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Diabetic foot is one of the main causes of non-traumatic amputation. However, there is still lack of effective drugs to treat diabetic foot in clinical practice. Kanglexin (KLX) is a new anthraquinone compound with cardiovascular protective effects. Here we report that KLX accelerates diabetic wound healing by promoting angiogenesis via FGFR1/ERK signaling. Firstly, KM mice were injected (ip) with streptozocin to establish type 1 diabetic model. The full thickness wound with the diameter of 5 mm was prepared on the back of each mice. The wounds were treated with KLX once a day for 14 consecutive days. Results showed that KLX significantly accelerated the closure of diabetic wounds. Pathological studies of skin tissues around the wounds showed that KLX promoted the formation of granulation tissue and new blood vessels, increased collagen deposition and reduced inflammatory cell infiltration. Besides, KLX significantly alleviated advanced glycation end products (AGEs) - induced abnormal proliferation, migration and tubule formation of human umbilical vein endothelial cells (HUVECs), and up-regulated phospho-ERK1/2 both in the diabetic wound tissue and AGEs - treated HUVECs. Moreover, molecular docking results indicated that KLX had the potential to bind with FGF receptor 1 (FGFR1), and subsequent experiments confirmed that FGFR1 inhibitor PD173074 reversed the effect of KLX on promoting the phosphorylation of ERK1/2 and angiogenesis, suggesting that KLX promoted angiogenesis through FGFR1/ERK signaling. In conclusion, our study provides a new effective compound for treating diabetic wounds. More importantly, KLX has the potential to be developed as a topical drug to promote diabetic wound healing.Centrosome amplification (CA) is a common feature of human tumors, but it is not clear whether this is a cause or a consequence of cancer. The centrosome amplification observed in tumor cells may be explained by a series of events, such as failure of cell division, dysregulation of centrosome cycle checkpoints, and de novo centriole biogenesis disorder. The formation and progression of breast cancer are characterized by genomic abnormality. The centrosomes in breast cancer cells show characteristic structural aberrations, caused by centrosome amplification, which include an increase in the number and volume of centrosomes, excessive increase of pericentriolar material (PCM), inappropriate phosphorylation of centrosomal molecular, and centrosome clustering formation induced by the dysregulation of important genes. The mechanism of intracellular centrosome amplification, the impact of which on breast cancer and the latest breast cancer target treatment options for centrosome amplification are exhaustively elaborated in this review.Communication and interpersonal skills are relevant to the health professions, so it is important to promote these competencies at university. This research assesses the effectiveness of teaching oral competence through simulation using face-to-face and blended methods. A public speaking workshop was conducted in a group of 144 first year nursing students. Three groups were obtained according to the teaching method (Group 1 traditional method-3 sessions, Group 2 traditional method-2 sessions, Group 3 blended method-2 sessions). Public speaking confidence was measured at the beginning and end of the training, and oral competence was assessed at the end. As a result, all groups achieved a good level of oral competence after the training. However, while students in Group 1 showed greater oral competence, with regard to confidence in public speaking, students in Group 1 showed significantly worst results than those in Group 3. We concluded that simulation is a useful strategy to improve cognitive learning, and behavioural and practical competencies such as public speaking. As for the teaching method, although blended learning did not offer better results than traditional learning, it seems useful provide there is at least one face-to-face session so that the student can perform a speech and receive corrective feedback.
Understanding the neurobiology of depression and the mechanism of action of therapeutic measures is currently a research priority. Zunsemetinib We have shown that the expression of the synaptic protein Homer1a correlates with depression-like behavior and its induction is a common mechanism of action of different antidepressant treatments. However, the mechanism of Homer1a regulation is still unknown.

We combined the chronic despair mouse model (CDM) of chronic depression with different antidepressant treatments. Depression-like behavior was characterized by forced swim and tail suspension tests, and via automatic measurement of sucrose preference in IntelliCage. The Homer1 mRNA expression and promoter DNA methylation were analyzed in cortex and peripheral blood by qRT-PCR and pyrosequencing.

CDM mice show decreased Homer1a and Homer1b/c mRNA expression in cortex and blood samples, while chronic treatment with imipramine and fluoxetine or acute ketamine application increases their level only in the cortex. The quantitative analyses of the methylation of 7 CpG sites, located on the Homer1 promoter region containing several CRE binding sites, show a significant increase in DNA methylation in the cortex of CDM mice. In contrast, antidepressant treatments reduce the methylation level.

Homer1 expression and promotor methylation were not analyzed in different blood cell types. Other CpG sites of Homer1 promoter should be investigated in future studies. Our experimental approach does not distinguish between methylation and hydroxymethylation.

We demonstrate that stress-induced depression-like behavior and antidepressant treatments are associated with epigenetic alterations of Homer1 promoter, providing new insights into the mechanism of antidepressant treatment.
We demonstrate that stress-induced depression-like behavior and antidepressant treatments are associated with epigenetic alterations of Homer1 promoter, providing new insights into the mechanism of antidepressant treatment.
Rare genetic functional variants can contribute to 30-40% of functional variability in genes relevant to drug action. Therefore, we investigated the role of rare functional variants in antidepressant response.

Mexican-American individuals meeting the Diagnostic and Statistical Manual-IV criteria for major depressive disorder (MDD) participated in a prospective randomized, double-blind study with desipramine or fluoxetine. The rare variant analysis was performed using whole-exome genotyping data. Network and pathway analyses were carried out with the list of significant genes.

The Kernel-Based Adaptive Cluster method identified functional rare variants in 35 genes significantly associated with treatment remission (False discovery rate, FDR <0.01). Pathway analysis of these genes supports the involvement of the following gene ontology processes olfactory/sensory transduction, regulation of response to cytokine stimulus, and meiotic cell cycleprocess.

Our study did not have a placebo arm. We were not able to use antidepressant blood level as a covariate.
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