Nasal Cycle in Patients with Septal Deviation: Evaluation by Acoustic Rhinometry

2000 ◽  
Vol 14 (3) ◽  
pp. 171-174 ◽  
Author(s):  
Yeol-Woong Sung ◽  
Min-Han Lee ◽  
In-Jung Kim ◽  
Dong-Woo Lim ◽  
Ki-Sang Rha ◽  
...  

The nasal cycle in patients with septal deviation was studied by acoustic rhinometric techniques. This study included 24 patients with anteriorly located septal deviations (mean age = 23.5), and 26 normal controls (mean age = 24.7). Data of MCA (minimum cross-sectional area) and NV (nasal volume), collected in 20-minute intervals, were plotted for each subject during 8 hours. Twenty of 24 patients (83%) with septal deviation and 20 of 26 normal subjects (77%) showed at least one complete cycle. Duration of the nasal cycle, which ranged from 100 minutes to 400 minutes, had no statistical difference between the septal deviation group (mean duration of 216 minutes) and the normal control group (mean duration of 227 minutes). The degrees of variation of MCA and NV, defined as Degree of Variation of MCA (%) = 100 (MCAmax – MCAmin)/MCAmax, Degree of Variation of NV (%) = 100 (NVmax – NVmin)/NVmax, which represent the percent change of MCA and NV throughout the study, showed no difference between the wide side and the narrow side, or between the septal deviation group and the normal control group. These findings suggest that the nasal cycle is relatively independent of peripheral anatomic factors for its generation. However, the amplitude of changes of MCA was greater in the wide side, and the sum of both MCAs tended to fluctuate in accordance with the fluctuation of MCA of the wide side. Thus, the nasal cycle seemed to be affected by septal deviation.

2021 ◽  
Vol 11 (5) ◽  
pp. 417
Author(s):  
Jung Geun Park ◽  
Bo Young Hong ◽  
Hae-Yeon Park ◽  
Yeun Jie Yoo ◽  
Mi-Jeong Yoon ◽  
...  

A stroke may be followed by central post-stroke pain (CPSP), which is characterized by chronic neuropathic pain. The exact mechanism has not yet been fully uncovered. We investigated alterations in the white matters in patients with CPSP, compared with stroke patients without CPSP and normal controls. Our retrospective cross-sectional, case-control study participants were assigned to three groups: CPSP (stroke patients with CPSP (n = 17)); stroke control (stroke patients without CPSP (n = 26)); and normal control (normal subjects (n = 34)). The investigation of white matter for CPSP was focused on the values of fiber numbers (FN) and fractional anisotrophy (FA) for spinothalamic tract (STT), anterior thalamic radiation (ATR), superior thalamic radiation (STR) and posterior thalamic radiation (PTR), and corticospinal tract (CST) was measured. The FA for the STT and STR of the CPSP group were lower than those for the stroke control and normal control groups. The FA of CST and ATR did not differ between the CPSP and stroke groups, but both differed from the normal control. The FA of PTR in the stroke control group differed from the normal control group, but not from the CPSP group. The FN of CST, STT, ATR, and STR for the CPSP and stroke control groups did not differ from each other, but both differed from those of normal controls. FN of PTR did not differ between the CPSP and normal control groups. The alterations in the spinothalamic tract and superior thalamic radiation after stroke would play a role in the pathogenesis of CPSP.


Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 709-709 ◽  
Author(s):  
Daniel B. Bellissimo ◽  
P.A. Christopherson ◽  
S.L. Haberichter ◽  
V.H. Flood ◽  
J.C. Gill ◽  
...  

Abstract Von Willebrand disease (VWD) is caused by quantitative (types 1 and 3) and qualitative (type 2) defects in von Willebrand factor (VWF). The TS Zimmerman Program for the Molecular and Clinical Biology of VWD is a multinational Program Project established to further the study of VWD in the United States and to contrast these studies with the studies initiated previously in the EU and Canada. As one of the components of this study we sought further insight into the clinical expression and penetrance of established types of VWD by performing full gene DNA sequence analysis in VWD patients and normal controls. This report is an interim report of the first 50 index cases and 113 normal individuals recruited into this study. Twenty four of these index cases were found to have known mutations, four of which had a second new mutation, and 11 cases had 1 or 2 new mutations. In cases where mutations were identified, 46% of the identified mutations were new mutations that have not been reported in the Sheffield VWF Mutation Database. In 15 patients, no mutations were identified in the coding region, although analysis of the non-coding regions is still in progress. Five of the mutations were deletions, insertions, or nonsense mutations that have clear functional consequences. The other 12 mutations were missense mutations. Since VWF polymorphisms are not well characterized in all exons, we have also completed studies of the first 113 normal control individuals in our study. These are individuals without a bleeding history and in whom full VWF laboratory testing and VWF sequencing was also undertaken. Since some estimates in the EU and Canadian studies have determined the prevalence of VWF mutations varies by the severity of type 1 VWD patients, we wanted to determine the frequency of VWF variation in a normal population and determine if sequence variations correlate with VWF levels. There were three linked common polymorphims identified in normal African Americans that are discussed elsewhere and are not included in this present analysis. We found 19 new sequence variations in the normal control group of which three (2900G>A, 6554G>A, 7997C>T) were found individually in 4–6% of the normal control samples. In addition, in 12 normal control samples we identified 6 sequence variations that were previously reported as VWF mutations. Four were reported as type 1 mutations (2220 G>A, 3686T>G, 3692A>C, 6859C>T) and two as type 2N mutations (2451T>A, 2771G>A). The 2220G>A and 2451T>A mutations were seen in 6 normal controls (5%) and 5 of these 6 normal controls had both mutations. In another normal control, both 3686T>G and 3692A>C were identified. Although the reported prevalence of VWD is 1% or greater, the frequency of these mutations in our normal controls is higher than expected (as high as 5%). In our normal control group, the mean VWF:Ag concentration in the patients with polymorphisms/mutations did not differ from the normal control group as a whole and did not cluster on the lower end of the normal range. Thus, the data on our normal individuals suggest that VWF gene variation is considerable and that many mutations and polymorphisms remain to be identified. Differentiation of those that affect the diagnosis of VWD and/or hemorrhagic risk continues to be difficult.


1974 ◽  
Vol 39 (2) ◽  
pp. 1003-1011 ◽  
Author(s):  
W. H. Moore ◽  
William E. Weidner

The present investigation examined the role of the right cerebral hemisphere in linguistic perception following left cerebral insult which had resulted in aphasia. Bilateral tachistoscopic procedures, employing a central fixation mark, were utilized to investigate the visual half-field preferences of 30 aphasic Ss, grouped relative to the amount of time since the onset of left cerebral insult, and a group of 10 normal, control Ss. Statistical analyses indicated a significant left visual half-field preference for the aphasic Ss. In contrast, a significant right visual half-field preference was revealed for the normal, control group. Results did not show a simple decrement in recognition scores of the aphasic Ss but rather a shift in visual-field preference relative to the normal Ss' preference.


2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Jesús K. Yamamoto-Furusho ◽  
Ilse Ascaño-Gutiérrez ◽  
Janette Furuzawa-Carballeda ◽  
Gabriela Fonseca-Camarillo

Background. Patients with UC have shown an important defect in the secretion and maintenance of the mucosal barrier as part of inadequate expression of mucin genes. The aim of the present study was to determine the expression of MUC12, MUC16, and MUC20 in colonic tissue from patients with UC in regard to their clinical outcomes.Methods. We included a total of 40 patients with UC and 30 normal controls. Mucin gene expression was performed by RT-PCR and protein expression was detected by immunohistochemistry.Results. Patients with active UC showed no significant expression of MUC12 gene in mucosa compared to the group of patients with UC in remission and the normal control group. MUC16 gene expression was significantly increased in the UC active and remission groups compared to the normal control group (P=0.03). MUC20 gene expression was found significantly decreased in patients with active UC compared to both remission group (P=0.001) and normal controls (P=0.001). Furthermore, an association was found between MUC20 gene expression and the presence of histological remission in patients with UC (P=0.003, OR = 0.37).Conclusions. An increased gene expression of MUC16 and MUC20 was found in patients with remission UC.


1993 ◽  
Vol 13 (3) ◽  
pp. 214-218 ◽  
Author(s):  
Roel E. Reddingius ◽  
Cornelis H. Schröder ◽  
Mohamed R. Daha ◽  
Leo A.H. Monnens

Objective During continuous ambulatory peritoneal dialysis (CAPD), the loss of complement factors via the dialysate may cause complement deficiencies. This hypothesis was tested in a group of children treated with CAPD. Design Classical (CH50) and alternative (AP50) complement activity and serum levels of factors C1 q, C3, C4, C3d, B, D, and P in CAPD patients were compared to normal controls and to children with preterminal renal failure. Setting Patients were seen in a university hospital; normal controls were seen in an outpatient clinic of a general hospital. Patients A group of 22 children on CAPD was compared to a normal control group of 44 children and to a group of 12 children with preterminal renal failure with a creatinine clearance below 25 mL/min/1.73 m2. Results CH50, AP50, C3, and B were not significantly different from the control group in both the CAPD and preterminal groups. Factors C1q (p=0.01) and C4, C3d, D, and P (p<0.001) were higher in the CAPD group in comparison to the normal control group. The factors D (p<0.001) and P (p=0.02) were also elevated in the preterminal group. For the measured factors there was no significant difference between the CAPD group and the preterminal group. Conclusions There is no deficiency of complement in children treated with CAPD. High levels of C3d and D can be explained by the reduction of their elimination by the kidney. The increased levels of the other factors are presumably due to increased synthesis in renal failure. This does not seem to be caused by CAPD.


Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4899-4899
Author(s):  
Zonghong Shao ◽  
Huaquan Wang ◽  
Jun Shi ◽  
Yanran Cao ◽  
Hong Liu ◽  
...  

Abstract Background Myelodysplastic syndromes (MDS) is a group of clone haematopoietic stem cell diseases. The burden of abnormal hematopoietic clone plays key roles in the development of this disease and needs to be further studied quantitively. Methods The ratio of the counted bone marrow cells with abnormal chromosomes to the total counted bone marrow cells was regarded as the index of MDS clone burden. The disease severity related parameters including white cell count, hemoglobin, platelet count, lactate dehydrogenase level, bone marrow blast, myeloid differentiation index, the ratio of cFU-GM to CFU-GM, micromegakaryocyte, transfusion, IL-2, TNF, CD4+ and CD8+ T cells of MDS patients were assayed and the correlations between those parameters and MDS clone burden were also analysed. Results The clone burden of MDS patients was (67.4±36.2)%. MDS clone burden correlated positively with bone marrow blasts(r =0.483, P=0.012), negatively with hemoglobin level(r = −0.445, P= 0.023); The number of blasts, hemoglobin and erythocytes in high clone burden(&gt;50%) and low clone burden(≤50%) groups were (7.78±5.51)% and (3.45±3.34)%(P=0.035), (56.06±14.28)g/L and (76.40±24.44)g/L(P=0.013), (1.82±0.12)×1012/L and (2.32±0.21)×1012/L(P=0.034)respectively. CD4+ T lymphcytes of MDS patients and normal controls were (274.18±71.85)×106/L and (454.82±205.88)×106/L(P=0.012)respectively. CD8+ T lymphcytes of MDS patients and normal controls were (240.45±150.01)×106/L an (305.27±145.14)×106/L(P=0.317)respectively. The serum level of interleukin 2 of MDS patients and normal control group were (6.29±3.58)ng/ml and (3.11±1.40)ng/ml (P=0.002) respectively. The serum level of tumor necrosis factor of MDS patients and normal control group were (2.42±1.79)ng/ml and (1.68±0.69)ng/ml(P=0.124)respectively. The ratio of CD4 to CD8 in high clone burden MDS patients was (1.90±0.52), and that in low clone burden patients was (0.97±0.44)(P=0.022). Conclusion The quantitive clonal karyotype abnormalities and deficient T cell immunity are important parameters for evaluating MDS severeity and prediciting it’s progression.


2003 ◽  
Vol 62 (1) ◽  
pp. 45-51 ◽  
Author(s):  
Marek Nieznanski

The aim of the study was to explore the basic features of self-schema in persons with schizophrenia. Thirty two schizophrenic patients and 32 normal controls were asked to select personality trait words from a check-list that described themselves, themselves as they were five years ago, and what most people are like. Compared with the control group, participants from the experimental group chose significantly more adjectives that were common to descriptions of self and others, and significantly less that were common to self and past-self descriptions. These results suggest that schizophrenic patients experience their personality as changing over time much more than do healthy subjects. Moreover, their self-representation seems to be less differentiated from others-representation and less clearly defined than in normal subjects.


Author(s):  
Xitong Yang ◽  
Pengyu Wang ◽  
Shanquan Yan ◽  
Guangming Wang

AbstractStroke is a sudden cerebrovascular circulatory disorder with high morbidity, disability, mortality, and recurrence rate, but its pathogenesis and key genes are still unclear. In this study, bioinformatics was used to deeply analyze the pathogenesis of stroke and related key genes, so as to study the potential pathogenesis of stroke and provide guidance for clinical treatment. Gene Expression profiles of GSE58294 and GSE16561 were obtained from Gene Expression Omnibus (GEO), the differentially expressed genes (DEGs) were identified between IS and normal control group. The different expression genes (DEGs) between IS and normal control group were screened with the GEO2R online tool. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses of the DEGs were performed. Using the Database for Annotation, Visualization and Integrated Discovery (DAVID) and gene set enrichment analysis (GSEA), the function and pathway enrichment analysis of DEGS were performed. Then, a protein–protein interaction (PPI) network was constructed via the Search Tool for the Retrieval of Interacting Genes (STRING) database. Cytoscape with CytoHubba were used to identify the hub genes. Finally, NetworkAnalyst was used to construct the targeted microRNAs (miRNAs) of the hub genes. A total of 85 DEGs were screened out in this study, including 65 upward genes and 20 downward genes. In addition, 3 KEGG pathways, cytokine − cytokine receptor interaction, hematopoietic cell lineage, B cell receptor signaling pathway, were significantly enriched using a database for labeling, visualization, and synthetic discovery. In combination with the results of the PPI network and CytoHubba, 10 hub genes including CEACAM8, CD19, MMP9, ARG1, CKAP4, CCR7, MGAM, CD79A, CD79B, and CLEC4D were selected. Combined with DEG-miRNAs visualization, 5 miRNAs, including hsa-mir-146a-5p, hsa-mir-7-5p, hsa-mir-335-5p, and hsa-mir-27a- 3p, were predicted as possibly the key miRNAs. Our findings will contribute to identification of potential biomarkers and novel strategies for the treatment of ischemic stroke, and provide a new strategy for clinical therapy.


1993 ◽  
Vol 5 (3) ◽  
pp. 303-316 ◽  
Author(s):  
Anne B. Sereno ◽  
Philip S. Holzman

Saccadic and smooth pursuit eye movements were recorded in three groups of subjects: a schizophrenic group, a non-schizophrenic psychotic patient comparison group, and a normal control group. Schizophrenic subjects demonstrated a greater decrease in saccadic response time than did normal controls in a gap task (when the fixation point was turned off 150 msec before the target appeared). The psychiatric comparison subjects did not differ from normal controls. Further, only schizophrenic subjects demonstrated a relation between smooth pursuit and saccadic eye movement performance, such that subjects with impaired smooth pursuit showed a larger decrease in saccadic response time in the gap task. The relation between performance on the gap task and quality of smooth pursuit and its relevance for a prefrontal deficit hypothesis of schizophrenia are discussed.


2014 ◽  
Vol 1033-1034 ◽  
pp. 220-223
Author(s):  
Xue Mei Han ◽  
Li Bo Wang ◽  
Ni Ni Li ◽  
Song Yan Liu

To examine the effect of GDM on the expression of MT1-MMP and u-PA genes in glioma cells. Glioma cell lines U251 and U87 were cultured in DMEM medium supplemented with 10% fetal bovine serum. RT-PCR was used to identify gene expression level. The level of u-PA mRNA was up-regulated significantly in the HGF group compared with the normal control group (P<0.05). The expression of MT1-MMP and u-PA was significantly lower in the GDM group than in the normal control and HGF groups (P<0.05). The expression of u-PA in the HGF+GDM group was down-regulated significantly compared with the normal control and HGF groups (P<0.05).GDM can inhibit expression of both MT1-MMP and u-PA in glioma cells.


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