The Functions of Selenium and Selenoproteins Relating to the Liver Diseases.

Selenium is an important trace element. Many studies have proved that selenium can protect liver tissues by reducing response of immune inflammation and inducing high levels of ROS to promote tumor apoptosis. It can also participate in metabolism and involve in expression of selenoproteins. Selenoproteins also play a key role in liver diseases with regulating ROS and relating factors. In this review, we summarized the metabolic pathways of selenium intake and their bio-functions on liver diseases (Hepatoma, Cirrhosis and hepatitis). Moreover, the related molecular mechanisms are analyzed and discussed. Selenoproteins may be a promising target for liver diseases treatment.

Quantitative Analysis of Multiple Proteins of Different Invasive Tumor Cell Lines at the Same Single-Cell Level.

Tumor cell invasion is pivotal to the development, metastasis, and prognosis of tumors. It is reported that the invasive ability of tumor cells is mainly dependent on the expression levels of membrane type-1 matrix metalloproteinase (MT1-MMP) and integrin αV ß3 proteins on cell membranes. To precisely distinguish between tumor cells with different invasive abilities, it is important to establish a highly sensitive and precise quantification method to differentiate the expression levels of MT1-MMP and integrin αV ß3 in the same single tumor cell at the same time. Herein, two functional peptides to construct red-emissive Au26 clusters and green-emissive Ag12 clusters are reported. Moreover, the Au26 clusters and Ag12 clusters have the ability to specifically target MT1-MMP and integrin αV ß3 , respectively, in the same single cell at the same time. By utilizing the fluorescent properties and metallic compositions of metal clusters, the MT1-MMP and integrin αV ß3 levels of the more invasive SiHa cells or the less invasive HeLa cells are simultaneously and quantitatively differentiated via laser ablation inductively coupled plasma mass spectrometry. This method of quantitatively detecting multiple invasive proteins on the same cell is of great value for accurately diagnosing aggressive tumors and monitoring the invasiveness of these tumors.

Neurosurgical management of cavernous malformations located at the foramen of Monro.

Cavernous malformations (CMs) located at the foramen of Monro (FM) are relatively rare benign vascular malformations. Knowledge of FM CM is poor. The aims of this study were to describe the incidence, clinical presentation, radiological features, surgical approaches, and neurological outcomes for FM CM patients and to discuss the treatment strategy for this disease. We present a series of nine FM CM patients (four males, five females; mean age 29.3 years) who were treated at a single neurosurgical center. FM CM accounted for 0.56% of the entire series of the central nervous system (CNS) CMs. Headache accompanied by nausea and vomiting was the most common initial symptom (55.6%). The mean preoperative Karnofsky Performance Scale (KPS) score was 84.4 (range 70-100). In all but one patient, the lesions were surgically resected. Postoperatively, two patients developed obstructive hydrocephalus, and one experienced motor aphasia and right hemiparesis. At the time of discharge, the KPS score improved to a mean of 88.9. Follow-up period after diagnosis was 18 to 131 months (mean 69.7 months); all the patients were considered to be in excellent clinical condition. FM CMs are rare and challenging lesions; they have a female predilection. The most common clinical manifestations of FM CM are the symptoms of mass effect. The seizure risk of FM CMs seems to be significantly lower than that of general intraventricular CMs. Early surgical intervention should be offered to symptomatic cases, and gross total resection is associated with favorable neurological outcomes.

Multifunctional aggregation network of cell nuclei segmentation aiming histopathological diagnosis assistance: A new MA-Net construction.

Automated diagnostic systems can enhance the accuracy and efficiency of pathological diagnoses, nuclear segmentation plays a crucial role in computer-aided diagnosis systems for histopathology. However, achieving accurate nuclear segmentation is challenging due to the complex background tissue structures and significant variations in cell morphology and size in pathological images. In this study, we have proposed a U-Net based deep learning model, called MA-Net(Multifunctional Aggregation Network), to accurately segmenting nuclei from H&E stained images. In contrast to previous studies that focused on improving a single module of the network, we applied feature fusion modules, attention gate units, and atrous spatial pyramid pooling to the encoder and decoder, skip connections, and bottleneck of U-Net, respectively, to enhance the network's performance in nuclear segmentation. The dice coefficient loss was used during model training to enhance the network's ability to segment small objects. We applied the proposed MA-Net to multiple public datasets, and comprehensive results showed that this method outperforms the original U-Net method and other state-of-the-art methods in nuclei segmentation tasks. The source code of our work can be found in https://github.com/LinaZhaoAIGroup/MA-Net.

Ependymoma with metastases to the gallbladder: A case report and literature review.

Metastatic ependymoma of the gallbladder is an exceptionally rare condition that remains relatively unreported in the scientific literature. The present study described a case involving a 42-year-old female patient who underwent right frontal lobe surgery for ependymoma in 2017 and subsequently received adjuvant chemotherapy. The histological examination of the surgical specimen confirmed the presence of ependymoma metastasis in the gallbladder. The presentation and outcome of this patient with regard to metastatic ependymoma in the gallbladder were evaluated. During a follow-up period of 10 months, the patient received targeted treatment following the surgery. Presently, the patient has developed lung and bone metastases. In the present report, the treatment and diagnostic approach utilized in this unique case were outlined with the aim of providing valuable insight for future clinical management and enhancing clinicians' understanding of the disease.

[Expression of proteins in serum and hippocampus after closed brain injury in rats].

OBJECTIVE: To explore the difference of expression of proteins between the serum and hippocampus after brain injury in rats. METHODS: Male SD rats were used to establish brain injury model. The changes of proteins expression profile in serum and hippocampus at different time after brain injury were analyzed using weak cationic exchanger (WCX2) chips and immobilized metal affinity capture arrays-Cu (IMAC-Cu) chips by surface-enhanced laser desorption/ionization time-of-flight mass spectrometry. RESULTS: A total of 436 protein peaks were detected in serum and 346 protein peaks were detected in hippocampus using WCX2 chips. A total of 229 protein peaks were detected in serum and 345 protein peaks were detected in hippocampus using IMAC-Cu chips. The same 10 protein peaks were respectively detected in serum and hippocampus using WCX2 chips. The same 13 protein peaks were respectively detected in serum and hippocampus using IMAC-Cu chips. CONCLUSION: The changes of protein expression profile in serum and hippocampus are obvious after closed brain injury and show a significant difference. The different proteins detected in serum and hippocampus using the same chip could be biochemical markers for determining brain injury.

Protein phosphatase 2 regulatory subunit B''Alpha silencing inhibits tumor cell proliferation in liver cancer.

AIM: To explore the effects of protein phosphatase 2 regulatory subunit B''Alpha (PPP2R3A) on the proliferation and migration of liver cancer cells. METHODS: Expression of PPP2R3A in tumor tissues of hepatocellular carcinoma (HCC) patients was detected by immunohistochemistry and western blotting. In two liver cancer cell lines (HepG2 and HuH7), PPP2R3A expression was silenced and then overexpression with PPP2R3A lentiviral vectors, and the effects of PPP2R3A knockdown or overexpression on the proliferation, cell cycle, migration, and invasion of HCC cells were determined in vitro. In a xenograft cancer model in nude mice, the in vivo effects of PPP2R3A knockdown on tumor growth and cancer cell proliferation were evaluated. RESULTS: PPP2R3A expression was found in tumor foci in six of eight HCC samples, at a level higher than that in the adjacent para-tumor tissues. PPP2R3A expression was observed primarily in the cytoplasm of the cancer cells. Knockdown of PPP2R3A resulted in significant inhibition of hepatoma cell proliferation (P < .05), migration (P < .01), and invasion (P < .01) as well as a significant delay in the G1/S transition in both liver cancer lines (P < .05) and increased p53 expression. Conversely, overexpression of PPP2R3A promoted the proliferation (P < .05) and altered cell cycle progression (P < .05) of both liver cancer cell lines. In vivo, PPP2R3A knockdown in liver cancer cells led to significant reductions in the tumor volume (P < .001) and the expression of Ki-67 in tumor tissues (P < .05). CONCLUSION: PPP2R3A may play a role in liver cancer via the regulation of tumor cell proliferation and invasion.

[Detection of differential proteins in white matter in brain injury in rat by using a WCX-2 protein chip].

OBJECTIVE: To study the alteration in cortex protein fingerprinting of cerebral cortex after closed brain injury in rat. METHODS: Seventy-two male Sprague-Dawley (SD) rats were randomly divided into sham operation group, 4, 8, 12, 24 and 48 hours postinjury groups. Eight rats in each group were used for WCX-2 protein chip research, and 4 rats in each group for pathological examination. Marmarou's weight-dropping model was reproduced, and brain cortex was harvested for study with hematoxylin-eosin (HE) staining, and Bradford method was adopted for WCX-2 protein chip research, and protein chip reading was obtained for protein fingerprinting analysis. RESULTS: (1) The pathological observation showed different degree of injury could be seen in all the injury groups. (2) The WCX-2 experiment found that 3 protein expressions had changed in cortex after brain injury compared with the sham operation group. The differential protein with molecular weight of 5,639 protein expression was found to be upregulated at 8 hours after injury (P<0.05). The 3,212 protein did not expressed in sham operation or 4, 8, 12 and 24 hours groups, but upregulated at 48 hours after injury (P<0.05). The expression of 7,536 protein was upregulated at 24 hours after injury (P<0.05), but not in sham operation or 4, 8, 12, and 48 hours groups. CONCLUSION: Alterations in protein expression in cerebral cortex could be induced after brain injury.

Expression profile of plasma microRNAs and their roles in diagnosis of mild to severe traumatic brain injury.

Traumatic brain injury (TBI) is associated with trauma-related death. In this study, we evaluated differences in the expression of plasma microRNAs (miRNAs) in patients with different degrees of TBI, and explored the potential of miRNAs for use as diagnostic TBI biomarkers. The miRNA microarray results showed upregulation of 65, 33, and 16 miRNAs and downregulation of 29, 27, and 6 miRNAs in patients with mild, moderate, and severe TBI, respectively, compared with healthy controls. Thirteen miRNAs (seven upregulated and six downregulated) were found to be present in all TBI groups. Seven upregulated miRNAs were selected for validation in an enlarged cohort of samples and showed good diagnostic accuracy. The expression levels of miR-3195 and miR-328-5p were higher in the severe TBI group than in the mild and moderate TBI groups. In summary, our study demonstrates different expression profiles in plasma miRNAs among patients with mild to severe TBI. A subset of seven miRNAs can be used for diagnosis of TBI. Moreover, miR-3195 and miR-328-5p may be utilized during diagnosis to distinguish mild and moderate TBI from severe TBI.

A case report on intermediate-grade malignant meningeal melanocytoma with elevated cell proliferation index.

Meningeal melanocytoma is a kind of extremely rare pigmented tumor of the central nervous system, which often occurs in the groove around the base of the brain and spinal pia mater. Age of onset is 40 to 50 years old, mostly presenting a benign course of disease and the prognosis is good. Case reports of partial invasion or metastasis from lesions are even rarer. This report described a case of 56-year-old meningeal melanoma patient with partial skull and muscle invasion at the lantooccipital transition zone. Intraoperative histological examination showed moderate malignancy and Ki-67 index was 10%.

Sequential expression of cyclooxygenase-2, glutamate receptor-2, and platelet activating factor receptor in rat hippocampal neurons after fluid percussion injury.

Traumatic brain injury causes gene expression changes in different brain regions. Occurrence and development of traumatic brain injury are closely related, involving expression of three factors, namely cyclooxygenase-2, glutamate receptor-2, and platelet activating factor receptor. However, little is known about the correlation of these three factors and brain neuronal injury. In this study, primary cultured rat hippocampal neurons were subjected to fluid percussion injury according to Scott's method, with some modifications. RT-PCR and semi-quantitative immunocytochemical staining was used to measure the expression levels of cyclooxygenase-2, glutamate receptor-2, and platelet activating factor receptor. Our results found that cyclooxygenase-2 expression were firstly increased post-injury, and then decreased. Both mRNA and protein expression levels reached peaks at 8 and 12 hours post-injury, respectively. Similar sequential changes in glutamate receptor 2 were observed, with highest levels mRNA and protein expression at 8 and 12 hours post-injury respectively. On the contrary, the expressions of platelet activating factor receptor were firstly decreased post-injury, and then increased. Both mRNA and protein expression levels reached the lowest levels at 8 and 12 hours post-injury, respectively. Totally, our findings suggest that these three factors are involved in occurrence and development of hippocampal neuronal injury.

VCP/p97, down-regulated by microRNA-129-5p, could regulate the progression of hepatocellular carcinoma.

Valosin containing protein (VCP)/p97 plays various important roles in cells. Moreover, elevated expression of VCP in hepatocellular carcinoma (HCC) is correlated with increased incidence of recurrence. But the role of VCP in HCC progression in vitro and in vivo is unclear. And there are few reports about the regulation mechanism on the expression of VCP in HCC. In this study, it was identified that the level of VCP was frequently increased in human HCC tissues. In addition, down-regulation of VCP with siRNAs could dramatically suppress the genesis and progression of tumor in vivo. It was found that miR-129-5p directly inhibited the expression of VCP in several HCC cell lines. Meanwhile, the level of VCP in HCC tissues was negatively associated with the level of miR-129-5p. Our further investigation showed that the enhanced expression of miR-129-5p also suppressed tumor growth in vivo. Moreover, it was revealed that miR-129-5p could inhibit the degradation of IκBα and increase the apoptosis and reduce the migration of HCC cells by suppressing the expression of VCP. Our results revealed that the expression of VCP was directly regulated by miR-129-5p and this regulation played an important role in the progression of HCC.

[Analysis of the common morphological characteristics of cancerous cells using atomic force microscope].

OBJECTIVE: To observe the surface ultrastructure of different tumor cells in vivo using atomic force microscope (AFM) and analyze their common characteristics. METHODS: We selected 60 specimens of each of normal liver cells, liver cancer, cervical squamous cells, cervical cancer cells, ductal epithelial cells and breast cancer cells for scanning using AFM. The cell surface scan images were analyzed using image analysis software to identify their common morphological features. RESULTS: From normal cervical squamous epithelial cells, intermediate cells, and basal cells to HPV-infected cells, CIN2-3 cells and cervical cancer cells, the membrane surface roughness became gradually increased (P<0.05). Similarly, the surface roughness increased significantly in the order of normal liver cells, hepatitis B cirrhosis liver cells, and hepatocellular carcinoma cells (P<0.05). The average surface roughness also tended to increase from normal mammary gland cells to mammary gland hyperplasia cells and breast cancer cells (P<0.05). CONCLUSION: Normal cells and tumor cells show different cell membrane morphologies, and such morphological features provide a reliable basis for clinical pathological diagnosis and differential diagnosis of malignancies.

[Detection of distinct proteins for brain injury rats serum using a protein chip].

AIM: To explore the alteration of serum protein fingerprinting of rats subjected brain injury. METHODS: Male Sprague-Dawley rats were randomly divided into seven groups, ie, normal control group, sham operation group, injury 4 h, 8 h, 12 h, 24 h and 48 h groups. The change of protein pattern in serum was monitored with weak cationic exchanger chip and surface-enhanced laser desorption ionization-time of flight-mass spectrometry. RESULTS: The reduction of 5648 Da protein expression was detected at 4 h, 8 h or 12 h after injury (P < 0.01, compared with control and sham operation) and recovery at 24 h or 48 h. The increase of 9681 Da protein expression was detected at 4 h, 8 h or 12 h after injury (P < 0.05, compared with control and sham operation) and recovery at 24 h or 48 h. CONCLUSION: The alteration of protein expression in serum could be induced after brain injury.