Endogenous ligand of the APJ receptor Apelin-13 inhibits cell apoptosis and oxidative stress of cardiomyocytes.

The present study aimed to investigate the effect of Apelin-13 on nicotine-induced injuries of cardiomyocytes. To establish an H9c2 cell model of nicotine-induced apoptosis, H9c2 cells were divided into the control group, nicotine group, and Apelin-13+nicotine group. The apoptosis rate of H9c2 cells was then detected by flow cytometry. Later, the expressions of indicators related to apoptosis, oxidative stress, and inflammatory responses were measured via Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR). The results revealed that the expression of B-cell lymphoma-2 (Bcl-2) was remarkably down-regulated (P<0.01), while the apoptosis rate and the expressions of apoptosis-related proteins (Bcl-2-associated X protein (Bax) and cysteinyl aspartate specific proteinase-3 (Caspase-3)) were significantly up-regulated (P<0.01) in the nicotine group. However, the variation trends of Bcl-2, Bax, and Caspase-3 in the Apelin-13+nicotine group were contrary to those in the nicotine group (P<0.01). Additionally, the expressions of interleukin-1 beta (IL-1ß) and tumor necrosis factor-alpha (TNF-α) obviously declined (P<0.01), while those of superoxide dismutase 1 (SOD1) and SOD2 dramatically rose in the Apelin-13+nicotine group (P<0.01). Furthermore, Apelin-13 treatment evidently elevated the expressions of phosphorylated protein kinase B (p-AKT) and phosphorylated phosphatidylinositol 3-kinase (PI3K). In conclusion, Apelin-13 inhibits nicotine-induced apoptosis and oxidative stress in H9c2 cells via the PI3K/AKT signaling pathway.

A sensitive fluorescence biosensor based on metal ion-mediated DNAzyme activity for amplified detection of acetylcholinesterase.

In this paper, we developed an amplified fluorescence biosensor for acetylcholinesterase (AChE) activity detection by taking advantage of the mercury ion-mediated Mgzyme (Mg2+-dependent DNAzyme) activity. The catalytic activity of Mgzyme can be inhibited by the formation of T-Hg2+-T base pairs between the Mgzyme and mercury ions. Therefore, the Mgzyme-Hg2+ complex has no activity on a molecular beacon (MB) substrate, which afforded a very weak fluorescence background for this biosensor. After the addition of acetylcholinesterase (AChE), the substrate acetylthiocholine could be hydrolyzed to thiocholine, which has a stronger binding power with mercury ions than T-Hg2+-T base pairs. Therefore, the Mgzyme activity was recovered. The activated Mgzyme could hybridize with the MB substrate and undergo many cleavage cycles, resulting in a significant increase of fluorescence intensity. This biosensor displayed high sensitivity with the detection limit as low as 0.01 mU mL-1. Moreover, this design did not require complex composition and sequence design; thus it is simple and convenient. This biosensor was also applied for the determination of AChE in human blood and showed satisfactory results.

[Impact of Pax-8 gene interference on mitochondrial function and cardiomyocyte apoptosis].

OBJECTIVE: To observe the effects of paired box gene 8 (Pax-8) silencing by RNA interference on mitochondrial function and cardiomyocytes apoptosis. METHODS: The cultured H9C2 (2-1) myocytes were divided into 3 groups: short interference RNA targeting Pax-8 (Pax-8 siRNA) group, non-specific siRNA group as the negative control (NC siRNA), and blank control group (BC siRNA). Fluorescence spectrophotometry was used to detect the activity of caspase-3. RT-PCR was performed to detect mRNA expression of Bcl2 and Bax. The protein expression of Bcl2, Bax and cytoplasm of Cytochrome was examined by Western blot. Changes of ΔΨm were detected by flow cytometry.ΔΨm with JC-1 monomer/polymer ratio was calculated for measuring mitochondrial depolarization proportion. RESULTS: Compared to NC siRNA and BC siRNA group (0.075 ± 0.021, 0.072 ± 0.019), the activity of caspase-3 in Pax-8 siRNA group (0.167 ± 0.012) was significantly increased (P < 0.05); Bcl2 mRNA and protein expression in Pax-8 siRNA group (0.61 ± 0.06, 0.94 ± 0.11) were significantly downregulated compared with NC siRNA group (0.90 ± 0.070, 1.39 ± 0.15) and BC siRNA group (0.94 ± 0.087, 1.49 ± 0.20) (P < 0.05); Bax mRNA and protein expression in Pax-8 siRNA group (1.05 ± 0.10, 1.25 ± 0.12) were markedly upregulated compared with NC siRNA group (0.72 ± 0.03, 0.99 ± 0.12) and BC siRNA group (0.64 ± 0.03, 0.92 ± 0.06), P < 0.05; cytosolic cytochrome expression in Pax-8 siRNA group (0.75 ± 0.14) was significantly upregulated compared with NC siRNA group (0.51 ± 0.06) and BC siRNA group (0.48 ± 0.07) (P < 0.05); JC-1 monomer/polymer ratio in Pax-8 siRNA group (0.163 ± 0.011) was significantly increased compared with NC siRNA group (0.092 ± 0.015) and BC siRNA group (0.072 ± 0.025) (P < 0.05) indicating mitochondrial membrane potential was significantly reduced in Pax-8 siRNA group. Above parameters were similar between NC siRNA group and BC siRNA group (P > 0.05). CONCLUSION: Inhibiting Pax-8 results in enhanced cardiomyocytes apoptosis through the mitochondrial pathway.

Using Mathematical and Statistical Analysis to Investigate the Correlation between Exacerbation of Chronic Obstructive Pulmonary Disease and Risk of Subclinical Atherosclerosis.

Purpose: As the number of patients with chronic obstructive pulmonary disease continues to increase, it is increasingly important to understand the impact of cardiovascular risk on the progression of chronic obstructive pulmonary disease, which can provide guidance for clinical medication and recommendations for patient care and rehabilitation. The purpose of this study was to investigate the relationship between cardiovascular risk and the progression of chronic obstructive pulmonary disease (COPD). Methods: Selected COPD patients admitted to hospital from June 2018 to July 2020 were included in the study for prospective analysis, and patients who showed more than two instances of moderate deterioration or severe deterioration within one year before the consultation were defined as COPD patients, and all participants underwent relevant tests and assessments. Results: Multivariate correction analysis showed that a worsening phenotype improved the risk of carotid artery intima-media thickness exceeding 75% by nearly three times, and it had no relation with the degree of COPD severity and global cardiovascular risk; in addition, the relationship between a worsening phenotype and high carotid intima-media thickness (c-IMT) was more pronounced in patients under 65 years of age. Conclusions: The existence of subclinical atherosclerosis is individually related to the worsening phenotype, and the difference is more obvious in young patients. Therefore, the control of vascular risk factors in these patients should be strengthened.

Aptamer-based fluorescent sensors for the detection of cancer biomarkers.

Aptamers are short single-stranded RNA or DNA molecules that can recognize a series of targets with high affinity and specificity. Known as "chemical antibodies", aptamers have many unique merits, including ease of chemical synthesis, high chemical stability, low molecular weight, lack of immunogenicity, and ease of modification and manipulation compared to their protein counterparts. Using aptamers as the recognition groups, fluorescent aptasensors provide exciting opportunities for sensitive detection and quantification of analytes. Herein, we give an overview on the recent development of aptamer-based fluorescent sensors for the detection of cancer biomarkers. Based on various nanostructured sensor designs, we extended our discussions on sensitivity, specificity and the potential applications of aptamer-based fluorescent sensors in early diagnosis, treatment and prognosis of cancers.

Continuous renal replacement therapy for haemodynamic collapse and rhabdomyolysis induced by pheochromocytoma crisis.

Pheochromocytoma associated with pregnancy is not common. Caesarean section may induce pheochromocytoma crisis, resulting in a lethal condition. The clinical picture of pheochromocytoma crisis is extremely variable. In this report, we describe a case of severe pheochromocytoma crisis induced by caesarean section presenting with hyperpyrexia, haemodynamic collapse, muscle weakness, heart failure, and acute kidney injury. Furthermore, we report that the muscle weakness was a manifestation of rhabdomyolysis, resulting from the pheochromocytoma crisis. Standard medical therapy failed to halt the patient's rapidly deteriorating condition. Continuous renal replacement therapy removed catecholamines from the circulation, resulting in improvement of haemodynamics and abrogation of rhabdomyolysis.

[Study on risk factors of lung cancer in non-smoking women].

BACKGROUND: Lung cancer is a serious health problem in public. Its morbidity and mortality have been increasing rapidly. The mortality of lung cancer in women also increases year by year, in which most of the cases are non-smoking women, and the risk factors still are unclear. The aim of this study is to explore the effects of air pollution in room, passive smoking and other factors on risk of lung cancer. METHODS: A total of 618 newly diagnosed female patients with primary lung cancer were enrolled. The controls were selected randomly in the general population in urban districts. Two trained interviewers performed this interview face-to-face using the same questionnaire. The content of questionnaire included the characteristics of demography, history of passive smoking, exposed history of cooking fume, fuel exposure, exposed history of coal fume, history of using 'Kang', pulmonary disease history, cancer history of relatives and occupational history. RESULTS: Passive smoking in childhood was related with lung cancer of non-smoking women (OR= 1.81 , 95%CI=1.46-2.24). The exposure to the cooking fume was of great significance (OR=3.18, 95%CI= 2.55 -3.97). The relationship between coal fume and lung cancer was significant (OR=2.56, 95%CI= 1.83 -4.55). The pulmonary disease history including tuberculosis, chronic bronchitis, asthma, pneumonia, emphysema was strongly associated with lung cancer (OR=1.80, 95%CI=1.43-2.27). The family history of cancer significantly increased the risk of lung cancer (OR=2.09, 95%CI=1.46-3.00), especially the lung cancer history in the first relatives (OR=2.46, 95%CI=1.55-3.90). After adjusting other factors, logistic analysis showed that cooking fume (OR=4.11, 95%CI=2.14-7.89), the pulmonary disease history (OR= 2.05 , 95%CI=1.08-3.93), and the family history of lung cancer (OR=2.89, 95%CI=1.30-6.41) were significant factors. CONCLUSIONS: The results show that passive smoking in childhood, cooking oil exposure, coal fume exposure, pulmonary disease history including tuberculosis and family history of lung cancer are risk factors of lung cancer in non-smoking women.

Reduced expression of FXYD domain containing ion transport regulator 5 in association with hypertension.

Experimental evidence indicates that hypertension is a multifactorial disorder and that the products of several genes may contribute to its development. The aim of this study was to investigate the expression of hypertension-related genes in spontaneous hypertensive rats (SHRs). A microarray screening for hypertension-related genes was conducted in SHRs and Wistar-Kyoto (WKY) rats using total-RNA extracted from second-order mesenteric arteries and kidneys. The FXYD5 mRNA expression in vascular smooth muscle cells (VSMCs) was silenced by RNA interference (RNAi). Meanwhile, the FXYD5 mRNA overexpression in renal tubular epithelial cells (RTECs) was induced by the recombinant plasmid pcDNA3.1(+)-FXYD5. The expression of FXYD5 mRNA was found to be 14.8-fold lower in SHR rats compared to that in WKY rats (P<0.01). The levels of FXYD5 mRNA expression were the highest in kidneys of SHR 13-week-old rats when the blood pressure reached the highest levels. The down-regulated FXYD5 mRNA expression inhibited the migration of smooth muscle cells (P<0.01) and cell membrane Na⁺-K⁺-ATPase activity (P<0.01). Up-regulated FXYD5 mRNA expression enhanced the renal tubular epithelial cell membrane Na⁺-K⁺-ATPase activity (P<0.05) and cell proliferation (P<0.05). FXYD5 is related to the migration of smooth muscle cells and cell membrane Na⁺-K⁺-ATPase activity in rodents. The results of the present study suggest that FXYD5 may have profound impact on the regulation of blood pressure, and that this gene may be a potential target for anti-hypertensive therapy.