Histone lactylation-related genes correlate with the molecular patterns and functions of cancer-associated fibroblasts and have significant clinical implications in clear cell renal cell carcinoma.

Recent research emphasised the indispensable role of histone lactylation in the activation of hepatic stellate cells. The VHL mutation is extremely common in clear cell renal cell carcinoma, which normally causes a metabolic shift in cancer cells and increases lactate production, eventually creating a lactate-enriched tumour microenvironment. Cancer-associated fibroblasts (CAFs) promote tumour progression, which is also vital in clear cell renal cell carcinoma. Therefore, this study investigated histone lactylation in CAFs and its impact on patient survival. Multiomics technology was employed to determine the role of histone lactylation-related genes in the evolution of CAFs which correlated with the function and molecular signatures of CAFs. The results suggested that TIMP1 was the hub gene of histone lactylation-related genes in clear cell renal cell carcinoma.

Diphenyl Ether Derivative Rhexocerins and Rhexocercosporins from the Endophytic Fungus Rhexocercosporidium sp. Dzf14 Active against Gram-Positive Bacteria with Multidrug-Resistance.

Ten new diphenyl ether polyketides, including rhexocerins A-D (1-4) and rhexocercosporins A-F (5-10), together with three known congeners (11-13), were isolated from the endophytic fungus Rhexocercosporidium sp. Dzf14 obtained from Dioscorea zingiberensis. Their structures were elucidated by analysis of NMR and HRESIMS data, and their absolute configurations were determined by quantum chemical ECD calculations and X-ray crystallography. Compounds 1-4 featured an unprecedented tetracyclic carbon skeleton (6/7/5/6). Among them, compounds 1 and 5-9 showed antibacterial activities against methicillin-resistant S. aureus T144 and vancomycin-resistant E. faecalis 10.

Identification of sugar transporter genes and their roles in the pathogenicity of Verticillium dahliae on cotton.

Introduction: Verticillium wilt (VW) caused by Verticillium dahliae is a soil-borne vascular fungal disease that severely affects cotton yield and fiber quality. Sugar metabolism plays an important role in the growth and pathogenicity of V. dahliae. However, limited information is known about the sugar transporter genes and their roles in the growth and pathogenicity of V. dahliae. Method: In this study, genome-wide identification of sugar transporter genes in V. dahliae was conducted and the expression profiles of these genes in response to root exudates from cotton varieties susceptible or resistant to V. dahliae were investigated based on RNA-seq data. Tobacco Rattle Virus-based host-induced gene silencing (TRV-based HIGS) and artificial small interfering RNAs (asiRNAs) were applied to investigate the function of candidate genes involved in the growth and pathogenic process of V. dahliae. Results: A total of 65 putative sugar transporter genes were identified and clustered into 8 Clades. Of the 65 sugar transporter genes, 9 were found to be induced only by root exudates from the susceptible variety, including VdST3 and VdST12 that were selected for further functional study. Silencing of VdST3 or VdST12 in host plants by TRV-based HIGS reduced fungal biomass and enhanced cotton resistance against V. dahliae. Additionally, silencing of VdST12 and VdST3 by feeding asiRNAs targeting VdST12 (asiR815 or asiR1436) and VdST3 (asiR201 or asiR1238) inhibited fungal growth, exhibiting significant reduction in hyphae and colony diameter, with a more significant effect observed for the asiRNAs targeting VdST12. The inhibitory effect of asiRNAs on the growth of V. dahliae was enhanced with the increasing concentration of asiRNAs. Silencing of VdST12 by feeding asiR815+asiR1436 significantly decreased the pathogenicity of V. dahliae. Discussion: The results suggest that VdST3 and VdST12 are sugar transporter genes required for growth and pathogenicity of V. dahliae and that asiRNA is a valuable tool for functional characterization of V. dahliae genes.

AURKB promotes tumorigenesis and carboplatin resistance by regulating the ERK pathway in neuroblastoma cells.

BACKGROUND: Previous research has revealed that activation or aberrant expression of kinases can lead to tumorigenesis of various cancers, including neuroblastoma (NB). Suppression of kinase expression can reduce drug resistance. We explored the potential role and mechanism of the aurora kinase B (AURKB) gene in the acquisition of carboplatin resistance in NB. METHODS: Immunohistochemistry (IHC) and qRT-PCR were used to explore the AURKB expression in NB patients. Subsequently, we structured Carboplatin-resistant NB cells. The potential biological functions of AURKB in carboplatin resistance were examined through knockdown of AURKB combined with CCK8, flow cytometry, immunohistochemistry, and western blot. Finally, overexpression of AURKB combined with ERK inhibitor (U0126) was carried out to explore the role of downstream signaling pathways. RESULTS: Overexpression of AURKB was closely correlated to poor prognosis in NB patients. In vitro, knockdown of AURKB could lead to a decline in IC50 value and restrain the invasion and the expression of MRP1 and Ki67, while promotes apoptosis in carboplatin-resistant cells (IMR-32-R and SK-N-AS-R). Additionally, AURKB overexpression could potentiate the invasion and the expression of MRP1 and Ki67, while suppresses apoptosis in SK-N-AS-R and IMR-32-R, whereas ERK inhibitor U0126 could reverse the phenomenon caused by AURKB overexpression. CONCLUSION: AURKB overexpression was strongly associated with poor prognosis and carboplatin resistant acquisition. Additionally, suppression of AURKB-ERK axis might be a potential therapy for carboplatin resistance in NB patients.

Evaluation of porcine GM-CSF during PRRSV infection in vitro and in vivo indicating a protective role of GM-CSF related with M1 biased activation in alveolar macrophage during PRRSV infection.

Granulocyte-macrophage colony stimulating factor (GM-CSF), participates in diverse biological processes associated with innate and adaptive immunity, has unknown effects during PRRSV infection. Here, a double-antibody sandwich ELISA for pGM-CSF was developed in-house for evaluation of pGM-CSF level during PRRSV infection both in vitro and in vivo. In in vitro assay, it was notable that PRRSV-infected porcine alveolar macrophages (PAMs) yielded inconsistent pGM-CSF protein- and mRNA-level, suggesting a post-transcriptional inhibition of pGM-CSF mRNA was employed by PRRSV. Meanwhile, concurrent analysis of pGM-CSF levels in serum samples from PRRSV-infected piglets suggested that effect of PRRSV infection demonstrated minimum effect on pGM-CSF levels regardless of PRRSV virulence phenotypes. Moreover, in vitro treatment of PAMs with pGM-CSF prior PRRSV inoculation did not inhibit PRRSV replication in PAMs although genes downstream of pGM-CSF in PAMs could be upregulated by pGM-CSF treatment. Meanwhile, knockdown of pGM-CSF using siRNA did not enhance PRRSV replication as well. Intriguingly, therapeutic antibody treatment of HP-PRRSV-infected piglets led to significantly increased serum pGM-CSF levels, thus aligning with low pneumonia incidence and low intracellular PRRSV-RNA levels in PAMs of therapeutic antibody treated piglets. Furthermore, transcriptome analysis of PAMs from infected piglets revealed increased serum pGM-CSF levels correlated with activation of downstream signal of pGM-CSF in PAMs as evidenced by a M1-like phenotypes of gene expression pattern, implying a potential host-protective role played by pGM-CSF for PRRSV infection in vivo. In conclusion, our results demonstrated developments of a highly sensitive and specific ELISA for pGM-CSF and revealed a potential protective role conferred by pGM-CSF during PRRSV infection.

Early Serum Metabolism Profile of Post-operative Delirium in Elderly Patients Following Cardiac Surgery With Cardiopulmonary Bypass.

Background: Cardiac surgery with cardiopulmonary bypass (CPB) is considered to be one of the surgical types with the highest incidence of post-operative delirium (POD). POD has been associated with a prolonged intensive care and hospital stay, long-term neurocognitive deterioration, and increased mortality. However, the specific pathogenesis of POD is still unclear. Untargeted metabolomics techniques can be used to understand the changes of serum metabolites in early POD to discover the relationship between serum metabolites and disease. Materials and Methods: The present study recruited 58 elderly patients undergoing cardiac surgery with CPB. Serum was collected within the first 24 h after surgery. The Confusion Assessment Method (CAM) and ICU-CAM assessments were used to identify patients who experienced POD. All patients with normal post-operative cognitive assessment were included in the non-POD groups. Moreover, we collected serum from 20 healthy adult volunteers. We performed untargeted analyses of post-operative serum metabolites in all surgical groups, as well as serum metabolites in healthy non-surgical adults by using liquid chromatography mass spectrometry (LC/MS) and analyzed metabolic profiles and related metabolites. Results: The probability of POD after cardiac surgery were 31%. There were statistically significant differences in post-operative mechanical ventilation time, ICU stay time and post-operative hospital stay between POD and non-POD group (P < 0.05). And ICU stay time was an independent risk factor for POD. The analysis revealed that a total of 51 differentially expressed metabolites (DEMs) were identified by comparing the POD and non-POD group, mostly lipids and lipid-like molecules. Three phosphatidylinositol (PI) were down-regulated in POD group, i.e., PI [18:0/18:2 (9Z, 12Z)], PI [20:4 (8Z, 11Z, 14Z, 17Z)/18:0], and PI [18:1 (9Z)/20:3 (8Z, 11Z, 14Z)]. The receiver operating characteristic (ROC) curve analysis showed that three kinds of PI metabolites had the highest area under the curve (AUC), which were 0.789, 0.781, and 0.715, respectively. Correlation analysis showed that the expression of three PIs was negatively correlated with the incidence of POD. Conclusion: Our findings suggest that lipid metabolism plays an important role in the serum metabolic profile of elderly patients with POD in the early post-operative period. Low serum lipid metabolic PI was associated with incidence of POD in elderly following cardiac bypass surgery, which may provide new insights into the pathogenesis of POD.

PD-1/PD-L1 checkpoint inhibitors in advanced hepatocellular carcinoma immunotherapy.

Hepatocellular carcinoma (HCC) has a high prevalence and mortality rate worldwide. Sorafenib monotherapy has been the standard of first-line treatment for advanced HCC for a long time, but there are still many shortcomings. In recent years, with the deepening of research on tumor immune microenvironment, researchers have begun to explore new approaches in immunotherapy, and the introduction of immune checkpoint inhibitors has brought fundamental changes to the treatment of HCC. Programmed cell death protein 1 (PD-1) is an immune checkpoint molecule that plays an important role in down-regulating immune system function and promoting tolerance. Programmed cell death ligand 1 (PDL-1) is involved in tumor immune evasion by binding to PD-1, resulting in failure of treatment. Currently, immunotherapy targeting the PD-1/PD-L1 axis has achieved unprecedented success in HCC, but it also faces great challenges, with its low remission rate still to be solved. For most patients with HCC, the PD-1/PD-L1 pathway is not the only rate limiting factor of antitumor immunity, and blocking only the PD-1/PD-L1 axis is not enough to stimulate an effective antitumor immune response; thus, combination therapy may be a better option. In this study, changes in the immune microenvironment of HCC patients were reviewed to clarify the feasibility of anti-PD-1/PD-L1 therapy, and a series of monotherapy and combination therapy clinical trials were summarized to verify the safety and efficacy of this newly developed treatment in patients with advanced HCC. Furthermore, we focused on hyperprogressive disease and drug resistance to gain a better understanding of PD-1/PD-L1 blockade as a promising treatment.

Recent Metabolomics Analysis in Tumor Metabolism Reprogramming.

Metabolic reprogramming has been suggested as a hallmark of cancer progression. Metabolomic analysis of various metabolic profiles represents a powerful and technically feasible method to monitor dynamic changes in tumor metabolism and response to treatment over the course of the disease. To date, numerous original studies have highlighted the application of metabolomics to various aspects of tumor metabolic reprogramming research. In this review, we summarize how metabolomics techniques can help understand the effects that changes in the metabolic profile of the tumor microenvironment on the three major metabolic pathways of tumors. Various non-invasive biofluids are available that produce accurate and useful clinical information on tumor metabolism to identify early biomarkers of tumor development. Similarly, metabolomics can predict individual metabolic differences in response to tumor drugs, assess drug efficacy, and monitor drug resistance. On this basis, we also discuss the application of stable isotope tracer technology as a method for the study of tumor metabolism, which enables the tracking of metabolite activity in the body and deep metabolic pathways. We summarize the multifaceted application of metabolomics in cancer metabolic reprogramming to reveal its important role in cancer development and treatment.

Extremely high titer of hepatitis B surface antigen antibodies in a primary hepatocellular carcinoma patient: A case report.

BACKGROUND: Hepatocellular carcinoma (HCC) may be caused by hepatitis B virus (HBV) infection. Post-infection recovery-associated changes of HBV indicators include decreased hepatitis B surface antigen (HBsAg) level and increased anti-HBsAg antibody titer. Testing to detect HBV DNA is conducted rarely but could detect latent HBV infection persisting after acute infection and prompt administration of treatments to clear HBV and prevent subsequent HBV-induced HCC development. Here, we present an HCC case with an extremely high anti-HBsAg antibody titer and latent HBV infection. CASE SUMMARY: A 57-year-old male patient with abdominal pain who was diagnosed with primary HCC presented with an extremely high level (over 2000 ng/mL) of serum alpha-fetoprotein. Abdominal B-ultrasonography and computed tomography scan results indicated focal liver lesion and mild splenomegaly. Assessments of serological markers revealed a high titer of antibodies against hepatitis B core antigen (anti-HBcAg antibodies), an extremely high titer (1000 mIU/mL) of hepatitis B surface antibodies (anti-HBsAg antibodies, anti-HBs) and absence of detectible HBsAg. Medical records indicated that the patient had reported no history of HBV vaccination, infection or hepatitis. Therefore, to rule out latent HBV infection in this patient, a serum sample was collected then tested to detect HBV DNA, yielding a positive result. Based on the aforementioned information, the final diagnosis was HCC associated with hepatitis B in a compensated stage of liver dysfunction and the patient was hospitalized for surgical treatment. CONCLUSION: A rare HCC case with high serum anti-HBsAg antibody titer and detectable HBV DNA resulted from untreated latent HBV infection.

Genome-Wide Identification and Functional Investigation of 1-Aminocyclopropane-1-carboxylic Acid Oxidase (ACO) Genes in Cotton.

ACO is one of the rate-limiting enzymes in the biosynthesis of ethylene, and it plays a critical role in the regulation of plant growth and development. However, the function of ACO genes in cotton is not well studied. In this study, a total of 332 GhACOs, 187 GaACOs, and 181 GrACOs were identified in G. hirsutum, G. arboretum, and G. raimondii, respectively. Gene duplication analysis showed that whole-genome duplication (WGD) and tandem duplication were the major forces driving the generation of cotton ACO genes. In the promoters of GhACOs, there were cis-acting elements responding to stress, phytohormones, light, and circadian factors, indicating the possible involvement of GhACOs in these processes. Expression and co-expression analyses illustrated that most GhACOs were not only widely expressed in various tissues but also coexpressed with other genes in response to salt and drought stress. GhACO106_At overexpression in Arabidopsis promoted flowering and increased salt tolerance. These results provide a comprehensive overview of the ACO genes of cotton and lay the foundation for subsequent functional studies of these genes.

Identifications of immune-responsive genes for adaptative traits by comparative transcriptome analysis of spleen tissue from Kazakh and Suffolk sheep.

Aridity and heat are significant environmental stressors that affect sheep adaptation and adaptability, thus influencing immunity, growth, reproduction, production performance, and profitability. The aim of this study was to profile mRNA expression levels in the spleen of indigenous Kazakh sheep breed for comparative analysis with the exotic Suffolk breed. Spleen histomorphology was observed in indigenous Kazakh sheep and exotic Suffolk sheep raised in Xinjiang China. Transcriptome sequencing of spleen tissue from the two breeds were performed via Illumina high-throughput sequencing technology and validated by RT-qPCR. Blood cytokine and IgG levels differed between the two breeds and IgG and IL-1ß were significantly higher in Kazakh sheep than in Suffolk sheep (p < 0.05), though spleen tissue morphology was the same. A total of 52.04 Gb clean reads were obtained and the clean reads were assembled into 67,271 unigenes using bioinformatics analysis. Profiling analysis of differential gene expression showed that 1158 differentially expressed genes were found when comparing Suffolk with Kazakh sheep, including 246 up-regulated genes and 912 down-regulated genes. Utilizing gene ontology annotation and pathway analysis, 21 immune- responsive genes were identified as spleen-specific genes associated with adaptive traits and were significantly enriched in hematopoietic cell lineage, natural killer cell-mediated cytotoxicity, complement and coagulation cascades, and in the intestinal immune network for IgA production. Four pathways and up-regulated genes associated with immune responses in indigenous sheep played indispensable and promoting roles in arid and hot environments. Overall, this study provides valuable transcriptome data on the immunological mechanisms related to adaptive traits in indigenous and exotic sheep and offers a foundation for research into adaptive evolution.

Tanning process promotes abiotic humification: separation and characterization of humic acid-like polymers complex.

Humic-like substances are essential components of soluble organic matter in tannery wastewater. However, the tannery process can promote the abiotic humification in wastewater. Therefore, it is of great significance to clarify the pathway and degree of abiotic humification and the properties of the as-derived humic acid-like (HAL) complex polymers in the tannery process in order to control the refractory organic compounds. In the present study, considering the catechol-Maillard system and commercial humic acid (HA) as control, the polyphenol-Maillard humification in the tannery process was simulated under the catalysis of MnO2. Moreover, physicochemical and spectroscopic techniques were used to characterize the separated fractions of HAL further. As a result, it was found that the catechol-Maillard system with small molecule organic matter as precursor had higher humification degree. Furthermore, the ultraviolet-visible (UV-Vis), Fourier transform infrared (FTIR), and excitation-emission matrix (EEM) fluorescence spectrum of humic acid-like 0 (HAL0) derived from it was different from those of humic acid-like 1 and 2 (HAL1 and HAL2) of polyphenol-Maillard system, indicating the differences of polymer structure between them. In the polyphenol-Maillard system, tannin was the skeleton of polymerization or polycondensation reaction, and the high content of N and the H/C value of HAL2 indicated that in adding to amino acids, proteins promoted the humification, forming industry-specific HAL polymers with a high degree of aliphatic nature. Therefore, it can be concluded that controlling the raw materials in the tannery process (especially tannins), in order to reduce the occurrence of abiotic humification may be the key to improve the efficiency of wastewater treatment.

Fenton reaction induced in-situ redox and re-complexation of polyphenol-Cr complex and their products.

In this study, in-situ Fenton oxidation was used for the de-complexation and degradation of tannin-Cr(III) complexes. Cr(III) can be oxidized into free Cr(VI) under the effect of ·OH and oxidation products of tannin can be used as reductant for Cr(VI) to establish a redox cycle of Cr(III)-Cr(VI)-Cr(III). Thus, it is crucial to investigate the interactions of Cr(III) with tannin derived oxidation products due to negligible accumulation of Cr(VI) during Fenton oxidation treatment. Here, sequential filtration/ultrafiltration was applied to reveal the distribution characteristics of TOC and Cr fractions during the oxidation of tannin-Cr(III). As the increase of colloidal size of tannic acid products, residual TOC and Cr mainly distribute in larger size range after the oxidation of tannin-Cr(III) which can be ascribed to re-complexation between oxidation products and Cr(III). Besides, analytical results indicate that carboxyl group and hydroxyl group in oxidation products may cause the re-complexation of Cr(III), resulting in the formation of highly conjugated materials containing Cr(III). It can be concluded that due attention should be paid to the efficient removal technology and mechanism for polymer-Cr complexes, as well as the oxidation intermediates in the role of conversion and removal of Cr species.

The Capsid Protein of Hepatitis E Virus Inhibits Interferon Induction via Its N-terminal Arginine-Rich Motif.

Hepatitis E virus (HEV) causes predominantly acute and self-limiting hepatitis. However, in HEV-infected pregnant women, the case fatality rate because of fulminant hepatitis can be up to 30%. HEV infection is zoonotic for some genotypes. The HEV genome contains three open reading frames: ORF1 encodes the non-structural polyprotein involved in viral RNA replication; ORF2 encodes the capsid protein; ORF3 encodes a small multifunctional protein. Interferons (IFNs) play a significant role in the early stage of the host antiviral response. In this study, we discovered that the capsid protein antagonizes IFN induction. Mechanistically, the capsid protein blocked the phosphorylation of IFN regulatory factor 3 (IRF3) via interaction with the multiprotein complex consisting of mitochondrial antiviral-signaling protein (MAVS), TANK-binding kinase 1 (TBK1), and IRF3. The N-terminal domain of the capsid protein was found to be responsible for the inhibition of IRF3 activation. Further study showed that the arginine-rich-motif in the N-terminal domain is indispensable for the inhibition as mutations of any of the arginine residues abolished the blockage of IRF3 phosphorylation. These results provide further insight into HEV interference with the host innate immunity.

Lung cancer cells release high mobility group box 1 and promote the formation of neutrophil extracellular traps.

Lung cancer is the leading cause of cancer-associated mortality. Tumor-associated neutrophils represent a large portion of inflammatory cells within the lung tumor microenvironment. However, the roles of neutrophil extracellular traps (NETs) in lung cancer remain unclear. In the present study, it was identified that Lewis lung carcinoma cells actively released the danger-associated molecular pattern protein high mobility group box 1 (HMGB1). Furthermore, HMGB1 in lung cancer cell supernatants promoted the formation of neutrophil extracellular traps (NETs), which was dependent on Toll-like receptor 4 (TLR4). The downstream molecules of TLR4, including myeloid differentiation factor 88, TIR-domain-containing adapter-inducing interferon-ß, p38 mitogen-activated protein kinases (p38 MAPKs) and extracellular signal-regulated kinases (ERKs), were activated during the formation of NETs. In addition, inhibition of p38 MAPKs or ERKs significantly decreased NETs. Morphine, an additional ligand for TLR4, aggravated the NETs induced by lung cancer cells. The present study revealed novel mechanisms in tumor-associated NET formation.

Extracellular RNAs from lung cancer cells activate epithelial cells and induce neutrophil extracellular traps.

Neutrophil infiltration is frequently observed in lung cancer tissues. Extracellular RNAs (exRNAs) may facilitate tumor progression. The present study investigated the cross­talk of tumor exRNAs and neutrophil extracellular traps (NETs) in lung cancer. Lewis lung carcinoma (LLC) cells were cultured with the deprived sera. And the cell culture supernatants (CCS) were analyzed in vitro and in vivo. The results revealed that exRNAs from lung cancer CCS promoted the inflammatory cytokine interleukin­1ß and reduced the vascular cell adhesion molecule­1 expression in lung epithelial cells. Lung cancer CCS­treated epithelial cells induced the production of NETs. By contrast, NETs reduced the tight junction protein claudin­5 in epithelial cells. Furthermore, NETs caused the necrosis of epithelial cells, which resulted in the release of exRNAs. In mice, lung cancer cells instilled in the lung recruited neutrophils and initiated NETs. In patients with lung cancer, NETs were also observed. These results suggested that exRNAs in the cell culture supernatant may indirectly induce NETs and contribute to lung cancer oncogenesis.

The comparison of reproductive hormone receptor expressions of the sheep ovary and hormone concentrations in two Chinese breeds.

The aim of this research was to investigate the changes in reproductive hormone receptor expressions of the ovary and hormone concentrations between oestrous cycle pattern of two different sheep breeds in China. Ovarian tissues were collected from Chinese Merino (Junken type) and Hu sheep with different reproductive states in spring and autumn. Serum samples were assayed for oestrogen (E2), progesterone (P), luteinizing hormone (LH) and follicle-stimulating hormone (FSH) concentrations by radioimmunoassay during spring. The ovarian expression of hormone receptors (ERα, ERß, PR, LHR and FSHR) was analysed using real-time reverse transcription polymerase chain reaction (RT-PCR). In Chinese Merino, there was no corpora lutea and ovulation point on the surfaces of ovaries in spring and low basal levels of both LH and P in serum. ERα, ERß and FSHR were expressed significantly higher in Merino ovaries during anoestrus compared with oestrous or luteal phases of Hu sheep (p < 0.05 or p < 0.01). However, both varieties of sheep exhibited a similar tendency to secrete E2 and FSH. Compared with Hu sheep, FSH levels were slightly higher in Merino serum. In Hu sheep, ERα, ERß, FSHR, LHR and PR expressed in luteal phase ovaries during spring were significantly lower (p < 0.05, p < 0.01 or p < 0.001) than autumn. Interestingly, LHR and PR expressed in anoestrous ovaries were similar to that in oestrous phase of both sheep breeds. The above results suggest that seasonal reproductive sheep increased the expression of E2 and FSH receptors in ovary during spring may enhance the effects of E2 and FSH on follicular development. It is likely that this enhancement prevents the ovary from progressing to the luteal phase.

Microsurgical Treatment of Ruptured True Posterior Communicating Artery Aneurysm in the Distal Portion of the Posterior Communicating Artery.

The true posterior communicating artery (PCoA) aneurysms in the distal portion of the posterior communicating artery are rare. The authors describe a 63-year-old woman with 1 true PCoA aneurysms in the distal portion of the PCoA, which was treated surgically through modified pterional approach. No neurologic deficit was present at the postoperative period. Although endovascular intervention is more and more widely used in the treatment of aneurysms, the authors have also emphasized that true PCoA aneurysms in the distal portion of the PCoA can also be surgically treated in suitable patients.

Application of Micromirror in Microsurgical Clipping to the Intracranial Aneurysms.

OBJECTIVE: The aim of the study was to explore the values and disadvantages of micromirror in the intracranial aneurysm clipping surgery. METHODS: Micromirror was used to assist microsurgical clipping to 36 intracranial aneurysms in 31 patients, of which 3 were carotid-ophthalmic artery aneurysms, 3 were anterior choroidal artery aneurysms, 11 were posterior communicating artery aneurysms, 7 were middle cerebral artery aneurysms, 10 were anterior communicating artery or anterior cerebral artery aneurysms, and the rest were a posterior cerebral artery aneurysm and a posterior inferior cerebellar artery aneurysm. The micromirror was used before and after clipping to observe the anatomic features of necks hidden behind and medial to aneurysms, to visualize surrounding neurovascular structures, and to verify the optimal clipping position. Intraoperative indocyanine green fluorescein angiography, postoperative computerized tomography angiography, and digital subtraction angiography confirmed the success of sufficient clipping. RESULTS: Intraoperative indocyanine green angiography, postoperative computerized tomography angiography , or digital subtraction angiography were performed and showed no case of wrong or insufficient clipping of aneurysm. CONCLUSIONS: Micromirror-assisted microsurgical clipping to the intracranial aneurysm is safe, sufficient, convenient, and practical.

MiR-145 inhibits the epithelial-to-mesenchymal transition via targeting ADAM19 in human glioblastoma.

In recent years, increasing studies demonstrated that miR-145 plays a tumor suppressor role in many human cancers. In the present study, we evaluated the expression of miR-145 and A Disintegrin and Metalloproteinase 19 (ADAM19) in glioblastoma multiforme (GBM) tissues and cells. Furthermore, we investigated the mechanisms underlying miR-145/ADAM19-induced GBM biology. Here, we found that miR-145 expression was down-regulated, while ADAM19 expression was up-regulated in GBM tissues and cells. Moreover, miR-145 mimics repressed U87 and U251 cell proliferation, migration and invasion. miR-145 mimics also inhibited the epithelial-to-mesenchymal transition (EMT) of U87 and U251 cells. Mechanically, the 3' untranslated region (3'-UTR) of ADAM19 mRNA was a direct target for miR-145. In addition, ADAM19 over-expression also partially abrogated miR-145-inhibited EMT. In conclusion, this work suggested that high miR-145 expression inhibited EMT of GBM cells by targeting ADAM19. Thus miR-145/ADAM19 can be suggested as a novel target for GBM patients.