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Potassium (K) deficiency has consequences not only on cellular ion balance and transmembrane potential but also on metabolism. In fact, several enzymes are K-dependent including enzymes in catabolism, causing an alteration in glycolysis and respiration. In addition, K deficiency is associated with the induction of specific pathways and accumulation of metabolic biomarkers, such as putrescine. However, such drastic changes are usually observed when K deficiency is established. Here, we carried out a kinetic analysis with metabolomics to elucidate early metabolic events when nutrient conditions change from K-sufficiency to K-deficiency in Arabidopsis rosettes from both wild type and mutants affected in both K absorption and low-K signalling (hak5 akt1 cipk23). Our results show that mutants have a metabolomics pattern similar to K-deficient wild-type, showing a constitutive metabolic response to low K. In addition, shifting to low K conditions induces (i) changes in sugar metabolism and (ii) an accumulation of salicylic acid metabolites before the appearance of biomarkers of K deficiency (putrescine and aconitate), and such an accumulation is more pronounced in mutants. Our results suggest that early events in the response to low K conditions involve salicylic acid metabolism.
Although preschool-age children who stutter report more negative attitudes toward communication than their typically fluent peers, few investigations have explored factors that may contribute to the differences observed in communication attitude. The purpose of the present study was to explore whether behavioral characteristics of stuttering severity (frequency, duration, physical concomitants) and time since onset of stuttering predict communication attitude in preschool-age children.
Fifty-nine preschool-aged children who stutter completed two speaking samples and the KiddyCAT, a self-report assessment of communication attitude. Speech samples were analyzed for stuttering frequency (measured by percentage of stuttered syllables), duration, and presence of physical concomitants. Linear regression models were used to assess if these behavioral measures of stuttering and time since onset of stuttering predicted self-reported communication attitude.
Results indicate stuttering behavioral measures and time since onset do not predict KiddyCAT scores of preschool-age children who stutter.
Preliminary data suggest children who have presented with stuttering for a longer period of time are no more likely to report a negative communication attitude than children who have a shorter time since onset. Additionally, in contrast to school-age children who stutter, but similar to adults and adolescents who stutter, communication attitude is not linearly related to stuttering severity in preschool-age children.
Preliminary data suggest children who have presented with stuttering for a longer period of time are no more likely to report a negative communication attitude than children who have a shorter time since onset. Additionally, in contrast to school-age children who stutter, but similar to adults and adolescents who stutter, communication attitude is not linearly related to stuttering severity in preschool-age children.
Poly (ADP-ribose) polymerase-inhibitors (PARPis) showed antitumour activity in BRCA1/2-mutated cancers, with more heterogeneous outcomes in tumours harbouring mutationsthat impair other genes involved in the DNA homologous recombination repair (HRR) or wild-type (wt).
We conducted a systematic review and meta-analysis to better assess the role of PARPis in the treatment of metastatic solid tumours, with and without BRCA1/2 mutations. The primary end-point was progression-free survival (PFS). The secondary end-points were overall response rate (ORR) and overall survival (OS). A random-effects model was applied.
Twenty-nine studies (8,839 patients) were included. PFS was significantly improved (hazard ratio [HR] 0.59, 95% confidence interval [CI] 0.51-0.68, p<0.001), without being affected by BRCA mutational status (p=0.65). Significant subgroup differences were observed with regard to the tumour site (p=0.001), line of therapy (p=0.002), control arm (p<0.001), type of PARPi(p<0.001) and trials' e studies are warranted.
Our results confirm the efficacy of already approved PARPi-based treatments in BRCA1/2-mutant solid tumours, support their role also in BRCA-independent HRR-deficient tumours and suggest a potentially broader efficacy in some wt tumours, perhaps with appropriate therapeutic partners. Prospective studies are warranted.The presistent increase of 12/15 lipoxygenase enzyme activity is correlated with uncontrolled inflammation, leading to organ dysfunction. ML351, a potent 12/15 lipoxygenase (12/15LOX) inhibitor, was reported to reduce infarct size and inflammation in a murine ischemic stroke model. selleck products In the presented work, we have applied three complementary experimental approaches, in-vitro, ex-vivo, and in-vivo, to determine whether pharmacological inhibition of 12/15LOX could dampen the inflammatory response in adult mice after Kdo2-Lipid A (KLA) as an endotoxin stimulator or post myocardial infarction (MI). Male C57BL/6 (8-12 weeks) mice were subjected to permanent coronary ligation thereby inducing acute heart failure (MI-d1 and MI-d5) for in-vivo studies. 12/15LOX antagonist ML351 (50 mg/kg) was subcutaneously injected 2 h post-MI, while MI-controls received saline. For ex-vivo experiments, ML351 (25 mg/kg) was injected as bolus after 5 min of inflammatory stimulus (KLA 1 μg/g) injection. Peritoneal macrophages (PMɸ) were harvested after 4 h post KLA. For in-vitro studies, PMɸ were treated with KLA (100 ng/mL), ML351 (10 µM), or KLA + ML351 for 4 h, and inflammatory response was evaluated. In-vivo, 5LOX expression was reduced after ML351 administration, inducing a compensatory increase of 12LOX that sensitized PMɸ toward a proinflammatory state. This was marked by higher inflammatory cytokines and dysregulation of the splenocardiac axis post-MI. ML351 treatment increased CD11b+ and Ly6Chigh populations in spleen and Ly6G+ population in heart, with a decrease in F4/80+ macrophage population at MI-d1. In-vitro results indicated that ML351 suppressed initiation of inflammation while ex-vivo results suggested ML351 overactivated inflammation consequently delaying the resolution process. Collectively, in-vitro, ex-vivo, and in-vivo results indicated that pharmacological blockade of lipoxygenases using ML351 impaired initiation of inflammation thereby dysregulated acute immune response in cardiac repair.