Preliminary clinical application of multimodal imaging combined with frameless robotic stereotactic biopsy in the diagnosis of primary central nervous system lymphoma.

Objective: To evaluate the clinical application of multimodal imaging combined with frameless robotic stereotactic biopsy in the diagnosis of primary central nervous system lymphoma (PCNSL). Methods: We retrospectively reviewed the clinical data of 8 patients who were considered suspected cases of PCNSL by multimodal imaging techniques. The final pathologic diagnosis were determined by the frameless robotic stereotactic biopsy. The postoperative related complications and pathological results were analyzed. Results: All patients underwent biopsies under general anesthesia with an average surgery time of 29.5 ± 4.5 min. The final pathological diagnostic accordant rate with the preoperative ones was 100%, and the pathologic examination of our patients showed features of diffuse large B-cell lymphoma. During the surgery, one patient suffered intratumoral hemorrhage without leading to serious cerebral edema, and conservative treatment was given. There was no death occurring during the study, and there were no significant differences in the Karnofsky Performance Scale Scores of all patients before and after surgery. Finally, they were transferred to the hematology department for standardized chemoradiotherapy according to the pathological results of PCNSL. Conclusion: This study shows that it may play a vital role in the early diagnosis of PCNSL with the technique of multimodal imaging. The technique of frameless robotic stereotactic biopsy for obtaining the pathology outcomes in suspected PCNSL patients has the advantages of safety, efficiency, and minimally invasiveness.

Clinical Study on a Modified Hematoma Puncture Drainage Treatment in Patients with Hypertensive Basal Ganglia Hemorrhage.

OBJECTIVE: We aim to investigate the clinical efficacy and safety of a modified hematoma puncture drainage treatment through the burr hole lateral to Kocher's point from the frontal lobe in patients with hypertensive basal ganglia hemorrhage. METHODS: Twenty-six patients were enrolled in the retrospective study. The volume of hematoma in those patients was between 25 and 35 mL, and the Glasgow Coma Scale scores were between 9 and 11; they were divided into a hematoma puncture drainage treatment group and a traditional conservative treatment group. The volume of remaining hematoma, neurological function defect scores, and life quality after treatment, duration of hospitalization, and cost of hospitalization were analyzed in these 2 groups. RESULTS: The volume of remaining hematoma was significantly less in the drainage group than that in the traditional group on the first day and the third day after treatment (P < 0.05). Posttreatment neurological function defect scores in the drainage group were statistically lower than those in the traditional group (P < 0.05). The duration of hospitalization was significantly shorter and the cost of hospitalization was also significantly less in the drainage group than that in the traditional group (P < 0.05). The Extended Glasgow Outcome Scale and Barthel Index scores were significantly higher in the drainage group than those in the traditional group (P < 0.05). There were no significant differences between the 2 groups in the complication rates (P > 0.05). CONCLUSIONS: The modified hematoma puncture drainage treatment represents an effective and safe way to treat hypertensive basal ganglia hemorrhage.

Differential expression of microRNAs in postoperative radiotherapy sensitive and resistant patients with glioblastoma multiforme.

Glioblastoma multiforme (GBM) is the most malignant primary brain tumor and more resistant to radiotherapy. However, hetero-radiosensitivity occurs in different patients. MicroRNAs (miRNAs) play important roles in the initiation and progression of a multitude of tumors. The study aims to examine the different microRNAs expression profiles of postoperative radiotherapy sensitive and resistant patients with GBM, to make an inquiry about their potential role and discover a certain set of radio-sensitivity markers. Three paired samples from six GBM patients who had only been treated with postoperative radiotherapy were selected, and then, they were divided into radiotherapy sensitive group and resistant group according to their overall survivals, local recurrence rates, and Karnofsky Performance Scale scores. Expression profiles of miRNAs in these two groups were determined by the method of microarray assay. Comparing with resistant patients, 13 miRNAs were significantly upregulated and 10 miRNAs were greatly downregulated in sensitive group. Among them, four miRNAs were validated by quantitative RT-PCR. The differentially expressed miRNAs and their putative target genes were revealed by bioformatic analysis to play a role in cell signaling, proliferation, aging, and death. High-enrichment pathway analysis identified that some classical pathways participated in numerous metabolic processes, especially in cell cycle regulation, such as mTOR, MAPK, TGF-beta, and PI3K-Akt signaling pathways. Our research will contribute to identifying clinical diagnostic markers and therapeutic targets in the treatment of GBM by postoperative radiotherapy.

Zinc as mediator of ubiquitin conjugation following traumatic brain injury.

Previous studies have shown that pathological zinc accumulation and deposition of ubiquitinated protein aggregates are commonly detected in many acute neural injuries, such as trauma, epilepsy and ischemia. However, the underlying mechanisms are poorly understood. Here we assessed the effect of zinc on ubiquitin conjugation and subsequent neurodegeration following traumatic brain injury (TBI). First, we found that scavenging endogenous Zn(2+) reduced trauma-induced ubiquitin conjugation and protected neurons from TBI insults in rat hippocampus. Second, we detected both zinc accumulation and increased ubiquitin conjugated protein following brain trauma in human cortical neurons. Our previous study has shown that zinc can induce ubiquitin conjugation in cultured hippocampal neurons. All these findings indicate that alterations in Zn(2+) homeostasis may impair the protein degradation pathway and ultimately cause neuronal injury following traumatic brain injury.

The expression of PGC-1α in the mice brain after traumatic brain injury.

BACKGROUND: Peroxisome proliferator activated receptor γ co-activator-1α (PGC-1α) is a transcriptional co-activator that co-ordinately regulates genes required for mitochondrial biogenesis and is a key contributor to the up-regulation of antioxidant activities in response to oxidative stress. The expression pattern of PGC-1α after traumatic brain injury (TBI) has not been studied. MATERIALS AND METHODS: Ninety male ICR mice (28-32 g) were randomly assigned to six groups: sham, 3, 6, 12, 24 and 48 hours after TBI. PGC-1α mRNA levels in mice brain were detected by reverse-transcriptase polymerase chain reaction and its nuclear protein levels by Western blot from 3-48 hours after TBI. PGC-1α distribution in the cerebral cortex after TBI was investigated by immunohistochemistry. MAIN OUTCOMES AND RESULTS: The PGC-1α mRNA level significantly increased from 3 hours after TBI, peaked at 6 hours and gradually decreased from 12 to 48 hours. The nuclear PGC-1α protein level increased from 6 to 24 hours after TBI and decreased at 48 hours after TBI. Increased PGC-1α immunostaining was detected in the neurons of the cerebral cortex at 12 hours after TBI. CONCLUSION: PGC-1α may play an important role in the brain after TBI.