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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]

Although exogenous calcitonin gene-related peptide (CGRP) protects against hyperoxia-induced lung injury (HILI), the underlying mechanisms remain unclear. The present study attempted to elucidate the molecular mechanism by which CGRP protects against hyperoxia-induced alveolar cell injury. Human alveolar A549 cells were treated with 95% hyperoxia to establish a hyperoxic cell injury model. ELISA was performed to detect the CGRP secretion. Immunofluorescence, quantitative (q)PCR, and western blotting were used to detect the expression and localization of CGRP receptor (CGRPR) and transient receptor potential vanilloid 1 (TRPV1). Cell counting kit-8 and flow cytometry were used to examine the proliferation and apoptosis of treated cells. Digital calcium imaging and patch clamp were used to analyze the changes in intracellular Ca2+ signaling and membrane currents induced by CGRP in A549 cells. The mRNA and protein expression levels of Cyclin D1, proliferating cell nuclear antigen (PCNA), Bcl-2 and Bax were detected by qPCR and western blotting. The expression levels of CGRPR and TRPV1 in A549 cells were significantly downregulated by hyperoxic treatment, but there was no significant difference in CGRP release between cells cultured under normal air and hyperoxic conditions. CGRP promoted cell proliferation and inhibited apoptosis in hyperoxia, but selective inhibitors of CGRPR and TRPV1 channels could effectively attenuate these effects; TRPV1 knockdown also attenuated this effect. CGRP induced Ca2+ entry via the TRPV1 channels and enhanced the membrane non-selective currents through TRPV1 channels. The CGRP-induced increase in intracellular Ca2+ was reduced by inhibiting the phospholipase C (PLC)/protein kinase C (PKC) pathway. Moreover, PLC and PKC inhibitors attenuated the effects of CGRP in promoting cell proliferation and inhibiting apoptosis. In conclusion, exogenous CGRP acted by inversely regulating the function of TRPV1 channels in alveolar cells. Importantly, CGRP protected alveolar cells from hyperoxia-induced injury via the CGRPR/TRPV1/Ca2+ axis, which may be a potential target for the prevention and treatment of the HILI. [ABSTRACT FROM AUTHOR]

We aim to establish a formula calculating the fetal cavum septi pellucidi (CSP) width Z-scores and compare CSP width between the normal fetus and 18-trisomy fetus. In this retrospective study, 608 normal fetuses and 71 fetuses with the 18-trisomy syndrome were included. Z-scores were calculated after the acquisition of CSP images. Normal CSP width Z-scores formulae were constructed based on gestational age (GA) by performing a standard regression analysis followed by weighted regression of absolute residual values. Subsequently, the Mann–Whitney U test was used to compare the CSP width Z-scores between normal and 18-trisomy groups. Formulae calculating CSP width Z-scores were constructed. Normal fetal CSP width was significantly correlated with GA (R2 = 0.50, p <.01). In 18-trisomy group, 69% (34/49) fetuses displayed enlarged fetal CSP width and CSP width Z-scores (p <.01). The CSP width Z-scores formulae established in the current study can provide a quantitative basis for the prenatal diagnosis of 18-trisomy syndrome. Enlarged CSP width Z-score may serve as a novel prenatal diagnostic marker for the 18-trisomy syndrome. [ABSTRACT FROM AUTHOR]