[Overexpression of NAT10 induced platinum drugs resistance in breast cancer cell].

Objective: To observe the platinum drugs resistance effect of N-acetyltransferase 10 (NAT10) overexpression in breast cancer cell line and elucidate the underlining mechanisms. Methods: The experiment was divided into wild-type (MCF-7 wild-type cells without any treatment) group, NAT10 overexpression group (H-NAT10 plasmid transfected into MCF-7 cells) and NAT10 knockdown group (SH-NAT10 plasmid transfected into MCF-7 cells). The invasion was detected by Transwell array, the interaction between NAT10 and PARP1 was detected by co-immunoprecipitation. The impact of NAT10 overexpression or knockdown on the acetylation level of PARP1 and its half-life was also determined. Immunostaining and IP array were used to detect the recruitment of DNA damage repair protein by acetylated PARP1. Flow cytometry was used to detect the cell apoptosis. Results: Transwell invasion assay showed that the number of cell invasion was 483.00±46.90 in the NAT10 overexpression group, 469.00±40.50 in the NAT10 knockdown group, and 445.00±35.50 in the MCF-7 wild-type cells, and the differences were not statistically significant (P>0.05). In the presence of 10 µmol/L oxaliplatin, the number of cell invasion was 502.00±45.60 in the NAT10 overexpression group and 105.00±20.50 in the NAT10 knockdown group, both statistically significant (P<0.05) compared with 219.00±31.50 in wild-type cells. In the presence of 10 µmol/L oxaliplatin, NAT10 overexpression enhanced the binding of PARP1 to NAT10 compared with wild-type cells, whereas the use of the NAT10 inhibitor Remodelin inhibited the mutual binding of the two. Overexpression of NAT10 induced PARP1 acetylation followed by increased PARP1 binding to XRCC1, and knockdown of NAT10 expression reduced PARP1 binding to XRCC1. Overexpression of NAT10 enhanced PARP1 binding to LIG3, while knockdown of NAT10 expression decreased PARP1 binding to LIG3. In 10 µmol/L oxaliplatin-treated cells, the γH2AX expression level was 0.38±0.02 in NAT10 overexpressing cells and 1.36±0.15 in NAT10 knockdown cells, both statistically significant (P<0.05) compared with 1.00±0.00 in wild-type cells. In 10 µmol/L oxaliplatin treated cells, the apoptosis rate was (6.54±0.68)% in the NAT10 overexpression group and (12.98±2.54)% in the NAT10 knockdown group, both of which were statistically significant (P<0.05) compared with (9.67±0.37)% in wild-type cells. Conclusion: NAT10 overexpression enhances the binding of NAT10 to PARP1 and promotes the acetylation of PARP1, which in turn prolongs the half-life of PARP1, thus enhancing PARP1 recruitment of DNA damage repair related proteins to the damage sites, promoting DNA damage repair and ultimately the survival of breast cancer cells.

Is intraoperative neurophysiological monitoring valuable predicting postoperative neurological recovery?

OBJECTIVES: We investigated the ability of intraoperative neurophysiological monitoring to predict postoperative neurological recovery in intradural-extramedullary spinal cord tumors. METHODS: From 2010 to 2014, we operated on 173 intradural-extramedullary spinal cord tumor patients with intraoperative neurophysiological monitoring. We retrospectively compared preoperative and postoperative clinical status using a modified McCormick grading scale and correlated with intraoperative neurophysiological monitoring. We followed patients for at least 1 year and correlated neurological outcomes with intraoperative changes in intraoperative neurophysiological monitoring. We then compared the degree of intraoperative neurophysiological monitoring change with the duration of the neurological deficit. RESULTS: Monitorability was 92% and 57% with transcranial motor-evoked potential and somatosensory-evoked potential modalities, respectively. Waveform attenuation on transcranial motor-evoked potentials was detected in 8.17% of cases. For somatosensory-evoked potentials, waveform attenuation was detected in 7% of the patients. A multimodality approach incorporating any transcranial motor-evoked potential changes had a sensitivity of 0.91 and a specificity of 0.98. The McCormick grade scale increased until 1 month in patients with alarm criteria on transcranial motor-evoked potentials (P<0.05). CONCLUSIONS: Patients suffered neurological deterioration in case of abolishment or >50% irreversible attenuation of the waveform in transcranial motor-evoked potentials. All patients gradually recovered after 1 postoperative month with alarm criteria from 50% to 80% irreversible amplitude drop on transcranial motor-evoked potentials.

Variability of neural activation during walking in humans: short heels and big calves.

People come in different shapes and sizes. In particular, calf muscle size in humans varies considerably. One possible cause for the different shapes of calf muscles is the inherent difference in neural signals sent to these muscles during walking. In sedentary adults, the variability in neural control of the calf muscles was examined with muscle size, walking kinematics and limb morphometrics. Half the subjects walked while activating their medial gastrocnemius (MG) muscles more strongly than their lateral gastrocnemius (LG) muscles during most walking speeds ('MG-biased'). The other subjects walked while activating their MG and LG muscles nearly equally ('unbiased'). Those who walked with an MG-biased recruitment pattern also had thicker MG muscles and shorter heel lengths, or MG muscle moment arms, than unbiased walkers, but were similar in height, weight, lower limb length, foot length, and exhibited similar walking kinematics. The relatively less plastic skeletal system may drive calf muscle size and motor recruitment patterns of walking in humans.

Application of ICHD-II criteria for headaches in a TMJ and orofacial pain clinic.

The aim of this study was to identify and diagnose headache in a temporomandibular joint and orofacial pain clinic population using the second edition of The International Classification of Headache Disorder criteria. In 502 temporomandibular disorder and orofacial pain patients, 246 patients (49%) were diagnosed with tension-type headache (TTH), followed by migraine without aura (14.5%), probable migraine (12.9%), migraine with aura (7%), probable TTH (4.8%) and cluster headache (0.2%). The prevalence of headaches was compared between male and female patients, and the prevalence of migraine was found to be higher in women than in men. In evaluating by age, the prevalence of migraine was highest in patients in their 20s and 30s and declined as age increased above 40. TTH showed the highest rate throughout all age groups, but it also decreased as age increased. In this study, the prevalence of migraine was lower than that reported in Dr Kim et al.'s study, and the prevalence of TTH much higher than that reported in the previous study. Of the headache patients, 81.1% presented with masseter muscle pain and 47.8% with temporal muscle pain. This finding suggests that pericranial muscle pain may be an inducing factor of primary headache.

Combined motor- and somatosensory-evoked potential monitoring for spine and spinal cord surgery: correlation of clinical and neurophysiological data in 85 consecutive procedures.

STUDY DESIGN: Prospective study. OBJECTIVES: The primary objective of neurophysiological monitoring during surgery is to prevent permanent neurological sequelae. To avoid neurological injury, we applied somatosensory-evoked potentials (SEPs) and/or motor-evoked potentials (MEPs). We evaluated whether the combination of SEP and MEP for spinal surgery may be beneficial. SETTING: Asian Medical Center, University of Ulsan College of Medicine, Seoul, Korea. METHODS: Combined SEP/MEP monitoring was attempted in 100 consecutive procedures for spinal operations. Trains of transcranial electrical stimulation over the motor cortex were used to elicit MEPs from the muscles of the upper/lower limbs. The tibial and median nerves were stimulated to record SEP. RESULTS: Combined SEP/MEP recording was successfully achieved in 85 of 100 operations. In 61 of 85 operations (71%), SEP and MEP were stable, and all patients remained neurologically intact after surgery. Significant MEP changes were recorded in 20 operations, either combined with (n=4) or without (n=16) SEP changes. In 7 of these 20 operations, MEP recovered to some extent after surgical intervention, and these patients showed no neurological changes. In the remaining 13 operations, MEP did not recover and the patients had a transient (n=4) or a permanent (n=3) motor deficit. Significant SEP changes with stable MEP were observed in four operations, all of which were not related to postoperative motor deficit. CONCLUSION: Combined SEP/MEP monitoring provided higher sensitivity and higher positive/negative predictive value than single-modality monitoring techniques. Detection of MEP changes and adjustment of surgical strategy may prevent irreversible pyramidal tract damage.

Aberrant GATA2 epigenetic dysregulation induces a GATA2/GATA6 switch in human gastric cancer.

Six GATA transcription factors play important roles in eukaryotic development. Among these, GATA2, an essential factor for the hematopoietic cell lineage, exhibits low expression in human gastric tissues, whereas GATA6, which is crucial for gastrointestinal development and differentiation, is frequently amplified and/or overexpressed in human gastric cancer. Interestingly, we found that GATA6 was overexpressed in human gastric cancer cells only when GATA2 expression was completely absent, thereby showing an inverse correlation between GATA2 and GATA6. In gastric cancer cells that express high GATA6 levels, a GATA2 CpG island is hypermethylated, repressing expression in these cells. In contrast, GATA6 expression is undetectable in GATA2-overexpressing gastric cancer cells, which lack GATA2 DNA methylation. Furthermore, PRC2 complex-mediated transcriptional silencing of GATA6 was observed in the GATA2-overexpressing cells. We also show that the GATA2 and PRC2 complexes are enriched within the GATA6 locus, and that the recruitment of the PRC2 complex is impaired by disrupting GATA2 expression, resulting in GATA6 upregulation. In addition, ectopic GATA2 expression significantly downregulates GATA6 expression, suggesting GATA2 directly represses GATA6. Furthermore, GATA6 downregulation showed antitumor activity by inducing growth arrest. Finally, we show that aberrant GATA2 methylation occurs early during the multistep process of gastric carcinogenesis regardless of Helicobacter pylori infection. Taken together, GATA2 dysregulation by epigenetic modification is associated with unfavorable phenotypes in human gastric cancer cells by allowing GATA6 expression.

Merlin facilitates ubiquitination and degradation of transactivation-responsive RNA-binding protein.

The Nf2 tumor suppressor codes for merlin, a protein whose function is largely unknown. We have previously demonstrated a novel interaction between merlin and TRBP, which inhibits the oncogenic activity of TRBP. In spite of the significance of their functional interaction, its molecular mechanism still remains to be elucidated. In this report, we investigated how merlin inhibits the oncogenic activity of TRBP in association with cell growth conditions. In the human embryonic kidney 293 cell line, the level of endogenous merlin increased, whereas that of endogenous TRBP significantly decreased along with the increase in cell confluence. We demonstrated that the carboxyl-terminal region of TRBP was responsible for this phenomenon using stable cell lines expressing deletion mutants of TRBP. The overexpression of merlin decreased the protein level of TRBP, and the ubiquitin-like subdomain of merlin's FERM domain was important for this activity. We also demonstrated that TRBP is ubiquitinylated and the ubiquitinylated forms of TRBP are accumulated by ectopically expressed merlin or cell confluence in the presence of MG132, a proteasome inhibitor. Furthermore, we showed that the regulation of TRBP in response to cell confluence was abolished upon knockdown of merlin expression by specific small interfering RNA. Finally, we showed that ectopically expressed merlin restored cell-cell contact inhibition in cells stably expressing TRBP but not in TRBPDeltac. These results suggest that merlin is involved in the regulation of TRBP protein level by facilitating its ubiquitination in response to such cues as cell-cell contacts.

Activation of NF-kappaB by HDAC inhibitor apicidin through Sp1-dependent de novo protein synthesis: its implication for resistance to apoptosis.

Histone deacetylase (HDAC) inhibitors are promising anti-cancer drugs, but these exert differential responses depending on the cell types. Here, we demonstrate a new mechanism for activation of nuclear factor-kappaB (NF-kappaB) by HDAC inhibitor apicidin and the role of NF-kappaB signaling pathway for mediating differential cellular responses, especially, apoptosis. Treatment of HeLa cells with apicidin increases transcriptional activity of NF-kappaB and its target gene IL-8 and cIAP-1 induction, which involves the activation of IKK-IkappaBalpha signaling pathway through Sp1-dependent de novo protein synthesis. In parallel, apicidin treatment leads to histone hyperacetylation in the IL-8 promoter region independent of NF-kappaB signaling pathway, which is not sufficient for full transcription of IL-8 gene. This NF-kappaB activation contributes to resistance of HeLa cells to apoptotic potential of apicidin. Collectively, our results suggest that activation of NF-kappaB signaling cascade functions as a critical modulator to determine cell fate on apoptosis in response to HDAC inhibitors.

Efficient inhibition of in vivo human malignant glioma growth and angiogenesis by interferon-beta treatment at early stage of tumor development.

Malignant gliomas are highly angiogenic and aggressive tumors. IFN-beta has been used for the treatment of patients with malignant glioma; however, its antitumor mechanism in vivo remains unclear. To understand the in vivo antitumor effect and mechanism of recombinant human IFN-beta (rhIFN-beta) depending on the stages of tumor development or progression, we used orthotopic xenograft brain tumors generated by stereotactic intracerebral implantation of U-87 human glioma cells in nude mice. Mice bearing tumors 7 days (group 1) and 21 days (group 2) postimplant were treated with 2 x 10(5) IU/day of rhIFN-beta or saline i.p. for 15 days, respectively. Tumor growth was suppressed by 69.6% in group 1 and 10.8% in group 2 compared with tumors of each control group treated with saline. rhIFN-beta-treated group 1 animals showed 38% reduction in vascularization along with a 2.5-fold increase of the apoptotic index and no change in the proliferative index as compared with untreated tumors. The expression level of vascular endothelial cell growth factor and basic fibroblast growth factor was not affected by rhIFN-beta treatment. rhIFN-beta showed inhibitory activity on proliferation of U-87 cells, human umbilical vein endothelial cells, and PAM 212 murine keratinocytes in vitro. Our results indicate that the in vivo antitumor effect of rhIFN-beta on malignant gliomas may be mediated, at least in part, via angiogenesis inhibition rather than antiproliferative activity and that rhIFN-beta may be more effective for the treatment of malignant glioma patients at an early stage with minimal or microscopic tumor burdens rather than at an advanced stage of tumor development.

Development of spontaneous hyperplastic skin lesions and chemically induced skin papillomas in transgenic mice expressing human papillomavirus type 16 E6/E7 genes.

Human papillomavirus type 16 (HPV16) has been known to be the major factor for the development of uterine cervical carcinomas. We have developed a line of transgenic mice that express the HPV16 E6 and E7 genes in certain organs using a fusion gene which consists of the tyrosinase promoter and E6/E7 of HPV16, and have chosen the tyrosinase minigene as a co-injected visual marker for the identification of transgenic mice. Our transgenic mice (1) expressed E6/E7 transgene mainly in skin and heart, and (2) showed skin and eye pigmentation profiles, and (3) raised incidence of hyperplastic skin lesions. We had performed two-stage skin carcinogenesis experiment to detect the susceptibility of skin papilloma development in our transgenic mice, using dimethylbenz-anthracene (DMBA) as a initiating agent and 12-O-tetradecanoyl-phorbol-13-acetate (TPA). After 1 week of DMBA treatment (25 microg dissolved in 0.2 ml acetone) and 15 consecutive weeks of TPA treatment (2.5 microg dissolved in 0.2 ml acetone) on the back of transgenic and non-transgenic control mice (Fv-1(b) strain mice which are Friend virus B-type susceptible (FVB)/N), papilloma incidence was increased in our transgenic mice approximately 2-fold higher than in control (in female mice, 69.2 vs. 30%, respectively). Thus our transgenic mice may be useful for the development of immunological or other therapies for HPV-associated cancers.

The expression of MHC class I, TAP1/2, and LMP2/7 gene in human gastric cancer cell lines.

Intracellular antigens are presented to CD8+ T cells through major histocompatibility complex (MHC) class I molecule. For stable MHC class I expression, several molecules as well as the MHC molecule itself have to express simultaneously and function well. To determine a gene associated with MHC class I surface expression, the expressions of LMP2/7 and TAP1/2 including MHC I gene were analyzed in ten human gastric cancer cell lines, using RT-PCR and Northern blot analysis. Although LMP2, TAP1/2, and MHC class I gene expression were reduced in some cells, this was not significantly associated with MHC class I surface expression. By comparison, the expression of LMP7 was significantly reduced in three of ten cell lines, which also showed low levels of MHC class I surface expression, and increased in four of ten cell lines, which also showed high levels of MHC class I surface expression. These results suggest that the level of MHC class I surface expression is associated, in most cases, with the expression of the LMP7 gene regardless of the LMP2, TAP1, TAP2, or MHC class I genes.

Potential of adenoviral p53 gene therapy and irradiation for the treatment of malignant gliomas.

We investigated the combined effects of p53 gene transfer and irradiation and its still unclear interaction mechanism in human gliomas. Four human glioma cell lines expressing mutant type p53 (U373 and A172) and wild-type p53 (D54MG and EFC-2) were transfected by adenoviral vectors bearing p53 gene at 50 multiplicity of infection. Two days after transfection, cells were irradiated (3, 6, and 9 Gy). The cytotoxicity was evaluated by clonogenic assay. The quantitative analysis of apoptosis and cell cycle analysis were performed using flow cytometry. Irradiation combined with adenoviral p53 transfection significantly increased cytotoxicity, which was additive in cell lines with wild-type p53 and more than additive in cell lines with mutant p53. The combination of two modalities increased the apoptotic population by 14% in A172 cells and 20% in D54 MG cells, which were the sum of apoptosis from each modality. Adenoviral p53 transfection increased the G1 phase fraction and concomitant decrease of radioresistant S phase fraction in A172 and D54MG cells. Our study demonstrated that p53 gene transfer combined with irradiation increased absolute cytotoxicity in human glioma cells used in this experiment. The interaction mechanism for increased cytotoxicity involved, in part, increased apoptosis and change of cell cycle profile.

Neuronal dysfunction in patients with closed head injury evaluated by in vivo 1H magnetic resonance spectroscopy.

RATIONALE AND OBJECTIVES: With the use of localized, water-suppressed in vivo 1H magnetic resonance spectroscopy (MRS), the proton metabolic alterations of white matter in patients with closed head injury (CHI) and healthy controls are evaluated, and metabolic alterations with Glasgow Outcome Scale (GOS) scores are compared. METHODS: Patients with CHI (n = 10) and healthy control subjects (n = 10) underwent MRS examinations using a stimulated-echo acquisition mode pulse sequence that provided 2 x 2 x 2 cm3 volume of interest in the left frontoparietal white matter. Proton metabolite ratios relative to creatine were obtained using a Marquart algorithm. RESULTS: The specific feature in patients with CHI was significant decrease of N-acetylaspartate (NAA)/creatine ratio compared with normal controls. No clear correlation of other metabolite ratios such as choline/creatine and inositols creatine was established. The level of NAA/creatine ratio was significantly correlated with GOS. CONCLUSIONS: Results of this preliminary study suggest that the reduction of NAA/creatine ratio may indicate neuronal loss in patients with CHI. The NAA/creatine ratio may serve as a metabolic criterion to predict the GOS of patients with CHI. Thus, in vivo 1H MRS may be a useful modality in the clinical evaluation of patients with CHI based on the proton metabolite concentrations of cerebral white matter.

Efficacy of D-CPPene, a competitive N-methyl-D-aspartate antagonist in focal cerebral ischemia in the rat.

The effect of a novel and potent competitive N-methyl-D-aspartate (NMDA) antagonist D-(E)-4-(3-phosphonoprop-2-enyl)piperazine-2-carboxylic acid (D-CPPene) upon ischemic brain damage has been examined in a rat model of focal cerebral ischemia. Focal cerebral ischemia was produced by permanent occlusion of the left middle cerebral artery (MCA). The animals were sacrificed 24 h after MCA occlusion and the amount of ischemic brain damage was assessed at 8 predetermined coronal planes. Pretreatment with D-CPPene (1.5, 4.5 or 15 mg/kg, i.v.), initiated 15 min prior to MCA occlusion (followed by constant infusion at 1, 3 or 10 mg/kg/h), produced dose-dependent reductions in the volumes of infarction; the dose of 4.5 mg/kg being the most effective (reduced by 37%; P < 0.01). These results indicate that systemic administration of the competitive NMDA antagonist D-CPPene has neuroprotective effects in a model of focal cerebral ischemia and define the dose dependency of its neuroprotective effects.

Expression of vascular endothelial growth factor mRNA following transient forebrain ischemia in rats.

Using a reproducible two-vessel occlusion model for forebrain ischemia in rats, we investigated the temporal and spatial changes of vascular endothelial growth factor (VEGF) expression after transient forebrain ischemia with Northern blot analysis and in situ hybridization. Northern blot analysis revealed that VEGF mRNA of the hippocampus was increased from 12 h after reperfusion, with a peak at 1 day. In situ hybridization and double labeling for VEGF mRNA and glial fibrillary acidic protein showed a transient induction of VEGF mRNA in the neurons of the hippocampus from 12 h of reperfusion with a peak at 1 day, and in the astrocytes of the hippocampus, caudoputamen, thalamus and cortical regions at 1 day. After 3 days, no more VEGF signal was detected. Our results demonstrate that astrocytes and neurons each upregulate VEGF mRNA in different temporal and spatial patterns after transient forebrain ischemia in the rat, and these patterns appear to be different from those in transient focal cerebral ischemia.

Cholangiographic appearance of multiseptate gallbladder: case report and a review of the literature.

A case of multiseptate gallbladder is described, with a review of the literature. This is the 24th such case report. The patient complained of right upper quadrant pain, colicky in nature. Abdominal ultrasonography showed multiple fine echoes within the gallbladder. On endoscopic retrograde cholangiography, multiple radiolucent lines crossing the gallbladder in various directions were noted within the gallbladder. The gallbladder was crisscrossed by numerous delicate septations and had a honeycomb appearance. These findings suggested multiseptate gallbladder.

Anterior thalamoperforating artery aneurysm associated with internal carotid artery occlusion: case report.

OBJECTIVE AND IMPORTANCE: We describe a rare case of a ruptured distal anterior thalamoperforating artery aneurysm associated with right internal carotid artery occlusion. CLINICAL PRESENTATION: A 59-year-old woman experienced sudden occipital headache, vomiting, and subsequent coma as a result of massive intraventricular hemorrhage. An initial angiogram revealed only an occlusion of the right internal carotid artery just distal to the posterior communicating artery. Repeat angiography 1 month later, however, revealed a saccular aneurysm at a distal anterior thalamoperforating artery in addition to the occlusion of the internal carotid artery. INTERVENTION: We approached this aneurysm through the right temporal horn after opening the ambient cistern. The aneurysm, which was located in the brain parenchyma just medial to the temporal horn, was successfully resected. CONCLUSION: This rare aneurysm probably developed as a result of hemodynamic stress on the anterior thalamoperforating artery after occlusion of the internal carotid artery and/or secondary to chronic hypertension.

Mucocele of the anterior clinoid process: case report.

OBJECTIVE AND IMPORTANCE: Of the primary intracranial mucoceles, those arising from the optic canal or anterior clinoid process are extremely rare. To our knowledge, only five cases have been reported. The pathogenesis of mucoceles at this unusual site is unclear, but the previously reported cases suggest that these mucoceles may originate from pneumatizing air cells in the anterior clinoid processes. CLINICAL PRESENTATION: A 43-year-old woman presented with diplopia. Magnetic resonance imaging showed a small mass, compressing the optic nerve, in the medial portion of the left anterior clinoid process. The medial portion of the anterior clinoid process surrounding the mass was eroded and the bony margins of the mass were well corticated in computed tomographic scans. There was no direct connection between any paranasal sinus and the mass cavity, as assessed in imaging studies and intraoperatively confirmed. The pathological diagnosis after the operation indicated a mucocele. CONCLUSION: Considering the absence of air cells in the anterior clinoid processes, the mucocele in this case might have originated from ectopic mucinous tissue that appeared during the development of the optic canal, rather than from a pneumatizing air cell.

Ventricular pressure monitoring during bilateral decompression with dural expansion.

OBJECT: The management of massive brain swelling remains an unsolved problem in neurosurgery. Despite newly developed medical and pharmacological therapy, the rates of mortality and morbidity caused by massive brain swelling remain high. According to many recent reports, surgical decompression with dural expansion is superior to medical management in patients with massive brain swelling. To show the quantitative effect of decompressive surgery on intracranial pressure (ICP), the authors performed a ventricular puncture and measured the ventricular ICP continuously during decompressive surgery and the postoperative period. METHODS: Twenty patients with massive brain swelling who underwent bilateral decompressive craniectomy with dural expansion were included in this study. In all patients, ventricular puncture was performed at Kocher's point on the side opposite the massive brain swelling. The ventricular puncture tube was connected to the continuous monitor via a transducer device. The ventricular pressure was monitored continuously, during the bilateral decompressive procedures and postoperative period. The initial ventricular ICP was variable, ranging from 16 to 65.8 mm Hg. Immediately after the bilateral craniectomy, the mean ventricular ICP decreased to 50.2+/-16.6% of the initial ICP (range 5-51.5 mm Hg). Additional opening of the dura decreased the mean ICP by an additional 34.5% and reduced the ventricular pressure to 15.7+/-10.7% of the initial pressure (range 0-15 mm Hg). Ventricular pressure measured postoperatively in the neurosurgical intensive care unit was lowered to 15.1+/-16.5% of the initial ICP. The ventricular ICP trend in the first 24 hours after decompressive surgery was an important prognostic factor; if it was greater than 35 mm Hg, the mortality rate was 100%. CONCLUSIONS: Bilateral decompression with dural expansion is an effective therapeutic modality in the control of ICP. To obtain favorable clinical outcomes in patients with massive brain swelling, early decision making and proper patient selection are very important.