Effect of SOCS3 on lung injury in rats with severe acute pancreatitis through regulating JAK2/STAT3 signaling pathway.

OBJECTIVE: To explore the effect of suppressor of cytokine signaling 3 (SOCS3) on the lung injury in rats with severe acute pancreatitis (SAP) by regulating the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway. MATERIALS AND METHODS: Sprague-Dawley rats were divided into control group (n=20) and SAP model group (established via injection of 5% sodium taurocholate, n=40). Then, SOCS3 was overexpressed using the adenovirus in 20 rats in SAP model group. The serum amylase (AMY) was detected, whether the transfection was successful was verified via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR), the hepatic function indexes were detected, the pathological changes were observed using hematoxylin-eosin (HE) staining, and the wet/dry weight ratio (W/D) was calculated. Moreover, the content of serum inflammatory factors was detected via enzyme-linked immunosorbent assay (ELISA) and the expression levels of JAK2/STAT3 signaling pathway genes and proteins were detected through RT-PCR and Western blotting. RESULTS: The content of AMY in SAP model group was significantly increased, indicating the successful modeling. SOCS3 was significantly increased in transfection group, suggesting that the transfection efficiency was significant. The content of alanine aminotransferase (ALT),  and aspartate aminotransferase (AST) in SOCS3 transfection group was significantly lower than in model group. According to the histopathological observation, there were lung injury, pulmonary edema, hemorrhage, severe inflammatory response, and alveolar congestion in SAP model group. There were almost no pathological changes in SOCS3 transfection group. In SOCS3 transfection group, the content of serum interleukin-6 (IL-6), IL-18 and tumor necrosis factor-α (TNF-α), the mRNA and protein expressions of IL-6, JAK2, and STAT3 were all remarkably declined. CONCLUSIONS: SOCS3 inhibits the activation of the JAK2/STAT3 pathway and the increase of inflammatory factors, promoting the repair of lung injury in SAP rats.

[Screening for hotspot mutations associated with genetic hearing impairment in pregnant women and subsequent prenatal diagnosis in high risk pregnancies].

Objective: To screen for hotspot gene mutations associated with genetic deafness in Chinese pregnant women, and to perform risk assessment and prenatal diagnosis in high-risk families. Methods: Between November 2012 and October 2017, 26 117 pregnant women were screened by molecular hybridization microarray for 9 hot-spot mutations in 4 hereditary deafness related genes (GJB2 c. 35 del G, c. 176_191 del 16 bp, c. 235 del G, c. 299_300 del AT, GJB3 c. 538 C>T, SLC26A4 c. 2168 A>G, IVS 7-2 A>G, mitochondrial DNA 12S rRNA m. 1494 C>T, m. 1555 A>G). Genotype analysis was carried out in husbands of women carrying mutations, and prenatal diagnosis was carried out in the fetuses with high risk of deafness. Results: Among all women tested, 1 208(4.63%) were carriers of genetic deafness mutations, 7 with hearing impairment were affected by homozygous or compound heterozygous mutations, 51 were mitochondrial gene mutation carriers, 103 were carriers of GJB3 c. 538 C>T heterozygous mutation, 1 026 were carriers of GJB2 or SLC26A4 heterozygous mutations, and 21 carried heterozygous mutations in two genes simultaneously. In 394 families, the husbands accepted gene sequence testing, and 27 in which were determined as carriers of mutations in identical genes as their wives. Among which, 18 families received prenatal diagnosis, and 5 fetuses were diagnosed as hereditary deafness. In 9 families who did not receive prenatal diagnosis, 1 neonate was diagnosed as compound heterozygote after delivery. Conclusion: In order to prevent birth defects with congenital hearing problems, it is effective to provide screening for hotspot mutations in pregnant women and to perform prenatal diagnosis on high risk pregnancies.

Genetic variability of ERCC1 and ERCC2 genes involved in the nucleotide excision repair pathway influences the treatment outcome of gastric cancer.

We conducted a prospective study to investigate whether ERCC1 rs11615 and rs3212986 and ERCC2 rs13181 and rs1799793 gene polymorphisms could serve as potential biomarkers for the prognosis of gastric cancer. Between January 2010 and December 2012, 246 patients with pathologically proven gastric cancer who were receiving platinum-based chemotherapy were recruited from the First Affiliated Hospital of Guangxi Medical University. The genotyping of the gene polymorphisms was conducted using the polymerase chain reaction coupled with restriction fragment length polymorphism. By logistic regression analysis, we found that the AA genotype of ERCC1 rs3212986 was associated with lower rates of complete remission and partial remission following chemotherapy in gastric cancer patients, and the OR (95%CI) was 0.19 (0.06-0.60). We found that the AA genotype of rs3212986 was correlated with higher risk of death from gastric cancer according to the Cox proportional hazards model, and the adjusted HR (95%CI) was 1.60 (0.81-3.16). However, we found no association between ERCC1 rs11615, ERCC2 rs13181, and ERCC2 rs1799793 and overall survival of gastric cancer. In conclusion, the results of the present retrospective study indicate that the ERCC1 rs3212986 gene polymorphism has a significant effect on the pharmacokinetics and treatment outcome of gastric cancer.

Magnetic properties in Co and Mn-doped ZnO powders and thin films.

Zn0.86Co0.14O powder and thin films were prepared by standard solid-state reaction processes and radio-frequency (RF) magnetron sputtering. Magnetic measurements indicate that the powder is paramagnetic for temperatures above 3 K, while the thin films annealed in vacuum are ferromagnetic at room temperature. The saturated magnetization was found to be about 0.6 microB/Co, while the coercive force was found to be 200 Oe at room temperature. The very similar results were also obtained in Zn0.96Mn0.04O powder and thin films. Such different results for the powder and thin films indicate that growth conditions and defects play an important role in producing ferromagnetism.