As a non-coding single-strand small RNA,microRNA (miRNA) plays an important role in post-translational regulation.Its role in tumor formation has become a study hotspot.A large body of studies in dicate that the abnormal expression of miRNA involves in the occurrence and development of liver cancer,which can be used for the diagnosis,therapy and prognosis evaluation of liver cancer.In-depth exploration of the molecular mechanism of miRNA and the relationship between miRNA and liver cancer could provide novel ideas and methods for the therapy and prevention of liver cancer.

This study aims to investigate the effect of total flavones of Fructus Chorspondiatis (TFFC) on the mRNA and protein expression of collagen type I and III of rat cardiac fibroblasts (CFs) induced by angiotensin II (Ang II), and explore its anti-myocardial fibrosis molecular mechanism. Neonatal rat CFs were prepared from Sprague-Dawley rats (1-3 d after birth). The expression of collagen type I and III mRNA and protein were measured by RT-PCR and Western blotting, respectively. The study showed that stimulation of neonatal rat CFs with 100 nmol.L-1 of Ang II for 72 h resulted in a significant increase of the expression of collagen type I and III mRNA and protein. The changes on the expression level were blocked by TFFC. The results demonstrated that TFFC can inhibit myocardial fibrosis induced by Ang II in rats, which is probably associated with the collagen type I and III mRNA and protein levels up-regulated by Ang II, and TFFC was shown to decrease the expression levels of collagen type I and III mRNA and protein.

Aim To investigate the effects of maternal chronic aluminum exposure on memorial behaviour and hippocampal intracellular Ca2+ concentration ([Ca2+]i)on their offspring after the induction of LTP(long-term potentiation). Methods Adult Wistar rats (150~200 g) were exposed to aluminum by drinking distilled water, the concentration of AlCl3 is 0.015 mol?L-1(2 g?L-1) and 0.03 mol?L-1(4 g?L-1) aluminum chloride (AlCl3) solution, respectively, for 30 days prior to mating and during the whole gestation and suckling period. Their offspring were distributed into three experimental groups: control group; two exposed groups (represented by 0.2%-Al and 0.4%-Al ) administrated aluminum exposure ended at postnatal day 21. The brain tissue and blood aluminum levels were measured by Atomic absorption spectrometry (AAS). Memorial ability of the offspring was tested by Step down test.[Ca2+]i was measured by the technique of Fura-2/AM calcium ions fluorescence indicator. Results The mean aluminum content in blood and brain tissue was significantly higher than the control group(P0.05), but was significantly decreased in 0.4%-Al exposed group(P

Objective To investigate the role of scavenger receptor class B type 1 (SR-B1) signaling pathway in serum amyloid A (SAA)-induced angiogenesis in rheumatoid arthritis (RA).Methods The expression and location of SR-B1 in RA and osteoarthritis (OA) synovial tissues were observed by immunohistochemistry.And SR-B1 expression in the resting human umbilical vein endothelial cells (HUVECs) was detected by immunoflourescence.Wound repair assessement and tube formation assessement were employed to evaluate the effect on cell migration and tube formation stimulated by SAA and/or anti-SR-B1 antibody.The t-test and one-way analysis of variance (ANOVA) were used for statistical analysis.Results ① SR-B1 was significantly highly expressed in RA tissue samples (A=6 788±819) when compared to the minimal expression in OA (A =31 849±6 977,t=3.567,P＜0.01).Positive staining of SR-B1 was observed in RA synovial vascular endothelial cells and perivascular areas.② Strong staining for SR-B1 was observed in all HUVECs tested.③ Significant wound healing induced by SAA (MI=2.50±0.17) was found compared with the untreated controls (MI=1.00±0.09,q=14.38,P＜0.01),and the effects were inhibited in the presence of anti-SR-B1 antibody (MI=1.16±0.14,q=13.02,P＜0.01).④ Compared to the untreated group (branch point number:6.6±0.8),there was an enhanced formation of branched and capillary-hke tube structure followed by SAA stimulation (branch point number:19.0±1.1,q=25.04,P＜0.01) after culturing for 72 h,whereas,tube formation decreased markedly upon pre-treated with anti-SR-B1 antibody (branch point number:7.6±1.3,vs SAA,q =23.32,P＜0.01).Conclusion Our present study suggests that serum amyloid A may induce angiogenesis via SR-B1 signaling pathway in RA.

Objective To explore whether serum amyloid A (SAA) can induce the formation of neutrophil extracellular traps(NETs)in neutrophils in vitro. Methods A stable method for inducing NETs formation in vitro was established, in-cluding isolation of peripheral blood neutrophils, cell culture, and NETs formation and observation. The neutrophils were iso-lated from peripheral blood of healthy volunteers. And cells were cultured in vitro and classified into three groups:negative control (NC) group, SAA group and lipopolysaccharide (LPS) group. Following the distinct stimulation in three groups, NETs formation was observed and its percentage was calculated. The concentration of hinstone (h) 3 in supernatant was detected by ELISA. Results The purification and vitality of isolated neutrophils were both more than 95%. The nuclei of neutrophils lost their shape and spread, NETs formation was found. More NETs formation was found in SAA group than that in NC group (P < 0.05). Moreover, the concentration of h3 in supernatant was significantly higher in SAA group than that in NC group (P<0.05). Conclusion SAA can induce the formation of NETs in vitro.

Objective To explore the biological basis of TCM syndromes from a biomolecules network perspective with qi deficiency syndrome as the breakthrough point. Methods A data dictionary of neuro-endocrine-immune (NEI) related genes and qi deficiency syndrome characterization terminology thesaurus were established. Literature about qi deficiency syndrome characterization was retrieved by using Genclip, to excavate the characteristic NEI gene, thereby to explore different bioactive substances of syndromes. Results The analysis of the genetic data, showed qi deficiency related cluster with the relevance of endocrine, signal transduction, hematopoietic cell and immune deficiencies etc. It is confirmed that the intrinsic biological features of TCM syndrome can effectively identify in the NEI level. Conclusion Literature mining method as a new way to discover syndromes biological indicators has certain feasibility, and it is recommended to be further expanded into other studies on syndromes to validate the universality and reliability of this method.

Objective To discuss key points of prevention and treatment of perioperative pulmonary hypertensive crisis in patients with serious pulmonary arterial hypertension associated with ventricular septal defect. Methods Retrospectively analyzed the nursing experience of perioperative pulmonary hypertensive crisis on 31 patients with serious pulmonary arterial hypertension associated with ventricular septal defect from March to December during 2016.Among these patients,7 patients occurred pulmonary hypertensive crisis.The prevention contained avoiding oxygen lack,keeping pH alkaloid in the body, application of pulmonary vasodilator, deep sedation. Results A total of 30 cases survived the perioperative period, and were discharged from the hospital, one died. Conclusions The patients with serious pulmonary arterial hypertension had more risks during the perioperative period,the main cause of death was pulmonary hypertensive crisis during this time.So prevention of pulmonary hypertension crisis is the key point of postoperative nursing.

OBJECTIVETo determine the genetic cause for two mentally retarded patients from a family, and to correlate their genotypes with clinical phenotypes.

METHODSRoutine G-banded karyotyping analysis was performed. Single nucleotide polymorphism (SNP) microarray analysis was used to detect microdeletions or microduplications. Fluorescence in situ hybridization (FISH) was used to ascertain the origin of chromosomal abnormalities.

RESULTSBoth proband and his uncle showed a normal karyotype. SNP microarray analysis has identified a 1.147-Mb microdeletion at 16p13.3 (85 880-1 233 819) and a 2.948-Mb microduplication at 19q13.42-q13.43 (56 008 597-58 956 816). FISH analysis confirmed that the patient has inherited a derivative chromosome 16 from his father. The proband presented with mental retardation, reduced speech, and facial dysmorphism (hypertelorism, down-slanting palpebral fissure, low nasal bridge and wide gap between front teeth). His uncle presented with a milder phenotype with mental retardation.

CONCLUSIONBoth the proband and his uncle have carried a chromosome microdeletion at 16p and microduplication at 19q, which were originated from their fathers carrying a balanced t(16;19) translocation. Combined SNP microarray analysis and FISH assay are useful for the detection the copy number variations and delineation of potential structural changes, which may help with evaluation of recurrence risk for this family.

Adult ; Child ; Chromosome Deletion ; Chromosome Duplication ; Chromosomes, Human, Pair 16 ; Chromosomes, Human, Pair 19 ; Humans ; In Situ Hybridization, Fluorescence ; Intellectual Disability ; genetics ; Karyotyping ; Male ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Single Nucleotide ; Translocation, Genetic

OBJECTIVETo explore the genetic cause for two familial Angelman syndrome cases and correlation between the clinical phenotypes and their genetic basis.

METHODSKaryotyping analysis and microarray assay were carried out to exclude chromosome anomalies and uniparental disomy. The UBE3A gene was analyzed for potential point mutations, deletions, insertions and splice site mutations. Reverse transcription PCR was used to evaluate splicing mutation of the RNA transcripts.

RESULTSDNA sequencing showed the proband of family 1 has carried a novel maternal UBE3A splice acceptor site mutation, resulting in a guanine-to-cytosine transversion (IVS15-1G>C). Reverse transcription PCR revealed the proband and his mother both carried heterozygous mutant transcripts with loss of 54 and 59 nucleotides in exon 16, respectively. The proband displayed severe mental retardation, ataxia, seizures and inappropriate laughter. The siblings of family 2 has carried a novel maternal missense mutation in exon 16 of the UBE3A gene (c.2540C>T). She also presented with mental retardation, absent speech, mild ataxia and inappropriate laughter.

CONCLUSIONThe novel IVS15-1G>C and c.2540 C>T mutations of the UBE3A gene probably underlie the AS in the two families. Compared with small-scale mutations, larger fragments mutations can produce more severe phenotypes.

Angelman Syndrome ; genetics ; Female ; Humans ; Karyotyping ; Male ; Mutation ; Ubiquitin-Protein Ligases ; genetics

Objective:To investigate the effect and mechanism of circular RNA (cirRNA) on the radiosensitivity of rectal cancer.Methods:The differential circRNAs in radiosensitive and radioresistant rectal cancer tissues (biopsy tissue before radiotherapy and chemotherapy) were detected by gene sequencing, and the effect of circRNAs on the radiosensitivity of colorectal cancer cells was further confirmed in vitro. Results:Through gene sequencing of rectal cancer tissue samples, 64 circRNAs were found to be highly expressed in radiosensitive rectal cancer tissues, and 36 circRNAs were lowly expressed in radiosensitive tissues. Ten differential circRNAs were selected and verified by qRT-PCR, and it was found that circATL2 was highly expressed in radiosensitive rectal cancer tissues. In vitro cell experiment indicated that up-regulation of circATL2 expression could significantly improve the radiosensitivity of rectal cancer. Subsequently, 8 miRNAs lowly expressed in radiosensitive rectal cancer tissues were analyzed. The direct binding relationship between miR-205 and circATL2 was confirmed by dual luciferase reporter assay. The rescue experiment confirmed that circATL2 in rectal cancer regulated the radiosensitivity of rectal cancer through miR-205. Conclusion:circATL2 regulates the radiosensitivity of rectal cancer by binding to miR-205.