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The effects of UVR on the skin include tanning, carcinogenesis, immunomodulation, and synthesis of vitamin D, among others. Melanocortin 1 receptor polymorphisms correlate with skin pigmentation, UV sensitivity, and skin cancer risk. This article reviews pathways through which UVR induces cutaneous stress and the pigmentation response. Modulators of the UV tanning pathway include sunscreen agents, MC1R activators, adenylate cyclase activators, phosphodiesterase 4D3 inhibitors, T oligos, and MITF regulators such as histone deacetylase (HDAC)-inhibitors. UVR, as one of the most ubiquitous carcinogens, represents both a challenge and enormous opportunity in skin cancer prevention.

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Objective Individuals with Parkinson disease are more likely to develop melanoma, and melanoma patients are reciprocally at higher risk of developing Parkinson disease. Melanoma is strongly tied to red hair/fair skin, a phenotype of loss-of-function polymorphisms in the MC1R (melanocortin 1 receptor) gene. Loss-of-function variants of MC1R have also been linked to increased risk of Parkinson disease. The present study is to investigate the role of MC1R in dopaminergic neurons in vivo. Methods Genetic and pharmacological approaches were employed to manipulate MC1R, and nigrostriatal dopaminergic integrity was determined by comprehensive behavioral, neurochemical, and neuropathological measures. Results MC1Re/e mice, which carry an inactivating mutation of MC1R and mimic the human redhead phenotype, have compromised nigrostriatal dopaminergic neuronal integrity, and they are more susceptible to dopaminergic neuron toxins 6-hydroxydopamine and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Furthermore, a selective MC1R agonist protects against MPTP-induced dopaminergic neurotoxicity. Interpretation Our findings reveal a protective role of MC1R in the nigrostriatal dopaminergic system, and they provide a rationale for MC1R as a potential therapeutic target for Parkinson disease. Together with its established role in melanoma, MC1R may represent a common pathogenic pathway for melanoma and Parkinson disease.

The variational quantum eigensolver (or VQE), first developed by Peruzzo et al. (Nature Comm.5, 4213 (2014)), has received significant attention from the research community in recent years. It uses the variational principle to compute the ground state energy of a Hamiltonian, a problem that is central to quantum chemistry and condensed matter physics. Conventional

Psoriasis is a common autoimmune and chronic inflammatory skin disorder globally affecting 0.51–11.43% of adults. Inflammation-associated cell death in keratinocytes plays a key role in the process of integrate inflammatory cascade in psoriasis. Necroptosis is a regulated necrotic cell death mediated by receptor interacting protein kinase 1 (RIPK1), RIPK3, and mixed lineage kinase domain-like pseudokinase (MLKL), which participates in many human inflammatory diseases. However, the mechanism and function of programmed necrosis in psoriasis is not well-illustrated. In the current study, we provide evidence for the involvement of necroptosis in psoriasis. RIPK1 and MLKL were significantly upregulated and localized in all layers of the epidermis in human psoriatic lesions, while RIPK3 and phosphorylated MLKL were mainly expressed in keratinocytes, which located in the upper layers. Increased tendency of necroptosis was also found in IMQ-induced psoriasiform skin of mice. Further, we discovered that both the inhibitor of RIPK1 R-7-Cl-O-Necrostatin-1 (Nec-1s) and MLKL-inhibitor necrosulfonamide (NSA) suppressed necroptosis in HaCaT cells and IMQ mouse models, powerfully blocked IMQ-induced inflammatory responses in vivo, and significantly downregulated the production of inflammatory factors like IL-1β, IL-6, IL-17A, IL-23a, CXCL1, and CCL20. These findings promote the development of new therapies for the treatment of necroptosis-activated pathologies for psoriasis.

SummaryPlasma is an ionized gas that consists of positively and negatively charged particles, neutral atoms, and photons. Recent developments in plasma sources have made it possible to generate room-temperature plasma in the "open air", thus enabling the application of plasma in vivo. Using nonthermal plasma, active agents can be efficiently delivered to target cells without creating thermal damage. Also known as cold atmospheric pressure plasma (CAP), nonthermal atmospheric pressure plasma offers innovative medical applications. In this context, it has also gained wide attention in the field of dermatology. The complex and variable mixture of active agents in plasma -predominantly reactive oxygen and nitrogen species (ROS, RNS) -can control or trigger complex biochemical reactions, achieving the desired effects in a dose-dependent manner. The objective of the present review is to present potential applications of plasma in dermatology and analyze its potential mechanisms of action.

Tantalum arsenide is experimentally verified as a Weyl semimetal recently. However, it is difficult to grow large TaAs single crystals due to the decomposition prior to reaching its melting point. Here we report an improved chemical vapor transport method using iodine as an agent to get large-size, high-quality TaAs single crystals up to 1 cm. X-ray diffraction confirmed that they are tetragonal TaAs. Specific heat of TaAs was measured from 2 K to room temperature, and hence the entropy and enthalpy were obtained, which are helpful in designing the optimal growth conditions. The as-grown crystals exhibit polyhedral morphology consisting of {101}, {001}, {103}, and {112} facets. The key points in crystal growth include using tantalum in the form of foils instead of powder as the starting material, tilting ampule to enhance convections and controlling the concentration of agent iodine. These measures should be applicable to the growth of other transition metal arsenides and phosphides.