Objective Our study aims to investigate the inhibitive effects of miR -124 on the growth of breast cancer cell MCF -7 induced by paclitaxel .Methods MTT was used to detect the growth inhibition of MCF-7 induced by paclitaxel .Flow cytometry was used to detect the effect of paclitaxel on cell cycle .Real-time quantitative PCR(qRT-PCR) was used to detect the expressive level of miR -124,while MCF -7 cells were treated with paclitaxel .MiR-124 inhibitor was transfected into MCF -7 breast cancer cells ,and growth in-hibition was detected by MTT .Results The results showed that paclitaxel could significantly inhibit the growth of breast cancer cell line MCF -7 by blocking the G2 phase.The results from qRT-PCR showed that the relative expression of miR-124 was increased when the dosage of paclitaxel was increased .When the expression of miR-124 was inhibited ,the cell growth inhibition caused by paclitaxel was also prominently decreased .Conclusion The higher expression of miR -124 in MCF-7 induced by paclitaxel was dose dependent .And miR-124 in-hibitor can significantly influence the cell growth inhibition caused by paclitaxel .These results indicat that miR -124 plays an important role in paclitaxel -induced chemotherapy drug resistance ,and provides a new direction to solve the problem .

Objective:To observe and identify the inhibitory effect of oncostatin M (OSM) combined with dacarbazine (DTIC) on mouse melanoma cells B16 in vitro and in vivo. Methods:The inhibitory effect of OSM combined with DTIC on the proliferation and apoptosis of B16 melanoma cell line B16 were determined through MTT assay and flow cytometry, respectively. The change in nu-cleus morphology of B16 cells was observed under a fluorescence microscope by Hoechst staining method. The effects of single agents OSM and DTIC, as well as OSM-DTIC joint treatments, on tumor in mice in vivo were observed by inoculating B16 cells into C57 BL of six mice. Results:The OSM, DTIC, and combined OSM-DTIC treatments inhibited the proliferation of B16 cells by (11.2±2.3)%, (25.3±4.6)%, and (32.5±3.8)%, respectively (P<0.05). Apoptosis of B16 occurred at (1.32±0.42)%, (10.64±2.13)%, and (15.86±2.76)%, respectively (P<0.05). Cell morphology showed a significant increase in nuclear fragmentation, as proven by OSM-DTIC combined treatment. In the in vivo experiment, DTIC caused an apparent inhibition on the growth of mouse melanoma compared with the control group, and the joint treatment showed that the addition of OSM enhanced the tumor suppression effect of DTIC. Conclusion: OSM combined with DTIC has a synergistic effect that inhibits proliferation and apoptosis of B16 in vitro. This approach suggests a new po-tential treatment for melanoma.

OBJECTIVETo explore the clinical value of the neonatal hearing combined with deafness gene screening.METHODSFrom February 2014 to August 2015, 1933 newborns were included in the study. We analyzed the effects of combined screening of hearing and deafness gene.RESULTSAmong all the 1933 neonates, 71.34% (1379/1933) passed and 28.66% (554/1933) failed the initial hearing screening.The hearing impairment rate was 4.14‰ (8/1933). Genetic screening mutation rate was counted. GJB2 mutation rate was 28.97‰ (56/1933). SLC26A4 mutation rate was 13.97‰ (27/1933). GJB3 mutation rate was 6.21‰ (12/1933). Mitochondrial 12 S rRNA gene mutation rate was 1.03‰ (2/1933). 1 case of 235 delc homozygous mutation did not pass the initial hearing screening and lost to follow-up rescreening. 2 cases of 12 S rRNA 1555A>G homogeneous mutations passed early hearing screening. 8 cases of auditory handicaps were all normal.CONCLUSIONDeafness gene screening can make up for the deficiencies of the universal newborn hearing screening. Joint use of both of them should complement each other and play the biggest role.

Objective To explore the changes of plasma melatonin(MT)level in hypoxic-ischemic encephalopathy(HIE)neonates,and elucidate the function of rnelatonin in the pathogenesis and the prognosis of HIE.Methods Fourty HIE neonates were divided into 2 groups,20 mild HIE neonates and 20 moderate or severe HIE ones.The femoral vein blood were collected in 48 h and on 7 d after birth in mild HIE group,and in 48 h,on 7 d and(14±4)d after birth in moderate on severe HIE group.Twenty normal term infants served as control group.The level of plasma MT was determined with enzyme-labeled immunosorbent assay.Results Compared with control group[(8.003±1.840)ng/L],The MT level in mild HIE group in 48 h after birth[(13.311±4.025)ng/L]was higher(P＜0.01),but there was no difference on 7 d[(6.605±1.269)ng/L](P＞0.05);The MT level in moderate or severe HIE group in 48 h after birth[(5.487±1.997)ng/L]was lower(P＜0.01),but it was higher on 7 d[(16.201±5.594)ng/L](P＜0.01),there was no difference on(14±4)d[(6.799±1.765)ng/L](P＞0.05).Conclusion MT may have protective action on HIE.The prognosis of HIE with rising MT level in 48 h after birth is better than that with lower MT level.

Objective: This work aimed to investigate the relationships of the serum levels of IL-17 and TGF-β with the carcinogenesis and progression of colorectal cancer (CRC), as well as the clinical significance of these serum levels. Methods: Data of 30 healthy subjects, 59 patients with simple CRC and 44 CRC patients with postoperative (post-op) metastasis were recruited in this study. The patients were respectively divided into group A (30 healthy subjects as the control group), group B (59 CRC patients without distant metastasis after surgery), and group C (44 CRC patients with post-op metastasis). The patients in each group had a mean age of 53.8 ± 20.8, 62.0 ± 11.8, and 64.0 ± 15.7 years, respectively. All patients were confirmed by pathological diagnosis. The serum levels of IL-17 and TGF-β were measured by enzyme-linked immunosorbent assay. All quantitative data were analyzed using SPSS 13.0. Results: The IL-17 serum level was significantly higher in groups B and C than in group A. The preoperative (pre-op) serum level of IL-17 was significantly higher than the post-op serum level in group B (P<0.05). No significant difference was observed in the TGF-β serum levels between groups A and B, as well as between the pre-op and post-op serum levels in group B (P>0.05). However, the TGF-β serum level in group C was significantly higher than that in groups A and B (P<0.05). No significant correlation was observed in the serum level IL-17 or TGF-β between colon and rectum cancers in groups B and C. Conclusion: The serum level of IL-17 is significantly correlated with that of CRC. The serum level IL-17 increases with the aggravation of CRC and increased tumor burden. A strong correlation exists between the serum level of TGF-β and metastasis of CRC. Cytokine IL-17 and TGF-β may play an important role in the progression and metastasis of CRC.

Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is an inflammatory lung injury induced by a variety of factors, and these diseases are associated with high rates of mortality due to the lack of effective treatments. Based on the latest research in ALI/ARDS, it is widely accepted that generalized inflammatory responses play a critical role in initiating and developing process of ALI/ARDS. We make a brief review on the immune-pathogenesis and the signaling pathways of ALI/ARDS from the perspective of inflammation, thereby helping develop novel therapeutic strategy for treatment of patients with ALI/ARDS.

Objective To investigate the effects of lncRNA FENDRR on the proliferation, migration, invasion and apoptosis of LUSC H226 cells and its molecular mechanism. Methods The expression levels of FENDRR in normal lung epithelial cells BEAS, lung adenocarcinoma A549 and H1299 cells and LUSC H226 cells were detected by qRT-PCR. H226 cells were transfected with FENDRR-siRNA as the experimental group, or with FENDRR-siNC as a negative control group. Cell proliferation was detected by CCK-8 assay. Cell migration and invasion were detected by Transwell assay. Cell apoptosis was detected by flow cytometry. The protein expression levels of MEK, p-MEK, ERK and p-ERK were determined by Western blot. Results FENDRR levels in H226 cells were significantly lower than those in normal lung epithelial cells. Compared with the negative control group, the knockdown of FENDRR could significantly promote the proliferation, migration and invasion of H226 cells, inhibit the cell apoptosis, and increase the protein levels of p-MEK and p-ERK. The addition of ERK inhibitor U0126 rescued the effect of FENDRR knockdown on H226 cells. Conclusions The knockdown of lncRNA FENDRR can promote the proliferation, migration and inhibit the apoptosis of H226 cells through ERK/MAPK pathway.

OBJECTIVETo explore the effect of recombinant human soluble CD(40) ligand (rhsCD(40)L) and CD(40)L cDNA transfected cell (CD(40)L-TC) on the behavior of malignant B lymphocytes, and investigate the possibility of using rhsCD(40)L as a new bio-factor in tumor immunotherapy.

METHODrhsCD(40)L and CD(40)L-TC were obtained by gene recombinant techniques. Multiple myeloma cell lines, XG2, XG7, U266 and 8226, B-lymphoma cell lines, Raji and Daudi were selected to detect responses to rhsCD(40)L and CD(40)L-TC stimulation. Cell growth curve, cell cycle, early apoptosis as well as membrane surface molecules on these cell lines were analyzed.

RESULTS(1) The expression levels of CD(40) molecule on malignant B lymphocytes showed heterogeneity. High level of CD(40) on XG2, moderate on 8266, Raji, and Daudi, and no expression on U266 and XG7 were detected. The rhsCD(40)L stimulation gave rise to a typical homo-type cell aggregation of XG2 and Daudi. Meanwhile, at least 10 to 20 of CD(40)(+) XG2 or CD(40)(+) Daudi cells were found adherent to one pre-treat ed CD(40)L-TC. (2) Co-incubation with rhsCD(40)L (5 micro g/ml), or CD(40)L-TC (tumor cell: CD(40) = 5:1) resulted in a significant inhibition of in vitro cell growth of XG2, Raji and Daudi, with G(1)-phase arrest for XG2 and G(2)-phase for Raji and Daudi. These two kinds of CD(40) stimulators induced XG2, Raji and Daudi cells to apoptosis in vitro. The apoptotic rate for XG2 was 23.3% (rhsCD(40)L) and 18.8% (CD(40)L-TC), for Daudi 14.2% and 15.9%, and for Raji 11.6% and 8.9% respectively. (3) Phenotype analysis showed that CD(95) expression levels were significantly up-regulated on XG2, Raji and Daudi after stimulation with rhsCD(40)L or CD(40)L-TC, and CD(80) and CD(18) expression levels on Raji were respectively enhanced and decreased.

CONCLUSIONThe abilities to directly inhibit XG2, Daudi and Raji cell proliferation, to induce themapoptosis, as well as to up-regulate immune co-stimulator molecule CD(80) expression on Raji cells would make rhsCD(40)L a potential bio-factor for tumor immuno-therapy.

B-Lymphocytes ; drug effects ; metabolism ; pathology ; CD40 Antigens ; metabolism ; CD40 Ligand ; genetics ; metabolism ; pharmacology ; Cell Division ; drug effects ; Coculture Techniques ; DNA, Complementary ; genetics ; Humans ; Lymphoma, B-Cell ; metabolism ; pathology ; Recombinant Proteins ; pharmacology ; Time Factors ; Transfection ; Tumor Cells, Cultured ; drug effects

OBJECTIVE: To explore the genetic basis for a child featuring delayed intellectual development. METHODS: The child and his parents were subjected to conventional G-banding karyotyping and single nucleotide polymorphism array (SNP-array) analysis. Suspected copy number variations (CNVs) were verified in both parents. RESULTS: No karyotypic abnormality was found with the child and his parents. SNP-array results for both parents were normal. The child was found to harbor a de novo 172 kb deletion at 18q21.2 with a physical position of 52 957 042-53 129 237. The deletion only involved one OMIM gene, namely TCF4, resulting in removal of its exons 6 to 8. CONCLUSION The SNP-array assay has facilitated with the diagnosis of this child. Deletion of 18q21.2 region probably accounts for the Pitt-Hopkins syndrome (PTHS) in this patient.
Child ; Chromosome Deletion ; Chromosomes, Human, Pair 18 ; genetics ; DNA Copy Number Variations ; Developmental Disabilities ; genetics ; Facies ; Humans ; Hyperventilation ; genetics ; Intellectual Disability ; genetics ; Phenotype ; Transcription Factor 4 ; genetics

Objective:To investigate the effects of β-glucan combined with agonistic anti-CD40 monoclonal antibody (5C11) on the immune functions of dendritic cells (DCs) and the possible molecular mechanism.Methods:Mononuclear cells were separated from fresh concentrated white cells (granulocytes) of healthy subjects using Ficoll density gradient centrifugation, and induced by GM-CSF and IL-4 to differentiate into immature DCs. Following various stimulation (5C11 alone, β-glucan alone, 5C11 combined with β-glucan), flow cytometry was used to detect the expression of CD40, CD80, CD83, CD86 and MHC-Ⅱ molecule HLA-DR on the surface of DCs. ELISA was used to detect the secretion of cytokines including IL-12, IL-6, TNF-α and IL-10. Western blot was used to detect the phosphorylation of proteins related to MAPK signaling pathway.Results:Flow cytometry suggested that β-glucan significantly induced the expression of co-stimulatory molecule CD40 on the surface of DCs ( P<0.05). After the DCs were co-stimulated with β-glucan and 5C11, CD80, CD83 and CD86 expression were further significantly increased, and a strong synergistic effect on CD83 expression, a key marker of DC maturation, was observed ( P<0.01). ELISA showed that β-glucan combined with 5C11 could significantly promote the secretion of cytokines such as IL-12, IL-6 and TNF-α by DCs, and have a synergistic effect on the secretion of IL-12, a critical cytokine in regulating DC functions ( P<0.01). Western blot indicated that the phosphorylation of p38 MAPK and p44/42 MAPK in DCs was increased significantly after combined treatment, and the phosphorylation started earlier and lasted longer compared to that in DCs stimulated with 5C11 or β-glucan alone ( P<0.01). Conclusions:This study suggested that β-glucan combined with 5C11 had a synergistic effect on promoting the maturation and improving the immune functions of DCs, providing a new strategy for the preparation of anti-tumor DC vaccines.