Fallopian canal arachnoid cyst with acute facial nerve paralysis in children: a report of two cases and literature review

IntroductionSymptoms induced by arachnoid cysts in the fallopian canal are uncommon, and facial nerve paralysis without cerebrospinal fluid otorrhea is comparatively rarer.MethodsHerein, we present two cases of arachnoid cysts in the fallopian canal with acute severe facial nerve paralysis and review the relevant literature.ResultsThe symptoms and imaging findings of these two cases resembled those of facial nerve schwannomas. Cerebrospinal fluid otorrhea occurred upon removal of the arachnoid cyst, and the facial nerve was observed to be separated into multiple filaments or compressed and atrophied. Facial-hypoglossal nerve anastomosis and decompression were conducted after packing the dehiscence of cerebrospinal fluid otorrhea for the two cases.ConclusionArachnoid cysts of the fallopian canal rarely cause facial nerve paralysis. Enhanced magnetic resonance imaging is vital for differentiating schwannomas. Different treatment strategies should be adopted for patients with different degrees of facial nerve paralysis; however, concurrent repair of cerebrospinal fluid otorrhea and facial nerves during surgery can occasionally be challenging

Guanxintai Exerts Protective Effects on Ischemic Cardiomyocytes by Mitigating Oxidative Stress

Oxidative stress participates in numerous myocardial pathophysiological processes and is considered a therapeutic target for myocardial ischemia and heart failure. Guanxintai (GXT), a traditional Chinese medicine, is commonly used to treat cardiovascular disease on account of its numerous beneficial physiological activities, such as dilating coronary arteries, inhibiting platelet aggregation, and reducing the serum lipid content. However, the antioxidative properties of GXT and potential underlying mechanisms remain to be established. In the present study, we investigated the protective effects of GXT on ischemic cardiomyocytes and the associated antioxidative mechanisms, both in vivo and in vitro. Notably, GXT treatment reduced the degree of cardiomyocyte injury, myocardial apoptosis, and fibrosis and partially improved cardiac function after myocardial infarction. Furthermore, GXT suppressed the level of ROS as well as expression of NADPH oxidase (NOX) and phospho-p38 mitogen-activated protein kinase (MAPK) proteins. Our results collectively suggest that the protective effects of GXT on ischemic cardiomyocytes are exerted through its antioxidative activity of NOX inhibition

Nonlinear Free Vibration Analysis of Axisymmetric Polar Orthotropic Circular Membranes under the Fixed Boundary Condition

This paper presents the nonlinear free vibration analysis of axisymmetric polar orthotropic circular membrane, based on the large deflection theory of membrane and the principle of virtual displacement. We have derived the governing equations of nonlinear free vibration of circular membrane and solved them by the Galerkin method and the Bessel function to obtain the generally exact formula of nonlinear vibration frequency of circular membrane with outer edges fixed. The formula could be degraded into the solution from small deflection vibration; thus, its correctness has been verified. Finally, the paper gives the computational examples and comparative analysis with the other solution. The frequency is enlarged with the increase of the initial displacement, and the larger the initial displacement is, the larger the effect on the frequency is, and vice versa. When the initial displacement approaches zero, the result is consistent with that obtained on the basis of the small deflection theory. Results obtained from this paper provide the accurate theory for the measurement of the pretension of polar orthotropic composite materials by frequency method and some theoretical basis for the research of the dynamic response of membrane structure

Testosterone Replacement Modulates Cardiac Metabolic Remodeling after Myocardial Infarction by Upregulating PPARα

Despite the importance of testosterone as a metabolic hormone, its effects on myocardial metabolism in the ischemic heart remain unclear. Myocardial ischemia leads to metabolic remodeling, ultimately resulting in ATP deficiency and cardiac dysfunction. In the present study, the effects of testosterone replacement on the ischemic heart were assessed in a castrated rat myocardial infarction model established by ligating the left anterior descending coronary artery 2 weeks after castration. The results of real-time PCR and Western blot analyses showed that peroxisome proliferator-activated receptor α (PPARα) decreased in the ischemic myocardium of castrated rats, compared with the sham-castration group, and the mRNA expression of genes involved in fatty acid metabolism (the fatty acid translocase CD36, carnitine palmitoyltransferase I, and medium-chain acyl-CoA dehydrogenase) and glucose transporter-4 also decreased. A decline in ATP levels in the castrated rats was accompanied by increased cardiomyocyte apoptosis and fibrosis and impaired cardiac function, compared with the sham-castration group, and these detrimental effects were reversed by testosterone replacement. Taken together, our findings suggest that testosterone can modulate myocardial metabolic remodeling by upregulating PPARα after myocardial infarction, exerting a protective effect on cardiac function

Transcript Profiles of Stria Vascularis in Models of Waardenburg Syndrome

Background. Waardenburg syndrome is an uncommon genetic condition characterized by at least some degree of congenital hearing loss and pigmentation deficiencies. However, the genetic pathway affecting the development of stria vascularis is not fully illustrated. Methods. The transcript profile of stria vascularis of Waardenburg syndrome was studied using Mitf-M mutant pig and mice models. Therefore, GO analysis was performed to identify the differential gene expression caused by Mitf-M mutation. Results. There were 113 genes in tyrosine metabolism, melanin formation, and ion transportations showed significant changes in pig models and 191 genes in mice models. In addition, there were some spice’s specific gene changes in the stria vascularis in the mouse and porcine models. The expression of tight junction-associated genes, including Cadm1, Cldn11, Pcdh1, Pcdh19, and Cdh24 genes, were significantly higher in porcine models compared to mouse models. Vascular-related and ion channel-related genes in the stria vascularis were also shown significantly difference between the two species. The expression of Col2a1, Col3a1, Col11a1, and Col11a2 genes were higher, and the expression of Col8a2, Cd34, and Ncam genes were lower in the porcine models compared to mouse models. Conclusions. Our data suggests that there is a significant difference on the gene expression and function between these two models

Microfluidic assay of circulating endothelial cells in coronary artery disease patients with angina pectoris - Fig 4

<p>(<b>A</b>) Immunofluorescence staining of isolated CECs. Captured CECs (DAPI⁺/CD146⁺/VEGFR1⁺/CD45^-) can be clearly observed at the single cell level, together with residuary leukocytes (DAPI⁺/CD45⁺). (<b>B</b>) Comparative CECs counts among HC group, CSA group and UA group. Data are expressed as the median with IQRs. (<b>C</b>) Comparative CEC counts with increasing TIMI UA/NSTEMI risk score. Data are expressed as the median with IQRs. P-value referred to the results of Mann-Whitney test between groups. Scale bar, 20μm.</p

Baseline characteristics and CEC count for the three comparison groups.

<p>Baseline characteristics and CEC count for the three comparison groups.</p

Correlations between CEC count and typical cardiac biomarkers.

<p>Spearman rank correlation coefficient (<i>ρ</i>) was used to assessed the correlation between CEC counts in CAD patients with angina pectoris and each initial presenting serum cardiac biomarkers. (<b>A</b>) No correlation was observed between CEC count and cTnI value (<i>ρ</i> = 0.01, <i>p</i> = 0.987). (<b>B</b>) No correlation was observed between CEC count and AST value (<i>ρ</i> = 0.02, <i>p</i> = 0.910). (<b>C</b>) No correlation was observed between CEC count and LDH value (<i>ρ</i> = 0.15, <i>p</i> = 0.271). (<b>D</b>) No correlation was observed between CEC count and CK value (<i>ρ</i> = 0.18, <i>p</i> = 0.181). (<b>E</b>) No correlation was observed between CEC count and CK-MB value (<i>ρ</i> = -0.14, <i>p</i> = 0.326). (<b>F</b>) No correlation was observed between CEC count and α-HBDH value (<i>ρ</i> = 0.17, <i>p</i> = 0.212).</p

Calculation of risk score using the TIMI NSTEMI/UA system.

<p>Calculation of risk score using the TIMI NSTEMI/UA system.</p