Objective To investigate the relationship between p62 expression,and occurrence and metastasis of nasopharyngeal carcinomas.Methods Immunohistochemical method was used to analyze p62 expression in 123 nasopharyngeal carcinoma (NPC) cases and 30 chronic nasopharyngitis cases.The clinical pathological characteristics were analyzed.Results The positive rate of p62 protein in chronic nasopharyngitis nasopharyngeal epithelium,non-metastatic NPC tissue,and metastatic NPC tissues was 13.3％,66.67％,and 84.72％,respectively,and the difference was statistically significant.The expression of p62 protein in nasopharyngeal carcinoma patients with lymph node metastasis or distant metastasis was significantly higher than non-metastatic NPC patients (P ＜ 0.01 or P ＜ 0.05).However,the expression of p62 was not related to age,gender,tumor size,and TNM stage (P ＞ 0.05).Conclusions High p62 protein expression in nasopharyngeal carcinoma tissue is closely related to the occurrence and metastasis of nasopharyngeal carcinomas.It provides good reference value to predict NPC malignancy and metastases.

The study aims at cloning the CDS fragment of erk2 gene cDNA in Inner Mongolia Cashmere Goat and analyzing its tissue-specific expression, erk2 gene cDNA was cloned by RT-PCR. The nucleotide sequence was analyzed by Blast and amino acid sequence was analyzed by online softwares SMART and Psite. The tissue-specific expression pattern of erk2 was analyzed by quantitative RT-PCR. The expression of erk2 in testis of goat was detected by Immunohistochemistry. The cloned erk2 gene cDNA (GenBank Accession No. JX569765) was 1 083 bp in length, including a complete ORF encoding 360 amino acids residues. The amino acid sequence shares 100% identity with the Bos Taurus ERK2 (Bos Taurus BC133588.1). Analysis by SMART suggests that the encoded protein contained a "TEY" structure and an S-TKc domain possessing serine/threonine kinase catalytic activity. Analysis with Psite indicates one cAMP-/cGMP-dependent protein kinase phosphorylation site, 3 protein kinase C phosphorylation sites, 5 casein kinase II phosphorylation sites, 2 protein kinases ATP-binding region signatures and one serine/threonine protein kinases active-site signature in this protein. Analysis by Psort (k-NN prediction) suggestes that this protein most probably is localized in cytoplasm. The results of quantitative RT-PCR show that the expression of erk2 mRNA was higher in heart, skin and breast, whereas lower in spleen and kidney. ERK2 protein was detected in testis by immunohistochemistry.
Amino Acid Sequence ; Animals ; China ; Cloning, Molecular ; DNA, Complementary ; genetics ; Goats ; genetics ; Male ; Mitogen-Activated Protein Kinase 1 ; genetics ; metabolism ; Molecular Sequence Data ; Real-Time Polymerase Chain Reaction ; Testis ; metabolism

Objective To explore a scientific and reasonable fiscal input mechanism for public hospitals, in order to fully leverage the policy guidance and efficiency of such funding.Methods With literature review, expert consultation and demonstration, a basic subsidy model for public hospitals was established.According to the past operation data of 4 public hospitals in Baoshan district of Shanghai, the study figured out specific subsidy standards.Results The basic subsidy for public hospitals should be determined according to the number of approved beds, the number of outpatients and emergency visits, hospital bed days, surgeries, key services, and the quality and efficiency of work.In Baoshan district, the standard reference value of subsidy for each approved bed, each outpatient and emergency visit, each bed-day, each surgical operation is 42 096 yuan, 27.9 yuan, 104.9 yuan and 244 yuan respectively.The standard value of subsidy is 100 yuan per bed for critically ill inpatients.For patients under clinical pathway management, the subsidy is 300 yuan per case, and for hospital maternal care, it is 150 yuan per person.Conclusions The basic subsidy model for public hospitals has overcome the shortcomings of fiscal input based on hospital scale or hospital workload, and established an incentive mechanism to promote the implementation of key services.These measures can improve the operation mechanism of public hospitals and encourage them to play their role of public welfare as designed.

Objective:To evaluate the effect of hydrogen on the expression of hippocampal cold-inducible RNA-binding protein (CIRP) after cardiac arrest-resuscitation in rats.Methods:Ninety clean-grade healthy male Sprague-Dawley rats, weighing 280-320 g, were randomly divided into 3 groups: sham group (group Sham, n=20), cardiac arrest-cardiopulmonary resuscitation group (group CPR, n=35), and hydrogen-rich saline group (group H 2, n=35). Cardiac arrest was induced by transoesophageal cardiac pacing followed by CPR in group CPR.Only femoral arteriovenous puncture and tracheal intubation were performed in group Sham.Hydrogen-rich saline 5 ml/kg was intraperitoneally injected immediately after recovery of spontaneous circulation (ROSC) and at 6 and 12 h after ROSC in group H 2 , while the equal volume of normal saline was given instead in the other two groups.Neuro-functional deficit was assessed using neurologic deficit scores (NDS) at 1 and 3 days after ROSC.The animals were sacrificed immediately after intubation in group Sham and at 6 h and 1, 2 and 3 days after ROSC in CPR and H 2 groups, and the hippocampal tissues were obtained to detect the expression of nuclear and cytoplasmic CIRP by Western blot. Results:Compared with group Sham, NDS was significantly decreased at each time point after ROSC in group CPR and group H 2, the expression of nuclear CIRP was significantly down-regulated at 1, 2 and 3 days after ROSC, and the expression of cytoplasmic CIRP was up-regulated at 1 and 2 days after ROSC in group CPR, and the expression of nuclear CIRP was significantly down-regulated at each time point after ROSC, and the expression of cytoplasmic CIRP was down-regulated at 2 and 3 days after ROSC in group H 2 ( P<0.05). Compared with group CPR, NDS was significantly increased at each time point after ROSC, the expression of nuclear CIRP was down-regulated at 6 h after ROSC, and the expression of cytoplasmic CIRP was down-regulated at 1 and 2 days after ROSC in group H 2 ( P<0.05). Conclusion:The nechanism by which hydrogen reduces brain injury after cardiac arrest-resuscitation may be related to down-regulating hippocampal CIRP expression in rats.

As the most aggressive breast cancer, triple-negative breast cancer (TNBC) is still incurable and very prone to metastasis. The transform growth factor β (TGF-β)-induced epithelial-mesenchymal transition (EMT) is crucially involved in the growth and metastasis of TNBC. This study reported that a natural compound isotoosendanin (ITSN) reduced TNBC metastasis by inhibiting TGF-β-induced EMT and the formation of invadopodia. ITSN can directly interact with TGF-β receptor type-1 (TGFβR1) and abrogated the kinase activity of TGFβR1, thereby blocking the TGF-β-initiated downstream signaling pathway. Moreover, the ITSN-provided inhibition on metastasis obviously disappeared in TGFβR1-overexpressed TNBC cells in vitro as well as in mice bearing TNBC cells overexpressed TGFβR1. Furthermore, Lys232 and Asp351 residues in the kinase domain of TGFβR1 were found to be crucial for the interaction of ITSN with TGFβR1. Additionally, ITSN also improved the inhibitory efficacy of programmed cell death 1 ligand 1 (PD-L1) antibody for TNBC in vivo via inhibiting the TGF-β-mediated EMT in the tumor microenvironment. Our findings not only highlight the key role of TGFβR1 in TNBC metastasis, but also provide a leading compound targeting TGFβR1 for the treatment of TNBC metastasis. Moreover, this study also points out a potential strategy for TNBC treatment by using the combined application of anti-PD-L1 with a TGFβR1 inhibitor.