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Atopic dermatitis (AD) is a chronic inflammatory skin disease with the highest incidence in the world. The main clinical manifestations are eczema-like skin lesions, pruritus and xeroderma. Recent studies have revealed that sensory neurons in the skin lesions of AD patients can interact abnormally with keratinocytes (KC) and immune cells, leading to neuroimmune disorders. Among them, there are two types of sensory neurons involved in neuroimmune disorders, including histaminergic and non-histaminergic sensory neurons. In neuroimmune disorders, KC and immune cells activate sensory neurons to induce pruritus by secreting proinflammatory cytokines such as interleukin-4 (IL-4), IL-13, IL-31, IL-33, and thymic stromal lymphopoietin, as well as chemokines such as C-X-C motif chemokine ligand 12 (CXCL12) and CXCL10. In addition, neuropeptides such as nerve growth factor, brain-derived neurotrophic factor and artemin secreted by KC and immune cells can induce overgrowth of sensory neurons, thereby promoting neuroimmune disorders. At the same time, the excessive release of neuropeptides such as calcitonin gene-related peptide and substance P by sensory neurons can act on KC and immune cells, thereby aggravating skin inflammation. In recent years, many drugs targeting neuroimmune disorders are in preclinical studies, clinical trials and other stages, or have been marketed for the treatment of AD. Among them, our research group has found that lidocaine, a local anesthetic, can target neuroimmune disorders and relieve pruritus and skin inflammation in AD patients. At present, the role of neuroimmune disorders in AD has not been systematically discussed. Based on this, this article reviews the types of sensory neurons involved in neuroimmune disorders, the role of KC, immune cells and sensory neurons in neuroimmune disorders, as well as the therapeutic strategies targeting neuroimmune disorders.

Atopic dermatitis (AD) is a chronic recurrent inflammatory skin disease characterized by intense pruritus. A satisfactory understanding of itch in AD has been proved difficult to reach and the relapsing itch is believed to be primarily a result of dysfunction of the skin barrier, dysregulation of the immune system and multiple environmental factors. Itch-scratch cycle exacerbates skin lesions, promotes inflammation and neurological disorders, and triggers the desire to continue scratching. The current methods of treatment for controlling AD pruritus symptoms include topical and systemic drugs. The exploration on the mechanisms of atopic pruritus has provided novel therapeutic targets, such as IL-4, IL-13, IL-31, JAK, IL-33. The new advances in the mechanism and treatment of itch in AD were systemically reviewed.

Objective: To analyze the clinic-pathological features, immunohistochemical phenotype and differential diagnosis of a child with fibroblastic connective tissue nevus（FCTN）. Methods: A 2-year-old girl developed bright red sclerotic plaque on her right thigh with clear boundary and irregular shape. Biopsy was performed on the lesion, and the pathological tissues were stained with HE and immunohistochemistry. The immunohistochemical phenotypes for differential diagnosis were analyzed along with literature review. Results: Histologically, the lesion was composed of bundles of bland spindle cells of fibroblastic/myofibroblastic lineage irregularly branching within the reticular dermis and along fibrous septa in the subcutis, without affecting the adnexal structures. The dermal adipocytes were entrapped by tumor cells, and elastic fibers were fragmented and decreased. Immunohistochemically, cells of FCTN were positive for CD34, and weak positive for SMA（smooth muscle actin） locally, while negative for S100, des, and low index of Ki-67(1%). Among the 45 cases reported, it was found that the patients generally had an early onset age (median 10 years old), and FCTN occured mostly in children’s trunk, head and neck, with painless spots or nodules as primary presentations. The clinic-pathological features and immunohistochemical phenotype of the patient described hereby were consistent with cases previously reported. Conclusions: FCTN is a rare variant of nevus of connective tissue, which could differentiate into myofibroblast and mechanocyte cells. Immunohistochemically, CD34 is usually positive and SMA is weakly positive in spindle cells. The FCTN should be differentiated with soft tissue tumor, such as dermatofibrosarcoma protuberans,congenital infantile fibrosarcoma and rhabdomyosarcoma.

This article discusses a rare case of primary cutaneous CD8+ aggressive epidermotropic cytotoxic T-cell lymphoma (pcAECyTCL) in a 4-year-old girl. The patient presented with non-healing cutaneous ulcers and multiple plaques on various regions of her body. The diagnosis was confirmed through clinical and histopathological features, and the patient was treated with recombinant human IFN-α2a. However, the lesions reappeared and the patient's condition rapidly deteriorated, leading to her death. The article emphasizes the importance of early diagnosis and highlights the challenges in distinguishing pcAECyTCL from other indolent types of CD8+ CTCLs. [Extracted from the article]

Linear morphea, also known as linear scleroderma, is a localized form of scleroderma characterized by the presence of lesions that follow a linear distribution pattern. Apart from the typical inflammation and fibrosis of the skin, the linear subtype of morphea often affects underlying structures such as muscles and bones, which can lead to functional limitations. Lichen striatus, a linear inflammatory skin condition, primarily affects children aged 5 to 15 years. Interestingly, both diseases can exhibit lesions that follow the lines of Blaschko. Here we report a case with linear morphea following the lines of Blaschko mimicking lichen striatus in a 4‐year‐old child. This unique case represents the first documented instance of linear morphea exhibiting a precise Blaschko pattern and being successfully treated with baricitinib. The patient received oral baricitinib at a daily dosage of 2 mg for a duration of 1 year, resulting in remarkable improvement. The majority of the lesions softened, and there was no significant disease progression or occurrence of adverse events throughout the treatment period. Recognizing linear morphea at an early stage is of utmost importance in ensuring effective treatment and preventing disfiguring sequelae. Patients suspected of lichen striatus should also be closely followed and linear morphea should be excluded during the follow‐up. The recent breakthrough in the application and the safety of baricitinib in scleroderma is also reviewed. [ABSTRACT FROM AUTHOR]

Thin films of transition metal oxides such as molybdenum oxide (MoOx) are attractive for application in silicon heterojunction solar cells for their potential to yield large short‐circuit current density. However, full control of electrical properties of thin MoOx layers must be mastered to obtain an efficient hole collector. Here, we show that the key to control the MoOx layer quality is the interface between the MoOx and the hydrogenated intrinsic amorphous silicon passivation layer underneath. By means of ab initio modelling, we demonstrate a dipole at such interface and study its minimization in terms of work function variation to enable high performance hole transport. We apply this knowledge to experimentally tailor the oxygen content in MoOx by plasma treatments (PTs). PTs act as a barrier to oxygen diffusion/reaction and result in optimal electrical properties of the MoOx hole collector. With this approach, we can thin down the MoOx thickness to 1.7 nm and demonstrate short‐circuit current density well above 40 mA/cm2 and a champion device exhibiting 23.83% conversion efficiency. [ABSTRACT FROM AUTHOR]

Excellent surface passivation induced by (i)a‐Si:H is critical to achieve high‐efficiency silicon heterojunction (SHJ) solar cells. This is key for conventional single‐junction cell applications but also for bottom cell application in tandem devices. In this study, we investigated the effects of (i)a‐Si:H deposition temperature on passivation quality and SHJ solar cell performance. At the lower end of temperatures ranging from 140°C to 200°C, it was observed with Fourier‐transform infrared spectroscopy (FTIR) that (i)a‐Si:H films are less dense, thus hindering their surface passivation capabilities. However, with additional hydrogen plasma treatments (HPTs), those (i)a‐Si:H layers deposited at lower temperatures exhibited significant improvements and better passivation qualities than their counterparts deposited at higher temperatures. On the other hand, even though we observed the highest VOCs for cells with (i)a‐Si:H deposited at the lowest temperature (140°C), the related FFs are poorer as compared to their higher temperature counterparts. The optimum trade‐off between VOC and FF for the SHJ cells was found with temperatures ranging from 160°C to 180°C, which delivered independently certified efficiencies of 23.71%. With a further improved p‐layer that enables a FF of 83.3%, an efficiency of 24.18% was achieved. Thus, our study reveals two critical requirements for optimizing the (i)a‐Si:H layers in high‐efficiency SHJ solar cells: (i) excellent surface passivation quality to reduce losses induced by interface recombination and simultaneously (ii) less‐defective (i)a‐Si:H bulk to not disrupt the charge carrier collections. [ABSTRACT FROM AUTHOR]

Photodynamic therapy (PDT) has emerged as a non-surgical, efficacious, and safe treatment for non-melanoma skin cancers, and has been reported to treat LyP in four cases (Table 1) resistant to conventional treatments. LyP lesion did not recur in the PDT-treated area.1 year310M/13Right forearmCA 4-year history of recurrent crops of red papules, nodules, and tumors. Refractory lymphomatoid papulosis successfully treated with IFN- 2a and photodynamic therapy. [Extracted from the article]

Passivating contacts are crucial for realizing high‐performance crystalline silicon solar cells. Herein, contact formation by plasma‐enhanced chemical vapor deposition (PECVD) followed by an annealing step is focused on. Poly‐SiOx passivating contacts by combining plasma‐assisted N2O‐based oxidation of silicon (PANO‐SiOx) with a thin film of phosphorus (n+) or boron (p+)‐doped hydrogenated amorphous silicon oxide (a‐SiOx:H) are manufactured. Postannealing is conducted for transitioning a‐SiOx:H into poly‐SiOx. The aim is to achieve a contact with low absorption and high‐quality passivation. It is demonstrated that by tuning the plasma oxidation process time and power, the PANO‐SiOx thickness and its passivation quality can be controlled. A higher SiO2 content is observed in PANO‐SiOx than in the nitric acid oxidation of silicon (NAOS‐SiOx) counterpart. PANO‐SiOx acts as a stronger diffusion barrier for both boron and phosphorus atoms compared to NAOS‐SiOx, affecting the dopant distribution during annealing. Implied open‐circuit voltages up to 751 and 710 mV for n+ and p+ flat symmetric samples, respectively, are demonstrated. With respect to standard thermally grown SiO2 tunneling oxide combined with (in/ex)situ‐doped low‐pressure chemical vapor deposition poly‐Si, this study presents a simple alternative for manufacturing passivating contact fully based on PECVD processes. [ABSTRACT FROM AUTHOR]