A 54-year-old woman presented with a five-year history of malaise with weight loss and arthralgia of both knee joints. Six months prior to the presentation, an indurated nodule developed at the site of an old scar on the temporal side of left eyebrow. Subsequently, erythema and nodules spread over the trunk and extremities, especially at the sites of old scars on the hands. Physical examination showed bilateral axillary lymphadenectasis, a plaque at the site of an old scar on the temporal side of left eyebrow, a subcutaneous mass at the extensor aspect of the right upper arm, multiple dark-erythematous nodules at the site of scars on the left hand and both soles, few small erythematous papules scattered on the left forearm and trunk. The serum angiotensin converting enzyme concentration was high (82 kU/L). Computer tomography of thorax showed multiple obscure tubercles in both lungs and swollen lymph nodes in mediastina and axillary fossa, but no hilum pulmonis lymphadenectasis was observed. Histopathology revealed non-caseating granulomas with multinucleated giant cells. Neither acid-fast bacilli nor PAS staining was positive. A diagnosis of scar sarcoidosis was established. The lesions obviously improved after one-month treatment with oral methylprednisolone. This case represents a rare subtype of sarcoidosis that arose in old sears and clinically manifests as scar, nodules,plaques, subcutaneous masses and papules. The reactivation of old scars, which manifests as erythematous swelling and nodules, may highly suggest the diagnosis of sarcoidosis.

ObjectiveTo determine the protein and mRNA expression levels of interleukin-17 (IL-17) and proportions of Th17 cells in peripheral blood of patients with atopic dermatitis (AD),and to analyze their clinical significance.MethodsVenous blood samples were obtained from 63 patients with AD and 30 normal human controls.Enzyme linked immunosorbent assay was performed to measure the plasma level of IL-17 protein,real time fluorescence reverse transcription (RT)-PCR to detect the mRNA expression level of IL-17 in peripheral blood,flow cytometry to determine the percentage of Th17 cells in peripheral blood mononuclear cells(PBMCs).Spearman's rank correlation analysis was performed to assess the relationship of peripheral blood Th17 cell percentage and IL-17 levels with disease severity in patients with AD.Results The percentage of Th17 cells in PBMCs was 1.83％ ± 0.47％ in patients with acute AD,significantly higher than that in normal human controls (0.85％ ± 0.45％,t =4.128,P ＜ 0.01 ) and in patients with chronic AD ( 1.12％ ± 0.69％,t =2.439,P ＜ 0.05).There was a significant increase in the plasma level (98.37 vs.63.75 ng/L,U =168,P ＜ 0.05) and mRNA expression level of IL-17 in peripheral blood in patients with AD compared with normal controls.Both the Th17 cell percentage and plasma IL-17 level were positively correlated with eczema area and severity index(EASI) score in patients with AD (r =0.681,P ＜ 0.01;r =0.427,P ＜ 0.05).ConclusionsThere is an elevated proportion of Th17 cells and an abnormal expression of IL-17 protein and mRNA in peripheral blood from patients with acute AD,which are positively correlated with disease severity,implicating the possible roles of IL-17 and Th17 cells in the pathogenesis of AD.

Many people affected by fragile X syndrome (FXS) and autism spectrum disorders have sensory processing deficits, such as hypersensitivity to auditory, tactile, and visual stimuli. Like FXS in humans, loss of Fmr1 in rodents also cause sensory, behavioral, and cognitive deficits. However, the neural mechanisms underlying sensory impairment, especially vision impairment, remain unclear. It remains elusive whether the visual processing deficits originate from corrupted inputs, impaired perception in the primary sensory cortex, or altered integration in the higher cortex, and there is no effective treatment. In this study, we used a genetic knockout mouse model (Fmr1^KO), in vivo imaging, and behavioral measurements to show that the loss of Fmr1 impaired signal processing in the primary visual cortex (V1). Specifically, Fmr1^KO mice showed enhanced responses to low-intensity stimuli but normal responses to high-intensity stimuli. This abnormality was accompanied by enhancements in local network connectivity in V1 microcircuits and increased dendritic complexity of V1 neurons. These effects were ameliorated by the acute application of GABA_A receptor activators, which enhanced the activity of inhibitory neurons, or by reintroducing Fmr1 gene expression in knockout V1 neurons in both juvenile and young-adult mice. Overall, V1 plays an important role in the visual abnormalities of Fmr1^KO mice and it could be possible to rescue the sensory disturbances in developed FXS and autism patients.
Animals ; Disease Models, Animal ; Fragile X Mental Retardation Protein/metabolism* ; Fragile X Syndrome/metabolism* ; Humans ; Mice ; Mice, Knockout ; Neurons/metabolism*