Wongvalenzuela2663

enterica Typhimurium SL1344 serve as a reference point for much of the discussion and, hopefully, as a resource for readers and for future experiments to address open questions raised in this review.Background Melanin in the skin is the defense against the harmful UV radiation, which is considered as one of the major risk factors for skin cancer. The compound 7,8-dimethoxycoumarin (DMC, C11H10O₄), a natural coumarin molecule present in several medicinal plants, possesses antioxidant and anti-inflammatory activities. However, the mechanism underlying its effects on melanogenesis in melanocytes is unclear. Therefore, we investigated the effect of DMC on melanogenesis activation in B16F10 melanoma cells. Methods We examined the cytotoxic range of DMC on B16F10 melanoma cells and increased effects of melanogenesis, and intracellular tyrosinase activity. In addition, regulation mechanisms were assessed by Western blot analysis. Results The results showed that DMC significantly increased melanin content and tyrosinase activity in the cells without being cytotoxic. Furthermore, DMC stimulated the expression of tyrosinase, TRP-1, TRP-2, and MITF thereby activating melanin production and Akt phosphorylation was increased in the Akt signaling pathway. on the contrary, interfering with the phosphorylation of ERK in the MAPKs pathway. Conclusions These results suggest that DMC may serve as a candidate for potential melanin-producing activator and anti-gray hair applications.The anti-inflammatory effects of Rg3 on the hypertrophic scar (HS) formation remain relatively obscure. Hence, this study aimed to explore the anti-inflammatory effects of Rg3 on the HS formation using a rabbit ear model and we assessed the involvement of the NF-κ B/IκB signaling pathway in this process. We constructed the Newland white rabbit ear HS model and treated it with Rg3. Using histological analyses, we evaluated scar hypertrophy based on the hematoxylin and eosin staining. The degree of scarring was evaluated using the scar elevation index (SEI). In addition, collagen I and collagen III expression levels were assessed by immunohistochemistry, while fibroblast apoptosis was examined using TUNEL assays. While MPO, IL-1β, IL-6, and TNF-α concentrations were quantified using ELISA, NF-κB and p-IκB activities were respectively measured using electrophoretic mobility shift assays (EMSAs) and western blots. SEI measurements and histological characteristics revealed that Rg3 could suppress the HS formation. Moreover, Rg3 could inhibit the HS formation by decreasing collagen I and collagen III synthesis and inducing fibroblast apoptosis. Besides, Rg3 treatment markedly inhibited the inflammatory cytokine production and ameliorated neutrophil infiltration. Notably, this study revealed that Rg3 inhibited NF-κB activation and the activity of p-IκB. Furthermore, this study suggested that the ability of Rg3 to decrease the scar formation might result from its ability to inhibit inflammation by modulating the NF-κB/IκB signaling. Overall, the findings of this study could support the use of Rg3 to prevent the HS formation.An octahedral Pt (IV) prodrug, Cis-wog, containing a wogonin derivative as a bioactive axial ligand was designed and prepared to suppress DDR (DNA damage repair)-related proteins. In vitro biological studies indicated that a Pt (IV) prodrug with axially functional groups (Cis-wog) showed cytotoxicity superior to cisplatin and reversed its resistance against two pairs of cisplatin sensitive and resistant cell lines. Further mechanistic research revealed that the powerful antitumor activity of Cis-wog resulted from its suppression of JWA and its multi-interaction with XRCC1 to repair DNA single strand breaks (SSBs) caused by the introduction of wogonin. It is concluded that Cis-wog is a promising cytotoxic agent, which could be used for enhancing the antitumor activity of its corresponding Pt(II)-based drugs and reversing cisplatin resistance via decaying JWA-mediated SSBs repair pathways and inducing apoptosis.MicroRNA-181c (miR-181c) has been reported to be highly expressed in the brain, but downregulated in acute ischemic stroke patients. However, the underlying mechanism of miR-181c in regulating cerebral ischemic injury (I/R) remains poorly understood. The aim of this study was to explore the molecular basis of miR-181c in regulating cerebral I/R. It was found that the overexpression of miR-181c mediated by recombinant adeno-associated virus (AAV) vector infection significantly promoted neuron death induced by oxygen-glucose deprivation (OGD)/ reoxygenation in hippocampal neuron, whereas the inhibition of miR-181c provided protective effects against OGD/reoxygenation-induced cell death. In addition, c-Fos expression was decreased and increased though overexpression or inhibition of miR-181c. c-Fos was further determined to a putative target of miR-181c by dual-luciferase reporter assay. miR-181c overexpression also inhibited the expression of the downstream gene of c-Fos, including AP-1 and NFATc1, whereas the inhibition of miR-181c upregulated the expression of AP-1 and NFATc1 in neurons after OGD/reoxygenation. Interestingly, c-Fos siRNA apparently abolished the protective effect of anti-miR-181c on OGD/reoxygenation-induced cell death. These observations determine that downregulated miR-181c ameliorates I/R via increasing the expression of c-Fos and its downstream genes, which will provide a new and promising therapeutic target for cerebral I/R.Background/aim In the convalescent rehabilitation ward, many elderly patients undergo rehabilitation. Histamine-2 receptor antagonists (H₂RA), which is a one of the acid secretion inhibitors, is frequently prescribed for the patients as a peptic ulcer prevention measure. At present, H₂RA are reported as being associated with factors that reduce cognitive function. However, little is known about the relationship H₂RA and rehabilitation outcome. Therefore, this study examined the relationship between H₂RA use and Functional Independence Measure (FIM) gain, which determines rehabilitation outcomes for patients admitted to the convalescent rehabilitation ward. check details Patients and methods We retrospectively investigated FIM gain on discharge by both the administration group (H₂RA (+)) (n = 118) and non-administration group (H₂RA (-)) (n = 118). Results The FIM gain scores of Motor FIM total, Cognition FIM total, and Total FIM were significantly lower in H₂RA (+) than in H₂RA (-) (Motor FIM total 8.0 [4.0-16.0] [Inter-Quartile Range] vs.