4 kinds of lectin receptors (PHA, DBA, PNA, ConA) in the tissues of a variety of lesions of the gastric mucosa are studied with the histochemical method (ABC technique) in 87 cases. The results are follows: the positive rates of 4 kinds of lectin-binding, the distribution of lectin receptors, the intensity of positiveness and the stained patterns are correlated to the histologic types and the grades of various mucosal lesions. The intensity of positive reaction of PHA, PNA and DBA shows a progressive rising, while that of ConA appears a gradual declining tendency with the change from normal gastric mucosa to intestinal metaplasia and cancer. The stained patterns of lectin are: type I is the main pattern for ConA, type I for PNA and type III for PHA and DBA .

Objective: To investigate the clinical significance of serum low-density lipoprotein receptor-related protein 6 (LRP6) level in patients with acute myocardial infarction (AMI). Methods: One hundred and fifty patients with AMI were selected as the AMI group and 150 patients with suspected coronary heart disease without coronary artery stenosis were selected as control group from January 2017 to December 2018 in Quzhou People′s Hospital of Zhejiang. The serum LRP6 levels were determined by Western blot. The serum B-type brain natriuretic peptide (BNP) and cardiac troponin I (cTnI) levels were determined by enzyme-linked immunosorbent assay (ELISA). Results: The levels of total cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C) in AMI group were higher than those in the control group [(4.42 ± 0.79) mmol/L vs. (3.79 ± 0.82) mmol/L, (1.52 ± 0.33) mmol/L vs. (1.37 ± 0.38) mmol/L, (3.15 ± 0.34) mmol/L vs. (2.91 ± 0.28) mmol/L], and the level of high-density lipoprotein cholesterol (HDL-C) was lower than that in control group [(0.95 ± 0.26) mmol/L vs. (1.21 ± 0.33) mmol/L], and there were significant differences (P<0.05). The level of serum LRP6 and left ventricular ejection fractionin in AMI group were lower than those in control group [0.12 ± 0.03 vs. 0.38 ± 0.07, (53.27 ± 6.89)% vs. (66.82 ± 7.35)%], and the BNP and cTnI levels were higher than those in control group [(78.16 ± 5.27) ng/L vs. (7.13 ± 1.24) ng/L, (125.83 ± 3.26) ng/L vs.(0.71 ± 0.24) ng/L], and there were significant differences (P<0.05). The serum LRP6 level was negatively correlated with LDL-C, BNP, cTnI and SYNTAX scores (r=- 0.587, - 0.523, - 0.542, - 0.583, P<0.05), and was positively correlated with left ventricular ejection fraction (r=0.515, P<0.05). Conclusions Serum LRP6 level is decreased in patients with AMI. Serum LRP6 is closely related to the severity of AMI and the extent of coronary artery disease.

[摘 要] 目的：探讨circFBXL5通过靶向miR-515-5p影响膀胱癌T24细胞的增殖、迁移、侵袭及其分子机制。方法： 收集2020年4月至2020年6月间在苏州市中西医结合医院手术切除的41例膀胱癌组织及其癌旁组织，采用qPCR法检测circFBXL5、miR-515-5p的表达；双荧光素酶报告实验验证circFBXL5与miR-515-5p之间的靶向关系，体外培养人膀胱癌T24细胞，实验分为si-NC组、si-circFBXL5组、anti-miR-NC+si-circFBXL5组和si-circFBXL5+anti-miR-515-5p组；MTT法、细胞克隆形成实验、FCM、Transwell实验和WB法分别检测转染后T24细胞的增殖、细胞克隆形成、迁移、侵袭和凋亡及BAX、Bcl-2蛋白水平。结果：膀胱癌组织中circFBXL5呈高表达，miR-515-5p呈低表达（均P<0.05）；circFBXL5靶向且负向调控miR-515-5p的表达；敲减circFBXL5后T24细胞的增殖抑制率、凋亡率和BAX蛋白水平均显著增高（均P<0.05），细胞克隆形成数和迁移、侵袭细胞数均显著减少（均P<0.05），Bcl-2蛋白水平显著降低（P<0.05）；同时敲减circFBXL5和miR-515-5p可部分逆转敲减circFBXL5对T24细胞增殖的抑制作用。结论：circFBXL5通过调控miR-515-5p表达影响膀胱癌T24细胞的增殖、迁移、侵袭，circFBXL5和miR-515-5p可能膀胱癌治疗的潜在分子靶标。

Adipose tissue is a promising target for treating obesity and metabolic diseases. However, pharmacological agents usually fail to effectively engage adipocytes due to their extraordinarily large size and insufficient vascularization, especially in obese subjects. We have previously shown that during cold exposure, connexin43 (Cx43) gap junctions are induced and activated to connect neighboring adipocytes to share limited sympathetic neuronal input amongst multiple cells. We reason the same mechanism may be leveraged to improve the efficacy of various pharmacological agents that target adipose tissue. Using an adipose tissue-specific Cx43 overexpression mouse model, we demonstrate effectiveness in connecting adipocytes to augment metabolic efficacy of the β ₃-adrenergic receptor agonist Mirabegron and FGF21. Additionally, combing those molecules with the Cx43 gap junction channel activator danegaptide shows a similar enhanced efficacy. In light of these findings, we propose a model in which connecting adipocytes via Cx43 gap junction channels primes adipose tissue to pharmacological agents designed to engage it. Thus, Cx43 gap junction activators hold great potential for combination with additional agents targeting adipose tissue.