Evidence suggests that prenatal maternal stress (PNMS) has long-term effects on several outcomes, yet effects on neuromotor function are relatively unknown. We aimed to determine whether disaster-related PNMS predicts motor functioning in young children and whether timing of exposure and sex of the child moderate these effects. Objective and subjective PNMS levels were assessed among pregnant women exposed to a natural disaster. Their children's bilateral coordination, balance, and visual motor integration (VMI) were assessed at 5½ years. Girls performed better than boys. Objective stress exposure and subjective distress interacted such that when subjective distress was high, no added effect of objective hardship was observed; when subjective distress was low, objective hardship showed a negative effect. In girls, late pregnancy exposure was associated with poorer outcomes. In conclusion, disaster-related PNMS is associated with relatively lower motor functions in exposed offspring. Exposure timing, sex, and type of stress influenced the effects.
Previous research has shown that antioxidant (butylated hydroxyanisole) treatment ameliorates respiratory syncytial virus (RSV)-induced disease and lung inflammation. Melatonin has been reported to exhibit a wide varieties of biological effects, including antioxidant and anti-inflammation, and has no evident toxicity and side effect. But it is not known whether melatonin would modify RSV-induced lung disease and oxidative stress. The present study was to establish the involvement of oxidative stress in the pathogenesis of RSV-induced lung inflammation, and to investigate the protective effect of administration of melatonin in mice with RSV-induced oxidative pulmonary injury for 4 days. Malondialdehyde (MDA), an end product of lipid peroxidation, and glutathione (GSH) and superoxide dismutase (SOD) and nitric oxide (NO) levels were evaluated in lung tissue homogenates by spectrophotometry. Hydroxyl radical (.-OH), one of the indicators of free radical formation, was also detected in lung homogenates by Fenton reaction. Tumor necrosis factor-a (TNF-a) concentrations in mouse serum were measured with ELISA assay. The results demonstrated that the mice intranasally inoculated with RSV resulted in oxidative stress changes by increasing NO, MDA and .-OH levels, and decreasing GSH and SOD activities, whereas administration of melatonin significantly reversed all these effects. Furthermore, melatonin inhibited production of proinflammatory cytokines such as TNF-a in serum of RSV-infected mice. These results suggest that melatonin ameliorates RSV-induced lung inflammatory injury in mice via inhibition of oxidative stress and proinflammatory cytokine production and may be as a novel therapeutic agent in virus-induced pulmonary infection.
Double-stranded (ds) RNA has been identified as a ligand for Toll-like receptor 3 (TLR3). Respiratory syncytial virus (RSV), a single-stranded RNA virus and a major respiratory pathogen and pneumovirus in human infants pathogenesis of which relies on early inflammatory and immune events of the host in response to RSV, could be recognized by TLR3 sensing viral dsRNA produced during replication. The downstream signaling pathway from TLR3 leads to activation of IFN regulatory factor (IRF)-3 and/or NF-kappaB and subsequent expression of numerous proinflammatory factors. Melatonin (MT) is an effective regulator of the immune system. To determine the molecular mechanisms responsible for the suppressive effect of MT on RSV infection, we analyzed signaling molecules involved in the TLR3-mediated activation of inflammatory factors in macrophages infected with RSV and the modulatory role of MT on these mediators. We report that RSV infection of RAW264.7 macrophages time-dependently stimulate the rapid activation of TLR3 and NF-kappaB, as well as subsequent NF-kappaB-dependent gene expression such as those encoding TNF-alpha and inducible nitric oxide synthase. Moreover, we demonstrate that MT decreased TLR3-mediated downstream gene expression in RSV-infected macrophages in a dose- and time-dependent manner, and that MT inhibition of NF-kappaB activity seemed to be the key event required to explain the reduction in inflammatory gene expression caused by MT. But MT did not influence TLR3 at either the protein or mRNA level or MyD88 transcription. These results could be related to the beneficial immunoregulatory role of MT in RSV-infected macrophages and address the possible therapeutic potential of this indoleamine in human RSV diseases.
The increasing evidences showed that adverse early life events have profound long lasting consequences in adult rats including neural, behavioral, and cognitive effects. Early maternal separation was one of the models of adverse early life stress, but which period acts critically was unknown until now. The purpose of this paper was to explore the effects of maternal separation in different periods, that is, postnatal Day 2-9 and postnatal Day 14-21, on spatial learning and memory and long-term potentiation (LTP) in hippocampus of adolescent rats. Rat pups were assigned to three groups: early maternal separation from postnatal Day 2-9 (EMS2-9), separation from postnatal Day 14-21 (EMS14-21), and control (Con)--rats stayed with their mother all the time before weaning. Morris water maze test (MWM) and electrophysiological test were performed at 40-50 days of age. The results indicated that EMS14-21 impaired spatial learning and memory ability. For the excitatory postsynaptic potential long-term potentiation (EPSP LTP), both the two maternal separation groups showed decreased values compared to control group. In terms of population spike long-term potentiation (PS LTP), both the two maternal separation groups also showed lower values compared with control group, but only EMS14-21 group had significant difference compared with control group. In conclusion, our results revealed that EMS14-21 showed worst in both escape latency in Morris Water Maze test and LTP compared to control group and EMS2-9 group.
There is little investigation on the independent effects of left-behind experience (LBE) on self-esteem and aggressive behavior in Chinese young adult populations, or the interaction effects of LBE and self-esteem on aggressive behavior. Thus, a school-based health survey was conducted in Anhui province in China in 2017. A total of 4,154 college students completed standard questionnaires which contain details of left-behind–related characters, self-esteem, aggressive behavior, and sociodemographic profile. Of included students, 55.3% were those with LBE (LBEs). Compared to students without left-behind experiences (NLBEs), LBEs had significantly increased scores of aggressive behavior and decreased score of self-esteem. The increased aggression in LBEs was highly related to longer left-behind duration, younger age of left-behind for the first time, and decreased self-esteem. On the other side, the aggressive behavior was demonstrated negatively correlated with self-esteem in both LBEs and NLBEs. There was an interaction effect of left-behind duration and self-esteem on physical aggression and of frequency of contacting with parents and self-esteem on verbal aggression. Besides, the interaction of primary caregiver and self-esteem on hostility and aggression toward self were also observed, respectively. Our results indicated LBEs and low self-esteem are associated with increased risk of aggressive behavior in Chinese young adults. The increased aggressive behavior in LBEs were highly related to longer left-behind duration, younger age of left-behind for the first time and decreased self-esteem. In those LBEs with some certain left-behind–related characters, aggressive behavior decreased more prominently with the increase of self-esteem. Strategies to improve self-esteem, particularly among young adults who have certain characters of LBE, should be a significant component of prevention and interventions of aggressive behavior.
Lead (Pb2+) exposure in children can induce long lasting deficits in cognitive function and has been modeled in experimental animals. Based on previous studies which demonstrated that learning impairments resulting from developmental Pb2+ exposure were reversible if the animals were provided with an enriched environment, here, we asked if environmental enrichment (EE) could also reverse long-term potential (LTP) impairment induced by lead. Rats drank 1,500 ppm lead acetate (PbAc) solution or distilled water throughout gestation and lactation. After weaning at postnatal Day 22, one half of the control and lead-exposed male offspring were given the environmental enrichment treatment through all the experiments until tested. Electrophysiological and Morris water maze test were performed at 8 weeks of age. The result showed that the impaired learning ability induced by lead could be reversed by EE. Furthermore, our results revealed that EPSP LTP and PS LTP impairments induced by lead were also reversible by EE experience.
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