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Aims: We intend to elucidate the alterations of cerebral networks in patients with insular glioma‐related epilepsy (GRE) based on resting‐state functional magnetic resonance images. Methods: We collected 62 insular glioma patients, who were subsequently categorized into glioma‐related epilepsy (GRE) and glioma with no epilepsy (GnE) groups, and recruited 16 healthy individuals matched to the patient's age and gender to form the healthy control (HC) group. Graph theoretical analysis was applied to reveal differences in sensorimotor, default mode, visual, and executive networks among different subgroups. Results: No significant alterations in functional connectivity were found in either hemisphere insular glioma. Using graph theoretical analysis, differences were found in visual, sensorimotor, and default mode networks (p < 0.05). When the glioma located in the left hemisphere, the degree centrality was reduced in the GE group compared to the GnE group. When the glioma located in the right insula, the degree centrality, nodal efficiency, nodal local efficiency, and nodal clustering coefficient of the GE group were lower than those of the GnE group. Conclusion: The impact of insular glioma itself and GRE on the brain network is widespread. The networks altered by insular GRE differ depending on the hemisphere location. GRE reduces the nodal properties of brain networks than that in insular glioma. [ABSTRACT FROM AUTHOR]

To explore the prognostic factors of patients with low-grade optic pathway glioma (OPG) and the optimal treatment to reduce the incidence of postoperative hydrocephalus. This single-center study retrospectively analyzed data from 66 patients with OPGs who underwent surgery. The patients were followed, and overall survival (OS) and progression-free survival (PFS) were determined. The effects of different treatments on the hydrocephalus of patients were compared. Postoperative hydrocephalus was identified as a factor to increase the risk of mortality by 1.99-fold (p =.028). And, 5-year survival rate was significantly lower among patients with postoperative hydrocephalus (p =.027). The main factors leading to preoperative hydrocephalus in patients are large tumor volume and invasion into the third ventricle. Gross total resections (GTR) could reduce the risk of long-term hydrocephalus (p =.046). Age younger than 4 years (p =.046) and tumor invasion range/classification (p =.029) are the main factors to reduce the five-year survival rate. Postoperative radiotherapy (RT) and chemotherapy (CT) had no significant effects on OS. Extraventricular drainage (EVD) was not associated with perioperative infection (p =.798 >.05) and bleeding (p =.09 >.05). Compared with 2 stage surgery (external ventricular drainage or ventriculoperitoneal shunt (VPS) was first placed, followed by tumor resection), 1 stage surgery (direct resection of tumor) had no complication increase. Postoperative hydrocephalus is mostly obstructive hydrocephalus, and it is an important factor that reduces the OS of patients with low-grade OPGs. Surgery to remove the tumor to the greatest extent improves cerebrospinal fluid circulation is effective at reducing the incidence postoperative hydrocephalus. For patients whose ventricles are still dilated after surgery, in addition to considering poor ventricular compliance, they need to be aware of the persistence and progression of hydrocephalus. [ABSTRACT FROM AUTHOR]

To investigate the association between loci rs3761847 and rs10818488 of tumor necrosis factor receptor-associated factor 1/complement C5 (TRAF1/C5) gene and the susceptibility to IgAV. 100 blood samples of children with IgAV and 100 blood samples of healthy children were collected from the Third Xiangya Hospital of Central South University from June 2017 to June 2019. The target gene fragment was amplified by polymerase chain reaction (PCR), and the single nucleic acid gene polymorphism of the gene loci was detected by PCR sequencing based typing technique. The association between gene polymorphism of each locus and susceptibility to IgAV was analyzed. There were significant differences in both genotype (P <.05) and allele frequencies （P <.05) of rs3761847 of TRAF1/C5 gene between the IgAV group and the control group.Besides, the risks of developing IgAV in children with the TT genotype was 0.495 times and in children with the C allele was 1.627 times of that in children with other genotypes and alleles, respectively (P <.05). For IgAV patients, renal involvement risk in children with CC genotype was 5.859 times of that in children with other genotypes (P <.05). There were no significant differences in genotype (P >.05) and allele frequencies (P >.05) of rs10818488 of TRAF1/C5 gene between the IgAV group and the control group. IgAV patients with TT genotype had a 3.2 times higher risk of renal involvement than those with other genotypes (P <.05). There is an association between locus rs3761847 of TRAF1/C5 gene single nucleotide polymorphisms and susceptibility to IgAV. The T allele at locus rs3761847 of TRAF1/C5 gene may be a protective factor for IgAV. The C allele at locus rs3761847 and the T allele at locus rs10818488 of TRAF1/C5 gene may be associated with kidney injury in IgAV. [ABSTRACT FROM AUTHOR]

Background: Previous research demonstrated the association between cyclooxygenase-2 (COX-2) gene polymorphisms and susceptibility to Kawasaki disease (KD). This study aims to detect the plasma concentration of COX-2 in different phases of KD patients and evaluate the relationship between COX-2 level and coronary artery lesion formation, therapeutic response to intravenous immunoglobulin. Methods: Plasma COX-2 levels were measured by enzyme-linked immunosorbent assay in KD patients during the acute (a-KD, n = 52), subacute (s-KD, n = 46), and convalescent (c-KD, n = 43) phase. Results: The concentration of COX-2 in the a-KD group was significantly higher than that in the s-KD, c-KD, healthy control or febrile control group, respectively. There was no difference in the levels of COX-2 between the KD with or without coronary artery lesion subgroups, intravenous immunoglobulin resistant, and sensitive subgroups in the a-KD group, respectively. Conclusions: The plasma concentration of COX-2 might be a novel potential biomarker of acute KD. [ABSTRACT FROM AUTHOR]

Object: This study aimed to explore the relationship between the aggressiveness and immune cell infiltration in pituitary adenoma (PA) and to provide the basis for immuno-targeting therapies. Methods: One hundred and three patients with PA who underwent surgery at a single institution were retrospectively identified. The infiltration of macrophages and T-lymphocytes was quantitatively assessed. Results: The number of CD68+ macrophages was positively correlated with Knosp (p = 0.003) and MMP-9 expression grades (p = 0.00). The infiltration of CD163+ macrophages differed among Knosp (p = 0.022) and MMP-9 grades (p = 0.04). CD8+ tumor-infiltrating lymphocytes (TILs) were also positively associated with Knosp (p = 0.002) and MMP-9 grades (p = 0.01). Interestingly, MGMT expression was positively correlated with MMP-9 staining extent (p = 0.000). The quantities of CD8+ TILs (p = 0.016), CD68+ macrophages (p = 0.000), and CD163+ macrophages (p = 0.043) were negatively associated with MGMT expression levels. The number of CD68+ macrophages in the PD-L1 negative group was significantly more than that in the PD-L1 positive group (p = 0.01). The rate of PD-L1 positivity was positively correlated with the Ki-67 index (p = 0.046) and p53 expression (p = 0.029). Conclusion: Targeted therapy for macrophages and CD8+ TILs could be a helpful treatment in the future for aggressive PA. Anti-PD-L1 therapy may better respond to PAs with higher Ki-67 and p53 expression and more infiltrating CD68+ macrophages. Multiple treatment modalities, especially combined with immunotherapy could become a novel therapeutic strategy for aggressive PA. [ABSTRACT FROM AUTHOR]

Kawasaki disease (KD)), also known as mucocutaneous lymph node syndrome (MCLS), is an autoimmune and systemic vasculitis syndrome. Its etiology and pathogenesis are still unclear. microRNAs (miRNA), a novel class of small non-coding RNAs, regulate the expression of multiple protein-encoding genes at the post-transcriptional level. We intend to study the change of miRNA-133a in the plasma of patients with KD, explore the role of miRNA-133a on HUVEC and define the pathogenesis of vascular dysfunction in KD. miRNA-133a expression and the mRNA and protein expression of protein phosphatase 2 catalytic subunit alpha (PPP2CA) were assessed by RT-qPCR and Western blot, respectively. The PPP2CA mRNA 3ʹUTR was predicted to be the potential target of miRNA-133a by using the miRNA databases and verified by the luciferase assay. The plasmids of miRNA-133a mimics and inhibitors were transfected into HUVEC cells. The plasma soluble vascular endothelial cadherin (sVE-cadherin, the excised extracellular part of VE-cadherin) levels were investigated by ELISA. The results suggested that miRNA-133a was increased by 3.8 times in the acute KD group and by 2.7 times in the convalescent KD group compared with the control group (both P =.000). PPP2CA is the target gene of miRNA-133a and its expression was inhibited by miRNA-133a acting on PPP2CA mRNA 3ʹUTR (P =.013). The plasma sVE-cadherin levels in the acute KD groups were increased compared with the control group (P =.024). The ROC curve analysis showed that the expression of miRNA-133a segregate acute KD patients from convalescent KD patients and healthy children. Our results suggest that miRNA-133a might be a new biomarker for KD. [ABSTRACT FROM AUTHOR]

A novel printed monopole antenna with simple, low-profile and convenient design is presented in this paper. The antenna composes of a printed monopole antenna and a folded-line stepped impedance resonator (SIR) loaded on the bottom of the substrate. The resonant frequency is decreased by the coupling between the folded-line SIR as the near-field resonant parasitic (NFRP) element and radiation patch of the monopole antenna. The stronger the coupling, the lower the frequency. At the same time, the introduction of the NFRP element does not require an additional circuit for impedance matching, a novel the printed monopole antenna can be achieved. After analyzing the principle of the proposed antenna, a sample antenna has been manufactured and measured to prove the estimated performance of the proposed antenna. The measured results of the proposed antenna are consistent with the simulation, which shows that the design method in this paper is accurate and effective. [ABSTRACT FROM AUTHOR]

Background: Kawasaki disease (KD) is an acute systemic vasculitis of unknown etiology. Cyclophilin A (CypA), also known as PPIA, has been identified to play a vital role in the pathogenesis of cardiovascular or inflammatory diseases. However, no studies have examined the relationship between single-nucleotide polymorphisms (SNPs) in the peptidylprolyl isomerase A (PPIA) and the development of KD and KD with or without coronary artery lesions (CALs). Objective: The present study was conducted to evaluate whether PPIA SNPs are associated with susceptibility to KD or CALs in KD. Methods: Three PPIA SNPs were genotyped in 101 KD patients and 105 healthy controls from a Chinese population. The allele and genotype frequencies were compared between the case and control groups, as well as in KD patients with and without CALs. Results: The data revealed a significant difference in the genotype and allele frequencies of rs17860041 A/C between KD patients and normal controls. Compared to the rs17860041 CC genotype, the AC genotype demonstrated a consistently beneficial roles in reducing the KD incidence. Furthermore, the allele frequency of C in the KD group was higher than that in the control group (P <.05). Haplotype analysis for PPIA polymorphisms (rs10951772 A/G, rs17860041 A/C, and rs4720485 A/T) also confirmed this association in KD patients and normal controls. Conclusion: A PPIA promoter SNP (rs17860041 A/C) confers susceptibility to KD in Chinese children and was identified as an important marker of KD in this study. [ABSTRACT FROM AUTHOR]

Objective: Central neurocytomas (CNs) are rare, and this has resulted in a paucity of information and a lack of clarity regarding their optimal management. This study aimed to explore individual treatment strategies for CNs and the benefits of these strategies for patients. Methods: This single-center study retrospectively analyzed data from 67 patients with CNs who underwent surgery. Based on the extent of resection, patients were divided into complete and incomplete resection groups. The patients were followed, and overall survival (OS) and progression-free survival (PFS) were determined. Results: Of 55 patients (82.1%) who underwent complete resections, 24 received radiotherapy (24/55, 43.6%). Of 12 patients who underwent incomplete resections, 9 (9/12, 75.0%) received radiotherapy. The OS (p = 0.003) and PFS (p = 0.006) intervals were significantly longer in the complete resection group than in the incomplete resection group. Postoperative radiotherapy did not affect OS (p = 0.129) or PFS (p = 0.233) in the complete resection group. In the incomplete resection group, postoperative adjuvant radiotherapy prolonged patient survival significantly (p = 0.021). PFS was significantly longer among patients who underwent complete resection without radiotherapy than in those who underwent incomplete resection followed by radiotherapy (p = 0.034). Functional dependence on admission, which was defined as a Karnofsky Performance Status score <70, was an independent risk factor associated with long-term survival in patients with CN. Postoperative complications were not associated with the amount of tumor resected. The prognosis of patients aged ≥ 50 years was relatively poor. The atypical CN recurrence rate was relatively high (7.8%). Conclusions: To protect function as much as possible, complete tumor resection should be the first choice of treatment for CN. After gross total resection, adjuvant radiotherapy is not acceptable. Postoperative adjuvant radiotherapy improves the prognosis of patients who have undergone incomplete tumor resections. Adjuvant radiotherapy is not recommended after complete resections of atypical CNs, and close follow-up with imaging is required. Our findings can help guide decision-making regarding the treatment of CNs and could potentially maximize the benefits of treatment for patients with CN. [ABSTRACT FROM AUTHOR]

The aim of the present study was to explore the clinical characteristics of repeated hemorrhages of meningioma and analyze the causes of hemorrhage. Meningiomas are mostly benign tumors that rarely manifest hemorrhagic strokes. In the present study, a case of sphenoid ridge meningioma with repeated hemorrhages is reported. Internal hemorrhage was first observed, which, on further aggravation, formed a hematoma in the brain parenchyma and finally led to the development of a hernia. No neurological deficit was present after surgery and rehabilitation. A postoperative pathological examination showed increased levels of Ki-67, abnormal blood vessels in the tumors and the presence of progesterone, which indicate possible causes of the hemorrhage. A review of associated previous studies revealed that hemorrhages originate mainly from inside the meningioma. Two cases of meningiomas with repeated hemorrhages have been reported; one in the foramen magnum region and the other in the pineal gland area. The foramen magnum tumor had an interval of 1.33 months between two hemorrhagic episodes. Collecting relevant data from the latter case was not possible. In the present case report, the interval between two bleeding episodes was 3 days. The literature review also revealed that the average age of onset of meningioma is relatively young at only 28.00±6.24 years. In conclusion, repeated hemorrhages in meningiomas are extremely rare and the causes have not yet been identified. Increased Ki-67 and abnormally proliferating blood vessels may be potential causes of hemorrhage. Early diagnosis and rapid surgical intervention are essential to prevent further episodes of bleeding, which may otherwise have fatal consequences for the patients. [ABSTRACT FROM AUTHOR]

Familial renal glucosuria (FRG) is a rare condition that involves isolated glucosuria despite normal blood glucose levels. Mutations in the solute carrier family 5 member 2 (SLC5A2) gene, which encodes sodium-glucose cotransporter 2 (SGLT2), have been reported to be responsible for the disease. Genetic testing of the SLC5A2 gene was conducted in a Chinese family with FRG. A number of online tools were used to predict the potential effect of the identified mutations on SGLT2 function. Additionally, the SLC5A2 mutations previously reported in PubMed were summarized. A novel compound heterozygous mutation (c.514T>C, p.W172R; c.1540C>T, p.P514S) of the SLC5A2 gene in a Chinese child with FRG was identified. In total, 86 mutations of the SLC5A2 gene have been reported to be associated with FRG. The novel compound heterozygous mutation (c.514T>C, p.W172R; c.1540C>T, p.P514S) of the SLC5A2 gene may be responsible for the onset of FRG. The present study provides a starting point for further investigation of the molecular pathogenesis of the SLC5A2 gene mutation in patients with FRG. [ABSTRACT FROM AUTHOR]

Background: Kawasaki disease (KD) is an acute systemic vasculitis that predominantly affects children, and it can result in coronary artery lesions. Cyclooxygenase-2 (COX-2) is involved in the conversion of arachidonic acid to prostaglandin H2, an important precursor of several prostaglandins. The aim of this study was to examine the association between COX-2 gene polymorphisms and susceptibility to KD. Methods: A total of 276 subjects (136 KD and 140 controls) were recruited. The analysis of two single nucleotide polymorphisms rs689466 (−1195G/A) and rs20417 (−765G/C) was respectively detected with polymerase chain reaction sequence-based typing methods. Results: Polymorphisms of rs689466 were significantly different between the normal controls and KD patients (χ2 = 6.070 and 5.435, both p < 0.05). The frequencies of AA genotype and A allele of rs689466 in Kawasaki disease group were higher than that of control group (χ2 = 4.832, p = 0.028, OR = 1.832, 95%CI = 1.064-3.124; χ2 = 5.435, p = 0.028, OR = 1.491, 95%CI = 1.065-2.088). Conclusion: This study provides the first evidence supporting an association between COX-2 gene polymorphisms and susceptibility of KD. The AA genotype and A allele of rs689466 confer predisposing factors to KD. [ABSTRACT FROM AUTHOR]

Background/Aims: Hereditary spherocytosis (HS) is a common pediatric hemolytic anemia caused by congenital red blood cell defects. HS due to ankyrin 1 (ANK1) mutations is the most common type. We explored an ANK1 mutation from an HS patient and reviewed the literature. Methods: We detected the mutation in a Chinese family in which 2 members were diagnosed with HS by next-generation sequencing. The proband was diagnosed with HS in the newborn period, based on clinical manifestations, laboratory data, and family history. The mutation spectrum of the ANK1 gene was summarized based on 85 patients diagnosed with HS carrying ANK1 mutations, and the ANK1 mutation spectrum was summarized and analyzed. Results: We identified a novel mutation affecting ANK1 gene splicing (a splicing mutation) in both the patient and her mother, which is a substitution of T>G 2 nt after exon 25 in intron 26. The study expands our knowledge of the ANK1 gene mutation spectrum, providing a molecular basis for HS. Conclusion: A novel ANK1 mutation (NM_000037.3, c.2960+2T>G, intron 26) that is potentially associated with HS was identified. To date, 80 ANK1 mutations have been reported to be associated with HS in humans. [ABSTRACT FROM AUTHOR]

Coxsackievirus B3 (CVB3) infection has been shown to stimulate autophagy. We have demonstrated that the inhibition of phosphoinositide 3-kinase (PI3K)/protein kinase B/mammalian target of rapamycin complex (mTORC) signaling pathway could affect the autophagic reaction induced by CVB3 infection in our previous study. However, the processes associating autophagy and CVB3 replication remain to be determined. In the present study, CVB3-induced autophagy and its impact on viral replication were investigated. Rapamycin (inhibitor of mTOR) and ZSTK474 (inhibitor of PI3K) were used to change the autophagic reaction caused by CVB3 in Hela cells at different post-infection (p.i.) time points (6, 9, 12 and 24 h p.i.), meanwhile, we detected the CVB3 mRNA replication and CVB3 capsid protein VP1 expression following the change of autophagy. Here, it was showed that ZSTK474 and Rapamycin promoted CVB3-induced autophagy, as well as decreasing CVB3 mRNA replication and CVB3 capsid protein VP1 expression at 6 and 9 h p.i. ZSTK474 also alleviated CVB3-induced autophagy, and decreased CVB3 mRNA replication and VP1 expression at 12 and 24 h p.i. However, Rapamycin continued to promote CVB3-induced autophagy and increase CVB3 mRNA replication at 12 and 24 h p.i, as well as increase VP1 expression at 12 h, but not at 24 h, p.i. In the present study, we found Rapamycin and ZSTK474 have differential effects at different p.i. time-points regarding CVB3 replication and CVB3-induced autophagy. This indicates that the association between CVB3-induced autophagy and viral replication depends on the infection time. During the early course of infection, autophagy may help host cells clear the virus, thereby providing protection, whereas when the infection time increases, autophagy may be exploited for viral replication. [ABSTRACT FROM AUTHOR]

Kawasaki disease (KD) is an acute systemic vasculitis that predominantly affects children and can result in coronary artery lesions (CALs). Thrombomodulin (TM) is a critical cofactor in the protein C anticoagulant system. The TM C1418T (rs1042579) polymorphism is associated with a high risk of cardiac-cerebral vascular diseases. But the association of the TM C1418T polymorphism with susceptibility to KD, CAL formation, and intravenous immunoglobulin (IVIG) resistance is still unclear. In our study, we examined the TM C1418T polymorphism in 122 children with KD and 126 healthy children and revealed the correlation between the TM C1418T polymorphism and KD, CAL formation, and IVIG resistance. [ABSTRACT FROM AUTHOR]

Background: PHKG2 gene mutation can lead to liver phosphorylase kinase (PhK) deficiency, which is related to glycogen storage disease type IX (GSD IX). GSD IXc due to PHKG2 mutation is the second most common GSD IX. Methods: We identified a novel mutation (c.553C>T, p.Arg185X) in PHKG2 in a Chinese family and verified it by next-generation and Sanger sequencing. The mutation spectrum of the PHKG2 gene was summarized based on 25 GSD IXc patients with PHKG2 mutations. Results: We found that missense mutation (39%) was the most common type of mutation, followed by nonsense mutation (23%). Mutations were more prevalent in Asian (12/25) and European (9/25) populations than in populations from elsewhere. The exons had more sites of mutation than the introns, and exons 3 and 6 were the most frequent sites of mutations. Conclusions: This study expands our knowledge of the PHKG2 gene mutation spectrum, providing a molecular basis for GSD IXc. [ABSTRACT FROM AUTHOR]

Background: Kawasaki disease (KD) is a childhood systemic vasculitis that exhibits a specific preference for the coronary arteries. The aetiology remains unknown and there are no especially diagnostic tests. microRNAs (miRNAs) are 18 to 23 nucleotides non-coding RNAs that are negative regulator of gene expression and play a crucial role in the regulatory network of the genome. Recently, circulating miRNAs have been found presentation in human plasma and displayed some characteristics of the ideal biomarker. However, few researches explored differentially expressed miRNAs in the plasma of KD patients. Our study is to identify circulating miRNAs in KD plasma which can serve as potential biomarkers of KD diagnosis. Materials and methods: The total of five pairs of acute KD and normal plasma samples were analyzed using ABI miRNAs TLDA Assay chip. Differentially expression of miR-125a-5p in plasma were confirmed by quantitative real-time PCR (qRT-PCR) in independent cohort (acute KD = 30, convalescent KD = 30 and healthy control = 32). After bioinformatics prediction, miR-125a-5p vector and inhibitor were transfected into HUVECs respectively, to observe MKK7 expression as a potential target gene. Flow cytometry was used to analyze apoptosis. The mRNA and protein levels of desired genes including MKK7, Caspase-3, Bax and Bcl2 were detected by qRT-PCR and western blotting. Results: Eighteen miRNAs were differentially expressed in acute KD’s plasma compared with healthy control. miR-125a-5p was significantly increased in plasma of KD patients (p = 0.000), but no variation between acute and convalescent KD (p = 0.357). Moreover, the results from the gain and loss functions of miR-125a-5p in HUVECs have shown that miR-125a-5p remarkably suppressed MKK7 expression, as a novel target gene. Importantly, miR-125a-5p also induced apoptosis in HUVECs through inhibition MKK7 levels to regulate Bax/Bcl2 pathway resulting to activate Caspase-3. Conclusion: Our study indicated that the circulating miR-125a-5p levels in KD’s plasma have remarkably evaluated compared with healthy individuals. miR-125a-5p might play a role in the development of KD by regulating target gene MKK7 to induce apoptosis in vascular endothelial cells. Therefore, our findings have suggested that detected miR-125a-5p levels in plasma could be used as a potential biomarker in early KD diagnosis. [ABSTRACT FROM AUTHOR]

Kawasaki disease (KD) is an acute systemic vasculitis complicated by development of coronary artery lesions. PECAM-1 is a kind of cell adhesion molecule, which plays an important role in coronary artery disease. The relationship between PECAM-1 gene polymorphisms and their susceptibility to Kawasaki diseases (KD) is still unclear. In our study, we examined the PECAM-1 gene polymorphisms in 44 KD patients and 59 healthy children and revealed the correlation of PECAM-1 gene polymorphisms in KD children with and without coronary artery lesions (CAL). [ABSTRACT FROM AUTHOR]

Postoperative venous thromboembolism (VTE) is a common complication for glioma patients, with an incidence rate of about 20 %. The purpose of this study was to explore the risk factors of acute VTE after glioma surgery, which may provide an essential reference for clinical guidance on the prevention of acute VTE. A total of 435 patients who underwent glioma surgery from 2012 to 2021 were included in this study. Duplex ultrasonography was performed routinely 3–5 days after the surgery to define VTE. Univariate and multivariate logistic regression analyses were performed to explore the independent predictor of acute VTE after glioma surgery and use these selected risk factors to construct and validate a nomogram. Several risk factors for predicting acute VTE after glioma surgery were identified and used to build the nomogram: age, operation time, systemic immune-inflammation index (SII), hypertension, and diabetes mellitus. The area under the curve of the nomogram was 0.834, indicating good discrimination. Hosmer-Lemeshow of the calibration curve was 3.05 (P = 0.98), showing a high degree of agreement between the prediction and actual outcome. Decision curve analysis indicated that the nomogram model was helpful when the incidence of VTE was 5–80 %. A nomogram to predict acute VTE after glioma surgery was constructed and validated. Clinicians can use this predictive model to achieve risk assessment and take different treatment measures to prevent acute postoperative VTE and improve patients' quality of life effectively. [ABSTRACT FROM AUTHOR]

This work illustrated the mechanism contributing to the process of Phosphatidylinostiol 3-kinase (PI3K)/protein kinase B (PKB)/mammalian target of rapamycin (mTOR) signaling pathway, which has been demonstrated to play an important role in virus-induced apoptosis, which contributes to the Viral Myocarditis (VMC) pathogeneses. We examined the expression of Bax, Bim, caspase-3, caspase-9, and viral replication after Coxsackievirus B3 (CVB3) infection using the mTOR inhibitor and PI3K inhibitor pretreated HeLa cells, respectively. Apoptosis in different groups was determined by flow cytometry. Bax, Bim, caspase-9, and caspase-3 were examined by semiquantitative polymerase chain reaction (PCR) and Western blot analysis. The expression of CVB3 mRNA and viral capsid protein VP1 were analyzed by semiquantitative PCR and Western blot analysis distinctively. We found that rapamycin and LY294002 promote CVB3-induced cytopathic effect (CPE) and apoptosis. CVB3 replication in host cells is mediated in mRNA and protein expression by rapamycin and LY294002. Moreover, comparing with controls, at 12 and 24 h of postinfection (p.i.), Bim and Bax expression increased in cells after treated with rapamycin or LY294002, which also stimulates the activation of procaspase-9, and the CVB3-induced caspase-3 self-cleavage. However, in the meantime, the mRNA expression of caspase-9 and caspase-3 did not have an obvious change. In summary, our results demonstrated that the mTOR-signaling pathway plays an important role in CVB3-induced CPE and apoptosis, which is indispensable in VMC, via regulating Bim, Bax, caspase-9, caspase-3, and viral replication. Our findings may provide a new perspective and a deeper understanding of the mechanism of CVB3-induced apoptosis which, in turn, may help with the development of new therapy for the CVB3 infection. The mammalian target of rapamycin and Phosphatidylinostiol 3 kinase pathways contribute to cellular apoptosis and cytopathology following infection of HeLa cells by Coxsackievirus B type 3 infection. This requires Bim, Bax, and caspases-3 and -9. [ABSTRACT FROM AUTHOR]

The present study aimed to compare the thickness of brain abscesses in the deep and the superficial brain and to investigate the factors that influence the capsule of brain abscesses. The thickness of the brain abscess wall was evaluated on imaging. Bacteriological examination was performed on the abscess pus and wall, and immunohistochemical staining was used to count the number of macrophages. Kaplan-Meier curves were used to analyze overall survival. The results indicated that the wall of deep-brain abscesses was thicker than that of superficial abscesses. There was a difference in the extent of macrophage infiltration of deep- and superficial-brain abscess walls, and differences in the extent of macrophage infiltration in the wall of brain abscesses caused by various microorganisms were statistically significant. Of note, among the brain abscesses caused by Staphylococcus, the extent of macrophage/microglia infiltration and the thickness of the wall of the deep-brain abscesses were greater than those of superficial-brain abscesses and there was a positive correlation between the number of macrophages and the thickness of the abscess wall. The overall survival (OS) of patients with deep-brain abscess was not significantly shorter than that of patients with superficial-brain abscess. Furthermore, OS was not significantly different among groups of patients receiving different types of treatment. In conclusion, the wall of deep-brain abscesses is thicker than that of superficial abscesses and the infiltration of macrophages is abundant. The thick wall of abscesses in the deep brain may be associated with macrophage infiltration. [ABSTRACT FROM AUTHOR]

Tourette syndrome (TS) is a complex neuropsychiatric disorder with chronic motor and vocal tics. Though the etiology is elusive, strong evidence for a genetic contribution to TS has been established. To date, various chromosomal or genetic alterations have been implicated in its pathogenesis. Recently, the deletion in the arylacetamide deacetylase gene ( AADAC ) was reported to be associated with TS. To investigate the association between the AADAC gene variants and TS, we conducted genetic analysis of the AADAC gene in 200 Han Chinese patients and 300 ethnicity-matched normal controls. Two variants, including a heterozygous splice-site variant, c.361 + 1G > A (rs762169706), and a missense variant, c.744A > T (p.R248S, rs186388618), were identified in two unrelated patients. The c.361 + 1G > A variant, absent in 300 ethnicity-matched controls, led to the deletion of exon 2 in AADAC mRNA, probably associated with development of TS. The c.744A > T variant, predicted to be damaging, was identified in two normal controls. The findings indicate that the AADAC gene c.361 + 1G > A variant may be a potential candidate factor for TS development, though further investigations are warranted. [ABSTRACT FROM AUTHOR]

Abstract: Tourette syndrome (TS), a neurological disorder with a reported prevalence frequency ranging from 0.7% to 4.2%, is manifested by motor and phonic tics and associated with a variety of behavioral abnormalities including impulsivity. Clinical, neuroimaging and other studies support dysfunction of the dopamine and 5-hydroxytryptamine neurotransmitter systems in TS. To determine whether TS is associated with mutation in the 5-hydroxytryptamine receptor 2B gene (HTR2B), which has been also implicated in impulsivity, we screened 132 Caucasian and 128 Chinese Han patients with TS. Two novel (c.188T>G, Met63Arg; c.1346G>A, Arg449Gln) and three known (rs61731726, Gly51Gln; rs200541113, Lys324Asn; rs61731723, Asn438Asn) nucleotide variants were found. Further analysis of sex, age, and ethnically matched normal controls (138 Caucasians and 248 Chinese Han individuals), as well as an affected family member, indicated that these variants may not be pathogenically relevant, suggesting that variants in the HTR2B gene may play little or no role in the development of TS. [Copyright &y& Elsevier]