A Preliminary Study of Neonatal Cranial Venous System by Color Doppler.

AIM: To present anatomic data in the ultrasound planes for the identification of the major veins and the venous sinuses in cerebrum and to establish the sonographic normal reference values for the visualization of vein vessels and vein sinuses and blood flow velocities. METHODS: This study involved 55 healthy full-term neonates for transfontanellar color Doppler sonography. The imaging included both sagittal and coronal planes with LA332E probe, supplemented with PA240 probe as necessary. As low as reasonably achievable (ALARA) principle was obeyed, limiting Doppler exposure time and maximizing signal intensity by increasing gain rather than outputting transducer power settings. The output power was kept at a minimum level consistent with recording an adequate signal. Keeping the newborns in calm state, the total examination time which every neonate required was less than 5 min. All images were stored also in a workstation for further analysis. The description statistics and t-test for statistical analysis were used. RESULT: In all studied cases (100% cases), subependymal veins (SV), internal cerebral veins (ICV), Galen vein (GV), straight sinus (SS), superior sagittal sinus (SSS), and transverse sinuses (TS) were visualized. The visualization percentages of inferior sagittal sinus (ISS) or basal veins/Rosenthal veins (BV/RV) were lower than 100%. Based on vessel visualization percentage from high to low, the vessels were ordered as follows: SV, ICV, BV, SS, TS, ISS, and SSS. In SSS and TS, the pulsation percentage was 100%. The descending percentages of vessel pulsation were noted in SS, BV, ICV, and SV. On the basis of the mean of maximum velocities of the vessels from low to high, the vessels were ordered as follows: ISS, BV-L, BV-R, ICV-R, ICV-L, SV-L, SV-R, SSS, TS-L, TS-R, and SS. CONCLUSION: The measurements percent of visualization of cerebral deep veins was higher than the percent of cerebral venous sinuses. The pulsation percent of measurement and the velocities of cerebral venous sinuses were absolutely higher than the cerebral deep venous system. The pairs of vascular blood flow velocities were nonsignificantly different from one another.

Repression of lncRNA NEAT1 enhances the antitumor activity of CD8+T cells against hepatocellular carcinoma via regulating miR-155/Tim-3.

BACKGROUND: Immunotherapy is a promising method for the treatment of hepatocellular carcinoma (HCC), in which CD8+T cells play a key role. The influence of long noncoding RNA (lncRNA) nuclear-enriched autosomal transcript 1(NEAT1) on the antitumor activity of CD8+T cells was clarified in this study. METHODS: Peripheral blood mononuclear cells (PBMCs) were isolated from HCC patients, and the expressions of NEAT1 and Tim-3 were determined by qRT-PCR and western blot, respectively. CD8+T cell apoptosis and cell percentage were analyzed via flow cytometry. The cytolysis activity of CD8+T cells against HCC cells was examined. RNA immunoprecipitation (RIP) and RNA pull-down assay were performed to explore the interaction between NEAT1 and miR-155. RESULTS: NEAT1 and Tim-3 were up-regulated in the PBMCs of patients with HCC (n = 20) compared with healthy subjects (n = 20). Down-regulation of NEAT1 restrained CD8+T cell apoptosis and enhanced the cytolysis activity, while interference of miR-155 showed the opposite effects by up-regulating Tim-3. Binding and interaction between NEAT1 and miR-155 were validated in CD8+T cells. Down-regulation of NEAT1 restrained CD8+T cell apoptosis and enhanced the cytolysis activity through the miR-155/Tim-3 pathway. Repression of NEAT1 suppressed tumor growth in HCC mice. CONCLUSION: Via modulating the miR-155/Tim-3 pathway, repression of NEAT1 restrained CD8+T cell apoptosis and enhanced the cytolysis activity against HCC, implying an effective target for improving the outcome of immunotherapy.

[Secondary mutation of c-kit/PDGFRα genotypes after imatinib mesylate therapy and its relationship with efficacy of sunitinib].

OBJECTIVE: To investigate the relationship between secondary mutations of c-kit/PDGFRα resistance to imatinib mesylate and the efficacy of sunitinib in patients with gastrointestinal stromal tumor (GIST). METHODS: Five pairs specimens were collected before and after imatinib mesylate resistance. DNA for molecular genetic investigation was extracted from formalin-fixed, paraffin-embedded tissues. Mutational analysis was performed by using PCR and direct sequencing. RESULTS: Five pairs of specimens were collected before and after imatinib mesylate resistance from 5 GIST patients. C-kit exon 11 mutations were detected in 3 patients, which were all acquired mutations, including c-kit exon 13 V654A, c-kit exon 13 V654E and c-kit exon 17 N822K, after imatinib mesylate resistance. Furthermore, after sunitinib treatment, 3 patients had stable disease and progression free survival (PFS) were 3.5 months, 4.4 months and 3.8 months, respectively. C-kit exon 9 mutations were detected in 2 patients with no acquired mutations after imatinib mesylate resistance. And the both had partial response from sunitinib, following with 13.1 months and 12.0 months PFS respectively. CONCLUSION: The c-kit/PDGFRα genotypes after imatinib mesylate resistance may both relate to primary mutations and efficacy of sunitinib treatment.