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Background: Combinational therapy such as taking tranexamic acid while using laser treatment has been proved potential efficacy by many experiments. However, there is few research which contains large samples and consistent observations. Objective: We evaluated clinical efficacy and safety of a new systemic treatment of drug‐laser‐photon therapy. Methods: Retrospective and randomized investigator‐blinded study of 75 patients with mixed type melasma was analyzed. At each visit, standardized photographs were taken using VISIA. Modified melasma area and severity index (mMASI) scores were marked using photographs by two dermatologists. Results: The mMASI score decreased significantly from 6.92 to 3.84 after the treatment. The VISIA analyze right cheek data shows: Spots (from 49.67 ± 3.43 to 56.09 ± 3.31), UV spots (from 41.39 ± 24.45 to 44.56 ± 25.86), and Brown spots (from 23.97 ± 17.89 to 28.16 ± 21.28) are statistically increased (p = 0.035, p = 0.018, p = 0.07). All patients feel varying degrees of improvement, about 10.17% felt very much improved, 30.51% felt much improved (51%–75%), 45.76% felt moderately improved (26%–50%), and 13.56% felt little improved (1%–25%). Limitations: This study was no control group. Conclusion: The efficacy and safety profile of the combination of drug‐laser‐photon therapy systemic treatment in melasma patients has been proved. It has potential possibility to become a new, reliable, widely suitable therapy strategy. [ABSTRACT FROM AUTHOR]

Abstract An amphiphilic disulfide-containing polyamidoamine was synthesized by Michael-type polyaddition reaction of piperazine to equimolar N, N′-bis(acryloyl)cystamine with 90% yield. The polycationic micelles (198 nm, 32.5 mV), prepared from the amphiphilic polyamidoamine by dialysis method, can condense foreign plasmid DNA to form nanosized polycationic micelles/DNA polyelectrolyte complexes with positive charges, which transfected 293T cells with high efficiency. Under optimized conditions, the transfection efficiencies of polycationic micelles/DNA complexes are comparable to, or even higher than that of commercially available branched PEI (Mw 25 kDa).

It is of urgency to develop novel and high-efficient visible-light photocatalysts to eliminate antibiotics and organic pollutants rapidly in sewage. Therefore, the silver molybdate/aluminum atoms-doped zinc oxide (Ag2MoO4/AZO) nanocomposite was prepared by in situ deposition, and then the Ag dots were decorated on this nanocomposite surface via photo-reduced reaction forming a multiple complementary Ag@Ag2MoO4/AZO hybrid nanocomposite. The photogenerated electrons of AZO transferred to Ag2MoO4 surface, which solved the optical instability of Ag2MoO4 material increasing the recyclability. The photocatalytic efficiency of Ag@Ag2MoO4/AZO nanocomposite still remained 90.0% after eight runs. Meanwhile, the Ag dots decorated on the Ag@Ag2MoO4/AZO nanocomposite surface decreased the band gap and broadened the visible-light absorption range, promoting the efficient separation of photogenerated carriers. Because of the synergistic complementary effect of Ag dots and AZO solid solution, the Ag@Ag2MoO4/AZO hybrid nanocomposite showed excellent photocatalytic activity on organic pollutants compared to AZO and Ag2MoO4 material (282.3% and 422.7% improvement, respectively). In addition, the gatifloxacin was completely degraded to CO2 and H2O within 40 min, indicating that the Ag@Ag2MoO4/AZO hybrid nanocomposite also has excellent application in the treatment of antibiotics. [ABSTRACT FROM AUTHOR]

Abstract Many cell death regulators physically or functionally interact with metabolic enzymes. These interactions provide insights into mechanisms of anticancer treatments from the perspective of tumor cell metabolism and apoptosis. Recent studies have shown that zinc and p53 not only induce tumor cell apoptosis, but also regulate tumor cell metabolism. However, the underlying mechanism is complex and remains unclear, making further research imperative to provide clues for future cancer treatments. In this study, we found that hexokinase 2 (HK2), which has dual metabolic and apoptotic functions, is downstream of zinc and p53 in both prostate cancer patient tissue and prostate cancer cell lines. Notably, the mitochondrial location of HK2 is crucial for its function. We demonstrate that zinc and p53 disrupt mitochondrial binding of HK2 in prostate cancer cells by phosphorylating VDAC1, which is mediated by protein kinase B (Akt) inhibition and glycogen synthase kinase 3β (GSK3β) activation. In addition, we found that zinc combined with p53 significantly inhibited tumor growth in a prostate cancer cell xenograft model. Therefore, interference of the mitochondrial localization of HK2 by zinc and p53 may provide a new treatment approach for cancer. Graphical abstract fx1 Highlights • HK2 expression is positively correlated with p53 in prostate cancer patients. • Zinc cooperates with p53 to increase HK2 expression in prostate cancer cells. • Zinc and p53 enhance GSK3β activation by inhibiting Akt. • GSK3β activation disrupts HK2 binding to VDAC1 by phosphorylating VDAC1. • Disrupting mitochondrial localization of HK2 may be a potential therapeutic target. [ABSTRACT FROM AUTHOR]

Platinum-based therapeutic strategies have been widely used in ovarian cancer treatment. However, drug resistance has greatly limited therapeutic efficacy. Recently, tolerance to cisplatin has been attributed to other factors unrelated to DNA. p62 (also known as SQSTM1) functions as a multifunctional hub participating in tumorigenesis and may be a therapeutic target. Our previous study showed that p62 was overexpressed in drug-resistant ovarian epithelial carcinoma and its inhibition increased the sensitivity to cisplatin. In this study, we demonstrate that the activity of the NF-κB signaling pathway and K63-linked ubiquitination of RIP1 was higher in cisplatin-resistant ovarian ( SKOV3/ DDP) cells compared with parental cells. In addition, cisplatin resistance could be reversed by inhibiting the expression of p62 using si RNA. Furthermore, deletion of the ZZ domain of p62 that interacts with RIP1 in SKOV3 cells markedly decreased K63-linked ubiquitination of RIP1 and inhibited the activation of the NF-κB signaling pathway. Moreover, loss of the ZZ domain from p62 led to poor proliferative capacity and high levels of apoptosis in SKOV3 cells and made them more sensitive to cisplatin treatment. Collectively, we provide evidence that p62 is implicated in the activation of NF-κB signaling that is partly dependent on RIP1. p62 promotes cell proliferation and inhibits apoptosis thus mediating drug resistance in ovarian cancer cells. [ABSTRACT FROM AUTHOR]