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Both high environmental heterogeneity and milder source site climates were associated with higher plasticity in various traits and co-expression gene networks. Associations between traits, trait plasticity, gene networks and the source site climate suggest that temperature may play a greater role in shaping these patterns when compared to precipitation, in line with recent changes in the region due to climate change. We also found that traits respond to climatic variation in an environment-dependent manner some associations between traits and climate were apparent only under certain growing conditions. Together, our results uncover common responses of P. repens populations to drought, and climatic drivers of population differentiation in functional traits, gene expression and their plasticity.Tacrolimus is a key drug in kidney transplantation (KT) with a narrow therapeutic index. The association between the tacrolimus metabolism rate and KT outcomes have not been investigated in large-scale multi-center studies. The Korean Organ Transplantation Registry (KOTRY) datasets were used. A total of 3456 KT recipients were analyzed. The tacrolimus metabolism rate was defined as blood trough concentration of tacrolimus (C0 ) divided by the daily dose (D). The patients were grouped into fast, intermediate, or slow metabolizers by the C0 /D measured 6 months after transplantation. The slow metabolism group was associated with a 2.7 ml/min/1.73 m2 higher adjusted estimated glomerular filtration rate (eGFR) at 6 months [95% confidence interval (C.I.) 1.2-4.3, P = 0.001], less acute rejection (AR) within 6 months [Odds ratio (OR) 0.744, 95% C.I. 0.585-0.947, P = 0.016], and less interstitial fibrosis and tubular atrophy [OR 0.606, 95% C.I. 0.390-0.940, P = 0.025]. Fast tacrolimus metabolism affected the 6-month post-KT eGFR through mediation of AR [natural indirect effect (NIE) -0.434, 95% C.I. -0.856 to -0.012, P = 0.044) and delayed graft function (DGF; NIE -0.119, 95% C.I. -0.231 to -0.007, P = 0.038). Slow tacrolimus metabolism was associated with better post-KT eGFR. AR and DGF were found to be significant mediators.In this review we show how the neuronal theory is relevant to the convergence theory for the mechanism causing vitiligo, especially the segmental type. Neuropeptides and neurotransmitters, such as neuropeptide Y and dopamine, can be central to the pathological mechanisms of melanocyte destruction. They link into a bidirectional network connecting cutaneous nerves, the neuroendocrine axis and the immune system, and through their local influence on cutaneous inflammation, to the antigen-specific regulatory T cells and the chemokine ligand type 9/chemokine receptor type 1 axis, which is thought to be the final pathway for melanocyte destruction.Single-parent expression (SPE) is defined as gene expression in only one of the two parents. SPE can arise from differential expression between parental alleles, termed non-presence/absence (non-PAV) SPE, or from the physical absence of a gene in one parent, termed PAV SPE. We used transcriptome data of diverse Zea mays (maize) inbreds and hybrids, including 401 samples from five different tissues, to test for differences between these types of SPE genes. Although commonly observed, SPE is highly genotype and tissue specific. A positive correlation was observed between the genetic distance of the two inbred parents and the number of SPE genes identified. CCT241533 Regulatory analysis showed that PAV SPE and non-PAV SPE genes are mainly regulated by cis effects, with a small fraction under trans regulation. Polymorphic transposable element insertions in promoter sequences contributed to the high level of cis regulation for PAV SPE and non-PAV SPE genes. PAV SPE genes were more frequently expressed in hybrids than non-PAV SPE genes. The expression of parentally silent alleles in hybrids of non-PAV SPE genes was relatively rare but occurred in most hybrids. Non-PAV SPE genes with expression of the silent allele in hybrids are more likely to exhibit above high parent expression level than hybrids that do not express the silent allele, leading to non-additive expression. This study provides a comprehensive understanding of the nature of non-PAV SPE and PAV SPE genes and their roles in gene expression complementation in maize hybrids.Pentatricopeptide repeat (PPR) proteins form a large family of proteins targeted to organelles, where they post-transcriptionally modulate gene expression through binding to specific RNA sequences. Among them, the mitochondria-targeted restorer-of-fertility (Rf) PPRs inhibit peculiar mitochondrial genes that are detrimental to male gametes and cause cytoplasmic male sterility (CMS). Here, we revealed three nuclear loci involved in CMS in a cross between two distant Arabidopsis thaliana strains, Sha and Cvi-0. We identified the causal gene at one of these loci as RFL24, a conserved gene encoding a PPR protein related to known Rf PPRs. By analysing fertile revertants obtained in a male sterile background, we demonstrate that RFL24 promotes pollen abortion, in contrast with the previously described Rf PPRs, which allow pollen to survive in the presence of a sterilizing cytoplasm. We show that the sterility caused by the RFL24 Cvi-0 allele results from higher expression of the gene during early pollen development. Finally, we predict a binding site for RFL24 upstream of two mitochondrial genes, the CMS gene and the important gene cob. These results suggest that the conservation of RFL24 is linked to a primary role of ensuring a proper functioning of mitochondria, and that it was subsequently diverted by the CMS gene to its benefit.We re-engineered a classic tool for mutagenesis and gene expression studies in Gram-negative bacteria. Our modified Tn5-based transposon contains multiple features that allow rapid selection for mutants, direct quantification of gene expression and straightforward cloning of the inactivated gene. The promoter-less gfp-km cassette provides selection and reporter assay depending on the activity of the promoter upstream of the transposon insertion site. The cat gene facilitates positive antibiotic selection for mutants, while the narrow R6Kγ replication origin forces transposition in recipient strains lacking the pir gene and enables cloning of the transposon flanked with the disrupted gene from the chromosome. The suicide vector pCKD100, a plasmid that could be delivered into recipient cells through biparental mating or electroporation, harbours the modified transposon. We used the transposon to mutagenize Pectobacterium versatile KD100, Pseudumonas coronafaciens PC27R and Escherichia coli 35150N. The fluorescence intensities of mutants expressing high GFP could be quantified and detected qualitatively. Transformation efficiency from conjugation ranged from 1600 to 1900 CFU per ml. We sequenced the upstream flanking regions, identified the putative truncated genes and demonstrated the restoration of the GFP phenotype through marker exchange. The mini-Tn5 transposon was also utilized to construct mutant a library of P. versatile for forward genetic screens.O-GlcNAcylation is a post-translational modification catalysed by O-GlcNAc transferase (OGT). Missense mutations in OGT have been associated with developmental disorders, OGT-linked congenital disorder of glycosylation (OGT-CDG), which are characterized by intellectual disability. OGT relies on the hexosamine biosynthetic pathway (HBP) for provision of its UDP-GlcNAc donor. We considered whether mutations in UDP-N-acetylhexosamine pyrophosphorylase (UAP1), which catalyses the final step in the HBP, would phenocopy OGT-CDG mutations. A de novo mutation in UAP1 (NM_001324114c.G685Ap.A229T) was reported in a patient with intellectual disability. We show that this mutation is pathogenic and decreases the stability and activity of the UAP1 isoform AGX1 in vitro. X-ray crystallography reveals a structural shift proximal to the mutation, leading to a conformational change of the N-terminal domain. These data suggest that the UAP1A229T missense mutation could be a contributory factor to the patient phenotype.Anti-inflammatory products may represent the future for depressive disorder therapies. Curcumin (CUR) is a polyphenol and an active component of the turmeric plant Curcuma longa. The aim of this study was to investigate the impact of CUR, as a natural anti-inflammatory agent, on neuro-inflammation related to depression and compare it with the effects of fluoxetine (FLX) and estradiol (E2 ) in ovariectomized (OVX) rats. The experimental animals were divided into the following five treatment groups (n = 10) sham-operated, OVX, OVX-E2 (100 μg/kg, im, every other day), OVX-FLX (20 mg/kg, ip, daily), and OVX-CUR (100 mg/kg, po, daily). The results indicated that CUR improved the animals' performances in the open field test and modulated dopamine (DA) and norepinephrine levels in several brain regions compared with the OVX group. CUR resulted in the down-regulation of monoamine oxidase b and up-regulation of tyrosine hydroxylase, as well asDA receptor mRNA in the limbic region. In addition, CUR significantly attenuated the production of serum corticosterone hormone, tumour necrosis factor-alpha, interleukin-β1, interleukin-6, and nitric oxide in the limbic system. Furthermore, CUR normalized malondialdehyde levels and led to a significant upsurge in total antioxidant capacity, compared with the OVX group. Consequently, CUR, besides being harmless, was efficient against inflammation and oxidative-nitrosative stress, showing a greater effect on DA receptor expression than FLX and E2 in OVX rats.Reports on abdominal tumours in koi carp are scarce and most are from the gonads. Their histological diagnosis is challenging due to the occurrence of mixed populations of neoplastic cells and the few availability of cross-reactive antibodies in fish tissues. The present study aims to provide a histopathological characterization of seventeen gonadal tumours, enriched by a wide antibody panel (vimentin, CD117, placental alkaline phosphatase-PLAP, AE1/AE3 cytokeratin, E-cadherin, proliferating cell nuclear antigen-PCNA, müllerian-inhibiting substance-MIS, GATA4 and Inhibin-α) applied on whole and tissue microarray (TMA) sections. Abdominal enlargement was associated with tumours filling 30%-80% of the abdominal cavity; frequently, the gonads had been completely replaced by neoplastic tissue. Twelve cases were characterized as sex cord-stromal tumours (SCSTs), three as germ cell tumours (GCTs), one as mixed germ cell sex cord-stromal tumour (MGCSCST) and one as carcinoma. By immunohistochemistry, PLAP enabled confirmation of GCTs, ovarian carcinoma and the objective identification of a further cell component in 8 out of the 12 SCSTs that were reclassified as mixed tumours. The use of an immunohistochemical panel can help in refining the histological diagnosis, but the morphological diagnosis still represents the main tool for the characterization of these tumours in koi carp.

Independent effects of gestational diabetes (GDM), maternal prepregnant obesity and gestational weight gain on offspring BMI and obesity are scarcely documented. We examined associations between GDM and children's BMI trajectories from birth to 4-5years age, and effects of prepregnant obesity and gestational weight gain not mediated through GDM.

We included 734 children from a population-based, multi-ethnic cohort of women and their offspring followed from early pregnancy. All women were screened for GDM. Using linear mixed models, we explored associations between maternal factors and children's BMI development through seven serial measurements.

At birth and age 4-5years, BMI of children exposed to GDM was similar to those not exposed. However, they had slower BMI growth (B=-0.1BMI units/month (95% CI -0.17, -0.04)) during first 6months, and faster BMI growth from 6months to 4-5years. Maternal prepregnant obesity was associated with higher child BMI at birth, and thereafter persistently higher BMI. High gestational weight gain was associated with faster BMI growth from 6months to 4-5years.

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