RGCC-mediated PLK1 activity drives breast cancer lung metastasis by phosphorylating AMPKα2 to activate oxidative phosphorylation and fatty acid oxidation.

BACKGROUND: More than 90% of the mortality of triple-negative breast cancer (TNBC) patients is attributed to cancer metastasis with organotropism. The lung is a frequent site of TNBC metastasis. However, the precise molecular mechanism for lung-specific metastasis of TNBC is not well understood. METHODS: RNA sequencing was performed to identify patterns of gene expression associated with lung metastatic behavior using 4T1-LM3, MBA-MB-231-LM3, and their parental cells (4T1-P, MBA-MB-231-P). Expressions of RGCC, called regulator of cell cycle or response gene to complement 32 protein, were detected in TNBC cells and tissues by qRT-PCR, western blotting, and immunohistochemistry. Kinase activity assay was performed to evaluate PLK1 kinase activity. The amount of phosphorylated AMP-activated protein kinase α2 (AMPKα2) was detected by immunoblotting. RGCC-mediated metabolism was determined by UHPLC system. Oxidative phosphorylation was evaluated by JC-1 staining and oxygen consumption rate (OCR) assay. Fatty acid oxidation assay was conducted to measure the status of RGCC-mediated fatty acid oxidation. NADPH and ROS levels were detected by well-established assays. The chemical sensitivity of cells was evaluated by CCK8 assay. RESULTS: RGCC is aberrantly upregulated in pulmonary metastatic cells. High level of RGCC is significantly related with lung metastasis in comparison with other organ metastases. RGCC can effectively promote kinase activity of PLK1, and the activated PLK1 phosphorylates AMPKα2 to facilitate TNBC lung metastasis. Mechanistically, the RGCC/PLK1/AMPKα2 signal axis increases oxidative phosphorylation of mitochondria to generate more energy, and promotes fatty acid oxidation to produce abundant NADPH. These metabolic changes contribute to sustaining redox homeostasis and preventing excessive accumulation of potentially detrimental ROS in metastatic tumor cells, thereby supporting TNBC cell survival and colonization during metastases. Importantly, targeting RGCC in combination with paclitaxel/carboplatin effectively suppresses pulmonary TNBC lung metastasis in a mouse model. CONCLUSIONS: RGCC overexpression is significantly associated with lung-specific metastasis of TNBC. RGCC activates AMPKα2 and downstream signaling through RGCC-driven PLK1 activity to facilitate TNBC lung metastasis. The study provides implications for RGCC-driven OXPHOS and fatty acid oxidation as important therapeutic targets for TNBC treatment.

Centralized health management based on hot spring resort improves physical examination indicators and sleep quality in people at high risk of chronic diseases: a randomized controlled trial.

We study the effects of centralized health management based on hot spring resorts on the physical examination index and sleep quality of people at high risk of chronic diseases. We recruited 114 volunteers at high risk of chronic diseases. We then divided them into 57 in the intervention group and 57 in the control group. The intervention group collectively received 4 weeks (28 days) of comprehensive health management interventions at Tongjing Hotspring Resort, including regular schedules, balanced diet, appropriate exercise, targeted health education, etc. The main outcomes are physical examination indicators (height, weight, waist circumference, blood pressure, lipids, and glucose) and sleep quality. Both groups underwent a questionnaire and physical examination at baseline, 2 weeks and 4 weeks. Intragroup comparisons grouped by exposure criteria showed decreases in BMI, waist circumference, triglycerides, total cholesterol, and blood glucose in the intervention group at both 2 and 4 weeks (all P < 0.05); however, in the control group, only triglycerides decreased at 4 weeks (P < 0.05). Intergroup comparisons showed BMI and waist circumference were significantly lower in the intervention group than in the control group at 4 weeks (all P < 0.05). Intragroup comparisons of insomnia severity index (ISI) scores showed a significant decrease in the intervention group at both 2 and 4 weeks (all P < 0.001) with no significant change in the control group (P > 0.05). Intergroup comparisons showed that the insomnia severity index (ISI) scores were significantly higher in the intervention group than in the control group at baseline (P = 0.006) but became significantly lower than the control group at 2 and 4 weeks (all P < 0.001). Thus, this pattern significantly improved BMI, waist circumference, triglycerides, and sleep in the intervention group. TRIAL REGISTRATION NUMBER: Chinese Clinical Trials Registry: ChiCTR2100053201, registered 14 Nov 2021. (Retroactive Registration).

An improved method for preparing stained ground teeth sections.

Objective: In oral histopathology teaching and research, there is a need for high-quality undemineralized tooth sections that are easy to handle, have controlled thickness, allow the observation of intact microstructures, and can be preserved for long periods of time. Methods: Teeth were collected under non-demineralizing conditions. Tooth sections (15-25 µm) were prepared using a diamond knife, then randomly divided into three groups: (1) stained with rosin, (2) stained with hematoxylin and eosin, or (3) not stained. The prepared tooth sections were evaluated by microscopy for clarity and microstructure visibility. Results: The use of a diamond knife in the sectioning and grinding process yielded high-quality ground sections of teeth. Rosin-stained ground sections allowed better identification of microstructures within the teeth, compared with unstained or hematoxylin and eosin-stained ground sections. Conclusion: The best results were obtained in the ground sections of teeth that were stained with rosin. Ground sections of teeth prepared using this staining method could be useful in oral histopathology teaching and research.

Study on nondrug intervention of 7 days of balneotherapy combined with various sleep-promoting measures on people with sleep disorders: preliminary and pilot study.

To preliminarily explore a nondrug intervention method and evaluate its effects (sleep quality, physical examination indicators, and general physical symptoms) on people with sleep disorders. The intervention was based on regular balneotherapy, coupled with targeted health education, appropriate exercise, diet management, and other sleep-promoting measures. It was the combined effects that we evaluated. We recruited 31 volunteers with sleep disorders to receive a 7-day sleep-promoting experience in Tianxing International Hot Spring City, Nanchuan District, Chongqing. The intervention adopted a plan that combined balneotherapy with various sleep-promoting measures. Persisting baths in hot springs 1-2 times per day targeted health lectures about 1 h every morning, appropriate exercise every day (sleep-aid yoga, forest hiking, morning exercises, etc.), and diet management (the principle is to control oil, salt, and sugar, diversify food, keep meat and vegetable balanced, and control total calories. The dinner is light and easy to digest). During the intervention period, all participants followed the above intervention plan, and they lived in the spa resort to accept unified arrangement. This study adopted a self-contrast method by comparing the changes in sleep quality, physical examination indicators, and general physical symptoms before and after the intervention through physical examinations and questionnaire surveys. After the intervention, the subjects' total score of Insomnia Severity Index (ISI) decreased significantly (P = 0.006), and all seven dimensions showed a decrease, four of which included early morning awakening, sleep dissatisfaction, noticeability of sleep problems by others, and distress caused by sleep problems decreased significantly (all P < 0.05). The subjects' body mass index, waist circumference, fasting blood glucose, and triglycerides decreased significantly (all P < 0.05), and systolic blood pressure increased significantly (P = 0.006). Total cholesterol, high-density lipoprotein, low-density lipoprotein, and diastolic blood pressure did not change significantly (all P > 0.05). To some extent, all general health problems were improved than before the intervention (the improvement rate was up to 70% or more). The non-pharmacological intervention of balneotherapy combined with various sleep-promoting measures showed positive effects on sleep quality, general physical symptoms, and some physical examination indicators of sleep disorders. This comprehensive intervention may be an effective way to improve people's health with sleep disorders.

Heterozygous disruption of beclin 1 alleviates neurotoxicity induced by sub-chronic exposure of arsenite in mice.

Arsenite is a well-documented neurotoxicant that widely exists in the environment. However, the detailed mechanisms of arsenite neurotoxicity are not fully clarified. Autophagy has been reported to be involved in many neurological problems induced by arsenite. Since beclin 1 is an essential mediator of autophagy, we herein used both adult wild-type (beclin 1+/+) and heterozygous disruption of beclin 1 (beclin 1+/-) mice for chronic administration of 50 mg/L arsenite via drinking water for 3 months. Our results demonstrated that exposure of arsenite caused the working memory deficit, anxiety-like behavior and motor coordination disorder in beclin 1+/+ mice, accompanied with pathological changes in morphology and electrophysiology in the cortical tissues. This treatment of arsenite significantly reduced the number of neuronal cells and induced microglia activation and synaptic transmission disorders in the wild-type mice as compared with vehicle controls. Intriguingly, by using beclin 1+/- mice, we found that heterozygous disruption of beclin 1 profoundly attenuated these neurotoxic effects induced by arsenite, mainly manifested by improvements in the neurobehavioral impairments, abnormal electrophysiologic alterations as well as dysregulation of synaptic transmission. These findings together indicate that regulation of autophagy via beclin 1 would be a potential strategy for treatment against arsenite neurotoxicity.

Prenatal exposure to titanium dioxide nanoparticles induces persistent neurobehavioral impairments in maternal mice that is associated with microbiota-gut-brain axis.

Gestational exposure to titanium dioxide nanoparticles (TiO2NPs) has been widely reported to have deleterious effects on the brain functions of offspring. However, little attention has been paid to the neurotoxic effects of TiO2NPs on maternal body after parturition. The pregnant mice were orally administrated with TiO2NPs at 150 mg/kg from gestational day 8-21. The potential effects of TiO2NPs on the neurobehaviors were evaluated at postnatal day 60. The gut microbiota, morphological alterations of intestine and brain, and other indicators that involved in gut-brain axis were all assessed to investigate the underlying mechanisms. The results demonstrated that exposure to TiO2NPs during pregnancy caused the persistent neurobehavioral impairments of maternal mice after delivery for 60 days, mainly including behavioural changes, pathological changes in hippocampus, cortex and intestine. Our data also showed that persistent dysfunction and tissue injuries were probably associated with the disruption of gut-brain axis, manifested by the shift in the composition of gut microbial community, alteration of Sstr1, inhibition of enteric neurons and reduction of diamine oxidase contents in maternal mice. These findings provide a novel insight that regulation of gut microecology may be an alternative strategy for the protection against the neurotoxicity of TiO2NPs in pregnant women.

Results of a 30-day safety assessment in young mice orally exposed to polystyrene nanoparticles.

Polystyrene nanoparticles (PSNPs) are a newly emerging pollutant in the natural environment. However, due to the lack of sufficient toxicological studies in mammals, the potential effects of PSNPs on human health remain largely undefined. Therefore, in this study, young mice aged four weeks old were subjected to oral administration of 0, 0.2, 1, or 10 mg/kg PSNPs for 30 days. Our results demonstrated for the first time that oral exposure to PSNPs affected the expressions of mucus secretion-related genes and altered the community composition of intestinal microbiota, although this treatment did not cause behavioral impairments in young mice. No significant alterations in inflammatory or oxidative stress-related indicators were observed in the liver, lung, intestine, cortex or serum of PSNPs-treated animals. Moreover, exposure to PSNPs did not cause pathological changes in the liver, lung, or cortex tissues. Notably, although oral administration of PSNPs did not produce obvious toxic effects in the major organs of young mice, the possible toxicity of PSNPs remains unresolved and it may depend on the dose, exposure route and species. The potential hazardous effects of PSNPs still need to be systematically assessed, especially for children who are susceptible to exposure to nanoparticles.

Treating Autoimmune Inflammatory Diseases with an siERN1-Nanoprodrug That Mediates Macrophage Polarization and Blocks Toll-like Receptor Signaling.

The clinical application of small interfering RNA (siRNA) drugs provides promising opportunities to develop treatment strategies for autoimmune inflammatory diseases. In this study, siRNAs targeting the endoplasmic reticulum to nucleus signaling 1 (ERN1) gene (siERN1) were screened. Two cationic polymers, polyethylenimine (PEI) and poly(ß-amino amine) (PBAA), which can improve the efficiency of the siRNA transfection, were used as siERN1 delivery carriers. They were implemented to construct a nanodrug delivery system with macrophage-targeting ability and dual responsiveness for the treatment of autoimmune inflammatory diseases. In terms of the mechanism, siERN1 can regulate the intracellular calcium ion concentration by interfering with the function of inositol 1,4,5-trisphosphate receptor 1/3 (IP3R1/3) and thus inducing M2 polarization of macrophages. Furthermore, siERN1-nanoprodrug [FA (folic acid)-PEG-R(RKKRRQRRR)-NPs(ss-PBAA-PEI)@siERN1] acts as a conductor of macrophage polarization by controlling the calcium ion concentration and is an inhibitor of MyD88-dependent Toll-like receptor signaling. The results revealed that the FA-PEG-R-NPs@siERN1 has universal biocompatibility, long-term drug release responsiveness, superior targeting properties, and therapeutic effects in mouse collagen-induced arthritis and inflammatory bowel disease models. In conclusion, this study reveals a potential strategy to treat autoimmune inflammatory disorders.

Prevalence and Phylogenetic Analysis of Microsporidium Enterocytozoon bieneusi in Diarrheal Patients.

Enterocytozoon bieneusi can cause severe diarrhea in children and adults. However, in China, there are scant studies on E. bieneusi in diarrheal children and adults, with the exception of prevalence and genotyping data in a small number of cities including Hubei, Shanghai, and Heilongjiang. In this study, 196 fecal samples (n = 132 in Chongqing, n = 44 in Shandong, n = 20 in Hubei) were collected, including 91 from children and 105 from adults. Through microscopic examination, 19 positive samples (11 from children and 8 from adults) were detected. Using PCR examination, the internal transcriptional spacer (ITS) region was utilized by nested PCR to detect and characterize E. bieneusi. Twenty positive samples were detected, including 14 from children (≤11 years of age) and 6 from adults. According to the sequence analysis of ITS data, one known zoonotic (D) and seven novel (CQH5-11) genotypes were identified. This is the first molecular epidemiological study of E. bieneusi in diarrheal patients in different regions of China. Therefore, this study can provide useful information for the molecular epidemiology and control of E. bieneusi infection in humans in the future.

Metabolic disturbance in hippocampus and liver of mice: A primary response to imidacloprid exposure.

Imidacloprid (IMI) is one of the most frequently used neonicotinoid insecticides, but recent studies have shown adverse effects on mammals. IMI was found to be neurotoxic and hepatotoxic. In the present study, the effects of repeated oral administration of two doses of IMI (5 and 20 mg/kg/day) for 28 days on hippocampus and liver of female KM mice were studied. The histopathological and biochemical experiments indicated obvious damages to the hippocampus and liver of mice in the high-dose group (20 mg/kg/day). Using a high-throughput metabolomics platform based on ultrahigh performance liquid chromatography/hybrid quadrupole time-of-flight mass spectrometry (UPLC/Q-TOF MS), we studied effects of IMI on metabolic profiles in the hippocampus and liver of mice. Significant differences among the control group, the low-dose group and the high-dose group were clearly presented using multivariate analysis. The changed metabolic profile in the low-dose group (5 mg/kg/day) revealed that the metabolic disturbance in the hippocampus and liver of mice had been induced by low-dose of IMI, although no significant histopathological changes were observed in the low-dose group. Six differential metabolites in the hippocampus and 10 differential metabolites in the liver were identified as the possible biomarkers to distinguish IMI exposure from the control group using the variable importance in projection (VIP) value and receiver operating characteristic (ROC) analysis. The metabolism disturbances of important biochemical pathways in the hippocampus and liver of mice in the exposed groups were elucidated, mostly concentrated in lipid metabolism, amino acid metabolism, nucleotide metabolism, carbohydrate metabolism, and energy metabolism (p < 0.05). Such investigations give out a global view of IMI-induced damages in the hippocampus and liver of mice and imply a health risk associated with early metabolic damage in mice.

Improvement of cell counting method for Neubauer counting chamber.

BACKGROUND: We compared the cell counting accuracy of the conventional method and the improved method by using Neubauer counting chamber. METHODS: In the improved method, all the border cells were counted and then divided by two; while, in the conventional method, only border cells on the two boundaries (top and left) were counted. RESULTS: About 55.814% of the samples showed more accurate results by improved counting method, about 38.372% had more accurate results by conventional counting method, and about 5.814% were counted with similar counting error by both methods. The improved method had significantly smaller counting error than conventional method (P < .05). The distribution ratio of the border cells was an independent factor for counting accuracy (P < .05). CONCLUSION: Together, the improved counting method can reduce the counting error of the Neubauer counting chamber to some extent, assess the distributing uniformity of border cells, and help to eliminate the samples with large differences in distribution.

BRF1 ameliorates LPS-induced inflammation through autophagy crosstalking with MAPK/ERK signaling.

Inflammation is indispensable for host defense, whereas excessive inflammation often develop inflammatory diseases. Autophagy is thought to be engaged in many extracellular stress responses, such as starvation and innate immunity. Thus, autophagy plays an important role in maintaining homeostasis. The purpose of this study was to elucidate the function of BRF1 in the regulation of inflammation and autophagy response in macrophages. We found that BRF1 inhibited the LPS-induced inflammatory factors expression and the autophagy flux in macrophage. Furthermore, inhibition autophagy with 3-MA can attenuate the suppressive effect of BRF1 on LPS-mediated inflammation. In addition, MAPK/ERK signaling pathway was involved in the BRF1 inhibition inflammation and autophagy in macrophages. These findings indicate that BRF1 attenuates LPS-induced inflammatory factors secretion through autophagy, at least in part, through MAPK/ERK signaling pathway.

m6A Demethylase FTO Regulates Dopaminergic Neurotransmission Deficits Caused by Arsenite.

Arsenite exposure is known to increase the risk of neurological disorders via alteration of dopamine content, but the detailed molecular mechanisms remain largely unknown. In this study, using both dopaminergic neurons of the PC-12 cell line and C57BL/6J mice as in vitro and in vivo models, our results demonstrated that 6 months of arsenite exposure via drinking water caused significant learning and memory impairment, anxiety-like behavior and alterations in conditioned avoidance and escape responses in male adult mice. We also were the first to reveal that the reduction in dopamine content induced by arsenite mainly resulted from deficits in dopaminergic neurotransmission in the synaptic cleft. The reversible N6- methyladenosine (m6A) modification is a novel epigenetic marker with broad roles in fundamental biological processes. We further evaluated the effect of arsenite on the m6A modification and tested if regulation of the m6A modification by demethylase fat mass and obesity-associated (FTO) could affect dopaminergic neurotransmission. Our data demonstrated for the first time that arsenite remarkably increased m6A modification, and FTO possessed the ability to alleviate the deficits in dopaminergic neurotransmission in response to arsenite exposure. Our findings not only provide valuable insight into the molecular neurotoxic pathogenesis of arsenite exposure, but are also the first evidence that regulation of FTO may be considered as a novel strategy for the prevention of arsenite-associated neurological disorders.

Genotype Identification and Phylogenetic Analysis of Enterocytozoon bieneusi Isolates from Stool Samples of Diarrheic Children.

Among approximately 14 human-pathogenic microsporidian species, Enterocytozoon bieneusi is the most common. It can inhabit the small intestines, causing chronic diarrhea and wasting syndrome. Prevalence and genotype data for E. bieneusi in humans is available for only a few provinces of China. In the current study, 93 fecal specimens were collected from diarrheic children in Chongqing. Polymerase chain reaction amplification and sequencing of the internal transcribed spacer ( ITS) region of the E. bieneusi rDNA sequence identified 11 (11.83%) positive specimens. Among them, 8 (8.60%) are from patients of ages ranging from 2 mo to 6 yr old and 3 (3.23%) from patients 7 to 11 yr old. In total, 6 genotypes (4 novel genotypes and 2 known genotypes) were identified in this study. Phylogenetic analysis showed that all the genotypes identified in the present study belong to group 1, which previously has been described as a zoonotic group. This could mean these infections were acquired zoonotically, and it may be prudent to warn those people having close contact with animals of this potential risk.

Spa therapy (balneotherapy) relieves mental stress, sleep disorder, and general health problems in sub-healthy people.

To investigate the relieving effects of hot spring balneotherapy on mental stress, sleep disorder, general health problems, and women's health problems in sub-healthy people, we recruited 500 volunteers in sub-health in Chongqing, and 362 volunteers completed the project, including 223 in the intervention group and 139 in the control group. The intervention group underwent hot spring balneotherapy for 5 months, while the control group did not. The two groups took questionnaire investigation (general data, mental stress, emotional status, sleep quality, general health problems, as well as some women's health problems) and physical examination (height, weight, waist circumference, blood pressure, blood lipid, blood sugar) 5 months before and after the intervention, respectively. After intervention, sleep disorder (difficulty in falling asleep (P = 0.017); dreaminess, nightmare suffering, and restless sleep (P = 0.013); easy awakening (P = 0.003) and difficulty in falling into sleep again after awakening(P = 0.016); and mental stress (P = 0.031) and problems of general health (head pain (P = 0.026), joint pain(P = 0.009), leg or foot cramps (P = 0.001), blurred vision (P = 0.009)) were relieved significantly in the intervention group, as compared with the control group. While other indicators (fatigue, eye tiredness, limb numbness, constipation, skin allergy) and women's health problems (breast distending pain; dysmenorrhea, irregular menstruation) were relieved significantly in the self-comparison of the intervention group before and after intervention (P < 0.05), but showed no statistically significant difference between two groups (P > 0.05). All indications (except bad mood, low mood, and worry or irritability) in the intervention group significantly improved, with effect size from 0.096 to 1.302. Multiple logistic regression analysis showed that the frequency, length, and location of balneotherapy in the intervention group were the factors influencing emotion, sleep, and health condition (P < 0.05). Relief of insomnia, fatigue, and leg or foot cramps was greater in old-age group than in young-aged group (P < 0.05). Physical examination found that waist circumferences in women of various ages under 55 years were significantly reduced in the intervention group (P < 0.05), while that in men did not significantly change (P > 0.05). Spa therapy (balneotherapy) relieves mental stress, sleep disorder, general health, and reduces women's waist circumferences in sub-healthy people.

Disruption of glutamate neurotransmitter transmission is modulated by SNAP-25 in benzo[a]pyrene-induced neurotoxic effects.

Benzo[a]pyrene (B[a]P), a ubiquitous chemical contaminant in the environment, is a well-established neurotoxicant to human. However, the molecular mechanisms for B[a]P neurotoxicity are still unclear. In the present study, after treating Sprague-Dawley rats with 0.02, 0.2 and 2.0mg/kg/day B[a]P for 7 weeks [from postnatal day (PND) 5 to PND54], our results showed that B[a]P exposure caused a significant deficits in learning and memory function. By using U87 cells as in vitro model, the significant cytotoxicity and the induction of apoptosis caused by B[a]P were further verified. More importantly, we demonstrated for the first time that B[a]P exposure caused the disruption of glutamate (Glu) neurotransmitter transmission by decreasing the level of Glu, reducing the expression of Glu receptors (GluR1 and GluR2), enhancing the level of SNAP-25, widening the synaptic cleft, and ultimately producing the neurotoxic effects in both cells and animals. Our results will provide novel evidence to reveal the possible role of SNAP-25 in B[a]P-induced neurotoxicity and may be helpful for searching the potential strategy for the prevention measures against B[a]P neurotoxicity.

[Health Qigong Wuqinxi improves hydrogen proton magnetic resonance spectra in prefrontal cortex and hippocampus in college students with mild depression].

OBJECTIVE: To investigate the effects of health Qigong Wuqinxi exercise on mild depression in college students and analyze the changes in hydrogen proton magnetic resonance spectra (1H-MRS) in the prefrontal cortex and hippocampus after the exercise. METHODS: Fifty-eight volunteer college students, including 30 with mild depression and 28 healthy students, were randomized into the intervention group and non-intervention group. The students in the intervention group were asked to practice health Qigong Wuqinxi training for 12 weeks and those in the non-intervention group did not engage in such training. For each subject, BECK Depression Self-reported questionnaire (BDI), Hamilton Depression rating scale (HAMD) score, and the metabolic parameters of 1H-MRS in the prefrontal cortex and hippocampus were evaluated before and after the intervention. RESULTS: Before the intervention, the scores of BDI and HAMD in the depression group were significantly higher than that in the control group (P<0.01), and were lowered obviously after the 12-week intervention (P<0.01). Compared with the control group, 1H-MRS in the depression group before intervention showed significantly increased NAA/Cr value in the left prefrontal cortex, Cho/Cr value in the bilateral hippocampus and the left frontal lobe, and Cho/Cr value of the left hippocampus and right frontal lobe (P<0.05) with significantly lowered NAA/Cho value in the bilateral prefrontal and Cho/NAA value in the right hippocampus (P<0.05). After 12 weeks of intervention, NAA/Cr value in the bilateral hippocampus and the NAA/Cho value in the right hippocampus were significantly lowered (P<0.05), and NAA/Cho value in the right prefrontal and Cho/NAA value in the right hippocampus were significantly increased (P<0.05) in the depression group. Before the intervention, Pearson correlation analysis showed that the scores of HAMD and BDI were positively correlated with Cho/Cr value in the hippocampus and NAA/Cr value in prefrontal lobe (P<0.01) and inversely with NAA/Cho in prefrontal lobe and Cho/NAA value in the hippocampus (P<0.05); after the intervention, the scores of HAMD and BDI were positively correlated with NAA/Cr value in the hippocampus and Cho/Cr value in the left hippocampus (P<0.05). CONCLUSION: Exercise of health Qigong Wuqinxi can reduce depression scale scores in patients with mild depression and improve the metabolic indexes (NAA/Cr and Cho/Cr values) in the prefrontal cortex and the hippocampus.

Cadmium Exposure is Associated with the Prevalence of Dyslipidemia.

BACKGROUND: Cadmium is a widespread environmental and occupational pollutant that accumulates in human body with a biological half-life exceeding 10 years. Cadmium exposure has been demonstrated to increase rates of cardiovascular diseases. Whether occupational cadmium exposure is associated with the increase in the prevalence of dyslipidemia and hence contributes to the risk of cardiovascular diseases is still equivocal. To test the hypothesis that exposure to cadmium is related to the prevalence of dyslipidemia, we examined the associations between blood cadmium concentration and the prevalence of dyslipidemia in workers occupationally exposed to cadmium in China. METHODS: A cross-sectional survey on demographic data, blood cadmium level and lipid profile in cadmium exposed workers from seven cadmium smelting factories in central and southwestern China was conducted. We measured blood cadmium concentration and lipid components of 1489 cadmium exposed workers. The prevalence of dyslipidemia was compared across blood cadmium quartiles. Associations between the blood cadmium concentrations and the prevalence of dyslipidemia were assessed using confounder adjusted linear and logistic regressions. RESULTS: The blood cadmium concentration was 3.61±0.84µg/L ( mean ±SD). The prevalence of dyslipidemia in this occupational population was 66.3%. Mean blood cadmium concentration of workers with dyslipedemia was significantly higher than that of workers without dyslipidemia (p <0.01). The prevalence of dyslipidemia increased dose-dependently with elevations in blood cadmium concentrations (p for trend <0.001). Elevated levels of blood cadmium were associated with BMI, education attainment, income, smoking status and duration of exposure (all p <0.01). Furthermore, the profile of blood lipid was obviously changed in this occupational population. The prevalence of high TC, high TG, Low HDL-C and high LDL-C rose with increases in blood cadmium levels dose-dependently (p for trend <0.001). The odds ratios (95% confidence interval) for dyslipidemia across the increasing blood cadmium quartiles were 1.21(1.16-1.55), 1.56(1.11-1.87), 1.79(1.26-2.25) respectively (referencing to 1.00; p for trend <0.001), after multivariate adjustment for BMI, education attainment, income, lifestyle factors and duration of exposure, the association between blood cadmium concentrations and the prevalence of dyslipidemia remained unchanged (all p for trend <0.001). CONCLUSION: Elevated blood cadmium concentration is associated with prevalence of dyslipidemia. Cadmium exposure could alter lipid metabolism in humans. It is imperative to control cadmium exposure of occupational population in cadmium related industries and reduce adverse health effects.

[Effect of Benzo [α]pryene and Butylated Hydroxylanisole on Learning and Memory in Rats].

OBJECTIVE: To investigate the neurotoxic effect of benzo[α]pryene (B[α]P) and protective effect of butylated hydroxyl anisole (BHA) on learning and memory in hippocampus of rats. METHODS: Ninety male, SD rats were randomly divided into blank control group, solvent control group, B[α]P exposed group [(2 mg/(kg x d)], BRA group [50 mg/(kg x d)] and B[α]P + BHA combined group. Rats were given the appropriate dose oral treatment according to body mass and group (the same volume of saline and peanut oil were given to blank and solvent control group, respectively) for 90 d. After 90 d exposer, Morris water maze (MWM) was conducted to estimate rats' learning and memory ability. The level of malonaldehyde (MDA), superoxide dismutase (SOD) activity, Na(+)-K(+)-ATPase and Ca(2+)-Mg(2+)-ATPase activity and Ca2+ concentration were measured after rats were sacrificed and brain tissue were removed. RESULTS: Behavioral test results showed that the escape latency of B[α]P exposed group were significantly increased than other groups (P < 0.05); however, the number of crossing platform (4.13 ± 0.78) were decreased significant. The level of MDA [( 2.46 ± 0.39) nmol/mg prot.] and Ca2+ concentration [(146.3 ± 16.68) nmol/L] in the B[α]P exposed group increased significant, while the activity of Na(+)-K(+)-ATPase and SOD [(76.1 ± 11.42) nmol/mg prot.] were significantly decreased. Compared with B[α]P group, each index in B[α]P+ BHA combined group improved significantly (P < 0.05), besides, there were no statistically difference when compared with solvent control group. CONCLUSION: The neurotoxic effect of B[α]P may be related to the decrease of ATPase activity and the increase of Ca2+ concentration in hippocampus, while BHA can prevent these damages.

[Effects of benzo(a)pyrene exposure on the ATPase activity and content of Ca²âº in the hippocampus of neonatal SD rats].

OBJECTIVE: To investigate the effect of benzo(α)pyrene on the ATPase activity and content of Ca²âº in the hippocampus of neonatal SD rats. METHODS: Sixty male and 60 female 4-days-old neonatal SD rats were randomly divided into 5 groups (n=24): a blank control group, a vehicle control group (peanut oil), 3 benzo(α)pyrene groups (0.02, 0.2 and 2 mg/kg, respectively). SD rats were given benzo(α)pyrene (dissolved in peanut oil) by gavage daily from postnatal day 4 (PND4) to PND20. The nerve reflex, the condition of neuro-muscle development and motion function were examined in the period of treatment. The colorimetric technique was used to detect the activity of Ca²âº-ATPase and Ca²âº-Mg²âº-ATPase in hippocampus after the treatment. The concentration of Ca²âº of synapse in the hippocampus of rats was detected by fluorescent labeling. RESULTS: The results from the behavior tests showed that duration of surface reflex latency in rats with medium dose of benzo(α)pyrene was longer compared with that in the control group in PND12. The duration of surface reflex latency in rats with high dose of benzo(α) pyrene is longer in PND 14 and PND 16 compared with that in the control group (P<0.05). Compared with the rats in the control group, the activities of Ca²âº-Mg²âº-ATPase and Ca²âº-ATPase in hippocampus in rats with high dose benzo(α) pyrene were significantly decreased, and the degree in the decrease of Ca²âº-ATPase activity was dose-dependent (P<0.05). The contents of Ca²âº in the hippocampus in rats with medium or high dose of benzo(α) pyrene were significantly increased compared with that in the control group (P<0.05), which showed a dose-dependent manner (P<0.05). CONCLUSION: Benzo(α)pyrene exposure led to the decrease in ATPase activity as well as Ca²âº overload of the synapse in the hippocampal tissue, which in turn results in the nerve damage of newborn SD rats.