Short-term and long-term effects of cesarean section on asthma and wheezing: A cohort study and meta-analysis.

OBJECTIVE: To describe the short-term and long-term effects of cesarean section on childhood asthma and wheezing. METHOD: Firstly, in the cohort study, 6640 infants were included in the cohort baseline from January 2018 to December 2019, in which 6501 children completed the follow-up study for respiratory diseases at age 2 years. The effect of cesarean section on asthma and wheezing was estimated by the logistic regression model. Secondly, we conducted a meta-analysis of studies with outcomes of childhood asthma and wheezing under 2 years of age and over 2 years of age, respectively, to investigate the short-term and long-term effects of cesarean section on asthma and wheezing. RESULTS: In our cohort study, the cumulative incidence of asthma and wheezing was 1.3% (84/6501). 45.5% of children (2961/6501) were born by cesarean section. The adjusted odds ratio for the effect of cesarean section on asthma and wheezing in children under 2 years of age was 1.14 (95%CI 0.73-1.78). Combining previous studies (outcomes of asthma and wheezing under 2 years of age) with our results for a meta-analysis, the odds ratio was 1.15 (95%CI 1.05-1.25, I2 = 46.82%). Meanwhile, cesarean section had a long-term effect on asthma and wheezing in the child population over 2 years of age (OR = 1.17, 95%CI 1.11-1.24, P < 0.001, I2 = 79.38%). CONCLUSION: Cesarean section had a short-term effect on asthma and wheezing before the age of 2, in addition, the long-term effect of cesarean section on asthma and wheezing persisted in the child population (under 18).

A life course approach to asthma and wheezing among young children caused by ozone: A prospective birth cohort in northern China.

BACKGROUND: Given differences in vulnerability of children in early life, a life course approach to asthma and wheezing (AW) in young children caused by ozone (O3) is not fully understood. METHODS: We conducted a birth cohort in Jinan, China from 2018 to 2021 to elucidate the onset model of childhood AW due to O3 exposure. An inverse distance weighted model was used for individual exposure assessment. The time-dependent Cox proportional-hazard model and logistic model were used to investigate the effects of O3 exposure on AW. Principal component analysis, interaction analysis, and distributed lag model were used to analyze the life course approach. RESULTS: The cumulative incidence rate for AW among 6501 children aged 2 was 1.4%. A high level of O3 was related to AW (HR: 2.10, 95% CI: 1.31, 3.37). Only O3 exposure after birth was associated with AW, with an OR of 1.82 (1.08, 3.12), after adjusting for the effect before birth. Furthermore, adjusting for other air pollutants, the HR for the individual effect of high O3 exposure on AW was 2.44 (1.53, 3.89). Interestingly, P values for interactions for O3 and the principal components of other pollutants, as well as the characteristic variable of open windows were less than 0.1. Moreover, an increase in the IQR of O3 exposure at the 31st to 37th weeks before birth and the 1st to 105th weeks after birth was associated with an increase in the HRs for AW. CONCLUSIONS: High-level of O3 exposure after birth could lead to AW among young children. Importantly, the AW onset model may include the risk factors accumulation and the sensitive period model. Specifically, there are two sensitive windows in early life, and the correlated insults between the high level of O3 and other pollutants as well as open windows in the asthma-inducing effect.

[Klinefelter syndrome: Advances in research].

Klinefelter syndrome (KS) is a most common chromosome abnormality and frequently leads to male infertility. In recent years, deeper insights have been gained into the treatment of KS in children, clinical manifestations of KS, as well as reproductive problems and pre- and postnatal screening of the disease. This article presents an overview of the epidemiology, clinical manifestations, pathophysiological mechanism, laboratory examination, drug therapy and application of assisted reproductive technology, and KS screening, aiming to provide some reference for KS-related clinical practice.

Influence of Assembly Gap Size on the Structure and Properties of SUS301L Stainless Steel Laser Welded Lap Joint.

The microstructure and properties of laser welding lap joints with different assembly gap sizes are experimentally investigated. The laser weld joint is composed of γ-austenite and δ-ferrite, and the strip ferrite phase is mainly distributed at the austenite grain boundary. The weld metal presents the austenitic-ferritic (AF) solidification mode. When there is a gap between the two plates, a triangular region composed of similar equiaxed crystals can be found, and the size of the cellular crystals in this region decreases significantly. When the assembly gap size increases from 0.1 mm to 0.4 mm, the weld penetration state of the joint changes from full penetration to semi-penetration, and the surface collapse increases. The excessive size of the gap leads to a decrease in the tensile-shear force and fatigue strength of laser welded joints. In order to ensure that the surface morphology and properties of the welded joint meet the quality standard and requirement, the assembly gap should be less than 0.1mm.

Exposure to O3 during pregnancy and offspring asthma induced by OVA: Sensitive window identification.

BACKGROUND: Evidence proved that gestational ozone (O3) exposure can increase the risk of neonatal adverse respiratory outcomes, but offspring asthma is unclear. OBJECTIVE: This study aimed to investigate whether gestational O3 exposure could exacerbate offspring asthma, and to research the differences in effects of O3 exposure at different gestational periods on offspring asthma. METHODS: The pregnant ICR mice were randomly grouped and were administered O3 (air as control) at gestational day (GD) 1-6, 7-12, and 13-18, respectively. The pups aged 2-4 weeks were treated with ovalbumin (OVA) to establish a model of early life asthma. Asthma characteristics such as pulmonary inflammation, goblet cell proliferation, airway remodeling, OVA-specific immunoglobulin (Ig) E secretion and cytokines were examined. RESULTS: OVA sensitization and challenge successfully induced asthma in offspring. Compared with the air control, pulmonary inflammation infiltration, mucous secretion, the concentration of OVA-specific IgE, the level of tumor necrosis factor (TNF)-α, and T helper (Th) 2-skewed response were significantly exacerbated when O3 exposure at GD13-18 following inhaling OVA, while pulmonary inflammatory infiltration, mucus secretion, and Th2-skewed response were not significantly changed when O3 exposure at both GD1-6 and GD7-12. What's more, the above indicators in asthmatic offspring due to O3 exposure at GD13-18 were more severe than at GD1-6 and GD7-12. Interestingly, the signs of asthma only appeared in the offspring after OVA inhalation. When offspring were not treated with OVA, the prenatal O3 exposure alone did not lead to asthmatic reactions in offspring. In addition, O3 exposure at GD13-18 markedly increased the number of neutrophils and macrophages in Bronchoalveolar Lavage Fluid (BALF) of asthmatic offspring, and significantly exacerbated Th2 immune imbalance in asthmatic offspring, but had no effect on Th17 immune imbalance. CONCLUSION: Exposure to O3 during pregnancy aggravated asthma in offspring, in which the third trimester is the most sensitive window.

Prenatal O3 exposure increases the severity of OVA-induced asthma in offspring.

BACKGROUND: Accumulating epidemiological studies showed that prenatal and early life exposure to ambient air pollution was important contributor to the development of childhood asthma. However, the effects and mechanisms of prenatal exposure to ozone (O3), a type of ambient air pollution, on the progression of asthma in offspring remain unclear. OBJECTIVE: This study aimed to determine the effects and mechanism of asthma in offspring after prenatal O3 exposure. METHODS: Pregnant BALB/c mice were exposed to O3 or air on gestational days (GDs) 13-18. Their offspring were sensitized and challenged to ovalbumin (OVA) to establish asthma model, and the asthma features were evaluated. The splenic natural killer (NK) cells in the offspring were measured to explore the mechanism on the effects of asthma in the offspring. The responses of the pregnant mice and dams after O3 exposure were evaluated. RESULTS: Airway inflammation, mucus secretion, OVA-specific immunoglobulin (Ig) E, T helper (Th) 2-skewed response, the frequency of CD3ε-CD49b+ splenic NK cells, the expression of tumor necrosis factor (TNF)-α, and IL (interleukin)-17 were significantly exacerbated in the OVA-induced asthma offspring after prenatal O3 exposure. In addition, airway inflammation, a lower number of CD3ε-CD49b+ splenic NK cells, and systemic oxidative stress were caused at the end of pregnancy after O3 exposure, which did not recover at the end of lactation for the first two responses. CONCLUSIONS: Prenatal O3 exposure increased the severity of OVA-induced asthma in the offspring, which might be directly induced by CD3ε-CD49b+ splenic NK cells in the offspring and indirectly related to the damaged maternal immune system.

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.

Presence of antibiotic residues in various environmental compartments of Shandong province in eastern China: Its potential for resistance development and ecological and human risk.

OBJECTIVES: To investigate the occurrence of antibiotic residues in different types of environmental samples including water samples in rural Shandong province, China. Further, to characterize the potential ecological risk for development of antibiotic resistance in the environment, and the potential direct human health risk of exposure to antibiotics via drinking water and vegetables. METHODS: Environmental samples (n = 214) (river water, waste water, drinking water, sediments, manure, soil and edible parts of vegetables) were collected in twelve villages in Shandong province in eastern China. High performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS) was used to determine the concentration of antibiotic residues. The ratio of the measured environmental concentrations (MEC) to the predicted no-effect concentrations (PNEC) was used to evaluate the ecological risk (risk quotient, RQ) for development of antibiotic resistance. The potential risks to human health through exposure to antibiotics in drinking water were assessed by comparing measured environmental concentrations (MEC) and predicted no-effect concentration in drinking water (PNECDW), and in vegetables by comparing estimated daily intake (EDI) to ADI. RESULTS: Sulfapyridine, sulfamethoxazole, ciprofloxacin, enrofloxacin, levofloxacin, norfloxacin, chloramphenicol, florfenicol, doxycycline, and metronidazole were detected at concentrations ranging between 0.3 and 3.9 ng/L in river water, 1.3 and 12.5 ng/L in waste water, 0.5 and 21.4 ng/L in drinking water, 0.31 and 1.21 µg/kg in river sediment, 0.82 and 1.91 µg/kg in pig manure, 0.1 and 11.68 µg/kg in outlet sediment, 0.5 and 2.5 µg/kg in soil, and 6.3 and 27.2 µg/kg in vegetables. The RQs for resistance development were >1 for enrofloxacin, levofloxacin, and ranged between 0.1 and 1 for ciprofloxacin. MECs/PNECDW ratios were <1 from exposure to antibiotics through drinking water for both adults and children. EDI/ADI ratios were <0.1 from exposure to antibiotics by vegetable consumption. CONCLUSIONS: Antibiotic pollutants were ubiquitous in various environmental compartments of Shandong province of China. Risk estimates indicated a potential for the measured levels of enrofloxacin, levofloxacin and ciprofloxacin in waste water to pose an ecological risk for resistance selection, and further studies are needed to validate this finding. The investigated antibiotics did not appear to pose an appreciable direct human health risk from environmental exposure through drinking water or vegetables consumption. However, they might still pose a risk for resistance development.

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.

Potential of Pteris vittata to Remove Tetracycline Antibiotics from Aquatic Media.

The role of combined arsenic and antibiotics pollution in the environment has recently gained more attention. In this study, a new approach to eliminate tetracycline antibiotics (TCs) from water, via the fern species Pteris vittata (L.), an arsenic hyperaccumulator, was investigated. The encouraging results showed that more than half of the TCs could be removed from the water solution (with the starting concentration of TCs about 1.0 mg kg(-1) respectively) after one day of treatment. No TCs (less than 0.01 mg kg(-1)) were detected in the solution after five days of treatment. The results showed that Pteris vittata has high ability to eliminate TCs, which makes it suitable for practical application. Further research found that TCs concentrations were very low in both the roots and the pinnae of Pteris vittata, which indicates that accumulation in the fronds is not the main removal mechanism and that degradation in the fronds might be the main cause. Present results provide a feasible method for simultaneous removal of arsenic and TCs from livestock-polluted wastewater. However, more research work should be done before any real-world application is made.

[Structural equation model analysis of risk factors for low back pain among greenhouse vegetable-planting farmers].

OBJECTIVE: To explore the risk factors of low back pain (LBP) among greenhouse vegetable planting farmers and estimate the level of the effects. METHODS: A self-made questionnaire based on the Dutch Musculoskeletal Questionnaire and the Nordic Questionnaire was conducted to 639 greenhouse vegetable planting farmers and then structural equation model was used to analyze the risk factors of LBP in SmartPLS software. RESULTS: The coefficient of determination of the model was 0.827, and the structural coefficients of dynamic loads, static loads, force exertion, ergonomic environment and repetitive loads on LBP were 0.21, 0.43,0.27, 0.045 and 0.034 respectively, and the total effects of the above latent variables on LBP were 0.21, 0.43,0.27, 0.33 and 0.034 respectively. CONCLUSION: The main risk factors of LBP among greenhouse vegetable planting farmers were static loads, ergonomic environment, force exertion and dynamic loads.

[Expression changes of cyclin dependent kinase 5/p35 in nerve tissues of 2, 5-hexanedione intoxicated rats].

OBJECTIVE: To explore the role of cyclin dependent kinase 5 (CDK5) in 2, 5-hexanedione (HD)-induced neuropathy. METHODS: Thirty male Wistar rats weighted 200 approximately 240 g were divided randomly into three groups, i.e. control group, 200 mg/kg HD group and 400 mg/kg HD group (n = 10 for each group). HD was administered to rats by intraperitoneal injection at dosage of 200 or 400 mg/kg for 8 weeks (five times per week) to establish the intoxicated rats model. The relative contents of CDK5, p35 and p25 were determined in cerebrum, spinal cord and sciatic nerve of rats by Western Blotting. RESULTS: Compared with that of the control group rats, p35 contents were significantly decreased (P < 0.01) in the cytosolic fractions of cerebrum and spinal cord in both the 200 and 400 mg/kg HD intoxicated rats, while in the membrane fractions of spinal cord and sciatic nerve, p35 contents were increased significantly (P < 0.01). The changes of p25 showed the same pattern with p35. P25 contents were significantly reduced (P < 0.05) in the cytosolic (cerebrum and spinal cord) and membrane (cerebrum) fractions of both HD-treated rats and were elevated (P < 0.01) in the membrane fraction of spinal cord and cytosolic fraction of sciatic nerve. The relative amounts of CDK5 were significantly decreased (P < 0.01) in the cytosolic and membrane fractions of cerebrum in both the 200 and 400 mg/kg HD intoxicated rats. Except for membrane fraction of sciatic nerve, the significant increased (P < 0.01) of CDK5 were observed in the spinal cord and sciatic nerve of both the 200 and 400 mg/kg HD treated rats. CONCLUSION: HD can induce significant changes of CDK5 and its activators p35, p25 in nerve tissues, which may be related to the neuropathy induced by HD.

Involvement of cyclin-dependent kinase 5 in 2,5-hexanedione-induced neuropathy.

Occupational exposure to n-hexane produces a neuropathy characterized as a central-peripheral distal axonopathy, which is mediated by 2,5-hexanedione (HD). To investigate the mechanisms of the neuropathy induced by HD, the contents and activities of cyclin-dependent kinase 5 (CDK5) and activators (p35 precursor, p35 and p25) in rats' cerebrum cortex (CC), spinal cord (SC) and sciatic nerve (SN) were determined. The results showed that the levels and activities of CDK5 in CC of 200 or 400mg/kg HD-treated rats were significantly decreased in both the cytosolic and membrane fractions and negatively correlated with gait abnormality in the cytosolic fraction. However, CDK5 contents and activities in SN of rats treated with 200 or 400mg/kg HD were significantly increased and positively correlated with gait abnormality in both the cytosolic and membrane fractions. Although increases of CDK5 contents in both the cytosolic and membrane fractions of SC in 200 and 400mg/kg HD-treated rats were also observed, CDK5 activities were significantly decreased in the cytosolic fraction and negatively correlated with gait abnormality. The changes of p35 precursor, p35 and p25 contents in CC, SC and SN showed the same pattern with that of CDK5 activities. Thus, HD intoxication was associated with deregulation of CDK5 and its activator p35 or p25 in nerve tissues. The inconsistent changes of CDK5 activities in CNS and PNS might delegate the different mechanisms of HD-induced peripheral neuropathy.