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BACKGROUND@#Chronic noise exposure is one environmental hazard that is associated with genetic susceptibility factors that increase Alzheimer's disease (AD) pathogenesis. However, the comprehensive understanding of the link between chronic noise stress and AD is limited. Herein, we investigated the effects of chronic noise exposure on AD-like changes in senescence-accelerated mouse prone 8 (SAMP8).@*METHODS@#A total of 30 male SAMP8 mice were randomly divided into the noise-exposed group, the control group, and aging group (positive controls), and mice in the exposure group were exposed to 98 dB SPL white noise for 30 consecutive days. Transcriptome analysis and AD-like neuropathology of hippocampus were examined by RNA sequencing and immunoblotting. Enzyme-linked immunosorbent assay and real-time PCR were used to further determine the differential gene expression and explore the underlying mechanisms of chronic noise exposure in relation to AD at the genome level.@*RESULTS@#Chronic noise exposure led to amyloid beta accumulation and increased the hyperphosphorylation of tau at the Ser202 and Ser404 sites in young SAMP8 mice; similar observations were noted in aging SAMP8 mice. We identified 21 protein-coding transcripts that were differentially expressed: 6 were downregulated and 15 were upregulated after chronic noise exposure; 8 genes were related to AD. qPCR results indicated that the expression of Arc, Egr1, Egr2, Fos, Nauk1, and Per2 were significantly high in the noise exposure group. These outcomes mirrored the results of the RNA sequencing data.@*CONCLUSIONS@#These findings further revealed that chronic noise exposure exacerbated aging-like impairment in the hippocampus of the SAMP8 mice and that the protein-coding transcripts discovered in the study may be key candidate regulators involved in environment-gene interactions.
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Objective@#To study the effects of different holding gun methods and gun weight on health when standing guard, and propose a way to support the health of long-term standing guard soldiers.@*Methods@#We created different percentile mannequins by Classic JACK, and adjusted the standing guard posture based on its standards for soldiers. The pressure on lumbar L4/L5 and moment on ankles and knees were analysied for different holding gun methods and gun weight. Then the mathematical models of joint load, gun weight and body mass index were studied by multiple regression analysis.@*Results@#Holding gun methods and gun weight influence the force characteristics on ankles, knees and lumbar L4/L5. Holding gun with a brace and hands applying downward force -2 kgf could significantly reduce lumbar L4/L5 pressure. When the hand force is -5, -3, -4, -3, -2, -1, 0, 1, 2 kgf, and the weight of the gun is 0, Lumbar vertebrae L4/L5 joint pressure of people with different body mass index(P1, P5, P55, P95, P99) are the smallest, respectively 269, 281, 321, 408, 444 N, and the same change trend occurs when the weight of the gun is 2, 4, and 8 kg.The moment on ankles and knees were less with the same holding gun method and the hands downward force ranged from 0 to -4 kgf, and the higher the body mass index is, the more the hands downward force needed to make the moment on ankles and knees zero. That is, the moment on ankles could be zero when the hands downward force ranged from -1 to -3 kgf, the moment on knees could be zero when the hands downward force ranged from -1.1 to -3.7 kgf.@*Conclusion@#To reduce the pressure on lumbar L4/L5 and moment on ankles and knees, so as to cut down occupational risk of long-standing operation, we advise the long-term standing guard soldiers holding gun with a brace and hands applying downward force -2 kgf.
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Objective To observe the effects of Coptidis Rhizoma on gastrointestinal motility functions, MTL and GAS in spleen-deficiency rats; To explore the dose-effect mechanism of “invigorating stomach” and “spoiling appetite”.Methods Fatigue and troublesome were used to establish exhausted spleen-deficiency models. 60 SD rats were randomly divided into blank control group, model group, positive medicine group, Coptidis Rhizoma high-, medium- and low-dose groups, with 10 rats in each group. Each medication group received relevant medicine for gavage, while the blank control group and model group received normal saline for gavage, once a day for 14 d. The general gastrointestinal motility functions, MTL and GAS of rats in each group were observed.Results Compared with blank control group, the gastric residual rate of model group was significantly higher; small intestinal propulsion rate, MTL, and GAS were significantly lower (P<0.05,P<0.01). Compared with model group, the gastric residual rate in Coptidis Rhizoma low-dose group was significantly lower; small intestinal propulsion rate, MTL and GAS increased significantly (P<0.05,P<0.01); small intestinal propulsion rate and MTL in Coptidis Rhizoma high-dose group were significantly lower (P<0.05).Conclusion High-doseCoptidis Rhizoma leads to “spoiling appetite”, and low-dose Coptidis Rhizoma leads to “invigorating stomach”, which may be related to adjusting gastrointestinal motility directly or adjusting the secretion of gastrointestinal hormones.
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Objective To investigate the carotid arterial stiffness in patients with coronary slow flow ( CSF) .Methods forty-five patients with CSF and Forty -five persons having normal coronary arteries ( NCA) detected by coronary angiography with a similar distri-bution of risk factors were recruited .Stiffness parameter (β), pressure-strain elastic modulus (Ep), arterial compliance (AC) and lo-cal pulse-wave velocity (PWV) were obtained at the level of bilateral carotid artery by a real time echo -tracking system.Serum levels of high-sensitivity C-reactive protein ( hs-CRP) were measured in two groups of subjects .Linear regression analysis were performed to evaluate the correlation between hs -CRP and the parameters of the carotid artery stiffness .Results We found that stiffness parameter (β), Ep and PWV were significantly higher in CSF group those that of control group (β:11.80 ±3.19 vs 9.70 ±3.76,P<0.01;Ep:149.90 ±44.47 vs 130.10 ±41.56,P<0.05;PWV:7.40 ±0.84 vs 7.00 ±1.08,P<0.05), AC was lower than that of control group (0.640 ±0.180 vs 0.760 ±0.192 ,P<0.01).The levels of high-sensitivity C-reactive protein (hs-CRP) was significantly higher in CSF group than that of control group (13.90 ±10.66 vs 9.30 ±6.33,P<0.05).The levels of hs-CRP was positively correlated with theβ(r=0.272,P=0.005), Ep(r=0.411,P=0.003), and PWV(r=0.452,P=0.001), but negatively correlated with AC (r=-0.293,P=0.025).Conclusion Echo-tracking technology is a simple practical method to evaluate carotid artery stiffness in patients with CSF and correlation well with coronary slow flow and artery stiffness .
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Objective To observe the influence of Cichorii extract on uric acid and lipid metabolic disorder and discuss the mechanism. Methods Quails were divided randomly into 5 groups by weight:normal group,model group,positive control group and Cichorii extract high and low dosage group,15 quails in each group. The normal group was fed with the common feeder,and the other groups were fed with the yeast powder. Positive control group was given Benzbromarone 20 mg/(kg?d). Cichorii extract high and low dosage group were given Cichorii extract 15,10 g/(kg?d) respectively. Normal and model group were given distilled water. UA,TG,FFA,TC,HDL,LDL level and XOD,ADA,GD activity related to uric acid metabolism were determined after 7 days. Results Compared with normal group,UA,TG,FFA of model group was significantly higher and HDL was significantly lower. Compared with model,Cichorii extract decreased UA,TG,FFA significantly. GD activity in model group increased significantly. Cichorii extract decreased GD activity. There was no significant variance of XOD and ADA activity in each group. Conclusion Cichorii extract had obvious effect in adjusting uric acid and lipid metabolic disorder. The possible mechanism was by decreasing GD activity and decreasing UA,FFA level.
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AIM: To observe the levels of triglyceridemia(TG),uricemia(UA),glycemia(GLU),the activity of 3-glyceraldehyde phosphate dehydrogenase(GAPDH) in blood and the gene expression in the liver in the animal model of hypertriglyceridemia,hyperuricemia and hyperglycemia.METHODS: SD rats were randomly divided into three groups,control group,fructose group,fructose and fenofibrate treated group.Rats in control group were fed with standard chow.Rats in fructose group were fed with high fructose diet.Rats in fructose and fenofibrate group were fed with high fructose diet,and treated with fenofibrate 100 mg?kg-1?d-1 by intragastric administration at the same time.Rats in control group and fructose group were given distilled water by intragastric administration.The levels of TG,UA and GLU were detected.Improved method was used to measure the activity of GAPDH.Quanti Gene technology was applied to determine the transcriptional level of GAPDH mRNA.RESULTS: During 7-28 d,the level of TG in fructose group was significantly and persistently high.During 14-28 d,the level of UA was higher.The level of GLU higher than that in control group was only observed at 28th day.The GAPDH activity change in blood and the expression in liver were significantly lower than that in norma1 during 7-28 d.Fenofibrate had the effect on reducing TG only at 7th day and reduced the level of GLU significantly at 28th day.Fenofibrate also increased the GAPDH activity in blood and the expression in liver at 7th day.CONCLUSION: ① The level of TG is significantly and persistently high in the early days by feeding with excessive fructose.The levels of UA and GLU are higher with the time cause of the model development.② The significantly higher level of TG,UA and GLU may be correlated with the reduction of the GAPDH activity in blood and the expression in liver.③ Fenofibrate has the effect of reducing the TG level only in the condition of hypertriglyceridemia,but not in the condition of accompanying hyperuricemia and hyperglycemia.④ The mechanism of reducing the TG level by fenofibrate may be correlated with the increase in GAPDH activity in blood and the expression in liver.