[Status and Influencing Factors of Hypertension in the Elderly Aged 60 and Above in Mianyang].

Objective To understand the prevalence and influencing factors of hypertension among the elderly aged 60 years and above in Mianyang City,Sichuan Province,so as to provide clues for targeted prevention and control of hypertension. Methods A total of 115 775 permanent residents aged 60 and above screened out from Mianyang demonstration sites from October 2017 to April 2019 were investigated by questionnaire and physical examination,and the data of personal basic information,lifestyle,body height,body weight,waist circumference,and blood pressure were collected.SPSS 22.0 was used for descriptive analysis,single factor analysis,and Logistic regression analysis. Results The prevalence rate of hypertension in the elderly aged 60 years and above in Mianyang was 50.60%.Specifically,the prevalence rates of hypertension in men and women were 50.27% and 50.85%,respectively.The prevalence rate of hypertension increased with the increase in age([Formula: see text]=370.199,P<0001).Multivariate Logistic regression analysis showed that the independent risk factors of hypertension included age of 70-79 years(OR=1.327,95%CI=1.292-1.363,P<0.001),the age of 80 years and above(OR=1.455,95%CI=1.386-1.527,P<0.001),widowhood(OR=1.343,95%CI=1.296-1.392,P<0.001),divorce(OR=1.255,95%CI=1.033-1.525,P=0.022),overweight(OR=1.431,95%CI=1.391-1.473,P<0.001),obesity(OR=2.171,95%CI=2.076-2.270,P<0.001),waist-to-height ratio>0.5(OR=1.317,95%CI=1.281-1.354,P<0.001),history of diabetes(OR=1.865,95%CI=1.791-1.941,P<0.001),history of smoking(OR=1.107,95%CI=1.068-1.148,P<0.001),and history of drinking(OR=1.950,95%CI=1.894-2.009,P<0.001).Living in urban-rural fringe areas(OR=0.628,95%CI=0.594-0.664,P<0.001),education background of junior high school and above(OR=0.942,95%CI=0.912-0.974,P<0.001),and low body weight(OR=0.785,95%CI=0.742-0.830,P<0.001) were protective factors for hypertension. Conclusions More than 50% of the elderly aged 60 years and above in Mianyang suffer from hypertension.The elderly with advanced age,widowhood,divorce,overweight,obesity,waist-to-height ratio>0.5,diabetes history,smoking history,and drinking history are the high-risk groups of hypertension.

[Current situation and influencing factors of the irritability of the elderly in Mianyang City in 2019].

OBJECTIVE: To understand the current situation of irritability in the elderly in Mianyang City, explore the influencing factors of irritability. METHODS: In 2019, 823 elderly people over 60 years old in Mianyang City were selected by multi-stage random sampling, including 351(42.65%) males and 472(57.35%) females, with a median age of 67 years and a interquartile interval of 8 years. The information was collected by self rating scale of irritability, depression and anxiety and questionnaire of influencing factors of negative emotion. Questionnaire surveys were used to investigate their irritability, health status, health-related behaviors, support for the elderly, characteristics of the elderly, and mental health knowledge. Describe the detection rate of irritability, and use two-class logistic regression model to analyze the influencing factors of their depressive symptoms. RESULTS: A total of 823 elderly people in Mianyang City were investigated, 178 were found to be irritable, and the prevalence of irritability was 21.63%. The result of Logistic regression model showed that: female(OR= 1.800, 95% CI 1.223-2.627), ill within two weeks(OR = 1.611, 95% CI 1.101-2.358), hospitalized within one year(OR = 2.045, 95% CI 1.327-3.048), no spouse(OR = 0.349, 95% CI 0.209-0.582), good self-rated health(OR = 0.389, 95% CI 0.243-0.625), emotional support for children(OR = 0.549, 95% CI 0.341-0.882), the old-age care model was self care(OR = 0.649, 95% CI 0.453-0.931), they were related to irritating emotions. CONCLUSION: A certain proportion of the elderly in Mianyang City have irritability. Gender, marital status, health status, pension support and characteristics are the influencing factors of irritability.

Magnoflorine Attenuates Cerebral Ischemia-Induced Neuronal Injury via Autophagy/Sirt1/AMPK Signaling Pathway.

Ischemic stroke is a common cause of permanent disability worldwide. Magnoflorine has been discovered to have good antioxidation, immune regulation, and cardiovascular system protection functions. However, whether magnoflorine treatment protects against cerebral ischemic stroke and the mechanism of such protection remains unknown. Here, we investigated the effect of magnoflorine on the development of ischemic stroke disorder in rats. A middle cerebral artery occlusion (MCAO) model followed by 24 h reperfusion after 90 min ischemia was used. The rats were treated with magnoflorine (10 mg/kg or 20 mg/kg) for 15 consecutive days. The neurological deficit scores, cerebral infarct volume, and brain water content were measured. The neuronal density was determined using Nissl and NeuN staining. The oxidative stress levels were determined using commercial kits. Immunofluorescence staining of LC3 and western blot assay for LC3 and p62 were used to assess autophagy. Magnoflorine treatment significantly reduced the cerebral infarct volume and brain water content and improved the neurological deficit scores in the rat MCAO model. In addition, magnoflorine ameliorated neuronal injury and neuron density in the cortex of rats. Magnoflorine also prevented oxidative damage following ischemia, reflected by the decrement of nitric oxide and malondialdehyde and the increase of glutathione (GSH) and GSH peroxidase. Moreover, the fluorescence intensity of LC3 and the ratio of LC3-II to LC3-I were remarkably downregulated in ischemic rat administration of magnoflorine. Finally, the expression levels of p62, sirtuin 1 (Sirt1), and phosphorylated-adenosine monophosphate-activated protein kinase (AMPK) were upregulated with magnoflorine. Magnoflorine attenuated the cerebral ischemia-induced neuronal damage, which was possibly associated with antioxidative stress, suppression of autophagy, and activation of the Sirt1/AMPK pathway in the rats.

Time series study on the effects of daily average temperature on the mortality from respiratory diseases and circulatory diseases: a case study in Mianyang City.

BACKGROUND: Climate change caused by environmental pollution is the most important one of many environmental health hazards currently faced by human beings. In particular, the extreme temperature is an important risk factor for death from respiratory and circulatory diseases. This study aims to explore the meteorological-health effect and find out the vulnerable individuals of extreme temperature events in a less developed city in western China. METHOD: We collected the meteorological data and data of death caused by respiratory and circulatory diseases in Mianyang City from 2013 to 2019. The nonlinear distributed lag model and the generalized additive models were combined to study the influence of daily average temperature (DAT) on mortality from respiratory and circulatory diseases in different genders, ages. RESULTS: The exposure-response curves between DAT and mortality from respiratory and circulatory diseases presented a nonlinear characteristic of the "V" type. Cumulative Relative Risk of 30 days (CRR30) of deaths from respiratory diseases with 4.48 (2.98, 6.73) was higher than that from circulatory diseases with 2.77 (1.96, 3.92) at extremely low temperature, while there was no obvious difference at extremely high temperature. The health effects of low temperatures on the respiratory system of people of all ages and genders were persistent, while that of high temperatures were acute and short-term. The circulatory systems of people aged < 65 years were more susceptible to acute effects of cold temperatures, while the effects were delayed in females and people aged ≥65 years. CONCLUSION: Both low and high temperatures increased the risk of mortality from respiratory and circulatory diseases. Cold effects seemed to last longer than heat did.

UPLC-Q-TOF/MS-Based Metabolomics Approach to Reveal the Hepatotoxicity of Emodin and Detoxification of Dihydromyricetin.

Dihydromyricetin (DMY), an important flavanone found in Ampelopsis grossedentata, plays a protective role in liver injury. Our previous research found that DMY protected L02 cells against hepatotoxicity caused by emodin. In this study, serum, urine, and liver samples from rats were systematically used for biochemical analysis, pathological observation, and nontargeted metabolomics to evaluate the toxicity of emodin and DMY intervention. After oral administration of DMY, DMY may alleviate liver injury by improving liver metabolism. Approximately, 8 of 15 metabolites in rat urine and serum were significantly regulated by DMY. Metabolic pathway analysis showed that glutathione metabolism, pyrimidine metabolism, and tryptophan metabolism were the most affected pathways, and 18 proteins were predicted to be potential targets of DMY during the alleviation of liver injury induced by emodin. This research is of great significance in confirming the liver-protective effect of DMY, especially during acute liver injury caused by traditional Chinese medicine.

Design, synthesis, and antitumor activity of desmosdumotin C analogues.

Desmosdumotin C (Des C), a natural product isolated from the roots of Desmos dumosus, has shown good antitumor activity. A three dimensional quantitative structure-activity relationship (QSAR) study using the comparative molecular field analysis (CoMFA) method was performed on 32 Des C analogues. Based on the QSAR, 18 new Des C analogues were designed and synthesized. An efficient three-step synthetic strategy toward Des C and its analogues was developed from commercial available 2, 4, 6-trihydroxyacetophenone. All synthesized compounds were evaluated against a panel of human cancer cell lines and showed ED50 values ranging from 1.1 to 25.1 µΜ.

Tunneling induced absorption with competing Nonlinearities.

We investigate tunneling induced nonlinear absorption phenomena in a coupled quantum-dot system. Resonant tunneling causes constructive interference in the nonlinear absorption that leads to an increase of more than an order of magnitude over the maximum absorption in a coupled quantum dot system without tunneling. Resonant tunneling also leads to a narrowing of the linewidth of the absorption peak to a sublinewidth level. Analytical expressions show that the enhanced nonlinear absorption is largely due to the fifth-order nonlinear term. Competition between third- and fifth-order nonlinearities leads to an anomalous dispersion of the total susceptibility.

Attenuation of reserpine-induced pain/depression dyad by gentiopicroside through downregulation of GluN2B receptors in the amygdala of mice.

Epidemiological studies demonstrate that pain frequently occurs comorbid with depression. Gentiopicroside (Gent) is a secoiridoid compound isolated from Gentiana lutea that exhibits analgesic properties and inhibits the expression of GluN2B-containing N-methyl-D-aspartate (NMDA) receptors in the anterior cingulate cortex of mice. However, the effects of Gent on the reserpine-induced pain/depression dyad and its underlying mechanisms are unclear. Reserpine administration (1 mg/kg subcutaneous daily for 3 days) caused a significant decrease in the nociceptive threshold as evidenced by the reduced paw withdrawal latency in response to a radiant heat source and mechanical allodynia. Behavioral detection indicated a significant increase in immobility time during a forced swim test, as well as decreased time in the central area and total travel distance in an open field test. Furthermore, reserpinized animals exhibited increased oxidative stress. Systemic Gent administration dose-dependently ameliorated the behavioral deficits associated with reserpine-induced pain/depression dyad. At the same time, the decrease in biogenic amine levels (norepinephrine, dopamine, and serotonin) was integrated with the increase in caspase-3 levels and GluN2B-containing NMDA receptors in the amygdala of the reserpine-injected mice. Gent significantly reversed the changes in the levels of biogenic amines, caspase-3, and GluN2B-containing NMDA receptors in amygdala. However, Gent did not affect the expression of GluN2A-containing NMDA receptors. The inhibitory effects of Gent on oxidative stress were occluded by simultaneous treatment of GluN2B receptors antagonist Ro25-6981. Our study provides strong evidence that Gent inhibits reserpine-induced pain/depression dyad by downregulating GluN2B receptors in the amygdala.

A rapid automatic processing platform for bead label-assisted microarray analysis: application for genetic hearing-loss mutation detection.

Molecular diagnostics using microarrays are increasingly being used in clinical diagnosis because of their high throughput, sensitivity, and accuracy. However, standard microarray processing takes several hours and involves manual steps during hybridization, slide clean up, and imaging. Here we describe the development of an integrated platform that automates these individual steps as well as significantly shortens the processing time and improves reproducibility. The platform integrates such key elements as a microfluidic chip, flow control system, temperature control system, imaging system, and automated analysis of clinical results. Bead labeling of microarray signals required a simple imaging system and allowed continuous monitoring of the microarray processing. To demonstrate utility, the automated platform was used to genotype hereditary hearing-loss gene mutations. Compared with conventional microarray processing procedures, the platform increases the efficiency and reproducibility of hybridization, speeding microarray processing through to result analysis. The platform also continuously monitors the microarray signals, which can be used to facilitate optimization of microarray processing conditions. In addition, the modular design of the platform lends itself to development of simultaneous processing of multiple microfluidic chips. We believe the novel features of the platform will benefit its use in clinical settings in which fast, low-complexity molecular genetic testing is required.

Gentiopicroside attenuates morphine rewarding effect through downregulation of GluN2B receptors in nucleus accumbens.

AIMS: Gentiopicroside (Gent) is one of the secoiridoid compound isolated from Gentiana lutea. This compound exhibits analgesic activities and inhibits the expression of GluN2B-containing N-methyl-D-aspartate (NMDA) receptors in the anterior cingulate cortex in mice. Nucleus accumbens (NAc) is a forebrain structure known for its role in drug addiction. However, little is known about the role of Gent on morphine dependence and synaptic transmission changes in the NAc. METHODS: Conditioned place preference (CPP) test and behavioral sensitization of locomotor activity were used to investigate drug-seeking related behaviors. Brain slices containing NAc were prepared, and whole-cell patch-clamp recordings were performed to record the excitatory postsynaptic currents (EPSCs). Expression of proteins was detected by Western blot analysis. RESULTS: Systemic administration of Gent attenuated the CPP effect induced by morphine, but had no effect on morphine-induced behavioral sensitization. Gent significantly reversed overexpression of GluN2B-containing NMDA receptors and dopamine D2 receptors in NAc during the first week of morphine withdrawal. However, the compound did not affect the overexpression of GluN2A-containing NMDA receptors, GluA1, and dopamine D1 receptors. Lastly, Gent significantly reduced NMDA receptors-mediated EPSCs in the NAc. CONCLUSION: Our study provides strong evidence that Gent inhibits morphine dependence through downregulation of GluN2B-containing NMDA receptors in the NAc.

Blocking α4ß2 and α7 nicotinic acetylcholine receptors inhibits the reinstatement of morphine-induced CPP by drug priming in mice.

Investigating the interaction between nicotinic and opioid receptors is of great interest for both basic mechanistic and clinical reasons. Morphine and nicotine, two common drugs of abuse, share several behavioral and rewarding properties. However, little is known about the subtypes of nicotinic acetylcholine receptors (nAChR) in the reinstatement of morphine-induced conditioned place preference (CPP). In this study, we found that a non-specific nAChR agonist, nicotine (0.5mg/kg), had no effects on the reinstatement of morphine-induced CPP. However, we found that pretreatment with specific α(4)ß(2) and α(7) nAChR subtype antagonists, dihydroxy-ß-erithroidine (DHßE, 5mg/kg) and methyllycaconitine (MLA, 4 mg/kg), 20 min prior to administration of morphine, inhibited the reinstatement of morphine-induced CPP by drug priming in mice. Furthermore, depression of the reinstatement of morphine-induced CPP by a single DHßE or MLA treatment lasted at least three days later when the reinstatement was induced by morphine priming. The data suggest that specific nAChR subtypes, i.e., α(4)ß(2) and α(7), may contribute to the reinstatement of morphine-induced CPP by drug priming in mice.

Role of 5-HT 2B receptors in cardiomyocyte apoptosis in noradrenaline-induced cardiomyopathy in rats.

1. Serotonin (5-hydroxytryptamine; 5-HT) plays important roles in the development of cardiac hypertrophy via activation of 5-HT receptors. The aim of the present study was to investigate the role of 5-HT(2B) receptors in the development of cardiomyocyte apoptosis and hypertrophy associated with noradrenaline (NA) overload. 2. Cardiac hypertrophy was induced in rats by intraperitoneal injection of 1.5 mg/kg NA for 4 weeks. Starting from Day 15, 5-HT2B receptor antagonist SB 204741 (i.p., 0.5 or 2 mg/kg) or SDZ SER 082 (i.p., 1 mg/kg) was injected twice daily for another 14 days. Whole-cell patch-clamp techniques were used to record ionic currents in freshly isolated ventricular cardiomyocytes. Western blot and terminal deoxyribonucleotidyl transferase-mediated dUTP-digoxigenin nick end-labelling (TUNEL) assays were used to assess myocardial apoptosis. 3. Expression of 5-HT(2B) receptors was enhanced in the hypertrophic left ventricle induced by NE overload in vivo. The 5-HT(2B) receptor antagonist SB 204741 partially reversed cardiac hypertrophy induced by NE overload (P < 0.05) and decreased L-type calcium currents in ventricular cardiomyocytes (P < 0.05). In addition, SB 204741 notably attenuated myocardial apoptosis, as evidenced by downregulation of Bax and caspase 3 (P < 0.05) and upregulation of the anti-apoptotic Bcl-2 protein (P < 0.05). 4. In conclusion, the data suggest an involvement of 5-HT(2B) receptors in the generation of apoptotic events associated with cardiac remodelling during increased adrenergic stimulation.

A role of periaqueductal grey NR2B-containing NMDA receptor in mediating persistent inflammatory pain.

The midbrain periaqueductal grey (PAG) is a structure known for its roles in pain transmission and modulation. Noxious stimuli potentiate the glutamate synaptic transmission and enhance glutamate NMDA receptor expression in the PAG. However, little is known about roles of NMDA receptor subunits in the PAG in processing the persistent inflammatory pain. The present study was undertaken to investigate NR2A- and NR2B-containing NMDA receptors in the PAG and their modulation to the peripheral painful inflammation. Noxious stimuli induced by hind-paw injection of complete Freund's adjuvant (CFA) caused up-regulation of NR2B-containing NMDA receptors in the PAG, while NR2A-containing NMDA receptors were not altered. Whole-cell patch-clamp recordings revealed that NMDA receptor mediated mEPSCs were increased significantly in the PAG synapse during the chronic phases of inflammatory pain in mice. PAG local infusion of Ro 25-6981, an NR2B antagonist, notably prolonged the paw withdrawal latency to thermal radian heat stimuli bilaterally in rats. Hyperoside (Hyp), one of the flavonoids compound isolated from Rhododendron ponticum L., significantly reversed up-regulation of NR2B-containing NMDA receptors in the PAG and exhibited analgesic activities against persistent inflammatory stimuli in mice. Our findings provide strong evidence that up-regulation of NR2B-containing NMDA receptors in the PAG involves in the modulation to the peripheral persistent inflammatory pain.