Characteristic features and proposed classification in 69 cases of intracranial microcystic meningiomas.

Microcystic meningioma (MM) is a rare subtype of intracranial meningiomas, with clinical and radiologic features not well characterized in the literature. Based on our experience, we propose a classification system of intracranial MMs. We reviewed the medical records, radiographic studies, and operative notes of a group of consecutive patients with intracranial MM. The mean age of the 69 patients was 46.8 ± 10.6 years (range, 21-75 years). Three types of intracranial MMs could be identified. Type 1 MMs presented as a solid lesion, hypointense or isointense on T1WI, hyperintense on T2WI, and homogeneous or heterogeneous enhancement, and were found in 43 patients (67.2%). Type 2 MMs represented signals similar to CSF both on T1WI and T2WI, and faint reticular enhancement with marginal enhancement, and these were found in 7 patients (10.9%). Type 3 MMs consisted of cystic-solid or cystic lesion and were found in 14 patients (21.9%). Significant differences were observed among the different types of MMs for the following variables: sex, presence of severe peritumoral brain edema (PTBE), and extent of tumor resection. Females were found in all of patients with type 2 MMs, but were only 35.7% of those with type 3 MMs (P = 0.018). Severe PTBEs were more common among patients with type 1 MMs (55.8%) than among those with type 2 (14.3%) and type 3 MMs (14.3%) (P = 0.007). Type 1 MMs (97.7%) were associated with a significantly higher rate of gross total resection compared with the other two types (71.4 and 78.6%) (P = 0.019). Total length of hospital stay after craniotomy ranged from 4 to 30 days (median, 8 days). There were no significant differences in progression-free survival among the three types of MMs (P = 0.788). The current classification identifies three distinct types of intracranial MM based on their radiological findings and growth patterns. The type 1 MMs are more commonly associated with severe PTBE. Type 2 and Type 3 MMs have a higher predilection towards parasaggital location with venous involvement and therefore have a lower rate of gross total resection.

Effect of urokinase-type plasminogen activator system in gastric cancer with peritoneal metastasis.

Peritoneal metastasis is a primary cause of mortality in patients with gastric cancer. Urokinase-type plasminogen activator (uPA) has been demonstrated to be associated with tumor cell metastasis through the degradation of the extracellular matrix. The present study aimed to investigate the mechanisms of the uPA system in gastric cancer with peritoneal metastasis. Expression of uPA, uPA receptor (uPAR) and plasminogen activator inhibitor-1 (PAI-1) in four gastric cell lines (AGS, SGC7901, MKN45 and MKN28) was measured by semiquantitative reverse transcription polymerase chain reaction, enzyme-linked immunosorbent assay and western blotting. uPA activity was detected using a uPA activity kit. Peritoneal implantation models of rats were established by injecting four gastric cancer cell lines for the selection of the cancer cells with a high planting potential. Biological behaviors, including adhesion, migration and invasion, were determined using a methyl thiazolyl tetrazolium assay. Expression of the uPA system was observed to be highest in the SGC7901 cells among the four gastric cell lines. uPA activity was observed to be highest in the MKN45 cells and lowest in the AGS cells. Furthermore, peritoneal implantation analysis demonstrated that no peritoneal tumors were identified in the AGS cells, whilst the tumor masses observed in the SGC7901 and MKN45 cells were of different sizes. The survival times of the rats injected with the MKN28 and SGC7901 cells were longer than those of the rats injected with the MKN45 cells. Antibodies for uPA, uPAR and PAI-1 in the uPA system had the ability to inhibit the adhesion, migration and invasion of peritoneal metastasis in the gastric cancer cells. The results of the present study demonstrated that the uPA system was positively associated with peritoneal metastasis in gastric cancer.

An improved electronic twist-drill craniostomy procedure with post-operative urokinase instillation in treating chronic subdural hematoma.

OBJECTIVE: Twist-drill craniostomy (TDC) with closed-system drainage is a less invasive surgical technique for the treatment of chronic subdural hematoma (CSDH), but results in a higher disease recurrence rate. Therefore, we aimed to modify the TDC procedure in order to reduce the recurrence rate and further decrease complications. METHODS: We retrospectively reviewed 230 cases of standard CSDH in 202 patients treated in our hospital between January 2006 and December 2013. We employed a new TDC device called micro-steel-needle-tube-bit for puncture and drainage. We chose an entry point 0.5cm anterior to the coronal suture at the superior temporal line and maintained post-operative drainage with urokinase instillation into the hematoma cavity. Clinical performance was assessed and compared by the Markwalder Grading Scale (MGS) score during the pre-operative period and at discharge. Recurrence of CSDH and complications were also recorded. RESULTS: Mean operation time was only 8.9 (6-13) min. Mean catheter indwelling duration and hospital stay were 1.18 (271/230, 1-3) and 2.27 (458/202, 2-9) days, respectively. The average frequency of urokinase instillation was 1.14 (262/230, 1-3) times. Intracerebral and sub-arachnoid hemorrhages were found in one patient, but were not in the puncture pathway. No perioperative deaths occurred. Recurrence was observed in only one patient at 28 days post-operation. Among 202 patients, 193 (95.54%) showed improved clinical symptoms and neurological function, and significantly lower MGS scores at discharge than pre-operation (0.13±0.45 vs. 1.37±0.55, P<0.01). CONCLUSION: In conclusion, electric TDC with micro-steel-needle-tube-bit at the pre-coronal suture entry point might be a safer, simpler, and faster mini-invasive surgical procedure for CSDH treatment. Post-operative drainage with instillation of urokinase could dramatically shorten drainage time and decrease recurrence rate.

Inhibition of hepatocellular carcinoma by fulvestrant involves the estrogen receptor α and Wnt pathways in vitro and in patients.

The aim of the present study was to investigate the effect of anti-estrogen treatment (fulvestrant) on the biological activity of hepatocellular carcinoma (HCC), involving the estrogen receptor α (ERα) and Wnt pathways, and to evaluate whether ERα and Wnt inhibitory factor-1 (WIF1) could be biomarkers for anti-estrogen clinical therapy. H22 and HepG2 cells were treated with 0.04 to 625 nM fulvestrant and the WST-8 method was used to assess the inhibition rate after 72 h. Furthermore, prolactin (PRL) secretion by HepG2 cells was assessed at 24 h using an enzyme immunoassay. Quantitative polymerase chain reaction and western blot analysis were used to analyze the mRNA and protein expression levels of ERα, ß-catenin and WIF1, respectively, in HepG2 cells. For clinical patient analysis, the tumor volume was analyzed by magnetic resonance imaging methods, and PRL in the blood was detected by an enzyme immunoassay. In HepG2 cells, the mRNA and protein expression levels of ERα were downregulated (P<0.01), while ß-catenin expression remained unchanged and WIF1 expression was upregulated (P<0.01). Analysis of samples from clinical patients demonstrated that there was a positive correlation between PRL levels and tumor volume. In addition, as compared with non-cancerous tissues, the ERα mRNA levels in tumor tissue were upregulated (P<0.05), particularly in that of male patients, while WIF1 expression was significantly downregulated (P<0.01). In conclusion, fulvestrant inhibited the proliferation of HepG2 cells, involving the ERα and non-canonical Wnt pathways, and it may be a promising therapeutic for HCC.

The expression and regulation of DFNA5 in human hepatocellular carcinoma DFNA5 in hepatocellular carcinoma.

Hepatocellular carcinoma is a primary malignancy of hepatocytes which accounts for 80 % of all primary liver cancers. DFNA5 has been identified as a tumor suppressor gene with an important role in several frequent forms of cancers, while little is known about its role in hepatocellular carcinoma. Through comparison of the DFNA5 protein expression in hepatocellular carcinoma cells (HepG2) with human fetal lung fibroblast cells (MRC5), we found that the DFNA5 protein expression in hepatocellular carcinoma cells was significantly lower than that in normal cells. The transfection of DFNA5 gene into HepG2 cells could increase DFNA5 protein expression, which subsequently led to inhibition of cell proliferation. Underlying mechanism study revealed that decreased proliferation was due to increased apoptosis and cell cycle arrest. In view of the important role of DFNA5 gene in carcinogenesis, these findings are expected to provide new understanding on development and treatment of human hepatocellular carcinoma.

Effect of combined treatment with recombinant interleukin-2 and allicin on pancreatic cancer.

This study aimed to evaluate the efficacy of combined treatment with recombinant interleukin-2 (rIL-2) and allicin on pancreatic cancer and explore the potential immunological mechanism. A total of 60 C57/BL6 nude mice pancreatic cancer xenograft models were randomized into four groups of 15 mice per group: control group, allicin treatment group, rIL-2 treatment group, combined treatment with allicin and rIL-2 group. Mice in each group were treated with saline, rIL-2, allicin, or combination of rIL-2 and allicin by weekly i.v injection for four weeks. After four weeks of treatment, eyeballs of the mice were extracted and blood was drawn, percentages of CD4+T, CD8+T and NK cell were analyzed by FACS, IFN-γ level was detected by ELISA. One mouse in each group was sacrificed to measure the weight and volume of the tumor and prepared to the paraffin section of tumor tissue. Apoptosis of the tumor cells was analyzed by TUNEL and FACS. Other mice continued to receive treatment, survival period were compared between each group. We observed a significant suppression of xenograft growth and a significant prolonged survival time in the combined treatment with allicin and rIL-2 group (P < 0.05). The most amount of apoptotic cells were observed in the combined therapy group (P < 0.05). The percentages of CD4+T, CD8+T and NK cell and serum IFN-γ level increased significantly in the combined treatment group compared with other groups (P < 0.05). Combined treatment with allicin and rIL-2 resulted in suppression of tumor growth and prolonged survival time possibly through activation of CD4+T, CD8+T and NK cell.

Bioinformatics method to analyze the mechanism of pancreatic cancer disorder.

Pancreatic cancer is an aggressive malignancy with a five-year mortality of 97-98% due to widespread metastatic disease. A better understanding of the molecular mechanism of pancreatic cancer is beneficial for the development of novel approaches for early detection and monitoring of pancreatic cancer. We aim to comprehensively identify the gene expression profile in pancreatic cancer and explore the molecular pathway of pancreatic cancer disorder. Using GSE15471 datasets downloaded from Gene Expression Omnibus data, we first screened the differentially expressed genes in pancreatic cancer using packages in R language. The key pathways of differentially expressed genes were investigated with the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis and synergetic network construction based on weighted Jaccard index. A total of 13,211 differentially expressed genes were identified, and they were enriched in several pathways, such as mitogen-activated protein kinase (MAPK) signaling pathway, transforming growth factor (TGF)-beta signaling pathway, Janus kinase-signal transducers and activators of transcription (JAK-STAT) signaling pathway, and calcium signaling pathway, as well as cell cycle, focal adhesion, complement and coagulation cascades, and leukocyte transendothelial migration. Synergetic pathway network analysis revealed that cytokine-cytokine receptor interaction pathway, calcium signaling pathway, and focal adhesion pathway were three important pathways in the development of pancreatic cancer. The method introduced here is helpful to screen the key pathways for controlling pancreatic cancer progression and provide potential therapeutic targets in the treatment of pancreatic cancer.

Habitat loss other than fragmentation per se decreased nuclear and chloroplast genetic diversity in a monoecious tree.

Generally, effect of fragmentation per se on biodiversity has not been separated from the effect of habitat loss. In this paper, using nDNA and cpDNA SSRs, we studied genetic diversity of Castanopsis sclerophylla (Lindl. & Paxton) Schotty populations and decoupled the effects of habitat loss and fragmentation per se. We selected seven nuclear and six cpDNA microsatellite loci and genotyped 460 individuals from mainland and island populations, which were located in the impoundment created in 1959. Number of alleles per locus of populations in larger habitats was significantly higher than that in smaller habitats. There was a significant relationship between the number of alleles per locus and habitat size. Based on this relationship, the predicted genetic diversity of an imaginary population of size equaling the total area of the islands was lower than that of the global population on the islands. Re-sampling demonstrated that low genetic diversity of populations in small habitats was caused by unevenness in sample size. Fisher's α index was similar among habitat types. These results indicate that the decreased nuclear and chloroplast genetic diversity of populations in smaller habitats was mainly caused by habitat loss. For nuclear and chloroplast microsatellite loci, values of F(ST) were 0.066 and 0.893, respectively, and the calculated pollen/seed dispersal ratio was 162.2. When separated into pre-and post-fragmentation cohorts, pollen/seed ratios were 121.2 and 189.5, respectively. Our results suggest that habitat loss explains the early decrease in genetic diversity, while fragmentation per se may play a major role in inbreeding and differentiation among fragmented populations and later loss of genetic diversity.