Adaptive compensation of arcuate fasciculus lateralization in developmental dyslexia.

Previous studies have reported anomalies in the arcuate fasciculus (AF) lateralization in developmental dyslexia (DD). Still, the relationship between AF lateralization and literacy skills in DD remains largely unknown. The purpose of our study is to investigate the relationship between lateralization of three segments of AF (AF anterior segment (AFAS), AF long segment (AFLS), and AF posterior segment (AFPS)) and literacy skills in DD. A total of 26 children with dyslexia and 31 age-matched control children were included in this study. High angular diffusion imaging, combined with spherical deconvolution tractography, was used to reconstruct the AF. Connectivity measures of hindrance-modulated orientational anisotropy (HMOA) were computed for each of the three segments of the AF. The lateralization index (LI) of each AF segment was calculated by (right HMOA - left HMOA)/(right HMOA + left HMOA). Results showed that the LIs of AFAS and AFLS were positively correlated with reading accuracy in children with dyslexia. Specifically, the LI of AFAS was positively correlated with nonword and meaningless text reading accuracy, while the LI of AFLS accounted for word reading accuracy. The results suggest adaptive compensation of arcuate fasciculus lateralization in developmental dyslexia and functional dissociation of the anterior segment and long segment in the compensation.

White matter connectivity in uncinate fasciculus accounts for visual attention span in developmental dyslexia.

The present study aimed to investigate the role of connectivity disruptions in two fiber pathways, the uncinate fasciculus (UF) and the frontal aslant tract (FAT), in developmental dyslexia and determine the relationship between the connectivity of these pathways and behavioral performance in children with dyslexia. A total of 26 French children with dyslexia and 31 age-matched control children were included. Spherical deconvolution tractography was used to reconstruct the two fiber pathways. Hindrance-modulated oriented anisotropy (HMOA) was used to measure the connectivity of each fiber pathway in both hemispheres. Only boys with dyslexia showed reduced HMOA in the UF compared to control boys. Furthermore, HMOA of the UF correlated with individual differences in the visual attention span in participants with dyslexia. All significant results found in HMOA of the UF were verified in fractional anisotropy (FA) of the UF using standard diffusion imaging model. This study suggests a differential sex effect on the connectivity disruption in the UF in developmental dyslexia. It also indicates that the UF may play an essential role in the visual attention span deficit in developmental dyslexia.

The ultra-early protective effect of ulinastatin on rabbit acute lung injury induced by paraquat.

OBJECTIVE: To study ultra-early pathophysiological changes of rabbit acute lung injury (ALI) caused by paraquat (PQ) and discuss the ultra-early protective effect of ulinastatin on rabbit ALI due to PQ. METHODS: 30 New Zealand white rabbits were randomly divided into a control group, a paraquat group and an ulinastatin intervention group with 10 rabbits in each group. For paraquat group and intervention group a single dose of paraquat (35 mg/kg) was injected intraperitoneally to establish rabbit models of ALI. The control group was injected an equal volume of saline. The intervention group was treated with 100 Ku/kg ulinastatin immediately after the establishment of the ALI model. The respective experimental groups underwent 320-slice CT perfusion scan of pleural at 2h, 4h and 6h time point after modeling to get CTP (CT Perfusion) images and related parameters. 2 mL blood was collected in the marginal ear vein to determine the mass concentration of the vascular endothelial growth factor (VEGF). The animals were killed by air embolism after 6h and lung tissue was taken for pathology observation. RESULTS: The reginal blood flow (rBF) and reginal blood volume (rBV) of paraquat group at 2,4,6 h time point were significantly (P <0.05) lower than those of control group. The intervention group rBF and rBV at 2, 4 and 6 h time points were significantly higher (P <0.05) compared to paraquat group. The permeability surface (rPS) and VEGF mass concentration of paraquat group at 2,4,6 h time point were significantly higher than the control group (P <0.05), and the intervention group rPS and VEGF mass concentrations at 2,4,6h time point were significantly lower (P <0.05) than those of paraquat group. Pathological detection indicators of paraquat group (congestive capillary percentage, the number of red blood cells outside of capillaries, percentage of capillaries with basement membrane damage) were significantly higher (P <0.05) at 6h time point compared with the control group, while significantly lower (P <0.05) in intervention group than in paraquat groups. Pathological observation under light microscope showed in paraquat group obvious inflammatory cell infiltration, alveolar epithelial cell hyperplasia, widened alveolar septum, visible focal hemorrhage, visible acute and chronic inflammatory cell infiltration in bronchioles cavity; under electron microscopy alveolar epithelial cell degeneration and necrosis, vascular welling of the endothelial cells, basement membrane rupture, a lot of exudates in alveolar space. In the intervention group, the above the symptoms were mitigated. CONCLUSION: In the ultra-early stage of rabbit ALI induced by PQ, pulmonary vascular endothelial cell is damaged and serum VEGF mass concentration and pulmonary vascular permeability increase. Early ulinastatin intervention can reduce serum VEGF level and PQ-induced vascular permeability amplitude, indicating that ulinastatin has a protective effect on pulmonary vascular endothelial cells.

Detection of p16INK4a promoter methylation status in non-small cell lung cancer by a fluorescence polarization assay.

The detection of the p16INK4a promoter methylation status has a good value for the prognosis, early detection, and individualized management of patients with non-small cell lung cancer. A novel method detecting the p16INK4a promoter methylation status of primary carcinoma tissue samples by a fluorescence polarization assay was developed in this research. A pair of general primers was used to amplify a 305-basepair fragment in the promoter region of p16INK4a. Two probes specific for either methylated p16INK4a or unmethylated p16INK4a DNA labeled with either tetramethyl 6-carboxyrhodamine or 6-carboxy-fluorescein hybridized, respectively, with their target amplicons, and the hybridization increased the fluorescence polarization values. The p16INK4a promoter methylation status was determined by the analysis of the fluorescence polarization values. One hundred and twenty-nine non-small cell lung cancer samples were analyzed in parallel with a fluorescence polarization assay and a gel-based methylation-specific polymerase chain reaction (PCR) assay. There was no significant difference between the results of the p16INK4a promoter methylation status obtained with the fluorescence polarization assay and the results obtained with the gel-based methylation-specific PCR assay. The minimum detection level of the fluorescence polarization assay was 25 copies/µL. The fluorescence polarization assay allowed the semiautomated detection of the methylated p16INK4a and unmethylated p16INK4a promoters directly in the solution with 1 PCR cycle, and it was much simpler than methylation-specific PCR and methylation-specific multiplex ligation-dependent probe amplification assays.

Imaging in detecting sites of pulmonary fibrosis induced by paraquat.

BACKGROUND: The most common cause of death from paraquat (PQ) poisoning is respiratory failure from pulmonary fibrosis, which develops through pathological overproduction of extracellular matrix proteins such as collagens. In this study, a MicroCT system was used to observe dynamic changes of pulmonary fibrosis in rats with PQ poisoning, and find the characteristics of interstitial lung diseases via density-based and texture-based analysis of CT images of the lung structure. METHODS: A total of 15 male SD rats were randomly divided into a control group (n=5) and a PQ poisoning group (n=10). The rats in the poisoning group were intraperitoneally administered with 4 mg/ mL PQ at 14 mg/kg, and the rats in the control group were administered with the same volume of saline. The signs of pulmonary fibrosis observed by the MicroCT included ground-glass opacity, nodular pattern, subpleural interstitial thickening, consolidation honeycomb-like shadow of the lung. RESULTS: Compared with the control group, the rats with acute PQ poisoning had different signs of pulmonary fibrosis. Ground-glass opacity and consolidation of the lung appeared at the early phase of pulmonary fibrosis, and subpleural interstitial thickening and honeycomb-like shadow developed at the middle or later stage. MicroCT images showed that fibrotic lung tissues were denser than normal lungs, and their density was up-regulated with pulmonary fibrosis. There was no difference in the progress of pulmonary fibrosis between the right lung and the left lung (P>0.05), but there were differences in fibrosis degree at different sites in the lung (P<0.05 or P<0.01). Pulmonary fibrosis was mainly seen in the exterior area of the middle-lower part of the lung. CONCLUSION: Imaging can show the development of pulmonary fibrosis in PQ poisoning rats, and this method may help to administer drugs more reasonably in treating pulmonary fibrosis.

Antinociceptive effects of systemic paeoniflorin on bee venom-induced various 'phenotypes' of nociception and hypersensitivity.

Paeoniflorin (PF), one of the active chemical compounds identified from the root of Paeonia lactiflora Pall, has been well-established to exhibit various neuroprotective actions in the central nervous system (CNS) after long-term daily administration. In the present study, by using the bee venom (BV) model of nociception and hypersensitivity, antinociceptive effects of PF were evaluated by intraperitoneal administration in conscious rats. When compared with saline control, systemic pre- and post-treatment with PF resulted in an apparent antinociception against both persistent spontaneous nociception and primary heat hypersensitivity, while for the primary mechanical hypersensitivity only pre-treatment was effective. Moreover, pre- and early post-treatment with PF (5 min after BV injection) could successfully suppress the occurrence and maintenance of the mirror-image heat hypersensitivity, whereas late post-treatment (3 h after BV) did not exert any significant impact. In the Rota-Rod treadmill test, PF administration did not affect the motor coordinating performance of rats. Furthermore, systemic PF application produced no significant influence upon BV-induced paw edema and swelling. Finally, the PF-produced antinociception was likely to be mediated by endogenous opioid receptors because of its naloxone-reversibility. Taken together, these results provide a new line of evidence showing that PF, besides its well-established neuroprotective actions in the CNS, is also able to produce analgesia against various 'phenotypes' of nociception and hypersensitivity via opioid receptor mediation.

[Different expression and significance of VEGF and PCNA in aorta and pulmonary artery smooth muscle cells of rats with hypoxia pulmonary hypertension].

AIM: To study the expression of vascular endothelial growth factor (VEGF) and proliferating cell nuclear antigen(PCNA) in aorta and pulmonary artery smooth muscle cells of rats with hypoxia pulmonary hypertension(HPH). METHODS: The rat chronically HPH models were set up in the hypobaric hypoxia cabin. The experimental rats were divided into 3 groups: control group (rearing in a normoxia environment), two hypoxia groups (oxygen-deficient time being 2 weeks and 3 weeks, respectively). Expression of VEGF and PCNA were detected by immunohistochemical staining and image analysis. RESULTS: There was VEGF expression in vascular smooth muscle cells of aorta, pulmonary artery trunk and pulmonary arteriole in control group. In two hypoxia groups VEGF expression in vascular smooth muscle cells of pulmonary artery, trunk and pulmonary arteriole increased significantly, while no difference was found in smooth muscle cells of aorta. Expression of PCNA was very little in vascular smooth muscle cells of aorta, pulmonary artery trunk and pulmonary arteriole in control group. In two hypoxia groups, the PCNA expression increased only in vascular smooth muscle cells of pulmonary arteriole; there was no difference of PCNA expression in vascular smooth muscle cells of aorta and pulmonary artery trunk between hypoxia groups and control group. CONCLUSION: There is difference of VEGF expression in pulmonary artery trunk and aorta smooth muscle cells during the formation of chronic HPH, suggesting that VEGF expression may play very important role in the formation of chronic HPH.