Microstructural brain abnormalities and associated neurocognitive dysfunction in obstructive sleep apnea: a pilot study with diffusion kurtosis imaging.

STUDY OBJECTIVES: To assess the possible brain abnormalities in adult patients with moderate and severe obstructive sleep apnea (OSA) using the mean kurtosis (MK) from diffusion kurtosis imaging (DKI) and analyze the correlation between MK and cognitive function. METHODS: A total of 30 patients with moderate and severe OSA and 30 healthy controls (HCs) evaluated by the Montreal Cognitive Assessment (MoCA) scale were enrolled. All subjects underwent DKI and 3D T1-weighted imaging (T1WI) on a 3.0T MR scanner. The MK values of gray and white matter brain regions were compared. Partial correlation analysis was used to analyze the correlation between respiratory sleep parameters/cognitive score and MK values in different brain regions. RESULTS: Compared with the HCs, the MK of 20 brain regions (13 after false discovery rate (FDR) correction) and cognitive scores in the OSA group were significantly lower. In the OSA group, the apnea-hypopnea index (AHI) was negatively correlated with the MK in the white matter of the right occipital lobe; the LSpO2 was positively correlated with the MK in the bilateral parietal, precentral, and right postcentral cortex; the total score of MoCA scale was positively correlated with MK in the left hippocampus; the language function was positively correlated with MK in the white matter of left parietal lobe, and the delayed recall was positively correlated with the MK in right insula cortex and bilateral cingulate. After FDR correction, only the correlations of LSpO2 with right precentral gyrus cortex, and bilateral parietal cortex were significant. CONCLUSIONS: MK values of DKI imaging may provide valuable information in assessing the neurological impacts of obstructive sleep apnea.

Quantitative Relaxometry Assessment of Brain Microstructural Abnormality of Preschool Children With Autism Spectrum Disorder With Synthetic Magnetic Resonance Imaging.

OBJECTIVE: This study aimed to perform an assessment of brain microstructure in children with autism aged 2 to 5 years using relaxation times acquired by synthetic magnetic resonance imaging. MATERIALS AND METHODS: Thirty-four children with autism spectrum disorder (ASD) (ASD group) and 17 children with global developmental delay (GDD) (GDD group) were enrolled, and synthetic magnetic resonance imaging was performed to obtain T1 and T2 relaxation times. The differences in brain relaxation times between the 2 groups of children were compared, and the correlation between significantly changed T1/T2 and clinical neuropsychological scores in the ASD group was analyzed. RESULTS: Compared with the GDD group, shortened T1 relaxation times in the ASD group were distributed in the genu of corpus callosum (GCC) ( P = 0.003), splenium of corpus callosum ( P = 0.002), and right thalamus (TH) ( P = 0.014), whereas shortened T2 relaxation times in the ASD group were distributed in GCC ( P = 0.011), left parietal white matter ( P = 0.035), and bilateral TH (right, P = 0.014; left, P = 0.016). In the ASD group, the T2 of the left parietal white matter is positively correlated with gross motor (developmental quotient [DQ] 2) and personal-social behavior (DQ5), respectively ( r = 0.377, P = 0.028; r = 0.392, P = 0.022); the T2 of the GCC was positively correlated with DQ5 ( r = 0.404, P = 0.018); and the T2 of the left TH is positively correlated with DQ2 and DQ5, respectively ( r = 0.433, P = 0.009; r = 0.377, P = 0.028). All significantly changed relaxation values were not significantly correlated with Childhood Autism Rating Scale scores. CONCLUSIONS: The shortened relaxometry times in the brain of children with ASD may be associated with the increased myelin content and decreased water content in the brain of children with ASD in comparison with GDD, contributing the understanding of the pathophysiology of ASD. Therefore, the T1 and T2 relaxometry may be used as promising imaging markers for ASD diagnosis.

Effects of amiloride on potassium and calcium currents in guinea pig ventricular myocytes / 药学学报

<p><b>AIM</b>To elucidate the possible mechanisms underlying antiarrhythmia of the non-selective Na+/H+ exchanger inhibitor--amiloride.</p><p><b>METHODS</b>Single ventricular cells were isolated using a double-enzyme method. Effects of amiloride on voltage-dependent potassium and calcium currents in isolated guinea pig ventricular myocyte were recorded by using whole-cell patch clamp techniques.</p><p><b>RESULTS</b>Exposure to amiloride (10 -100 micromol x L(-1)), the L-type and T-type calcium currents were depressed. Amiloride resulted in a concentration-dependent inhibition of peak (Ca,L), But amiloride did not change the shape of their I - V curves. It only decreased the amplitudes of the currents of the two types. When myocytes were incubated with 100 micromol x L(-1) amiloride, I(Kr) was slightly depressed and I(Ks) did not change. Amiloride (1 - 100 micromol x L(-10) depressed I(K1) in a concentration-dependent manner.</p><p><b>CONCLUSION</b>Amiloride depressed potassium and calcium currents, which may give support to its uses in some diseases of the cardiovascular system.</p>

Effects of benzyltetrahydropalmatine on the rapidly activating component of delayed rectifier potassium current in guinea pig ventricular myocytes / 药学学报

<p><b>AIM</b>To investigate the effect of benzyltetrahydropalmatine (BTHP) on the rapidly activating component of delayed rectifier K+ current (Ikr) in single guinea pig ventricular myocytes.</p><p><b>METHODS</b>Whole-cell patch clamp technique was used to record Ikr.</p><p><b>RESULTS</b>Ikr was blocked by 1-100 mumol.L-1 BTHP in concentration-, voltage-, and specifically frequency-dependent fashion, with IC50 of 13.5 mumol.L-1 (95% confidence range: 11.2-15.8 mumol.L-1). 30 mumol.L-1 BTHP reduced Ikr and Ikr.tail by (31 +/- 4)% and (36 +/- 5)% (n = 6, P < 0.01), respectively. The time constant for deactivation (tau') of the tail current was decreased by 30 mumol.L-1 BTHP from (238 +/- 16) ms to (196 +/- 14) ms, while drug had no any effect on the time constant for activation (tau) of Ikr,tail.</p><p><b>CONCLUSION</b>BTHP inhibited Ikr in a frequency-dependent fashion.</p>