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.

Objective:To investigate the effects of 40 Hz and 70 Hz frequency flash stimulation on the ability of learning memory and autonomous exploratory in young rats.Methods:Twenty-seven SPF grade male SD rats aged 19-21 days were divided into control group (Ctr group), 40 Hz group and 70 Hz group with 9 in each group according to the random number table.The rats in Ctr group were not given flash stimulation, while rats in the 40 Hz and 70 Hz group were received 40 Hz, 70 Hz flash stimulation (1.5 h/d for 39 days), respectively.The Morris water maze experiment was used to assess the learning and memory ability of rats, and the open field experiment was used to evaluate the ability of autonomous exploratory of rats.Nissl staining was used to assess the morphology of Nissl bodies in the hippocampus CA1 region of the rats.The local field potentials (LFPs) collected from the primary visual cortex (V1 area) region by electrophysiological experiments was used to verify the synchronization of flash evoked neural oscillations.SPSS 23.0 software was used for statistical analysis.The repeated measures ANOVA and one-way ANOVA were used to analyze normal distribution measurement data, and LSD and Tamhane tests were used for further pairwise comparison.The Kruskal-Wallis test was used for non-normal distribution measurement data.Results:(1) The flash stimulation of 40 Hz and 70 Hz both can effectively caused synchronization of neural oscillations in the primary visual cortex of healthy young rats.(2) The results of repeated measures ANOVA analysis showed that there was no interaction effect of grouping and time in the escape latency of young rats in the Morris water maze positioning navigation phase( F=1.326, P>0.05 ). The escape latency had time main effect ( F=40.025, P<0.05), but no grouping main effect ( F=2.039, P>0.05). With the increase of learning days, the escape latency of young rats in each group decreased significantly.There was no interaction effect of grouping and time in the total distance of young rats ( F=2.029, P>0.079). It had time main effect ( F=32.052, P<0.05), but not grouping main effect ( F=2.390, P>0.05) on total distance.With the increase of learning days, the total distance of young rats in each group significantly shortened.On the 6th day of the Morris water maze experiment, there was no statistically significant difference among groups in terms of time in the target quadrant and the number of crossing platforms ( F=2.511, 0.802, both P>0.05). The results of the open field experiment showed that the total distance traveled in the center of young rats in each group was statistically significant ( H=8.935, P<0.05), the total distance traveled in the center in the 70 Hz group (3.80 (2.25, 6.93) m)was significantly longer than that in the 40 Hz group (0.80 (0.72, 1.46) m), P<0.05). The percentage of time spent in the center was statistically significant in the three groups ( H=11.050, P<0.05). Young rats in the 70 Hz group spent significantly higher percentage of time in the center(3.20(2.43, 8.30)) than those in the 40 Hz group (0.95 (0.37, 1.06 ), P<0.05 ). (3) Nissl staining results showed that Nissl bodies in the hippocampal CA1 area of young rats in Ctr, 40 Hz and 70 Hz group were all arranged neatly and tightly, no edema was found in the surrounding stroma, and no obvious inflammatory cell infiltration was found. Conclusion:70 Hz frequency flash stimulation may promote the ability of learning memory and autonomous exploratory of young rats.

Background Noise has multiple negative effects on the organism, and gut microbes are influenced by the environment and are closely associated with the development of diseases. Currently, the effects of chronic noise exposure on intestinal microbiota are poorly understood. Objective To investigate the effects of noise exposure on the structure of rat gut microbiota and to make predictions of gut microbiota function. Methods Male Wistar rats (6 weeks old, 160-180 g) were randomly divided into control, NE_95dB, and NE_105dB groups, 10 rats in each group. Rats in the NE_95dB and the NE_105dB groups were exposed to noise at 95 dB sound pressure level (SPL) and 105 dB SPL, respectively, 4 h per day for consecutive 30 d, while the control group was exposed to background noise. Feces were collected after the last noise exposure for intestinal microbiota detection. Based on the 16S ribosomal RNA (rRNA) gene sequencing method, the diversity and structure of microbiota in rat intestinal contents were analyzed and compared. Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt) was applied to predict functions of the identified intestinal microbiota genes. Results Significant differences were found in the microbial structure of the rat gut after the designed noise exposure. In the α diversity results, there was a statistically significant difference in the Chao1 index between the NE_95dB group and the NE_105dB group (P=0.02), while there were no statistically significant differences in the Shannon and Simpson indexes between the noise exposure groups and the control group (P>0.05). The β diversity analysis results showed significant differences in species abundance between the control group and the noise exposure groups (P=0.001). Further species analysis results showed that the relative abundances of the Ruminococcaceae_NK4A214_group (P<0.05) and Peptococcaceae_unclassified (P<0.01) at the genus level were significantly higher in the NE_105dB group, and the relative abundance of Parasutterella (P<0.05) was significantly higher in the NE_95dB group compared to the control group. In addition, the Ruminococcaceae_NK4A214_group (P<0.05) was also significantly higher in the NE_105dB group compared to the NE_95dB group. The PICRUSt functional prediction analysis results showed that there were eight differential pathways between the control group and the NE_95dB group, in which D-arginine and D-ornithine metabolism, ascorbate and aldarate metabolism, carotenoid biosynthesis, glycerophospholipid metabolism, mineral absorption, NOD-like receptor signaling pathway and non-homologous end-joining were significantly down-regulated, and nucleotide metabolism was significantly up-regulated. There were 38 differential pathways between the control group and the NE_105dB group. Among them, D-arginine and D-ornithine metabolism, and mineral absorption were the differential metabolic pathways in both noise exposure groups, and both were down-regulated relative to the control group. Conclusion Chronic noise exposure could alter structure of rat gut microbiota and may affect metabolic functions of multiple microbiota genes.

Background Noise can cause not only auditory system injury, but also liver damage. However, the biomarkers and pathological mechanism of noise-induced liver injury are not clear yet. Objective To observe the effect of noise on the morphological structure and functions of rat liver. Methods A total of 30 Wistar rats were randomly divided into a normal control group, a low noise exposure group [(95 dB sound pressure level (SPL)], and a high noise exposure group (105 dB SPL). After 30 days of noise exposure, blood was collected, and livers were harvested and fixed. The pathological changes of livers were observed. The levels of biochemical indicators of liver function, blood glucose, and blood lipid were measured. Serum metabolites were detected by ultra-high-pressure liquid chromatography-tandem quadrupole time-of-flight mass spectrometry (UPLC/Q-TOF-MS). Differential metabolite markers and metabolic pathways were identified. Results Compared with the control group, the body weight gain decreased in the low noise group and the high noise group after noise exposure (P<0.001, P<0.05). The pathological results showed that noise caused the rat livers’ morphological and structural damage at various degrees, and damage of the high noise exposure group was more serious. Compared with the control group, the serum levels of aspartate aminotransferase, albumin, and glycosylated serum protein in the low noise exposure group were increased (P<0.05), but the total bile acid level was decreased (P<0.05). The serum levels of alanine aminotransferase, aspartate aminotransferase, albumin, triglyceride, low density lipoprotein, and glycosylated serum protein in the high noise group exposure were increased (P<0.05), but the glucose level was decreased (P<0.05). In the serum metabolomics analysis, 11 differential metabolites were screened out in the low noise exposure group, which were mainly enriched in 3 pathways (thiamine metabolism, primary bile acid biosynthesis, and bile secretion) related to liver metabolism. Four differential metabolites were screened out in the high exposure noise group, which were mainly enriched in four significantly different metabolic pathways (insulin signaling pathway, non-alcoholic fatty liver disease, bile secretion, and insulin secretion). All the metabolic pathways involved in bile acid secretion and metabolism. Conclusion Nosie exposure can not only damage the liver structure of rats, but also affects the metabolism functions of liver. The mechanism may be related to bile acid secretion metabolic pathway.

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.

Background Long-term exposure to noise during sleep may has adverse effects on metabolic system, and liver lipid metabolism is closely related to circadian clock genes. Objective To investigate the effects of long-term noise exposure during sleep on liver circadian clock and lipid metabolism in mice and its related mechanism. Methods Twenty C57BL/6J male mice were randomly divided into two groups: a noise exposure group and a control group with 10 mice in each group. The mice in the noise exposure group were exposed to white noise at 90 dB sound pressure level (SPL) for 30 consecutive days, 8 h a day, from 9:00 to 17:00. The mice in the control group were exposed to background noise ≤40 dB SPL. After noise exposure, the animals were neutralized at 14:00 (ZT6) and 2:00 (ZT18), 5 animals at each time spot, and the liver tissues were collected. Total cholesterol and triglyceride in liver were determined by cholesterol oxidase method and glycerol phosphate oxidase method respectively. The expressions of circadian clock genes (Clock, Bmal1, Rev-erbα, and Rev-erbβ) and lipid metabolism genes (Srebp1c, Hmgcr, Fasn, Lxrα, Acc1, and Chrebp) in liver were detected by quantitative real-time PCR. Results Compared with the control group, the content of total cholesterol in liver in the noise exposure group increased by 48% (P<0.05) and the content of liver triglyceride increased by 61% (P<0.05) at ZT18. The mRNA expression levels of circadian clock genes Clock and Bmal1 in the noise exposure group was significantly increased at ZT18 and decreased at ZT6 (P<0.05). The mRNA expression level of Rev-erbα decreased at both ZT6 and ZT18 (P<0.05). The mRNA expression level of Rev-erbβ had no significant change at ZT6 and ZT18. The mRNA expression levels of liver lipid metabolism related genes Srebp1c, Hmgcr, Chrebp, and Lxrα in the noise exposure group were higher than those in the control group at ZT18 (P<0.05). The mRNA expression levels of Acc1 and Fasn showed no significant change at ZT6, then an upward trend at ZT18, but no significant difference between the two time spots (P>0.05). Conclusion Long-term noise exposure during sleep can cause circadian clock and lipid metabolism disorders in mice. Among them, suppression of key circadian clock genes may be associated with Rev-erbα-mediated upregulation of the nuclear receptors Srebp1c and Chrebp for lipid synthesis and deposition in the liver, resulting in lipid metabolism disorder.

Background Environmental noise pollution is serious, and there are few studies on the effects of long-term noise exposure during sleep on cognitive function and possible biological clock mechanism. Objective To explore the cognitive impairment induced by noise exposure during sleep in mice and possible biological clock mechanism, and to provide a theoretical basis for the protection against noise exposure. Methods Twenty male C57BL/6J mice were randomly divided into a control group and a noise-exposed group, 10 mice in each group. The noise-exposed group was exposed to sleep-period noise using a noise generator for 12 h (08:00–20:00) per day for a total of 30 d. The calibrated noise intensity was set at 90 dB. No intervention was imposed on the control group. At the end of the noise exposure, cognitive function of mice was examined using the new object recognition experiment and the open field test, and the hippocampal tissue damage of mice were evaluated by Nissl staining, ionized calcium binding adaptor molecule 1 (Iba1) immunofluorescence staining, and real-time fluorescence quantitative PCR for inflammatory factors and biological clock genes. Oxidative stress indicators in the hippocampus of mice were also detected by assay kit. Results After noise exposure during sleep period, the results of new object recognition experiment showed that the discrimination index of mice in the noise-exposed group was 0.06±0.04, which was significantly lower than that of the control group (0.65±0.13) (P<0.05). The results of open field test showed that the central activity distance of the noise-exposed group was (242.20±176.10) mm, which was significantly lower than that of the control group, (1548.00±790.30) mm (P < 0.05), and the central activity time of the noise-exposed group was (0.87±0.64) s, which was significantly lower than that of the control group, (6.00±2.86) s (P < 0.05). The Nissl staining results showed that compared with the control group, neurons in the hippocampus of the noise-exposed mice were shrunken, deeply stained, disorganized, and loosely connected. The immunofluorescence results showed that microglia in the hippocampus of the noise-exposed mice were activated and the expression of Iba1 was significantly increased compared with those of the control group (P<0.05). The real-time PCR results of showed that the mRNA levels of the biological clock genes Clock, Per2, and Rev-erbα were significantly increased compared with those of the control group (P<0.05), and the mRNA level of Per1 was significantly decreased compared with that of the control group (P<0.05); and the mRNA levels of IL-18, IL-6, iNOS, and NLRP3 in the hippocampal tissues of mice were significantly increased compared with those of the control group (P<0.05). The results of oxidative stress evaluation showed that compared with the control group, reduced glutathione content was significantly reduced in the noise-exposed group (P<0.001). Conclusion Noise exposure during sleep period can lead to the destabilization of biological clock genes in hippocampal tissues and trigger hippocampal neuroinflammation, which can lead to the activation of microglia and cause cognitive impairment in mice.