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1.
Contrast Media Mol Imaging ; 2022: 1430380, 2022.
Article in English | MEDLINE | ID: mdl-35360267

ABSTRACT

This study was aimed to investigate the craniocerebral magnetic resonance imaging (MRI) measurement and clinical characteristics of patients with neuromyelitis optica (NMO) and multiple sclerosis (MS). 50 patients with NMO (NMO group) and 50 patients with MS (MS group) were studied. The clinical manifestations, brain injury morphology, MRI signal characteristics, brain distribution characteristics, and related laboratory tests (serum aquaporin 4 [AQP4] antibody) were statistically analyzed. The results showed that the analysis of clinical manifestations of patients revealed that optic neuritis (37 cases) was the most common disease in NMO patients, and myelitis (16 cases) was more common in MS patients than NMO patients. There were significant differences in gender ratio, abnormal expression of brain MR1, positive serum AQP4-IgG, and other immune diseases and symptoms between the two groups (P < 0.05). When the lesions measured by MRI were located in the white matter area of the cerebral hemisphere, the image showed blurred edges and a relatively symmetrical distribution. When the lesions measured by MRI were located around the medulla oblongata, the lesions mainly involved the central gray matter and white matter of the spinal cord, with patchy and line-like long T1 and long T2 signals. Moreover, in the late stage of recurrence of spinal cord disease, severe spinal cord atrophy may occur. In conclusion, craniocerebral MRI measurement in NMO patients can provide more basis for the diagnosis and differential diagnosis of the disease, so as to improve the diagnostic level of NMO.


Subject(s)
Multiple Sclerosis , Neuromyelitis Optica , Aquaporin 4/metabolism , Humans , Magnetic Resonance Imaging , Multiple Sclerosis/diagnosis , Multiple Sclerosis/pathology , Neuromyelitis Optica/diagnostic imaging , Spinal Cord
2.
Shanghai Kou Qiang Yi Xue ; 28(2): 179-183, 2019.
Article in Chinese | MEDLINE | ID: mdl-31384905

ABSTRACT

PURPOSE: To study the effect of adolescent premolar scissor bite on the sagittal position of mandible and provide proper reference for correct orthodontic diagnosis and right time to treatment. METHODS: One hundred adolescents (54 females, 46 males) with scissor bite of premolars(70 were unilateral,30 were bilateral) were selected as experimental group between 2004 to 2017 from the Department of Orthodontics, Stomatological Hospital of China Medical University. Among them, 54 females served as female group, 46 males served as male group; 30 were bilateral and 70 were unilateral. Lateral cephalograms were recorded before treatment. 16 sagittal hard tissue variables on maxilla and mandible were measured cephalometrically by Winceph 9.0 software, and the cephalometric data were analyzed statistically by using SPSS 21.0 software package. RESULTS: Compared with normal occlusion, Beta angle, SNB, SND, ANB, AB-Plane angle, APDI, convexity angle, facial angle, Wits, Co-Po showed statistically significant difference in both unilateral group and bilateral group (P<0.05). In addition, Go-Pog showed statistically significant difference between normal occlusion and unilateral group(P<0.05). CONCLUSIONS: Adolescents with premolar scissor bite restricts the sagittal position of mandible and tend to have skeletal Ⅱ sagittal jaw relationship. Scissor bite affects the growth of mandible and makes mandibular body length and mandibular length less than normal. More attention should be paid to scissor bite as early as possible to decrease the harmful effects on growth of mandible and sagittal jaw relationship.


Subject(s)
Bicuspid , Dental Occlusion , Mandible , Adolescent , Cephalometry , China , Female , Humans , Male , Mandible/anatomy & histology , Maxilla
3.
Intervirology ; 60(1-2): 19-27, 2017.
Article in English | MEDLINE | ID: mdl-28877517

ABSTRACT

Trionyx sinensis hemorrhagic syndrome virus (TSHSV) is a pathogen that causes severe hemorrhagic syndrome and irreversible damage to different infected tissues of Pelodis cus sinensis, ending in the death of affected organisms. In the present study, the histopathological characteristics of TSHSV-infected P. sinensis were analyzed and compared by HE staining. Relative and absolute quantification (iTRAQ)-based proteomic analysis was employed to explore the molecular pathology of liver injury. Anatomical features indicated that TSHSV caused obvious congestion in the liver, kidney, intestine, and other tissues of P. sinensis. The typical clinical symptoms included hepatomegaly, fragility, spotty and severe congestion in liver tissue, and also obvious intestinal bleeding. The histopathological studies corroborated such lesions in the liver and kidney, etc. iTRAQ-based proteomic analysis revealed that there were 252 differentially expressed proteins in the liver tissue between healthy and infected P. sinensis, of which 118 proteins were upregulated and 134 proteins were downregulated. GO enrichment analysis and KEGG pathway analysis initially revealed the molecular mechanism of pathological changes in P. sinensis by TSHSV infection. The expression of some differentially expressed proteins was further confirmed by qRT-PCR. These results provided important information for the pathological diagnosis of TSHSV-caused disease, as well as the mechanism underlying TSHSV-caused disease.


Subject(s)
Arteriviridae , Liver/pathology , Liver/virology , Proteins/genetics , RNA Virus Infections/veterinary , Reptilian Proteins/metabolism , Turtles/virology , Amino Acid Sequence , Animals , Host-Pathogen Interactions , Kidney/pathology , Kidney/virology , Metabolic Networks and Pathways/genetics , Pathology, Molecular , Proteins/isolation & purification , Proteomics , RNA Virus Infections/metabolism , RNA Virus Infections/pathology , RNA Virus Infections/virology , Real-Time Polymerase Chain Reaction , Turtles/anatomy & histology , Turtles/metabolism
4.
Mol Autism ; 5: 52, 2014.
Article in English | MEDLINE | ID: mdl-25694804

ABSTRACT

BACKGROUND: Autism spectrum disorder (ASD) is characterized by persistent deficits in social communication and interaction, and restrictive and repetitive patterns of behavior, interests or activities. This study aimed to analyze trends in ASD diagnosis and intervention in 20 years of data from the Beijing Stars and Rain Education Institute for Autism (SR), the first autism intervention center in mainland China, and from a recent survey of members of the Heart Alliance, an industry association of autism intervention centers in China. METHODS: We analyzed the registration data at the SR from 1993 to 2012 for a total of 2,222 children who had a parent-reported diagnosis of ASD and 612 of 'autistic tendencies'. Most of the children who were the primary focus of our analyses were age six and under. We also analyzed results of a survey we conducted in 2013 of 100 member centers of the Heart Alliance. Generalized Estimating Equations, multiple linear regression and the Mann-Whitney test were used for data analysis. Statistically significant findings are reported here. RESULTS: The number of hospitals where SR children received their diagnosis increased from several in the early 1990s to 276 at present. The proportion of 'autistic tendencies' diagnosis increased 2.04-fold from 1998 to 2012 and was higher for children diagnosed at a younger age. The mean age at first diagnosis of ASD or 'autistic tendencies' decreased by 0.27 years every decade. A higher level of parental education was statistically significantly associated with an earlier diagnosis of the child. The mean parental age at childbirth increased by about 1.48 years per decade, and the mean maternal age was 1.40 and 2.10 years higher than that in the national population censuses of 2000 and 2010, respectively. At the time of the survey 3,957 children with ASD were being trained at the 100 autism intervention centers. Ninety-seven of these centers opened after the year 2000. Economically underdeveloped regions are still underserved. CONCLUSIONS: This study revealed encouraging trends and remaining challenges in ASD diagnosis and intervention among children at the SR over the past 20 years and the 100 autism intervention centers in China at present.

5.
PLoS Comput Biol ; 6(3): e1000734, 2010 Mar 26.
Article in English | MEDLINE | ID: mdl-20376170

ABSTRACT

To understand whether any human-specific new genes may be associated with human brain functions, we computationally screened the genetic vulnerable factors identified through Genome-Wide Association Studies and linkage analyses of nicotine addiction and found one human-specific de novo protein-coding gene, FLJ33706 (alternative gene symbol C20orf203). Cross-species analysis revealed interesting evolutionary paths of how this gene had originated from noncoding DNA sequences: insertion of repeat elements especially Alu contributed to the formation of the first coding exon and six standard splice junctions on the branch leading to humans and chimpanzees, and two subsequent substitutions in the human lineage escaped two stop codons and created an open reading frame of 194 amino acids. We experimentally verified FLJ33706's mRNA and protein expression in the brain. Real-Time PCR in multiple tissues demonstrated that FLJ33706 was most abundantly expressed in brain. Human polymorphism data suggested that FLJ33706 encodes a protein under purifying selection. A specifically designed antibody detected its protein expression across human cortex, cerebellum and midbrain. Immunohistochemistry study in normal human brain cortex revealed the localization of FLJ33706 protein in neurons. Elevated expressions of FLJ33706 were detected in Alzheimer's brain samples, suggesting the role of this novel gene in human-specific pathogenesis of Alzheimer's disease. FLJ33706 provided the strongest evidence so far that human-specific de novo genes can have protein-coding potential and differential protein expression, and be involved in human brain functions.


Subject(s)
Alzheimer Disease/genetics , Brain/physiopathology , Models, Genetic , Mutation/genetics , Nerve Tissue Proteins/genetics , Computer Simulation , Humans
6.
BMC Evol Biol ; 9: 252, 2009 Oct 15.
Article in English | MEDLINE | ID: mdl-19832993

ABSTRACT

BACKGROUND: New genes generated by retroposition are widespread in humans and other mammalian species. Usually, this process copies a single parental gene and inserts it into a distant genomic location. However, retroposition of two adjacent parental genes, i.e. co-retroposition, had not been reported until the hominoid chimeric gene, PIPSL, was identified recently. It was shown how two genes linked in tandem (phosphatidylinositol-4-phosphate 5-kinase, type I, alpha, PIP5K1A and proteasome 26S subunit, non-ATPase, 4, PSMD4) could be co-retroposed from a single RNA molecule to form this novel chimeric gene. However, understanding of the origination and biological function of PIPSL requires determination of the coding potential of this gene as well as the evolutionary forces acting on its hominoid copies. RESULTS: We tackled these problems by analyzing the evolutionary signature in both within-species variation and between species divergence in the sequence and structure of the gene. We revealed a significant evolutionary signature: the coding region has significantly lower sequence variation, especially insertions and deletions, suggesting that the human copy may encode a protein. Moreover, a survey across five different hominoid species revealed that all adaptive changes of PSMD4-derived regions occurred on branches leading to human and chimp rather than other hominoid lineages. Finally, computational analysis suggests testis-specific transcription of PIPSL is regulated by tissue-dependent methylation rather than some transcriptional leakage. CONCLUSION: Therefore, this set of analyses showed that PIPSL is an extraordinary co-retroposed protein-coding gene that may participate in the male functions of humans and its close relatives.


Subject(s)
Carrier Proteins/genetics , Evolution, Molecular , Retroelements , Selection, Genetic , Animals , Gene Expression Profiling , Gene Expression Regulation , Genetics, Population , Humans , INDEL Mutation , Male , Methylation , Pan troglodytes/genetics , Phosphotransferases (Alcohol Group Acceptor)/genetics , Polymorphism, Single Nucleotide , Primates/genetics , Proteasome Endopeptidase Complex/genetics , RNA-Binding Proteins , Sequence Analysis, DNA , Species Specificity , Testis/metabolism , Transcription, Genetic
7.
Zhongguo Shi Yan Xue Ye Xue Za Zhi ; 9(2): 149-152, 2001 Jun.
Article in Chinese | MEDLINE | ID: mdl-12578623

ABSTRACT

Cytomegalovirus infection (CMV-I) and CMV related diseases (CMV-D) occurred after allogeneic hematopoietic stem cell transplantation (Allo-HSCT) seem to be with high morbidity and mortality. This study is a retrospective analysis of the incidence of CMV infection and diseases in Allo-HSCT patients known to be CMV seropositive before transplantation. To review the efficacy of CMV pp65 antigen-guided ganciclovir prophylaxis in preventing CMV infection and to search the optimal determination methods, 45 consecutive Allo-HSCT patients have been observed. Using the CMV pp65 antigenemia assay and serological analysis monitored blood samples from 23 patients with chronic myeloid leukemia (CML), 7 acute myeloblastic leukemia (AML), 6 acute lymphoblastic leukemia (ALL); other: 4 myelodysplastic syndrome (MDS), 3 non-Hodgkin's lymphoma (NHL) and 2 aplastic anemia. Forty-three patients received HLA-identical siblings transplantation and 2 from their HLA-haploidentical donors. Forty-five cases included Allo-PBPCT (38 cases), Allo-BMT (2 cases) and Allo-PBPCT + BMT 5 cases. Before transplantation, all donors/recipients have taken CMV serological detection. All donor/recipients were CMV IgG positive and one donor and one recipient with CMV IgM positive, respectively. After transplantation, all patients developed CMV antigenemia during monitoring period. Twenty-five patients developed CMV related interstitial pneumonia (CMV-IP). Patients have been followed from 6 to 28 months (median of 18 months) after transplantation. The patients who received preemptive therapy had a significantly better outcome than patients who did not received preemptive therapy. CMV related mortality was 1/29 cases in preemptive group vs. 12/16 cases in non-preemptive group. The results suggest that prompt and early institution of effective therapy with ganciclovir upon detection of CMV pp65 antigenemia, provides optimal protection against progress of CMV disease for patients undergoing Allo-HSCT.

8.
Zhongguo Shi Yan Xue Ye Xue Za Zhi ; 8(3): 176-179, 2000 Sep.
Article in Chinese | MEDLINE | ID: mdl-12578677

ABSTRACT

To investigate the significance of GATA-2 and immunoglobulin heavy chain germline gene C( micro ) (IgH germline gene C( micro )) expression and coexpression in various leukemia cells, GATA-2 and IgH germline gene C( micro ) mRNA in bone marrow and peripheral blood cells from 63 leukemia patients were detected by reverse transcription-polymerase chain reaction (RT-PCR). No GATA-2 or IgH germline gene C( micro ) mRNA were detected in normal bone marrow and peripheral blood. GATA-2 mRNA were be detected in 91.3% patients with acute myeloid leukemia (AML), 75% patients with acute lymphoblastic leukemia (ALL) as well as 83.3% patients with chronic myeloid leukemia (CML-CP); IgH germline gene C( micro ) mRNA were be identified in 47.8% AML, 41.6% ALL, as well as 5.6% CML-CP. All patients with CML-AP and CML-BC expressed GATA-2 mRNA and partly expressed IgH germline gene C( micro ) mRNA. 47.8% AML and 41.6% ALL patients coexpressed GATA-2 and IgH germline gene C( micro ) mRNA. GATA-2(+) IgH germline gene C( micro )(+) cells of AML and ALL were mainly HLA-DR positive. As aberration of the transcription factors, GATA-2 and germline IgH germline gene C( micro ) gene might been linked to leukemogenesis. Various expression of GATA-2 and germline IgH germline gene C( micro ) gene in leukemia might correlated with the heterogeneous differentiation level of leukemia cells. The fact that leukemia with GATA-2(+) IgH germline gene C( micro )(+) coexpression indicated multilineage impairment of hematopoietic cells.

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