Different functional connectivity optimal frequency in autism compared with healthy controls and the relationship with social communication deficits: Evidence from gene expression and behavior symptom analyses.

Studies have reported that different brain regions/connections possess distinct frequency properties, which are related to brain function. Previous studies have proposed altered brain activity frequency and frequency-specific functional connectivity (FC) patterns in autism spectrum disorder (ASD), implying the varied dominant frequency of FC in ASD. However, the difference of the dominant frequency of FC between ASD and healthy controls (HCs) remains unclear. In the present study, the dominant frequency of FC was measured by FC optimal frequency, which was defined as the intermediate of the frequency bin at which the FC strength could reach the maximum. A multivariate pattern analysis was conducted to determine whether the FC optimal frequency in ASD differs from that in HCs. Partial least squares regression (PLSR) and enrichment analyses were conducted to determine the relationship between the FC optimal frequency difference of ASD/HCs and cortical gene expression. PLSR analyses were also performed to explore the relationship between FC optimal frequency and the clinical symptoms of ASD. Results showed a significant difference of FC optimal frequency between ASD and HCs. Some genes whose cortical expression patterns are related to the FC optimal frequency difference of ASD/HCs were enriched for social communication problems. Meanwhile, the FC optimal frequency in ASD was significantly related to social communication symptoms. These results may help us understand the neuro-mechanism of the social communication deficits in ASD.

Penehyclidine Hydrochloride Alleviates Lipopolysaccharide-Induced Acute Lung Injury by Ameliorating Apoptosis and Endoplasmic Reticulum Stress.

BACKGROUND: Penehyclidine hydrochloride (PHC), a novel anticholinergic reagent, has been shown to exert anti-endoplasmic reticulum stress (ERS), antioxidant, and antiinflammation functions in various rat models. However, the definite pathogenesis of lung defensive roles of PHC remains unclear. This study measured the functions of PHC on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats. METHODS: In this research, the LPS-induced ALI model was assessed through the branchial injection of LPS for 24 h. Male Sprague-Dawley rats were randomly allocated into 5 groups: sham, LPS, LPS + PHC (0.5 mg/kg), LPS + PHC (1 mg/kg), and LPS + PHC (2.5 mg/kg). The concentrations of superoxide dismutase, malondialdehyde, myeloperoxidase, and glutathione peroxidase were measured by enzyme-linked immunosorbent assay and immunohistochemistry analysis. Western blotting, real-time PCR, and immunofluorescence analysis were used to determine the ERS-associated protein levels and mRNA expression. The protein levels of Bax, Bcl-2, caspase-3, and caspase-9 were used to measure lung tissue apoptosis. RESULTS: The results revealed that PHC administration inhibited LPS-induced ALI as indicated by the loss in the ratio of injury production evaluated through hematoxylin-eosin staining, in particular the lung sample sections, compared with the LPS group. PHC administration inhibited LPS-induced lung myeloperoxidase and serum concentrations of malondialdehyde, superoxide dismutase, and glutathione peroxidase in rats. PHC administration repressed the LPS-activated ERS-correlated pathway and apoptosis-associated protein levels in rats. CONCLUSIONS: In summary, our findings indicated that PHC has a defensive effect on LPS-induced ALI by inhibiting oxidative stress, attenuating PERK and ATF6 signals, and suppressing ERS-mediated apoptosis.

Blast-Burn Combined Injury Followed by Immediate Seawater Immersion Induces Hemodynamic Changes and Metabolic Acidosis: An Experimental Study in a Canine Model.

BACKGROUND: Severe burn-blast combined injury often causes systematic dysfunction related to blood coagulation, anticoagulation, and fibrinolysis. However, studies of burn-blast combined injury followed by immersion in seawater are rarely reported. METHODS: A canine burn-blast combined injury model was established including blast injury caused by explosion immediately followed by burning with gelatinized gasoline flames. The dogs were randomly divided into four groups: burn-blast injury (BB group); burn-blast injury followed by seawater immersion for four hours (BBI group); only immersed in seawater (I group); and sham treatment with no injury or immersion (S group). Rectal temperature, hemodynamic parameters, arterial blood gas levels, and respiratory function were measured. RESULTS: The dogs in the BB group showed relatively more stable hemodynamic features than those in the BBI group. The pH, base excess (BE), HCO3-, PaO2, and PaCO2 levels in the S, I, and BB groups after injury did not differ from those before injury (p > 0.05). The PaO2 level in the BBI group decreased initially after injury and returned to a normal level by 10 hours after injury. The pH, BE, HCO3-, and PaCO2 values in the BBI group decreased continuously after injury and were significantly less than those in the other groups (p < 0.05). CONCLUSIONS: Burn-blast combined injury followed by seawater immersion induced hemodynamic changes and metabolic acidosis. Knowledge of the early symptoms and unique pathophysiology of the combined injury will be valuable in determining the appropriate management of such patients. Level of evidence: Prognostic study, level IV.