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Primary immunodeficiency diseases (PID) is a congenital disease caused by single gene germline mutation related to the immune system. PID patients have immune dysregulation, and are susceptible to infectious diseases, autoimmune diseases, autoimmune diseases, allergic diseases, and malignant tumors. The first symptom of some PID patients is atopic disease, therefore they go to the department of allergy, department of pediatrics and other relevant departments. How to identify and diagnose PID in allergic patients, to reduce diagnosis delay and prevent disease aggravation are the abilities that allergists, pediatricians, and doctors in other relevant departments need to master. This article summarizes the warning signs of PID in allergic patients and the mechanism of allergy combined with PID, and then summarizes the common types of PID in allergic patients, the evaluation, treatment and prevention in patients with PID and allergy.原发性免疫缺陷病（primary immunodeficiency diseases，PID）是由免疫系统相关的单基因胚系突变导致的先天性疾病。PID患者存在免疫过程失调，对感染性疾病、自身免疫病、自身炎症性疾病、过敏性疾病和恶性肿瘤的易感性增加。部分PID患者以可疑过敏表现（如湿疹样皮损）为首发症状，或因严重的过敏性疾病就诊于变态反应科。如何在有可疑表现的过敏患者中识别并诊断出PID、减少诊断延误、预防疾病加重，是变态反应科、儿科及相关临床科室医生需要掌握的能力。本文总结归纳过敏患者中提示PID的警示征象和过敏合并PID的机制，同时概述过敏患者中常见的PID类型、PID伴发过敏患者的评估、治疗及预防。.

A young male patient with abdominal pain and fever was diagnosed as acute hyper-triglyceridemicpancreatitis is clear. During the recovery of pancreatitis, the patient developed acute acalculous cholecystitis, as well as carbapenem-resistant Enterobacter infection and Cytomegaloviremia, and had anaphylaxis for several times after the use of antibiotics, which cannot be completely explained by drug allergy. This paper analyzes the possible causes of multiple diseases in the same patient in detail.本文报道1例以腹痛、发热起病的青年男性患者，临床诊断高甘油三酯血症性急性胰腺炎明确。在胰腺炎恢复过程中，患者出现急性非结石性胆囊炎、耐碳青霉烯类抗生素的大肠杆菌感染及巨细胞病毒血症，并在使用抗生素后多次发生严重过敏反应，但亦不能完全以药物过敏解释。本文通过对同一患者中出现多种疾病的病程进行详细分析，分析相互之间的可能原因。.

In the present study the melatonin receptor 1A gene (MTNR1A) was proposed to be a candidate gene for egg production in Yangzhou geese. A total of 210 goose blood samples were collected to investigate the association of the MTNR1A gene with the number of eggs produced. Using a direct sequencing method, a single nucleotide polymorphism (SNP; g.177G>C) was detected in the 5' regulatory region of the MTNR1A gene (Genbank ss1985399687). Two alleles (G and C) and three genotypes were identified. Association analysis results showed that the g.177G>C SNP significantly affected the level of egg production within a 34-week egg-laying period (P

Methyl-CpG-binding domain protein 2, a target gene of miR-221and miR-222, plays a crucial role in a large body of human cancers. In this study, we aim to explore the mechanism by which miR-221/222 promotes cervical cancer.We have analyzed mRNA expression of MeCP2 and MBD2 in cervical cancer tissues by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and examined the expression of miR-221/222 in C33A, HeLa, and CaSki cells by Western blot.We found that the expression levels of MBD2 and MeCP2 were significantly reduced in cervical cancer samples as detected by the analysis of MeCP2 in matched tumor-normal samples of patients with cervical cancer, indicating a reduction in a significant percentage of patients. At the same time, we found that miR-221 and miR-222, which targeted MBD2, were upregulated in cervical cancer samples. To further elucidate the relation between miR-221/222 and MBD2, we used a lot of cell lines such as C33A, HeLa, and CaSki. Surprisingly, we found that the expression levels of MBD2 and MeCP2 were significantly lower in HeLa and CaSki than in C33A, as detected by qRT-PCR. Western blot analysis of MeCP2 of HeLa and CaSki was significantly lower than in C33A. MiR-221/222 was significantly higher in HeLa and CaSki than in C33A by qRT-PCR. The knockdown of miR-221/222 in HeLa and CaSki resulted in the downregulation of miR-221/222 levels, which rescued the expression levels of MBD2 and MeCP2 in HeLa and CaSki. However, transfection of miR-221/222 on C33A could upregulate the expression levels of miR-221/222 and decrease the expression levels of MBD2 and MeCP2.Our results demonstrate that the upregulated miR-221/222 promotes cervical cancer by repressing MBD2 and MeCP2.

Wnt/β-catenin pathway plays a critical role in modulating embryonic development, cell growth, and differentiation. The over-expression of β-catenin activates this pathway and up-regulates expression of matrix metalloproteinase-13 (MMP-13), and promotes matrix degradation and occurrence of osteoarthritis (OA). This study aims to explore the effect of miR-320 expression in OA chondrocyte and underlying mechanisms.Chondrocyte tissues from OA patients and normal individuals were collected for the detection of expression levels of miR-320, β-catenin, MMP-13, and alpha-1 chain of type II collagen (COL2A1). Dual luciferase reporter assay was performed to test targeted regulation between miR-320 and β-catenin. IL-1β was used to simulate in vitro cultured chondrocytes, which were transfected with miR-320 mimic and/or si-β-catenin, followed by quantification of miR-320, β-catenin, MMP-13, and COL2A1.In chondrocytes of OA patients, expression of microRNA (miR)-320 is decreased. Bioinformatics analysis revealed complementary binding sites between miR-320 and β-catenin. Compared to control group, increasing levels of β-catenin and MMP-13 expression with reduction of miR-320 and COL2A1 expressions were observed in OA chondrocytes. Transfection of miR-320 mimic and/or si-β-catenin depressed expression of β-catenin and MMP-13 inside chondrocytes, accompanied with elevation of COL2A1 expression.MiR-320 expression in OA chondrocyte is decreased, accompanied with up regulation of β-catenin and MMP-13. MiR-320 can inhibit β-catenin and MMP-13 expressions, elevates COL2A1 expression, which provides novel insights for the treatment of osteoarthritis.

We investigated the effect of progranulin (PGRN) expression on the proliferation and senescence of cervical cancer cells. PGRN small interfering RNA (siRNA) was introduced into the SiHa and HeLa cell lines of human cervical carcinoma using liposome-mediated transfection. The expression levels of PGRN in each cell line after transfection of PGRN siRNA were detected by reverse transcription-polymerase chain reaction (RT-PCR). Senescence in the cell lines was detected using the β-galactosidase-staining test, and proliferation was detected by clone formation. The RT-PCR assay showed that the expression of PGRN in all of the cell lines transfected with PGRN siRNA markedly decreased. In the clone-forming test, compared with the control group, the colony-forming ability in all cell lines decreased significantly after transfection with PGRN siRNA. The β-galactosidase-staining experiments showed that the phenomenon of cell aging in the PGRN interference group was more obvious than in the control group. After the cervical cancer cells had been transfected with PGRN siRNA, cell senescence was accelerated and clone-forming ability was markedly reduced. This suggests that PGRN can promote the proliferation of the cervical cancer cell line; proliferation of cervical cancer cells is achieved by inhibiting their senescence.