Automatic Detection Method of Dairy Cow Feeding Behaviour Based on YOLO Improved Model and Edge Computing.

The feeding behaviour of cows is an essential sign of their health in dairy farming. For the impression of cow health status, precise and quick assessment of cow feeding behaviour is critical. This research presents a method for monitoring dairy cow feeding behaviour utilizing edge computing and deep learning algorithms based on the characteristics of dairy cow feeding behaviour. Images of cow feeding behaviour were captured and processed in real time using an edge computing device. A DenseResNet-You Only Look Once (DRN-YOLO) deep learning method was presented to address the difficulties of existing cow feeding behaviour detection algorithms' low accuracy and sensitivity to the open farm environment. The deep learning and feature extraction enhancement of the model was improved by replacing the CSPDarknet backbone network with the self-designed DRNet backbone network based on the YOLOv4 algorithm using multiple feature scales and the Spatial Pyramid Pooling (SPP) structure to enrich the scale semantic feature interactions, finally achieving the recognition of cow feeding behaviour in the farm feeding environment. The experimental results showed that DRN-YOLO improved the accuracy, recall, and mAP by 1.70%, 1.82%, and 0.97%, respectively, compared to YOLOv4. The research results can effectively solve the problems of low recognition accuracy and insufficient feature extraction in the analysis of dairy cow feeding behaviour by traditional methods in complex breeding environments, and at the same time provide an important reference for the realization of intelligent animal husbandry and precision breeding.

Acrylamide treatment alters the level of Ca2+ and Ca2+-related protein kinase in spinal cords of rats.

This study aimed to analyze the neurological changes induced by acrylamide (ACR) poisoning and their underlying mechanisms within the spinal cords of male adult Wistar rats. The rats were randomly divided into three groups (n = 9 rats per group). ACR was intraperitoneally injected to produce axonopathy according to the daily dosing schedules of 20 or 40 mg/kg/day of ACR for eight continuous weeks (three times per week). During the exposure period, body weights and gait scores were assessed, and the concentration of Ca2+ was calculated in 27 mice. Protein kinase A (PKA), protein kinase C (PKC), cyclin-dependent protein kinase 5 (CDK5), and P35 were assessed by electrophoretic resolution and Western blotting. The contents of 3'-cyclic adenosine monophosphate (cAMP) and calmodulin (CaM) were determined using ELISA kits, and the activities of calcium/calmodulin-dependent protein kinase II (CaMKII), PKA, and PKC were determined using the commercial Signa TECTPKAassay kits. Compared with control rats, treatment with 20 and 40 mg/kg of ACR decreased body weight and increased gait scores at 8 weeks. Intracellular Ca2+ levels increased significantly in treated rats; CaM, PKC, CDK5, and P35 levels were significantly decreased; and PKA and cAMP levels remained unchanged. CaMKII, PKA, and PKC activities increased significantly. The results indicated that ACR can damage neurofilaments by affecting the contents and activities of CaM, CaMKII, PKA, cAMP, PKC, CDK5, and P35, which could result in ACR toxic neuropathy.

Silencing of NONO inhibits abdominal aortic aneurysm in apolipoprotein E-knockout mice via collagen deposition and inflammatory inhibition.

The role of Non-POU-domain-containing octamer-binding protein (NONO) in the formation and development of angiotensin II (Ang II)-induced abdominal aortic aneurysm (AAA) in apolipoprotein E-knockout (ApoE-/- ) mice is still unknown. In Part I, the protein level of NONO was suggestively greater in the AAA tissues compare to that in the normal abdominal aortas. In Part II, 20 ApoE-/- male mice were used to examine the transfection efficiency of lentivirus by detecting GFP fluorescence. In Part III, mice were arbitrarily separated into two groups: one was the control group without Ang II infusion, and another was the Ang II group. Mice treated with Ang II were further randomly divided into three groups to receive the same volume of physiological saline (NT group), sh-negative control lentivirus (sh-NC group) and si-NONO lentivirus (sh-NONO group). NONO silencing suggestively reduced the occurrence of AAA and abdominal aortic diameter. Compare to the NT group, NONO silencing markedly augmented the content of collagen and vascular smooth muscle cells but reduced macrophage infiltration in AAA. In addition, knockdown of NONO also increased the expression of prolyl-4-hydroxylase α1, whereas also decreased the levels of collagen degradation and pro-inflammatory cytokines in AAA. We detected the interface of NONO and NF-κB p65, and found that NONO silencing inhibited both the nuclear translocation and the phosphorylation levels of NF-κB p65. Silencing of NONO prevented Ang II-influenced AAA in ApoE-/- mice through increasing collagen deposition and inhibiting inflammation. The mechanism may be that silencing of NONO decreases the nuclear translocation and phosphorylation of NF-κB.

The neurotoxicity of nanoparticles: A bibliometric analysis.

The aim of this study was to evaluate the global scientific output of neurotoxicity of nanoparticles (NPs) and explore their hot spots and research trends. Articles about the neurotoxicity of NPs between 2008 and 2017 were taken from the Web of Science Core Collection database. The VOSviewer was used to analyze annual publications, countries/institutions, funding agencies, research objects, major journals, and international cooperation. The reference co-citation map and keywords were used to analyze the mechanisms of neurotoxicity of NPs. Six hundred and forty-one eligible studies were included for analysis, and the annual publications increased with time in the past decade. Based on the bibliometric analysis, China and the United States were the main countries in this field. Metals and metal oxides were the main types of NPs. Cell, rat, and mouse were the primary research objects of NPs. The main research hot spots might focus on the pathogenesis of NPs, such as oxidative stress and apoptosis. This study will help researchers understand the research status, hot spots, and trends of neurotoxicity of NPs.

Association between alcohol consumption and amyotrophic lateral sclerosis: a meta-analysis of five observational studies.

The purpose of this study is to examine the association between alcohol consumption and amyotrophic lateral sclerosis. Published literature on the association between alcohol consumption and amyotrophic lateral sclerosis was retrieved from the PubMed and Embase databases. Two authors independently extracted the data. The quality of the identified studies was evaluated according to the Newcastle-Ottawa scale. Subgroup and sensitivity analyses were performed and publication bias was assessed. Five articles, including one cohort study and seven case-control studies, and a total of 431,943 participants, were identified. The odds ratio for the association between alcohol consumption and amyotrophic lateral sclerosis was 0.57 (95 % confidence interval 0.51-0.64). Subgroup and sensitivity analyses confirmed the result. Evidence for publication bias was detected. Alcohol consumption reduced the risk of developing amyotrophic lateral sclerosis compared with non-drinking. Alcohol, therefore, has a potentially neuroprotective effect on the development of amyotrophic lateral sclerosis.

Neuroprotective Effect of Calpeptin on Acrylamide-Induced Neuropathy in Rats.

Acrylamide (ACR) is a vinyl monomer with established human neurotoxic effects, which is characterized by the accumulation of neurofilaments (NFs) in the distal swellings of large axons in peripheral and central nervous systems. However, the mechanisms of neurotoxicity remain unclear. The objective is to investigate the neuroprotective effect of calpeptin (CP) on ACR-induced neuropathy and its mechanism. Female adult Wistar rats were randomly divided into four groups (control, CP, ACR, and ACR + CP group). Control group received 0.9 % saline, ACR and ACR + CP groups received 30 mg/kg ACR by intraperitoneal injection. In addition, CP and ACR + CP groups also received 200 µg/kg CP. Gait analysis and hind limb splay were measured weekly to analyze neurobehavioral changes. The calpain activity and the changes of NFs protein levels in spinal cord are determined. Compared with control group, body weight of rats in ACR group decreased by 11.3 % (P < 0.01), while in ACR + CP group body weight increased significantly by 8.3 % (P < 0.01) compared with ACR group by the end of the 4th week; gait score of rats in both ACR and ACR + CP groups increased significantly by 167 % and 100 % (P < 0.01) compared with control group, while it decreased significantly by 25.1 % (P < 0.01) in ACR + CP group compared with ACR group; the distance of hind limb splay in both ACR and ACR + CP groups increased by 76.7 % and 49.5 % (P < 0.01) compared with control group, while it decreased by 15.4 % (P < 0.01) in ACR + CP group compared with ACR group; calpain activity of spinal cord at ACR and ACR + CP groups increased significantly by 14.9 % and 10.0 % (P < 0.01) compared with control group, while it decreased 4.2 % (P < 0.01) in ACR + CP group compared with ACR group; compared with control group, the levels of light NF (NF-L), medium NF (NF-M) and heavy NF (NF-H) subunits increased by 81.2 %, 263.6 % and 22.6 % (P < 0.01) in the supernatant of ACR group in spinal cord tissue and increased by 28.4 %, 96.6 % and 10.6 % (P < 0.01) in ACR + CP group, while the levels of NF-L, NF-M and NF-H subunits decreased by 29.1 %, 45.9 % and 9.8 % (P < 0.01) in ACR + CP group compared with ACR group. The present results suggested that CP can relieve ACR neuropathy by decrease calpain activity and NFs degradation. The changes of calpain activity and NFs may be one of the mechanisms of ACR-induced neuropathy.

[Analysis of risk factors for hypertension among taxi drivers on different shifts].

OBJECTIVE: To investigate the incidence and risk factors for hypertension among taxi drivers working different shifts. METHODS: Using the cluster sampling method, 415 day-shift and 304 night-shift taxi drivers in Jinan, China were selected and investigated. The influencing factors for hypertension were analyzed. RESULTS: The incidence of hypertension in all taxi drivers was 33.2%. The incidence of hypertension in night-shift drivers was significantly higher than that in day-shift drivers (37.8% vs 29.9%, P<0.05). According to multivariate analysis, the incidence of hypertension in day-shift drivers was closely related to body mass index (BMI), working years, working hours, sleep duration, rest days, diet quality, water intake, and smoking, while the incidence of hypertension in night-shift drivers was closely related to BMI, working years, working hours, part-time job, sleep duration, rest days, and drinking. CONCLUSION: BMI, working years, and working hours are the common risk factors for hypertension in day-shift and night-shift drivers. Sleep duration and rest days are the common protective factors. The risk factors for hypertension in taxi drivers vary with different shifts.

[Analyzing the factors of influencing the musculoskeletal disorders of greenhouse vegetable farmers].

OBJECTIVE: To study the prevalence of musculoskeletal disorders (MSDs) among greenhouse vegetable farmers and to explore the risk factors of MSDs. METHODS: A household questionnaire survey was conducted to investigate 203 greenhouse vegetable farmers and 127 non-greenhouse vegetable farmers in February, 2011. RESULTS: The one-year prevalence rates of MSDs were 70.0% and 33.9% among greenhouse vegetable farmers and non-greenhouse vegetable farmers, respectively. The three main positions of MSDs in greenhouse farmers were low back, knee (s) and shoulder (s). Age, working years, body weight and usage of rolling machine were statistically associated with MSDs of greenhouse farmers, ORadj values were 1.17, 1.82, 1.08 and 0.07, respectively. CONCLUSIONS: The prevalence of MSDs is high in greenhouse workers. Low back pain, knee (s), and shoulder (s) disorders are the main disorders. Age, working years, body weight and usage of rolling machine are main risk factors for the development of MSDs in greenhouse farmers.

Cognitive decline trajectories and influencing factors in China: A non-normal growth mixture model analysis.

BACKGROUND: With the increase in the aging population worldwide, cognitive decline has become an important research topic. The purpose of this study is to examine the cognitive development trajectories and influencing factors of different latent classes of Chinese elderly people. This will provide us with effective guidance for prevention and intervention. METHODS: Four waves of data from the Chinese Longitudinal Healthy Longevity Survey (CLHLS) were collected and included 2440 Chinese elderly individuals. The cognitive function of elderly individuals was measured using the Mini Mental State Examination (MMSE). A nonnormal Growth Mixture model (GMM) with five time-invariant covariates was used to identify the different trajectories of cognitive decline in elderly individuals. RESULTS: Three latent decline trajectory groups were identified: stable cognitive group (SCG), high initial level - cognitive decline group (HIL-CDG), and high initial level - cognitive decline group (LIL-CDG). Elderly women were more likely to be assigned to a lower level subgroup than men. People who smoked and played cards or mahjong were more likely to be assigned to a cognitively stable group. CONCLUSION: Education may help raise the upper limit of cognition. Smoking may impair cognitive upper limit. A small amount of alcohol intake and participation in cognitive and physical activities may help the elderly to delay cognitive decline in their later years.

Impact of intracoronary nicorandil before stent deployment in patients with acute coronary syndrome undergoing percutaneous coronary intervention.

The present study aimed to clarify the effect of bolus intracoronary nicorandil on inflammatory, oxidative and adherent indicators in patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI). This randomized controlled trial (RCT) was performed to detect the inflammation and oxidative stress in intracoronary blood both before and after PCI. In total, 65 consecutive patients undergoing PCI were classified into a nicorandil therapy group (n=32) or a placebo group (n=33). All procedures were performed at Shandong University Qilu Hospital, China, during the period from March, 2016 to May, 2017. Intracoronary blood from patients who received nicorandil therapy during PCI showed no change in soluble CD40 ligand (sCD40L) concentration (1.86±0.08 vs. 1.90±0.09 ng/ml, P=0.12) but a significant increase was noted in the control group (1.87±0.17 vs. 2.82±0.26 ng/ml, P<0.01). This indicated a relative reduction in sCD40L level after PCI in the nicorandil group. We further demonstrated an increase in superoxide dismutase (SOD) activity (29.37±0.81 vs. 31.03±0.60 U/ml, P<0.001) and a reduction in lipid peroxidation (3.84±0.99 vs. 4.23±0.13 U/ml, P=0.001) in the nicorandil group but observed no change in the placebo group. ICAM-1 levels showed no change in the nicorandil group (69.54±6.89 vs. 72.01±8.25 ng/ml, P=0.83) but a significant increase in the control group after PCI in intracoronary blood (56.57±4.96 vs. 76.81±6.88 ng/ml, P=0.002). No changes were found in hs-CRP, TNFα and sVCAM-1 levels in coronary blood for both groups before and after PCI in ACS patients. Our findings demonstrate that intracoronary bolus nicorandil therapy has a significant effect on the inhibition of inflammatory indicators and oxidative stress in patients with ACS during PCI. This suggests a possible medical application of nicorandil for reducing inflammation and oxidative stress.

The Effect of Flavonoids on Chronic Prostatitis: A Meta-analysis of Published Randomized Controlled Trials.

OBJECTIVE: To assess the effect of flavonoids on chronic prostatitis, a meta-analysis of randomized controlled trials was performed. METHODS: Through using subject word and random word, PubMed, Scopus, Web of Science, and Cochrane Library were searched for related records up to July 2018. The response rate and National Institutes of Health-Chronic Prostatitis Symptom Index (NIH-CPSI) were used to evaluate the therapeutic efficacy of the flavonoids. The Cochrane handbook for systematic reviews of interventions version was used to evaluate the quality of included studies. The model of determining odds ratio (OR) was chose according to the value of I2. RESULTS: A total of 11 studies involving 975 subjects (experiment 516, control 459) were included. The overall OR of response rate was 0.31 (95%CI 0.11-0.89, P = 0.03). At the subgroup analysis, the OR of response rate of chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) was 0.57 (95%CI 0.18-1.77, P = 0.33), while the OR of response rate of chronic bacterial prostatitis (CBP) was 0.08 (95%CI 0.02-0.33, P = 0.0005). The OR of response rate of CP/CPPS (control was placebo) was 0.29 (95%CI 0.16-0.52, P < 0.0001). The overall OR of baseline NIH-CPSI was -0.1 (95%CI -0.61-0.41, P = 0.70). The overall OR of posttreatment NIH-CPSI was -6.96 (95%CI -8.32∼ -5.60, P < 0.00001). CONCLUSIONS: This meta-analysis indicates that the flavonoids may be clinically beneficial through significantly improving the response rate and NIH-CPSI in chronic prostatitis patients and short-lasting antibiotics therapy in association with the flavonoids could be a better choose for CBP. Moreover, the flavonoids therapy has an excellent safety profile with minor adverse effects.

Occurrence patterns of black water and its impact on fish in cutover areas of Eucalyptus plantations.

Black runoff occasionally flows from cutover areas of Eucalyptus plantations, polluting rivers and ponds, and resulting in fish death in severe cases. However, the occurrence patterns and environmental impacts of this black water remain unclear. Herein, we analyzed the major characteristics of black water at the occurrence sites, tested the complexation reaction of ground eucalyptus leaves with a solution of Fe3+, and determined the color and absorbance of the complex solution. The results showed that the water was dark blue, with weak acidity and strong light absorbance. The water contained a high level of dissolved organic matter content, while its chemical oxygen demand, total N, total P, NO3--N, and NH4+-N concentrations were significantly higher than those in the stream water from Eucalyptus, Pinus massoniana Lamb., and Cunninghamia lanceolata stands during the growth period. Additionally, the tannic acid concentration in the black water was 1.0 mg L-1 higher than that in the stream water from the Eucalyptus stand. The input of black water increases the concentration of tannic acid and NH4+-N, and the degradation of organic matter consumes dissolved oxygen in downstream ponds, leading to fish deaths. The presence of fresh logging residues and hot, humid weather also enable black water formation. Field investigations and simulation experiments revealed fresh Eucalyptus residues decompose rapidly under high-temperature and rainfall conditions, releasing large amounts of tannic acid, which reacts with Fe3+ to form a dark blue tannic acid­iron complex and results in black water. These results indicate that the rich Fe3+ in runoff may be a key factor in the occurrence of black water. The logging of Eucalyptus plantations during the dry season or on non-rainy days and a reduction in the logging area could prevent the occurrence of black water or mitigate the extent of its environmental hazards.

The reversibility of neurofilaments decline induced by 2,5-hexanedione in rat nerve tissues.

To investigate the reversibility of the neuropathy induced by 2,5-HD, adult male rats were administered at a dosage of 400 mg/kg/day 2,5-HD (five times per week) for 2, 4, and 8 weeks, respectively. After stopping HD exposure, half of 8-week treated animals were allowed to naturally recover for 16 weeks. The relative levels of NF-H, NF-M, and NF-L in spinal cords and sciatic nerves of rats were determined by immunoblotting during the HD neuropathy. The results showed that NFs content in nerve tissues demonstrated a progressive decline as the intoxication continued. Furthermore, after a recovery of 16 weeks, the levels of three NF subunits in spinal cords of treated rats returned to normal while those in sciatic nerves displayed an inconsistent reversal. Among them, the level of NF-H in sciatic nerves returned to normal completely, and NF-L also showed a significant improvement, whereas NF-M did not demonstrate an obvious reversal. These findings suggest that HD-induced NFs decline is at least partially irreversible within the time frame of this study, which might be associated with the incomplete recovery of neurological dysfunctions of HD-treated rats.

2,5-hexanedione (HD) treatment alters calmodulin, Ca2+/calmodulin-dependent protein kinase II, and protein kinase C in rats' nerve tissues.

Calcium-dependent mechanisms, particularly those mediated by Ca(2+)/calmodulin (CaM)-dependent protein kinase II (CaMKII), have been implicated in neurotoxicant-induced neuropathy. However, it is unknown whether similar mechanisms exist in 2,5-hexanedione (HD)-induced neuropathy. For that, we investigated the changes of CaM, CaMKII, protein kinase C (PKC) and polymerization ratios (PRs) of NF-L, NF-M and NF-H in cerebral cortex (CC, including total cortex and some gray), spinal cord (SC) and sciatic nerve (SN) of rats treated with HD at a dosage of 1.75 or 3.50 mmol/kg for 8 weeks (five times per week). The results showed that CaM contents in CC, SC and SN were significantly increased, which indicated elevation of Ca(2+) concentrations in nerve tissues. CaMKII contents and activities were also increased in CC and were positively correlated with gait abnormality, but it could not be found in SC and SN. The increases of PKC contents and activities were also observed in SN and were positively correlated with gait abnormality. Except for that of NF-M in CC, the PRs of NF-L, NF-M and NF-H were also elevated in nerve tissues, which was consistent with the activation of protein kinases. The results suggested that CaMKII might be partly (in CC but not in SC and SN) involved in HD-induced neuropathy. CaMKII and PKC might mediate the HD neurotoxicity by altering the NF phosphorylation status and PRs.

Effects of acrylamide on the nervous tissue antioxidant system and sciatic nerve electrophysiology in the rat.

To investigate the time-dependent effects of acrylamide (ACR) on the antioxidative status in rat nerve tissues, adult male Wistar rats were given ACR (40 mg/kg, i.p., 3 times/week) for 2, 4, 6 and 10 weeks, respectively. The time-dependent changes of the lipid peroxidation (malondialdehyde, MDA) and antioxidative status (glutathione, GSH; glutathione peroxidase, GSH-Px; glutathione reductase, GR; superoxide dismutase, SOD and anti-reactive oxygen species, anti-ROS) in nerve tissues were investigated. The electrophysiology indices (nerve conduction velocity, NCV; compound action potential duration, CAPD; compound action potential amplitude, CAPA; compound action potential latency, CAPL) in the sciatic nerve were determined using BL-420E Biologic Function Determining System. The results showed that MDA levels increased significantly (P < 0.05) in nerve tissues, while GSH levels markedly decreased (P < 0.05) in a time-dependent manner. SOD activity (in the spinal cord and sciatic nerve) and GR activity (in the sciatic nerve) increased significantly after 4 weeks ACR treatment (P < 0.01), but then decreased (P < 0.05). The anti-ROS activity in the sciatic nerve was markedly decreased at the end of week 6 and 10 (P < 0.01). The above indices changed most in the sciatic nerve. The levels of GSH, MDA and anti-ROS in rat sciatic nerve were in high correlation (P < 0.05, |r| > 0.80) with the electrophysiology indices according to the exposure time. Thus, ACR-induced neurotoxicity may be associated with the enhancement of lipid peroxidation and reduction of the antioxidative capacity. Depletion of neural GSH level might be one of the primary events in ACR-induced neuropathy.

Protective effect of calpeptin on acrylamide-induced microtubule injury in sciatic nerve.

The present study aimed to investigate the protective effect and mechanism of calpeptin (CP) on acrylamide (ACR)-induced microtubule (MT) injury in the sciatic nerve of rats. All rats were divided into four groups (control, CP, ACR, and ACR + CP):1 ml/kg saline, 200 µg/kg CP, 30 mg/kg ACR, and 30 mg/kg ACR plus 200 µg/kg CP were administered to the corresponding rats for 4 weeks through intraperitoneal injection. Body weight and neurobehavioral indicators were measured weekly and α-tubulin, ß-tubulin, and other concerned proteins were estimated by western blotting and immunohistochemistry. At 4 weeks, decreased body weight, increased gait scores, increased hindlimb splay, and decreased time of fall of ACR rats were observed compared with those of control rats. All these mentioned changes were restored in the ACR + CP group compared with the ACR group. After 4 weeks of administration, western blotting and immunohistochemistry revealed significant increase in the protein levels of ß-tubulin, calpain I, calpain II, Tau, microtubule-associated protein 2 (MAP2), protein kinase C, and cyclin-dependent kinase 5 in the ACR group compared with the control group; these increases were significantly lower in the ACR + CP group than in the ACR group. Furthermore, histopathological examination revealed loose arrangement, disorganised structure, uneven density, and exfoliated perineurium in the ACR group, and CP administration improved these changes significantly. The present results suggest that CP has an intervening effect on ACR-induced MT injury. A possible mechanism is that calpain maintains the stability of MTs by regulating the metabolism of Tau and MAP2.

The relation of passive smoking with cervical cancer: A systematic review and meta-analysis.

BACKGROUND: Published studies about passive smoking and cervical cancer have found inconsistent results. Hence, the present meta-analysis was performed to assess this association. METHODS: A systematical search was performed to identify eligible cohort and case-control studies in PubMed, Scopus, Elsevier ScienceDirect, and Web of Science databases (up to March, 2018). The quality of included studies was assessed by the Newcastle-Ottawa quality scale (NOS). The random effects model (REM) was used to calculate the pooled odds ratio (ORs). Subgroup and sensitivity analyses were performed. Publication bias was assessed by funnel plot, using Begg's test and Egger's test. RESULTS: Around 14 eligible studies were included for analysis, which included a total of 384,995 participants. The pooled ORs of passive smoking with cervical cancer risk was 1.70 (95% CI: 1.40-2.07, I = 64.3%). Subgroups stratified by continent, study design, quality score, and cervical cancer types/phases suggested that the result was robust. For instance, the pooled ORs for the cohort and case-control studies was 1.37 (95% CI: 1.16-1.62, I = 0%) and 2.09 (95% CI: 1.52-2.89, I = 76.6%), respectively. The pooled ORs ranged from 1.61 (95%CI: 1.34-1.92) to 1.77 (95%CI: 1.44-2.16) after one study was removed each time in the sensitivity analyses, indicating that the result was stable. Publication bias was detected by funnel plot and Egger's tests. The recalculated ORs were 1.33 (95% CI: 1.21-1.47). CONCLUSIONS: This meta-analysis provides evidence that passive smoking is associated with an increased risk of cervical cancer.

Calpeptin is neuroprotective against acrylamide-induced neuropathy in rats.

The aim of this study is to explore the potent neuroprotective effect of calpeptin (CP) on neuron damage induced by acrylamide (ACR) and its mechanism. Behavioural indicators such as hind limb splay, rota-rod performance, and gait analysis were assessed weekly to evaluate neurobehavioural changes after ACR and/or CP administration. The histopathological alterations and the changes of µ-calpain, m-calpain, microtubule-associated protein 2 (MAP2), and α-tubulin and ß-tubulin protein levels in spinal cord were determined. Results showed that after administration of 30 mg/kg ACR, decreased body weight, attenuated neurobehavioural function, injury of motor neuron, increased protein levels of m-calpain and ß-tubulin, suppressed MAP2 protein level, and no significant changes of µ-calpain and α-tubulin protein levels were observed compared with the control group rats. After administration of 200 µg/kg CP, partially restored body weight and neurobehavioural function, improvement of motor neuron injury, decreased protein levels of m- calpain and ß-tubulin, and reversed effects of MAP2 protein level were observed compared with the ACR group rats. Our results suggested that CP alleviates neuropathy induced by ACR in rats. The calpain's overactivation causes the degrading of MAP2 and eventually leads to the destruction of microtubules (MTs), which may be one of the mechanisms of cytoskeletal damage induced by ACR.

Malondialdehyde and catalase as the serum biomarkers of allyl chloride-induced toxic neuropathy.

Chronic exposure to allyl chloride (AC) is known to produce a central-peripheral distal axonopathy. To access the biomarker of exposure and elucidate the mechanism of neuropathy induced by AC, we performed a longitudinal observational study of malondialdehyde (MDA), anti-reactive oxygen species (anti-ROS), glutathione (GSH), catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD) in rats serum and sciatic nerve after 0, 3, 6, 9 and 12 weeks of AC administration. AC was administrated to Wistar rats by gavage at a single dosage of 200 mg/kg/per dose (three times per week). Rats were sacrificed after 0, 3, 6, 9 and 12 weeks of AC treatment, serum and sciatic nerves were quickly collected at 4 degrees C. The results showed that MDA levels in serum (115.4 and 126.2%) and sciatic nerve (130.5 and 145.3%) significantly increased (p<0.05) on 3rd week of AC treatment and at gait score of 2, and further changes of MDA levels were observed after 6, 9 and 12 weeks and at gait score of 3 and 4. While a decrease (p<0.05) in the activities of CAT on 6th week of AC intoxication and at gait score of 2 was observed in serum (81.2 and 72.8%) and sciatic nerve (71.7 and 70.7%). The other antioxidants also decreased in serum and sciatic nerve after 3, 6 and 9, 12 weeks' intoxication and at gait score of 2, 3 and 4. Significant (p<0.05) positive correlations were observed between serum and sciatic nerve in MDA levels (r=0.9162 and 0.9551, respectively) and CAT (r=0.9410 and 0.9557, respectively) activities as time went on and symptoms developed. Thus, AC intoxication was associated with elevation of lipid peroxidation and reduction of antioxidative status, and the time dependent changes of these indexes in Wistar rats' serum and sciatic nerve occurred. The misbalance of lipid peroxidation and antioxidation status might be one of mechanisms of toxic neuropathy induced by AC. MDA and CAT could be served as the biomarkers of AC exposure to afford the early diagnosis of AC-induced toxic neuropathy.