Arachnoid granulations of middle cranial fossa: a population study between cadaveric dissection and in vivo computed tomography examination.

PURPOSE: Although arachnoid granulations (AGs) were initially described by Pacchioni more than 300 years ago, they are still poorly described, especially those in middle cranial fossa. The aim of this study was to identify anatomical features of AGs in middle cranial fossa of cadaver and compare such features with that of 64-slice computed tomography. METHODS: The study involved anatomical dissection of 33 adult cadaveric heads and computed tomographic (CT) examinations of 40 patients with various intracranial diseases. The number, size, distribution, and morphology of the AGs in middle cranial fossa of the cadavers and patients were examined and compared. RESULTS: The number of AGs observed on the middle cranial fossa of the cadaveric specimens was greater than that of the patients (P < 0.05). While anatomic dissection revealed a total of 228 AGs in 24 of 33 cadaveric heads, CT scans demonstrated only 80 AGs in 23 of 40 patients. In cadavers, the AGs occurred in the following sites in order of frequency: the middle meningeal sinus (144 AGs, 63.2%), sphenoparietal sinus (47 AGs, 20.6%), lateral foramen rotundum (19 AGs, 8.3%), and cavernous sinus (18 AGs, 7.9%). In CT images, the AGs occurred in the following sites in order of frequency: the middle meningeal sinus (50 AGs, 62.5%), sphenoparietal sinus (23 AGs, 28.8%), and lateral foramen rotundum (7 AGs, 8.8%). The AGs of cavernous sinus and venous lacunae adjacent to the middle meningeal sinus were hardly identified on CT images. Most of the AGs were spherical or finger-like in shape. Histologically, the AGs can be divided into two types: single type and lobulated type. CONCLUSIONS: The study provides a detailed description of AGs in or near the middle meningeal sinus, sphenoparietal sinus, lateral foramen rotundum, and cavernous sinus. It also reveals a difference in the ability of detecting cranial AGs between microanatomy and CT scans.

The long non-coding RNA CRNDE acts as a ceRNA and promotes glioma malignancy by preventing miR-136-5p-mediated downregulation of Bcl-2 and Wnt2.

The colorectal neoplasia differentially expressed (CRNDE) gene encodes a long non-coding RNA (lncRNA) that is the most unregulated among 129 lncRNAs differentially expressed in gliomas. In this study, we confirmed high CRNDE expression in clinical glioma specimens and observed through experiments in human glioma cell lines a novel molecular mechanism by which CRNDE may contribute to glioma pathogenesis. By inducing or silencing CRNDE expression, we detected a positive correlation between CRNDE levels and the proliferative, migratory, and invasive capacities of glioma cells, which were concomitant with a decreased apoptosis rate. Our experiments also suggest that these effects are mediated by downregulation of miR-136-5p, which correlated with the glioma WHO grade. Based on predicted CRNDE/miR-136-5p/mRNA interactions, both the mRNA and protein expression analyses suggested that miR-136-5p-mediated repression of Bcl-2 and Wnt2 underlies the pro-tumoral actions of CRNDE. We therefore propose that CRNDE functions as a competing endogenous RNA (ceRNA) that binds to and negatively regulates miR-136-5p, thereby protecting Bcl-2 and Wnt2 from miR-136-5p-mediated inhibition in glioma.

Inhibitory effect of recombinant human endostatin on the proliferation of hypertrophic scar fibroblasts in a rabbit ear model.

Hypertrophic scar (HS) is a pathological scar that particularly occurs after traumatic injuries, surgical procedures and burning. Abnormal activation of hypertrophic scar fibroblasts (HSFs) intensifies fibrosis during wound healing. Our previous studies demonstrated that recombinant human endostatin (rhEndostatin) prevented synovial thickening in adjuvant arthritis (AA) rats via inhibition of proliferation and enhancement of apoptosis in synovial fibroblasts. However, the effect of this protein on HSF proliferation is not known. This study investigated the inhibitory effect of rhEndostatin on the proliferation of cultured HSFs in a rabbit ear model. MTT assay and flow cytometric detection were performed to investigate HSF proliferation and cell cycle progression, respectively. The expression levels of p53, p21, cyclinD1, cyclin-dependent kinase 4 (CDK4) and proliferating cell nuclear antigen (PCNA) in HSFs were detected using real-time PCR and Western blotting. Our data revealed that HSFs treated with rhEndostatin were significantly inhibited in a concentration-dependent manner with an IC50 value of 100mg/L. Also, rhEndostatin (100mg/L) primarily induced G0/G1 and partially G2/M cell cycle arrest of HSFs. There were significant decreases in the expression levels of p53, p27, CDK4, cyclinD1 and PCNA in HSFs treated with rhEndostatin. In conclusion, rhEndostatin inhibited HSF proliferation via G0/G1 and/or G2/M phase arrest of the cell cycle, which was partially due to the down-regulation of cyclinD1, CDK4 and PCNA. These findings suggest that rhEndostatin may reduce scar hypertrophy in vivo via inhibition of HSF proliferation and may be a novel agent for HS treatment.

Anti-proliferative effect of recombinant human endostatin on synovial fibroblasts in rats with adjuvant arthritis.

Rheumatoid arthritis (RA) is characterized by pronounced synovial hyperplasia resulting in pannus formation, cartilage erosion and ultimately joint destruction. Activated RA synovial fibroblasts (SFs) mediate the invasion and destruction of cartilage and bone. We previously demonstrated that recombinant human endostatin (rhEndostatin) is sufficient to induce SF apoptosis in adjuvant arthritis (AA) rats. However, the effect of this protein on SF proliferation is unknown. This study was designed to assess the inhibitory effect and mechanisms of rhEndostatin on the proliferation of cultured AA SFs. MTT assay and flow cytometric detection were performed to investigate SF proliferation and cell cycle progression, respectively. Also, the expression levels of p53, p21, cyclin D1, CDK4 and PCNA in AA SFs were detected by real-time PCR and western blotting assays. Our data revealed that AA SF proliferation was significantly inhibited by rhEndostatin in a concentration-dependent manner. In addition, rhEndostatin (50µg/ml) caused the G0/G1 cell cycle arrest of AA SFs. There were significant decreases in the expression levels of p53, p21, cyclin D1 and PCNA in AA SFs treated with rhEndostatin, and a significant increase in CDK4 expression. Collectively, our data suggest that rhEndostatin inhibits AA SF proliferation, which is preceded by cell cycle arrest at the G0/G1 phase. This is partly due to the inhibitory effect of rhEndostatin on cyclin D1 and PCNA by a p53-p21-CDK4-independent mechanism. Taken together, these findings highlight the potential use of rhEndostatin for RA treatment.

[Anatomical observation of the 'holy plane' for total mesorectal excision].

OBJECTIVE: To provide anatomic evidence for identification of "holy plane" between fascia propria and its adjacent fascia in total mesorectal excision. METHODS: A total of 26 pelvic specimens of adult male preserved in 10% formalin solution were used in this study. Twenty pelvis were employed for topographic anatomy, six for sectional anatomy. RESULTS: Rectovesical septum was formed by the ventral part of the fascia propria and Denonvilliers' fascia, with no blood vessel and nerve coursed between two layers. Dorsal part of the fascia propria parallelled with the presacral fascia, with no blood vessel and nerve coursed between two layers in 80% of the pelvis. However, anatomic variations was encountered occasionally--with muscle-like tissue or fusion of presacral fascia interposed between them for 20%. The lateral space of rectum was between lateral part of the fascia propria and parietal fascia which witnessed pelvic nerve plexus and lateral ligament of the rectum traveling. Pelvic nerve plexus was categorized as two types according the relation between fascia propria and nerve plexus: fusion type accounting for 85% and rarefaction type for 15%. CONCLUSION: 'holy plane' is sandwiched between the fascia propria and its adjacent fascia--ventrally Denonvilliers fascia, dorsally presacral fascia and laterally parietal fascia.