Free Triiodothyronine Is Associated With Hepatic Steatosis and Liver Stiffness in Euthyroid Chinese Adults With Non-Alcoholic Fatty Liver Disease.

Objective: The association between non-alcoholic fatty liver disease (NAFLD) and thyroid hormones in euthyroid subjects is unclear. We investigated the relationship between thyroid function and the severity of hepatic steatosis and liver fibrosis in a large cohort of euthyroid Chinese adults. Methods: A total of 3496 participants were enrolled. Liver ultrasonography was used to define the presence of NAFLD (n=2172) or the absence of NAFLD (n=1324). Anthropometric and biochemical measurements were made and thyroid function parameters including free triiodothyronine (FT3), free thyroxine (FT4), thyroid-stimulating hormone (TSH) were measured. The severity of hepatic steatosis and liver stiffness was assessed by transient elastography. Results: Levels of FT3 were significantly higher in the severe NAFLD group and moderate NAFLD group than in the mild NAFLD group (5.18 ± 0.58 vs 5.11 ± 0.57 vs 4.98 ± 0.60 pmol/L, P<0.001). Participants with F4 and F3 liver fibrosis had higher FT3 levels than those with F2 fibrosis (6.33 ± 0.39 vs 5.29 ± 0.48 vs 5.20 ± 0.50 pmol/L, P<0.001). However, FT4 and TSH levels did not correlate with hepatic steatosis or liver fibrosis severity. In addition, the proportions of participants with NAFLD (46.0% vs 63.1% vs 73.3%, P<0.001) and liver fibrosis (11.5% vs 18.6% vs 20.8%, P<0.001) increased as FT3 levels increased. Logistic regression analysis showed that FT3 levels were positively associated with the severity of hepatic steatosis and liver fibrosis presence, even after adjustment for metabolic risk factors including BMI. In non-obese participants, the FT3 level was an independently risk factor for the severity of hepatic steatosis. Conclusions: There are positive associations of FT3 levels with the severity of hepatic steatosis and the presence of liver fibrosis in NAFLD with euthyroidism.

Serum alkaline phosphatase is associated with arterial stiffness and 10-year cardiovascular disease risk in a Chinese population.

BACKGROUND: Serum alkaline phosphatase (ALP) has been recognized as a biomarker of cardiovascular disease (CVD) risk, recently. This study aimed to explore the association of ALP with arterial stiffness and 10-year CVD risk. METHODS: A total of 12 539 participants without CVD who underwent health examinations including serum ALP level were retrospectively analysed. Arterial stiffness was measured by brachial-ankle pulse wave velocity (baPWV), and 10-year CVD risk was evaluated by Framingham risk score. RESULTS: All participants were stratified into four groups according to the quartile of serum ALP. Participants with high ALP quartiles had higher cardiovascular parameters and baPWV, as well as an increase 10-year CVD risk. There was a dose-response relationship between serum ALP level and baPWV (OR = 1.134, 95% CI 1.103-1.165, P < .001). Logistic regression analysis showed that serum ALP was positively associated with elevated baPWV and 10-year CVD risk after adjustment for traditional CVD risk factors in both women and men. In receiver operating characteristic (ROC) curve analysis, the optimal cut-off point of serum ALP for elevated baPWV was 84U/L and the area under the ROC curve (AUROC) was 0.740 (95% CI 0.726-0.754, P < .001), with 71.2% and 63.4% sensitivity and specificity, respectively, in women. The AUROC of serum ALP in women was larger than that in men [0.575 (95% CI 0.559-0.590), P < .001]. CONCLUSIONS: Serum ALP is independently associated with arterial stiffness and 10-year CVD risk. Our results imply that serum ALP may be a promising marker to identify an increased risk for subclinical atherosclerosis in women needing further evaluation.

Enhanced positive functional connectivity strength in left-sided chronic subcortical stroke.

Patients with stroke often exhibit evidence of abnormal functional connectivity (FC). However, whether and how anatomical distance affects FC at rest remains unclear in patients with chronic subcortical stroke. Eighty-six patients with chronic (more than six months post-onset) subcortical stroke (44 left-sided patients and 42 right-sided patients) with different degrees of functional recovery, and 75 matched healthy controls underwent resting-state functional magnetic resonance imaging scanning. Positive functional connectivity strength (FCS) was computed for each voxel in the brain using a data-driven whole-brain resting state FCS method, which was further divided into short- and long-range FCS. Compared with healthy controls, patients with left-sided infarctions exhibited stronger global- and long-range FCS in the left sensorimotor cortex (SMC), and no significant intergroup difference was found for short-range FCS. No significant differences were found between the patients with right-sided infarctions and healthy controls for global, long- and short-range FCS. These findings suggested that the positive FCS alteration was connection-distance dependent within patients with left-sided chronic subcortical stroke. Also, a positive correlation was found between the FCS in the left SMC and the accuracy of the Flanker test, reflecting a compensatory FCS alteration for altered attention and executive function abilities exhibited by those with left-sided stroke.

Connection Disruption Underlying Attention Deficit in Subcortical Stroke.

Purpose To investigate neural substrates underlying attention deficit in patients with chronic subcortical stroke by combining voxel-based lesion-symptom mapping (VLSM) and diffusion-tensor (DT) tractography. Materials and Methods Institutional review board approval and written informed consent were obtained. Diffusion magnetic resonance imaging data were prospectively acquired from August 1, 2014, to March 30, 2015, in 49 patients (32 men, 17 women; mean age, 55.7 years ± 8.0; age range, 40-71 years) with subcortical infarctions in the basal ganglia and neighboring regions and 52 control subjects (30 men, 22 women; mean age, 54.4 years ± 7.5; age range, 40-68 years). A modified version of the attention network test was used to assess visual attention function. On the basis of the lesion map at the acute stage, VLSM was used to identify lesion locations related to attention deficit in patients with stroke. DT tractography then was used to determine the responsible impaired connections by using diffusion data at the chronic stage (>6 months after stroke). Results When compared with control subjects, patients with chronic stroke exhibited prolonged reaction time (RT) of correct responses (P = .009). VLSM revealed that acute stroke lesion in the right caudate nucleus and nearby white matter (found in seven patients) was correlated with the prolonged RT (P < .05). DTT showed that the responsible lesion was located in the right thalamic- and caudate-prefrontal pathways in control subjects. The subgroup with right-sided brain damage had significantly decreased fractional anisotropy in these pathways (P < .001), which were correlated with the prolonged RT (P = .009 for the thalamic-prefrontal pathway, P < .001 for the caudate-prefrontal pathway). Conclusion Thalamic-prefrontal and caudate-prefrontal pathways impaired by stroke lesions appear to underlie attention deficit in patients with subcortical stroke in the right hemisphere.

Regional structural impairments outside lesions are associated with verbal short-term memory deficits in chronic subcortical stroke.

BACKGROUND AND PURPOSE: We aimed to explore the neural mechanisms of verbal short-term memory (VSTM) impairment in subcortical stroke by evaluating the contributions of lesion and remote grey matter volume (GMV) reduction. RESULTS: There was no significant correlation between lesions and VSTM. In stroke patients with left lesions, GMV reductions in the right middle frontal gyrus and in the left inferior frontal gyrus were positively correlated with VSTM impairment. In patients with right lesions, GMV reduction in the right dorsal posterior cingulate cortex was positively correlated with VSTM impairment. MATERIALS AND METHODS: Ninety-seven patients with chronic subcortical ischemic stroke and seventy-nine healthy controls underwent VSTM and structural MRI examinations. Voxel-based lesion symptom mapping was used to identify correlations between lesions and VSTM. Voxel-wise comparisons were used to identify brain regions with significant GMV reduction in patients with left and right lesions. These regions were used in correlation analyses between GMV and VSTM in each patient subgroup. CONCLUSIONS: These findings suggest that VSTM impairment in subcortical stroke is associated with secondary regional structural damage in non-lesion regions, rather than with the lesion itself. Moreover, different neural substrates may underlie VSTM impairment in stroke patients with left and right lesions.

Gray matter volume changes in chronic subcortical stroke: A cross-sectional study.

This study aimed to investigate the effects of lesion side and degree of motor recovery on gray matter volume (GMV) difference relative to healthy controls in right-handed subcortical stroke. Structural MRI data were collected in 97 patients with chronic subcortical ischemic stroke and 79 healthy controls. Voxel-wise GMV analysis was used to investigate the effects of lesion side and degree of motor recovery on GMV difference in right-handed chronic subcortical stroke patients. Compared with healthy controls, right-lesion patients demonstrated GMV increase (P < 0.05, voxel-wise false discovery rate correction) in the bilateral paracentral lobule (PCL) and supplementary motor area (SMA) and the right middle occipital gyrus (MOG); while left-lesion patients did not exhibit GMV difference under the same threshold. Patients with complete and partial motor recovery showed similar degree of GMV increase in right-lesion patients. However, the motor recovery was correlated with the GMV increase in the bilateral SMA in right-lesion patients. These findings suggest that there exists a lesion-side effect on GMV difference relative to healthy controls in right-handed patients with chronic subcortical stroke. The GMV increase in the SMA may facilitate motor recovery in subcortical stroke patients.