Disruption of the peripheral biological clock may play a role in sleep deprivation-induced dysregulation of lipid metabolism in both the daytime and nighttime phases.

STUDY OBJECTIVES: This study aimed to examine the effect of sleep deprivation (SD) on lipid metabolism or lipid metabolism regulation in the liver and white adipose tissue (WAT) during the light and dark phases and explored the possible mechanisms underlying the diurnal effect of SD on lipid metabolism associated with clock genes. METHODS: Male C57BL/6J mice aged 2 months were deprived of sleep daily for 20 h for ten consecutive days with weakly forced locomotion. The body weights and food consumption levels of the SD and control mice were recorded, and the mice were then sacrificed at ZT (zeitgeber time) 2 and ZT 14. The peripheral clock genes, enzymes involved in fat synthesis and catabolism in the WAT, and melatonin signalling pathway-mediated lipid metabolism in the liver were assessed. Untargeted metabolomics and tandem mass tag (TMT) proteomics were used to identify differential lipid metabolism pathways in the liver. RESULTS: Bodyweight gain and daily food consumption were dramatically elevated after SD. Profound disruptions in the diurnal regulation of the hepatic peripheral clock and enzymes involved in fat synthesis and catabolism in the WAT were observed, with a strong emphasis on hepatic lipid metabolic pathways, while melatonin signalling pathway-mediated lipid metabolism exhibited moderate changes. CONCLUSIONS: In mice, ten consecutive days of SD increased body weight gain and daily food consumption. In addition, SD profoundly disrupted lipid metabolism in the WAT and liver during the light and dark periods. These diurnal changes may be related to disorders of the peripheral biological clock.

Melatonin protects against body weight gain induced by sleep deprivation in mice.

Sleep deprivation is an epidemic phenomenon in modern society. Lack of sleep has been shown to result in metabolic and endocrine disorders that predispose to obesity and other chronic metabolic diseases. Melatonin is a sleep-related neurohormone and affected by the circadian rhythm and light/dark cycles. Melatonin has recently been used to ameliorate diet-induced or night light-induced energy metabolic imbalance. However, the effect of melatonin on sleep deprivation-induced obesity has been poorly characterized. This study focuses on the protective effects of melatonin on lipid metabolism and body weight homeostasis in sleep-deprived mice. Mice subjected to sleep deprivation had significantly decreased plasma melatonin content and increased food intake and body weight gain compared to that of control. Meanwhile, the transcription factor PPARγ protein in liver increased, but there were no significant changes in hepatic circadian proteins BMAL1 and REV-ERBα after 10 consecutive days of sleep deprivation. Moreover, melatonin supplementation increased liver AMPKα/PPARα signaling pathway activity, which leads to lipid catabolism and reduced fat accumulation. These findings suggested that melatonin may be a potential agent for protecting against sleep deprivation-induced obesity.

Recent Development of Graphene Based Electrochemical Sensor for Detecting Hematological Malignancies-Associated Biomarkers: A Mini-Review.

Hematologic malignancies are a group of malignant diseases of the hematologic system that seriously endanger human health, mainly involving bone marrow, blood and lymphatic tissues. However, among the available treatments for malignant hematologic diseases, low detection rates and high recurrence rates are major problems in the treatment process. The quantitative detection of hematologic malignancies-related biomarkers is the key to refine the pathological typing of the disease to implement targeted therapy and thus improve the prognosis. In recent years, bioelectrochemical methods for tumor cell and blood detection have attracted the attention of an increasing number of scientists. The development of biosensor technology, nanotechnology, probe technology, and lab-on-a-chip technology has greatly facilitated the development of bioelectrochemical studies of cells, especially for blood and cell-based assays and drug resistance differentiation. To improve the sensitivity of detection, graphene is often used in the design of electrochemical sensors. This mini-review provides an overview of the types of hematological malignancies-associated biomarkers and their detection based on graphene assisted electrochemical sensors.

Integrated metabolomics and proteomics analysis reveals energy metabolism disorders in the livers of sleep-deprived mice.

Sleep deprivation (SD) has been linked to impaired mental and physical health, obesity, and various diseases. However, the molecular mechanism underlying the effects of SD in the liver is still unclear. To investigate the metabolome and proteome alterations in the liver, an in vivo model of SD was established based on automated random motion platform techniques by applying a strategy of 10 consecutive days of 20 h of sleep deprivation +4 h of resting. The liver's altered metabolites and proteins were detected by liquid chromatography-tandem mass spectrometry (LC-MS/MS), and data analyses were performed with MetaboAnalyst 5.0. This study found 15 differential metabolites, including 12 upregulated- metabolites and 3 downregulated- metabolites. A total of 493 proteins were differentially regulated, including 377 upregulated- proteins and 116 downregulated- proteins. The glutathione metabolism, fructose and mannose metabolism, and pyruvate metabolism pathways had significant effects on the sleep-deprived mouse livers. These three active pathways cause energy metabolism disorder and may induce obesity. In conclusion, this study demonstrates that SD could change the metabolism of glucose, and specific fatty acids, amino acids, and critical enzymes in the liver, providing a reference for the health effects of insufficient sleep. SIGNIFICANCE STATEMENT: So far, little is known about the changes in metabolites and proteins in the liver of individuals who suffer from SD. Metabolites and proteins in serum, urine and hypothalamus do not entirely reflect the effects of sleep deprivation on the whole body. In addition, many SD-induced models used the multiplatform water environment method, which causes mice to fall into the water frequently. Under this condition, the physical exertion of mice is extremely high, and it is not suitable for long-term sleep deprivation. The SD induction process has caused some influence on the model. Finally, few studies have elucidated the imbalance of energy metabolism caused by SD to induce obesity from the molecular mechanism. This study used a rotary table deprivation apparatus to trigger SD. This method will not cause excessive consumption and stimulation of mice. Furthermore, this study analyzed the metabolic and proteomic changes in the liver and enriched the range and means of metabolic and proteomic changes in sleep deprived mice. Finally, this research provides reference for elucidating the molecular mechanism of sleep deprivation causing energy metabolism disorders in the liver of mice.

Nurse-led interventions on quality of life for patients with cancer: A meta-analysis.

BACKGROUND: To compare the quality of life outcome between nurse-led and non-nurse-led interventions for patients with cancer using a meta-analysis. METHODS: A systematic literature review was performed by searching randomized controlled trials about nurse-led interventions in PubMed, EMBASE, and Cochrane Library databases until June 2017. Pooled summary estimates for quality of life outcome was calculated as standardized mean difference (SMD) either on a fixed- or random-effect model via Stata 13.0 software. RESULTS: Seven literatures involving 1110 patients (554 in the nurse-led group and 556 in the control group) were included. Pooled analysis showed there were no differences in the global quality of life, cognitive, emotional, role, social and physical functions, appetite loss, diarrhea, and dyspnea scales of Quality of Life Questionnaire C30 version 3.0 core (QLQ-C30) questionnaires between the nurse-led and control groups. However, the nurse-led management program significantly decreased the occurrence of constipation (SMD = -0.36, 95% CI = -0.71 to -0.00; P = .001) and insomnia (SMD = -0.33, 95% CI = -0.99 to 0.32; P = .011) and reduced the financial difficulty (SMD = -0.34, 95% CI = -0.65 to -0.03; P = .033) for patients with cancer. CONCLUSION: The nurse-led disease management strategy seemed to be effective to improve constipation, insomnia, and financial impacts for patients with cancer in quality of life assessment.

Acupuncture Improves Intestinal Absorption of Iron in Iron-deficient Obese Patients: A Randomized Controlled Preliminary Trial.

BACKGROUND: Obesity has an adverse effect on iron status. Hepcidin-mediated inhibition of iron absorption in the duodenum is a potential mechanism. Iron-deficient obese patients have diminished response to oral iron therapy. This study was designed to assess whether acupuncture could promote the efficacy of oral iron supplementation for the treatment of obesity-related iron deficiency (ID). METHODS: Sixty ID or ID anemia (IDA) patients with obesity were screened at Beijing Hospital of Traditional Chinese Medicine and were randomly allocated to receive either oral iron replacement allied with acupuncture weight loss treatment (acupuncture group, n = 30) or oral iron combined with sham-acupuncture treatment (control group, n = 30). Anthropometric parameters were measured and blood samples were tested pre- and post-treatment. Differences in the treatment outcomes of ID/IDA were compared between the two groups. RESULTS: After 8 weeks of acupuncture treatment, there was a significant decrease in body weight, body mass index, waist circumference, and waist/hip circumference ratio of patients in the acupuncture group, while no significant changes were observed in the control group. Oral iron supplementation brought more obvious improvements of iron status indicators including absolute increases in serum iron (11.08 ± 2.19 µmol/L vs. 4.43 ± 0.47 µmol/L), transferrin saturation (11.26 ± 1.65% vs. 1.01 ± 0.23%), and hemoglobin (31.47 ± 1.19 g/L vs. 21.00 ± 2.69 g/L) in the acupuncture group than control group (all P < 0.05). Meanwhile, serum leptin (2.26 ± 0.45 ng/ml vs. 8.13 ± 0.55 ng/ml, P < 0.05) and hepcidin (3.52 ± 1.23 ng/ml vs. 6.77 ± 0.84 ng/ml, P < 0.05) concentrations declined significantly in the acupuncture group than those in the control group. CONCLUSION: Acupuncture-based weight loss can enhance the therapeutic effects of iron replacement therapy for obesity-related ID/IDA through improving intestinal iron absorption, probably by downregulating the systemic leptin-hepcidin levels.

Moderate exercise prevents neurodegeneration in D-galactose-induced aging mice.

D-galactose has been widely used in aging research because of its efficacy in inducing senescence and accelerating aging in animal models. The present study investigated the benefits of exercise for preventing neurodegeneration, such as synaptic plasticity, spatial learning and memory abilities, in mouse models of aging. D-galactose-induced aging mice were administered daily subcutaneous injections of D-galactose at the base of the neck for 10 consecutive weeks. Then, the mice were subjected to exercise training by running on a treadmill for 6 days a week. Shortened escape latency in a Morris water maze test indicated that exercise improved learning and memory in aging mice. The ameliorative changes were likely induced by an upregulation of Bcl-2 and brain-derived neurotrophic factor, the repression of apoptosis factors such as Fas and Bax, and an increase in the activity of glucose transporters-1 and 4. The data suggest moderate exercise may retard or inhibit neurodegeneration in D-galactose-induced aging mice.

[The changes of gene expression of iron transporters for duodenal iron uptake and export in diet-induced obese mice].

OBJECTIVE: This study aims to determine the gene expression changes of iron transporters-divalent metal transporter 1 (DMT1) and ferroportin 1 (Fpn1) in the duodenal tissue of diet-induced obese mice. METHODS: C57BL/6J mice were randomly divided into normal control (NC) and obesity model (OM) group, 6 in each, and fed on conventional and high-fat diet respectively for 14 weeks by table of random number. Then the DMT1 and Fpn1 mRNA contents in duodenal tissues of the animals were measured by Real-time PCR method, and the protein expression levels were analyzed by Western blot test. RESULTS: The Real-time PCR detection results showed that, compared with the NC group for which the mRNA expression level was defined as 1.0, the Fpn1 mRNA expression in OM group (0.58±0.11) was reduced significantly (t = 6.71, P = 0.014), whereas the relative expression level of DMT1 mRNA in OM group (0.89±0.26) showed no obvious alteration (t = 2.01, P = 0.122). Western blot results showed that the relative protein expression levels of Fpn1 in OM and NC group were 0.32±0.06 and 0.65±0.19, respectively, and the difference was statistically significant (t = 5.37, P = 0.026). The DMT1 protein relative abundance was 0.88±0.21 in OM group and 0.92±0.17 in NC group, and the difference has no statistical significance (t = 1.84, P = 0.185). CONCLUSION: Fpn1 gene expression is inhibited in the duodenum of diet-induced obesity mouse while DMT1 expression keeps unchanged, and this implies that decreased iron export from enterocytes into circulation might be responsible for the impaired iron absorption in obesity.

Calorie restriction down-regulates expression of the iron regulatory hormone hepcidin in normal and D-galactose-induced aging mouse brain.

It has been shown that iron progressively accumulates in the brain with age. Calorie restriction (CR) may allay many of the adverse effects of aging on the brain, yet the underlying mechanisms, in particular in relation to brain iron metabolism, remain unclear. This study aimed to investigate the role of CR in the regulation of cerebral cellular iron homeostasis. C57BL/6 mice were randomly divided into four groups of eight. The control group was fed a conventional diet ad libitum; the CR group received 70% of the calories of the control mouse intake per day; the D-galactose (D-gal) group received subcutaneous injection of D-gal at a dose of 100 mg/kg once daily to produce mouse model of aging; the D-gal plus CR group received both of the two interventions for 14 weeks. The Morris water maze (MWM) was employed to test the cognitive performance of all animals, and the expression of iron regulatory genes, ferroportin and hepcidin, in the cortex and hippocampus were detected by quantitative real-time PCR. Compared to the controls, the D-gal group mice showed significant spatial reference memory deficits in the MWM test, whereas the D-gal-CR group mice exhibited almost normal cognitive function, indicating that CR protects against D-gal-induced learning and memory impairment. Hepcidin mRNA expression was increased in the D-gal group, decreased in the CR group, and was basically unchanged in the D-gal-CR group. There was no statistical difference in the transmembrane iron exporter ferroportin expression between control and any of the experimental groups. The results suggest that the anti-aging effects of CR might partially lie in its capacity to reduce or avoid age-related iron accumulation in the brain through down-regulating expression of brain hepcidin--the key negative regulator for intracellular iron efflux--and that facilitating the balance of brain iron metabolism may be a promising anti-aging measure.

Child Health and Nutrition: Getting better and facing new challenges in China.

BACKGROUND: Child healthcare practices in China over the last 60 years have extensively improved children's health and growth, yet new challenges lie ahead. This review aims to summarise the successful experiences and the newly identified problems in child healthcare in China. METHOD: Information, available to the public, was obtained from Chinese databases and Chinese Government websites,chiefly the Chinese National Knowledge Infrastructure database, the Chinese Biomedical Literature database, the Ministry of Health website and the National working committee on children and Women website RESULTS: During its poverty-stricken 1950s-1970s, China protected children's health mainly through prevention and control of common infectious diseases and severe malnutrition within a comprehensive healthcare system. After the subsequent 30 years of rapid socio-economic development, China has achieved great success in reducing childhood mortality rates and promoting child growth, meeting the Millennium Development Goal 4 targets and the WHO child growth standards. Meanwhile, new challenges for children's healthcare emerged, including: large disparities in the health, growth and nutritional status of children,and in the accessibility and quality of child healthcare, between urban and rural areas and across different regions of China; the nutritional and healthcare concerns of the fast-expanding population of migrant children and rural left-behind children; the burgeoning epidemic of childhood obesity in urban and economically developed areas; micronutrient deficiencies such as calcium, iron, zinc and vitamin A; and increasing prevalence of mental and behavioural disorders. CONCLUSION: Under poor economic conditions, healthcare plays a key role in protecting children against diseases. With the development of social economy, new challenges present to healthcare services, specifically, to comprehensively promote and optimise childrens' health and nutrition.

[Effects of exercise on spatial learning and hippocampal synaptic plasticity in brain aging mice].

OBJECTIVE: To examine the effects and mechanism of exercise on resisting brain aging from the aspect of synaptic plasticity. METHODS: Forty male ICR mice were randomly divided into 4 groups: the D-galactose-induced brain aging, brain aging plus exercise, exercise only and normal controls. Mice were subjected to treadmill running at intensity (25 m/min for 20 min daily, 6 days a week) level of exercise and were given 100 mg x kg(-1) x d(-1) subcutaneous injection of D-galactose to prepare brain aging model for 9 weeks. The Morris water maze (MWM) test was employed to determine their spatial learning and memory ability. Flow cytometry (FCM) was used to analyze the amount of hippocampal synaptosomes. Membrane fluidity of synaptosomes was measured by fluorescence polarization technique. Acetylcholinesterase (AChE) activity in brain was determined by hydroxylamine colorimetric assay. RESULTS: (1) In Morris water maze test, brain aging mice showed a significant longer escape latency (EL) than the normal control mice (P < 0.05). Brain aging mice plus exercise exhibited a significant shorter EL than brain aging mice (P < 0.05), but no difference was found when compared with normal control mice (P > 0.05). There were no statistical difference in EL between the controls and exercise group (P > 0.05). (2) The number of synaptosomes in brain aging mice and brain aging mice plus exercise were less than those in non-brain aging mice (the exercise and the control mice) (P < 0.05). The number of synaptosomes in brain aging mice plus exercise was more than brain aging mice (P < 0.05). There were no statistical difference in the number of synaptosomes between the controls and exercise group (P > 0.05). (3) Membrane fluidity of synaptosomes: the viscosity of membrane in brain aging group was higher than in non-brain aging group, and higher than brain aging plus exercise group (P < 0.05). There were no statistical difference in viscosity of membrane between brain aging group and non-brain aging group, and between the controls and exercise group (P > 0.05). (4) The AChE activity in brain aging and brain aging plus exercise group were higher than those in control and exercise group (P < 0.05). There were no statistical difference in AChE activity between the controls and exercise group (P > 0.05). CONCLUSION: Exercise can effectively protect against decline in the capacity of learning and memory in brain aging mice.