydrate diet (acute) with the well-recognized traditional Mediterranean type of alimentation (chronic), which includes lifestyle changes; third, the particular metabolic characteristics induced by the low-carbohydrate (high fat) diet, namely, the scramble up of ketone bodies production.