Purpose To evaluate the predictive performance of mean apparent propagator-magnetic resonance imaging(MAP-MRI)combined with habitat analysis for determining O6-methylguanine-DNA methyltransferase(MGMT)promoter methylation status in glioma.Materials and Methods This retrospective study analyzed MRI and clinical data from 55 patients with surgically confirmed glioma at Fujian Medical University Union Hospital from January 2019 to December 2023.All patients underwent structural and diffusion-weighted imaging.Three-dimensional volumes of interest were delineated in the tumor solid region using ImageJ software.The nn-FAE tool was used to segment the tumor solid region into two habitat subregions based on mean diffusivity(MD)maps:high-MD and low-MD habitats.Average diffusion parameter values were extracted from the entire tumor solid region and each habitat subregion.Differences in parameters between methylated and unmethylated groups were compared,and the area under the curve was calculated.Results Among 55 patients,significant differences were observed in all MAP-MRI parameters and MD in the tumor solid region and low-MD habitat,as well as all parameters in the high-MD habitat between methylated and unmethylated groups(t/Z=-3.780-3.153,all P<0.05).The return-to-origin probability(RTOP)in the low-MD habitat demonstrated the highest diagnostic performance,with the area under the curve improving from 0.771 before habitat analysis to 0.827 after habitat analysis.In the high-grade subgroup,significant differences were observed in return-to-axis probability(RTAP)and RTOP in the tumor solid region;RTOP,non-Gaussianity,non-Gaussianity axial,and RTAP in the low-MD habitat;and non-Gaussianity in the high-MD habitat(t/Z=-2.820--1.976,all P<0.05).RTOP in the low-MD habitat again showed optimal diagnostic efficacy(the area under the curve 0.725 before habitat analysis,0.798 after).Multivariate analysis identified RTAP and RTOP in the tumor solid region and low-MD habitat as independent predictors of MGMT methylation.Conclusion MAP-MRI diffusion parameters demonstrate the ability to predict MGMT promoter methylation status in glioma,with superior performance compared with diffusion tensor imaging.Habitat imaging further enhances the predictive efficacy of MAP-MRI parameters for MGMT promoter methylation.

Purpose To evaluate the predictive performance of mean apparent propagator-magnetic resonance imaging(MAP-MRI)combined with habitat analysis for determining O6-methylguanine-DNA methyltransferase(MGMT)promoter methylation status in glioma.Materials and Methods This retrospective study analyzed MRI and clinical data from 55 patients with surgically confirmed glioma at Fujian Medical University Union Hospital from January 2019 to December 2023.All patients underwent structural and diffusion-weighted imaging.Three-dimensional volumes of interest were delineated in the tumor solid region using ImageJ software.The nn-FAE tool was used to segment the tumor solid region into two habitat subregions based on mean diffusivity(MD)maps:high-MD and low-MD habitats.Average diffusion parameter values were extracted from the entire tumor solid region and each habitat subregion.Differences in parameters between methylated and unmethylated groups were compared,and the area under the curve was calculated.Results Among 55 patients,significant differences were observed in all MAP-MRI parameters and MD in the tumor solid region and low-MD habitat,as well as all parameters in the high-MD habitat between methylated and unmethylated groups(t/Z=-3.780-3.153,all P<0.05).The return-to-origin probability(RTOP)in the low-MD habitat demonstrated the highest diagnostic performance,with the area under the curve improving from 0.771 before habitat analysis to 0.827 after habitat analysis.In the high-grade subgroup,significant differences were observed in return-to-axis probability(RTAP)and RTOP in the tumor solid region;RTOP,non-Gaussianity,non-Gaussianity axial,and RTAP in the low-MD habitat;and non-Gaussianity in the high-MD habitat(t/Z=-2.820--1.976,all P<0.05).RTOP in the low-MD habitat again showed optimal diagnostic efficacy(the area under the curve 0.725 before habitat analysis,0.798 after).Multivariate analysis identified RTAP and RTOP in the tumor solid region and low-MD habitat as independent predictors of MGMT methylation.Conclusion MAP-MRI diffusion parameters demonstrate the ability to predict MGMT promoter methylation status in glioma,with superior performance compared with diffusion tensor imaging.Habitat imaging further enhances the predictive efficacy of MAP-MRI parameters for MGMT promoter methylation.

Objective:To explore the genetic basis for a patient with factor XIII (FXIII) deficiency.Methods:All exons of the F13A1 and F13B genes were amplified by PCR and sequenced directly. The sequencing was performed with a reverse primer if a variant was found. Conservation of variant site was analyzed by the ClustalX software. Four online bioinformatic software including MutationTaster, PolyPhen-2, PROVEAN and SIFT were used to predict the function of the mutation site. The Swiss-PdbViewer software was applied to analyze the changes in the protein model and intermolecular force. Results:The proband was found to harbor a novel c. 515G>C (p.Arg171Pro) variant of the F13A1 gene. The corresponding amino acid Arg171 is conserved among homologous species. Bioinformatic analysis indicated that Arg171Pro variant may affect the protein function. Protein model analysis showed that in the wild-type, there is one hydrogen bond between Arg171 and Pro27; one hydrogen bond between Arg171 and Thr28; two hydrogen bonds between Arg171 and Glu102. When Arg171 was mutated to Pro171, the three hydrogen bonds between Arg171 and Pro27, Glu102 are all disappeared and formed a new benzene ring which might affect the stability of the protein structure. No variant was found in the F13B gene. Conclusion:The Arg171Pro variant may account for the decreased FXIII level. Above finding has enriched the spectrum of F13A1 gene variants.

Objective To study the spinal neurocyte apoptosis and the changes of p53 in chronic fluorosis rats,and the improvement after drinking no fluoride water.Methods One hundred twenty Wistar rats were divided into 4 groups by random number table method according to body mass,30 rats in one group fed with high concentration NaF water (200 mg/L) to make fluorosis model and classified as high fluoride group;other 30 rats were fed with distilled water as control group;another 30 rats were fed with high concentration NaF water (200 mg/L) for 12 weeks,then fed with distilled water for 12 weeks and classified as defluorination group;the rest 30 rats were classified as defluorination control group.The content of fluoride in urine was tested after the 4th,8th,and 12th weeks.Then the content of fluoride in urine of defluorination group and defluorination control group was tested.The high fluoride group rats and control group rats were killed after 12th week.Defluorination group rats and defluorination control group rats were killed after 24th week.Their spinal cord was collected.The expression of p53 protein in spinal cord was detected by immunohistochemistry and Westem blotting.Apoptosis of the neurocyte was quantitatively analyzed by flow cytometry (FCM).Results By FCM,apoptosis of neurocyte was increased in both high fluorosis group rats and defluorination group rats compared with those in control group rats [(3.36 ± 0.71)％ vs.(0.78 ± 0.65)％;(3.47 ± 0.56)％ vs.(0.83 ± 0.64)％,t =14.680,17.003,all P ＜ 0.01)],but no difference was found between these two groups [(3.47 ± 0.56)％ vs.(3.36 ± 0.71)％,P ＞ 0.05)].Immunohistochemistry and Western blotting revealed that p53 expression in spinal cord of high fluorosis group rats was increased compared with those in control group rats (422.69 ± 12.35 vs.177.82 ± 14.16;253.37 ± 10.42 vs.87.14 ± 7.39,t =77.212,72.988,all P ＜ 0.01).And p53 expression in spinal cord of defluorination group rats was increased compared with those in control group rats (418.75 ± 11.84 vs.163.47 ± 8.57;248.29 ± 10.23 vs.98.74 ± 11.52,t =95.663,53.167,all P＜ 0.01).But the differences were not statistically significant (418.75 ± 11.84 vs.422.69 ± 12.35;248.29 ± 10.23 vs.253.37 ± 10.42,t =1.261,1.906,all P ＞ 0.05).Conclusions There is apoptosis of neurocytes in the spinal cord of chronic fluorosis rats;overexpression of p53 probably plays an important role in the mechanism of damage induced by excessive fluorine.Apoptosis can not be recovered after defluorination for a short time,and persistent overexpression of p53 may be one of the reasons that apoptosis of neurocytes in the spinal cord can not decrease.

Objective To study the causes of hematoma-induced spinal cord injury after surgical treatment of fluorosis cervical canal stenosis (FCCS) so as to conclude the methods for early diagnosis and treatment.Methods A retrospective review was conducted on 329 cases of FCCS undergone expansive laminoplasty (ELOP) between 2006 and 2009.Eighteen out of the 329 cases presented with neural deterioration in postoperative 2 weeks,including l 1 males and 7 females at age of 45-73 years (mean 56.9 years).MRI scan at postoperative 1-5 days confirmed that the injury cause was hematoma formation (incidence of 5.47％).Once the definite diagnosis was made,immediate local puncture decompression,immobilization in the prone position as well as a timely second surgical probe and spinal decompression were performed.Results Nerve symptom of the 18 cases obtained different degree of recovery.Japanese Orthopedic Association (JOA) score promoted from preoperative (7.44 ± 1.25) points to (12.6 ± 2.1)points at 12 months after second operation.Scatter plot between time of definite diagnosis and improvement value in JOA score before and after the second operation was drawn so as to establish linear equation (Y =6.240 7-0.777 8X(F =9.89,P ＜0.01).As a result,the two variables presented a negative linear relationship,which suggested a better outcome after early treatment than delayed treatment.Conclusions Hematoma compression is the main cause of spinal cord injury following operation for FCCS patients.Strict hematosis and alternate lateral clinostatism after operation were effective prevention methods.Besides,early diagnosis and timely treatment are critically important.

In this paper is proposed a new method for functional connectivity detection using regression analysis. First, the resting state functional magnetic resonance imaging (fMRI) data from each voxel is passed through a bandpass filter to obtain frequencies between 0.01 Hz and 0.1 Hz. Then, the region of interest (ROI) is defined and the mean time course of all voxels in ROI is used as a regressor. Finally, the linear relationship between the time course of other voxels and the regressor in the resting brain is estimated. By the application of this new method in simulation data and fMRI data, the relevant validity and reliability are demonstrated.
Brain ; physiology ; Humans ; Image Processing, Computer-Assisted ; Magnetic Resonance Imaging ; methods ; Regression Analysis ; Signal Processing, Computer-Assisted

Objective: Combining spatial independent component analysis (sICA) with temporal correlation analysis to investigate the functional connectivity of human brain using resting state fMRI. Methods: First, activated area was localized by performing sICA on the data from block design run, then one of the activated brain areas was chosen as a region of interest (ROI)and low frequency correlations between ROI and other regions were calculated in resting state to detect the functional connectivity networks. To validate the method, neural connectivity to primary motor cortex was assessed using this method during a resting state. Results: Functional connectivity network of motor cortex was detected, including primary motor cortex (M1), supplementary motor area (SMA), primary sensory cortex (S1), dorsal premotor cortex (PMd) and posterior parietal somatosensory association area (PSAAp). The connectivity implied by the resting state correlation was far more similar to the connectivity established by non-imaging methods. Conclusion: Functional connectivity of human motor primary cortex was investigated by combining sICA with temporal correlation using resting fMRI data. It provided a simple and noninvasive method for the research of brain functional connectivity.

The aim of this work was to investigate guar gum/ethylcellulose mix coated pellets for potential colon-specific drug delivery. The coated pellets, containing 5-fluorouracil as a model drug, were prepared in a fluidized bed coater by spraying the aqueous/ethanol dispersion mixture of guar gum and ethylcellulose. The lag time of drug release and release rate were adjustable by changing the ratio of guar gum to ethylcellulose and coat weight gain. In order to find the optimal coating formulation that was able to achieve drug targeting to the colon, the effect of two independent variables (the ratio of guar gum to ethylcellulose and the coat weight gain) on drug release characteristics was studied using 3×4 factorial design and response surface methodology. Results indicated that drug release rate decreased as the proportion of ethylcellulose in the hybrid coat and the coat weight gain increased. When the ratio of guar gum to ethylcellulose was kept in the range of 0.2 to 0.7, and the coat weight gain in the range of 250% to 500%, the coated pellets can keep intact for about 5 h in upper gastrointestine and achieve colon-specific drug delivery. The pellets prepared under optimal conditions resulted in delayed-release sigmoidal patterns with T5% (time for 5% drug release) of 5.1-7.8 h and T90% (time for 90% drug release) of 9.8-16.3 h. Further more, drug release was accelerated and T90% of the optimum formulation pellets decreased to 9.0-14.5 h in pH 6.5 phosphate buffer with hydrolase. It is concluded that mixed coating of guar gum and ethylcellulose is able to provide protection of the drug load in the upper gastrointestinal tract, while allowing enzymatic breakdown of the hybrid coat to release the drug load in the colon.

Objective To inquire into the changes of learning and memory ability and the level of SP, VIP in the brain of the model of Spleen insufficiency. To observe the influence invigorating spleen and restoring virility on above changes. Methods Establishing the spleen insufficiency model of rat by adopting bitter decline diarrhea, wild eating and overworking, to examine influence of invigorating spleen and restoring virility on the ability of learning and memory with the change of SP and VIP in the brain. Results In the period of study and remember of the water maze experiment, the swim whole distance time was long and mistake number was many in the model group; the swim whole distance time was short and the mistake number was little in the group of invigorating the Spleen and restoring virility. In the period of study and remember of the diving platform experiment, the mistake number of times is more and the incubation period was short in the model group; the mistake number was less and the incubation period was long in Spleen invigrating group. At the period of remember mistake number was more. In the model group, the immunoreaction masculine substance of SP level decrease obviously in the hypothalamus ventral kernel, the hippocampi CA1 area and forehand cortex; on above mentioned parts, the group of invigorating spleen and restoring virility increases distinctly, in the group of restoring virility increases distinctly in the hippocampi CA 1 area and forehead cortex, but decreased in hypothalamus ventral kernel. In the model group, the immunoreaction masculine substance of VIP level decreased obviously;in the hippocampi CA1 area and cortex;on above mentioned parts, the groups of invigorating spleen and restoring virility increases obviously. Conclusion In the model group, the ability of learing and memory with SP and VIP level in the brain changed. Invigorating spleen and restoring virility can improve above changes remarkably.

0.05). Yet, the activity of NF-?B (female: 12.10?2.89; male: 19.53? 2.12) and the level of TNF-? female: (4.10?0.72) ng/ml; male: (6.37?1.29) ng/ml were significantly increased after injection of lipopolysaccharide (P