Objective To investigate the expression of vascular endothelial growth factor(VEGF) in human skin ulcer margin. Methods Ulcer biopsy samples were stained with anti VEGF and CD34 antibodies by immunohistochemistry .Results VEGF was not expressed in normal epidermis. The ulcer specimen was divided into normal,peripheral,marginal and central parts. Epidermis of normal part was not stained. VEGF was obviously expressed in peripheral upper epidermis of ulcer and lower epidermis of ulcer margin. Central part was not stained due to shedding of epidermis. And also CD34 staining demonstrated that dermal capillaries increased obviously and lumen dilated, which was marked in the periphery and the margin of ulcer. Conclusions VEGF is secreted in skin ulcerous epidermis and promotes angiogenesis and vascular dilataion which play a role in ulcer healing.

Objective To determine the content of total flavonoids and luteolin from Pteris multifida Poir. Methods The content of total flavonoids was determined by gradient elution of macroporous resin D101 and ultraviolet spectrophotometry. The content of luteolin was determined by HPLC. The analysis was performed on a RP-C18 column(4.6 mm×250 mm, 5 μm) with aceconitrile-0.2% phosphoric acid (35:65) as the mobile phase at a flow rate of 1.0 ml/min, and 30 ℃ temperature. Results The detection of wave length was set at 349 nm. The content of luteolin was 0.015%, 0.019%, 0.016%, and the content of total flavonoids was 0.015%, 0.019%, 0.016%, respectively. Conclusions The method is suitable for the determination of flavonoids componets from Pteris multifida Poir.

From the perspectives of the pathogenesis, diagnosis and treatment of cardiac graft vasculopathy(CGV), this review summarized the current understanding and cognition of its pathology, monitoring, diagnosis and treatment to provide rationales for better survivals of CGV.

Patent foramen ovale (PFO) is the most prevalent congenital heart disease, often accompanied by neurological symptoms as migraine, unexplained dizziness, and even anxiety and depression. Recent research findings indicate that the pathogenesis of neurological complications related to PFO involves abnormal embolism hypothesis, vasoactive substance hypothesis, impaired cerebral blood flow regulation and genetic inheritance. Treatments include primarily encompass pharmacological intervention and foramen ovale occlusion. This article summarizes the aforementioned research progress in order to provide clinical guidance for managing nervous system complications related to PFO.

OBJECTIVE: To explore the genetic basis of a patient with clinically suspected Loeys-Dietz syndrome (LDS). METHODS: A child who had presented at Beijing Anzhen Hospital in September 2018 was selected as the study subject. Clinical data and family history of the patient were collected, along with peripheral blood samples of the proband and his parents. Whole exome sequencing (WES) was carried out through next-generation sequencing. RESULTS: Candidate variants were searched through bioinformatic analysis focusing on genes associated with hereditary aortic aneurysms. Candidate variant was verified by Sanger sequencing. The patient was found to have cardiovascular abnormalities including early-onset aortic dilatation and coarctation, and LDS syndrome was suspected. WES revealed that he has harbored a heterozygous c.1526G>T missense variant of the TGFBR2 gene. The same variant was not found in either parent and was predicted as likely pathogenic (PM1+PM2_Supporting+ PM6+PP3+PP4) based on the guidelines from the American College for Medical Genetics and Genomics (ACMG). CONCLUSION The TGFBR2 c.1526G>T variant probably underlay the LDS in this patient and was unreported previously in China. Above finding has enriched the mutational spectrum of the TGFBR2 gene associated with the LDS and provided a basis for the genetic counseling for the patient.
Child ; Humans ; Male ; China ; Computational Biology ; Family ; Loeys-Dietz Syndrome/genetics* ; Mutation ; Receptor, Transforming Growth Factor-beta Type II/genetics*

Objective:To evaluate the effect of obesity factor on myocardial ischemia-reperfusion injury and the role of transient receptor potential ankyrin 1 (TRPA1) expression in mice.Methods:Twenty-four SPF healthy male C57BL/6J mice, aged 6-7 weeks, weighing 18-21 g, were divided into 2 groups ( n=12 each) using a random number table method: common diet group (CD group) and high fat diet group (HFD group). CD group was fed a common diet and HFD group was fed a high-fat diet supplied with 60% fat for 12 weeks, and the body weight of mice was recorded every week. The mice in CD group were then divided into 2 groups ( n=6 each) using a random number table method: CD+ solvent group (CD+ C group) and CD+ TRPA1 agonist allyl isothiocyanate (AITC) group (CD+ A group). The mice in group HFD were divided into 2 groups ( n=6 each) using a random number table method: HFD+ solvent group (HFD+ C group) and HFD+ AITC group (HFD+ A group). At 13th week, AITC 25 mg·kg -1·d -1 was intragastrically administered based on the original diet in CD+ A group and HFD+ A group, and the equal volume of solvent was given in CD+ C and HFD+ C groups. At 14th week, myocardial I/R injury was established by occlusion of the left coronary artery for 30 min followed by 120-min reperfusion. The body weight, epididymal fat, mesenteric fat and perirenal fat were recorded, and the levels of LDH, triglyceride and cholesterol in serum were determined. The percentage of myocardial infarct size was calculated. The expression of TRPA1, Bax and Bcl-2 was detected by Western blot, and the ratio of Bax/Bcl-2 was calculated. Results:Compared with CD+ C group, the expression of TRPA1 in myocardial tissues was significantly up-regulated ( P<0.05), and no significant differences were found in the other parameters in CD+ A group ( P>0.05), and the concentrations of serum triglyceride and cholesterol, body weight, weight of epididymal fat, mesenteric fat, perirenal fat and percentage of myocardial infarct size were significantly increased, the expression of TRPA1 in myocardial tissues was down-regulated, and the concentration of LDH and ratio of Bax/Bcl-2 were increased in HFD+ C group ( P<0.05). Compared with HFD+ C group, the concentrations of serum triglyceride and cholesterol, body weight, weight of epididymal fat, mesenteric fat, perirenal fat and percentage of myocardial infarct size were significantly decreased, the expression of TRPA1 in myocardial tissues was up-regulated, and the concentration of LDH and ratio of Bax/Bcl-2 were decreased in HFD+ A group ( P<0.05). Conclusions:Obesity can aggravate myocardial ischemia-reperfusion injury in mice, and the down-regulated myocardial TRPA1 expression is involved in this process.

The mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway is widely activated by a variety of extracellular stimuli, and its dysregulation is associated with the proliferation, invasion, and migration of cancer cells. ERK1/2 is located at the distal end of this pathway and rarely undergoes mutations, making it an attractive target for anticancer drug development. Currently, an increasing number of ERK1/2 inhibitors have been designed and synthesized for antitumor therapy, among which representative compounds have entered clinical trials. When ERK1/2 signal transduction is eliminated, ERK5 may provide a bypass route to rescue proliferation, and weaken the potency of ERK1/2 inhibitors. Therefore, drug research targeting ERK5 or based on the compensatory mechanism of ERK5 for ERK1/2 opens up a new way for oncotherapy. This review provides an overview of the physiological and biological functions of ERKs, focuses on the structure-activity relationships of small molecule inhibitors targeting ERKs, with a view to providing guidance for future drug design and optimization, and discusses the potential therapeutic strategies to overcome drug resistance.