Professor YAN Huimin's Experience in Pattern Identification and Treatment of Chest Tightness Variant Asthma in Children Based on the Method of Regulating Qi Movement / 中医杂志

To summarize the clinical experience of Professor YAN Huimin in pattern identification and treatment for chest tightness variant asthma in children with the method of regulating qi movement. It is believed that children's chest tightness variant asthma is mainly located in lungs and involves liver and spleen， and the core mechanism of the disease is disturbance of qi movement. On the basis of regulating qi， syndrome differentiation and treatment is conducted： for pattern of lung qi deficiency and cold， phlegm-fluid retention， the treatment is appropriate to tonify the lung and benefit qi， and warm phlegm-fluid， which commonly used in modified Yupingfeng Powder （玉屏风散） and Xiaoqinglong Decoction （小青龙汤）； for pattern of phlegm and qi binding constraint， the treatment is appropriate to soothe the liver and resolve constraint， and dissolve phlegm and dissipate masses， which commonly used in modified Banxia Houpo Decoction （半夏厚朴汤） and Jinlingzi Powder （金铃子散）； for pattern of qi deficiency and blood stasis， the treatment is appropriate to tonify the deficiency to reinforce healthy qi， and move qi to invigorate blood， which commonly used in modified Xuefu Zhuyu Decoction （血府逐瘀汤）. It is emphasised that during the treatment process， the developmental dynamics of the disease should be grasped， patterns and treat should be identified， and special attention to the changes of qi movement should be paid.

Imbalance between Th1 and Th2 cells in cord blood is influenced by maternal allergic rhinitis and associated with atopic dermatitis during the first two years of life / 中华耳鼻咽喉头颈外科杂志

<p><b>OBJECTIVE</b>To investigate the influence of maternal atopy on cord blood effector T cells and to identify these biologic markers as predictors of atopic dermatitis (AD).</p><p><b>METHODS</b>Seventy mother-infant pairs were recruited in this prospective birth cohort study. Suspected factors for allergy, including maternal allergic history, total serum IgE, and maternal age at birth, were collected. Mother peripheral blood samples and cord blood were obtained and assayed for the percentage of interferon-γ (IFN-γ) and interleukin 4 (IL-4) producing T cells(Th1 and Th2 respectively) using flow cytometry. Their offspring at the age of 2 years old were evaluated by their dermatologist whether they had AD. Statistical analysis was performed using multiple logistic regression models and receiver-operating characteristic curve was employed to predict atopic dermatitis.</p><p><b>RESULTS</b>Twenty-one allergic and 49 nonallergic mothers were recruited in this study. During the first two years of life, 15.7% children (n = 11) developed a physician-diagnosed AD (all children were the only child in the family). In group with maternal allergic rhinitis, a significantly increased percentage of Th2 was observed in peripheral blood of mother (7.10[1.18;16.1]% vs. 0.37[0.25;0.72]%, U = 10.0, P < 0.05) and cord blood of newborns (1.02[0.57;1.34]% vs. 0.21[0.15;0.42]%, U = 127.5, P < 0.05), respectively. Maternal atopic history did not affect the percentage of Th1 cells in cord blood (0.69[0.40;1.12]% vs.0.50[0.31;0.66]%, U = 361.0, P > 0.05). Children with reduced Th1/Th2 ratio in cord blood had a higher risk to develop AD (OR = 1.72, P = 0.001) . The model including Th1/Th2, maternal allergy, maternal age at birth and maternal total IgE showed high ability to discriminate children with and without AD. AUC was 0.907 (95% CI: 0.804-1.011, P < 0.001).</p><p><b>CONCLUSIONS</b>Elevated IL-4⁺CD4⁺ T cells in cord blood were of relevance with maternal allergic history. Imbalance between Th1 cell and Th2 cell at birth are associated with maternal allergy and promoted subsequent AD development.</p>

Expression of cyclin D1 and p16 protein in vulvar white lesion / 中华妇产科杂志

0.05). Conclusions Cyclin D1 and p16 are important factors modulating cell cycle. The interrupt of balance between these two factors derived from abnormal expression of cyclin D1 may be one of the causes of vulvar white lesion.