Objective:To evaluate the efficacy and safety of baricitinib combined with ruxolitinib cream in the treatment of progressive nonsegmental vitiligo.Methods:Clinical data were retrospectively collected from patients with progressive nonsegmental vitiligo in Boao Super Hospital. All the patients were treated with oral baricitinib daily (2 mg/day for patients weighing ≤ 50 kg; 4 mg/day for those > 50 kg) in combination with topical application of ruxolitinib cream twice daily for 24 consecutive weeks. Disease severity was assessed using the facial vitiligo area scoring index (F-VASI) and total body VASI (T-VASI) at baseline, week 12, and week 24. Adverse reactions were monitored throughout the treatment course.Results:Six patients with progressive nonsegmental vitiligo were collected, including 3 males and 3 females, aged 26 - 42 years, with the disease duration ranging from 0.5 to 25 years. At week 12, 3 patients achieved a 50% ~ < 75% improvement in facial vitiligo lesions (F-VASI 50), 1 patient achieved F-VASI 75 (75% ~ < 90% improvement), and 1 patient achieved T-VASI 50; at week 24, 4 patients achieved F-VASI 50, 1 patient achieved F-VASI 75, 1 patient achieved F-VASI 90 (≥ 90% improvement), and 3 patients achieved T-VASI 50. During the treatment, upper respiratory infection occurred in 1 patient, acne in 1 patient, pruritus in 2 patients, elevation of total cholesterol levels in 2 patients, and increase of high-density lipoprotein levels in 2 patients. No severe adverse events were observed during the treatment.Conclusion:The combination therapy with baricitinib and ruxolitinib cream may have potential efficacy and safety in the treatment of progressive nonsegmental vitiligo.

Objective:To evaluate the efficacy and safety of baricitinib combined with ruxolitinib cream in the treatment of progressive nonsegmental vitiligo.Methods:Clinical data were retrospectively collected from patients with progressive nonsegmental vitiligo in Boao Super Hospital. All the patients were treated with oral baricitinib daily (2 mg/day for patients weighing ≤ 50 kg; 4 mg/day for those > 50 kg) in combination with topical application of ruxolitinib cream twice daily for 24 consecutive weeks. Disease severity was assessed using the facial vitiligo area scoring index (F-VASI) and total body VASI (T-VASI) at baseline, week 12, and week 24. Adverse reactions were monitored throughout the treatment course.Results:Six patients with progressive nonsegmental vitiligo were collected, including 3 males and 3 females, aged 26 - 42 years, with the disease duration ranging from 0.5 to 25 years. At week 12, 3 patients achieved a 50% ~ < 75% improvement in facial vitiligo lesions (F-VASI 50), 1 patient achieved F-VASI 75 (75% ~ < 90% improvement), and 1 patient achieved T-VASI 50; at week 24, 4 patients achieved F-VASI 50, 1 patient achieved F-VASI 75, 1 patient achieved F-VASI 90 (≥ 90% improvement), and 3 patients achieved T-VASI 50. During the treatment, upper respiratory infection occurred in 1 patient, acne in 1 patient, pruritus in 2 patients, elevation of total cholesterol levels in 2 patients, and increase of high-density lipoprotein levels in 2 patients. No severe adverse events were observed during the treatment.Conclusion:The combination therapy with baricitinib and ruxolitinib cream may have potential efficacy and safety in the treatment of progressive nonsegmental vitiligo.

Brain size abnormality is correlated with an increased frequency of autism spectrum disorder (ASD) in offspring. Genetic analysis indicates that heterozygous mutations of the WD repeat domain 62 (WDR62) are associated with ASD. However, biological evidence is still lacking. Our study showed that Wdr62 knockout (KO) led to reduced brain size with impaired learning and memory, as well as ASD-like behaviors in mice. Interestingly, Wdr62 Nex-cKO mice (depletion of WDR62 in differentiated neurons) had a largely normal brain size but with aberrant social interactions and repetitive behaviors. WDR62 regulated dendritic spinogenesis and excitatory synaptic transmission in cortical pyramidal neurons. Finally, we revealed that retinoic acid gavages significantly alleviated ASD-like behaviors in mice with WDR62 haploinsufficiency, probably by complementing the expression of ASD and synapse-related genes. Our findings provide a new perspective on the relationship between the microcephaly gene WDR62 and ASD etiology that will benefit clinical diagnosis and intervention of ASD.
Mice ; Animals ; Microcephaly/genetics* ; Autistic Disorder/metabolism* ; Autism Spectrum Disorder/metabolism* ; Nerve Tissue Proteins/metabolism* ; Brain/metabolism* ; Mice, Knockout ; Cell Cycle Proteins/metabolism*

Objective:To analysis the expression of CD7 in NK/T-cell lymphoma as well as study the correlations between CD7 and clinical survival and prognosis.Methods:The clinical and pathological indicators of 112 NKTCL patients who were admitted to or consulted at the First Affiliated Hospital of Zhengzhou University between May 2008 and December 2019 were analyzed retrospectively. The CD7 expression in the tumor tissues was detected using immunohistochemistry staining, and the influence of CD7 expression on the survival and prognosis in the patients was analyzed.Results:The CD7 expression rate was 84.82% in 112 NKTCL patients, and its expression was not influenced by sex, age, and the primary site. An analysis of the complete clinical data of 72 patients showed that the CD7 expression was significantly correlated with the PINK score, tumor metastasis, and peripheral blood EBV-DNA level. However, the Ann Arbor stage, bone marrow involvement, B symptoms, IPI/aaIPI score, Ki-67, EBER, TIA-1, Granzyme B, LDH, and β 2-MG were not associated with the CD7 expression. The 1-year, 3-year, and 5-year overall survival (OS) rates of the 72 patients were 81.2%, 61.8%, and 58.8%, respectively, and the progression-free survival (PFS) rates were 53.5%, 29.4%, and 24.0%, respectively. The median overall survival (median-OS, mOS) was 81 mon, and the median progression-free survival (median-PFS, mPFS) was 14 mon. The 3-year OS rates in the CD7-positive group and the CD7-negative group were 58.1% and 83.9%, respectively, ( P>0.05) . The 3-year PFS rates were 21.7% and 51.9%, respectively ( P<0.05) . The univariate analysis showed that age, primary tumor site, Ann Arbor stage, IPI/aaIPI score, PINK score, LDH, β 2-microglobulin, EBV-DNA, Ki-67, and CD7 influenced patient prognosis. The multivariate analysis showed that Ann Arbor stage and CD7 were independent prognostic factors for PFS, while PINK score and Ki-67 were independent prognostic factors for OS. Conclusions:The expression rate of CD7 in NKTCL was high and was closely related to poor patient prognosis. The patients with high levels of EBV-DNA, metastatic disease, or high PINK score were more likely to express CD7.