Platelet count and clinical outcomes among ischemic stroke patients with endovascular thrombectomy in DIRECT-MT.

OBJECTIVES: The prognostic role of baseline platelet count (PLT) in acute ischemic stroke patients with large vessel occlusion undergoing endovascular thrombectomy is unclear. Whether PLT modifies alteplase treatment effect on clinical outcome in those patients is also uncertain. METHODS: We derived data from a multicenter randomized clinical trial (DIRECT-MT) comparing intravenous alteplase before endovascular treatment vs. endovascular treatment only. The 654 patients with available PLT data were included. Primary outcome was the ordinal modified Rankin Scale (mRS) score evaluated at 90 days. We also assessed various secondary and safety outcomes. RESULTS: After adjusting for confounding factors, patients in the top tertile of PLT had a significantly lower risk of a worse shift in the distribution of mRS score (Odds Ratio: 0.671, 95% Confidence Interval: 0.473-0.953, p for trend=0.025), major disability and death (Odds Ratio: 0.617, 95% Confidence Interval: 0.393-0.97, p for trend=0.037) as well as death (Odds Ratio: 0.544, 95% Confidence Interval: 0.313-0.947, p for trend=0.031), respectively, compared with the bottom one. Among patients in the bottom tertile of PLT, combination therapy was associated with a better imaging outcome of eTICI score of 2b, 2c or 3 on final angiogram (Odds Ratio: 3.23, 95% Confidence Interval: 1.49-7.002) with a marginally significant interaction effect. CONCLUSIONS: Participants with higher baseline PLT had a decreased risk of poor functional outcomes. Low baseline PLT modified alteplase treatment effect on the eTICI score on final angiogram. Combination therapy was beneficial for patients with low baseline PLT to have a better reperfusion status.

Age Does Not Affect Metoprolol's Effect on Perioperative Outcomes (From the POISE Database).

BACKGROUND: Perioperative ß-blockade reduces the incidence of myocardial infarction but increases that of death, stroke, and hypotension. The elderly may experience few benefits but more harms associated with ß-blockade due to a normal effect of aging, that of a reduced resting heart rate. The tested hypothesis was that the effect of perioperative ß-blockade is more significant with increasing age. METHODS: To determine whether the effect of perioperative ß-blockade on the primary composite event, clinically significant hypotension, myocardial infarction, stroke, and death varies with age, we interrogated data from the perioperative ischemia evaluation (POISE) study. The POISE study randomly assigned 8351 patients, aged ≥45 years, in 23 countries, undergoing major noncardiac surgery to either 200 mg metoprolol CR daily or placebo for 30 days. Odds ratios or hazard ratios for time to events, when available, for each of the adverse effects were measured according to decile of age, and interaction term between age and treatment was calculated. No adjustment was made for multiple outcomes. RESULTS: Age was associated with higher incidences of the major outcomes of clinically significant hypotension, myocardial infarction, and death. Age was associated with a minimal reduction in resting heart rate from 84.2 (standard error, 0.63; ages 45-54 years) to 80.9 (standard error, 0.70; ages >85 years; P < .0001). We found no evidence of any interaction between age and study group regarding any of the major outcomes, although the limited sample size does not exclude any but large interactions. CONCLUSIONS: The effect of perioperative ß-blockade on the major outcomes studied did not vary with age. Resting heart rate decreases slightly with age. Our data do not support a recommendation for the use of perioperative ß-blockade in any age subgroup to achieve benefits but avoid harms. Therefore, current recommendations against the use of ß-blockers in high-risk patients undergoing noncardiac surgery apply across all age groups.

The effects of halogen elements on the opening of an icosahedral B12 framework.

The fully halogenated or hydrogenated B12X122- (X = H, F, Cl, Br and I) clusters are confirmed to be icosahedral. On the other hand, the bare B12 cluster is shown to have a planar structure. A previous study showed that a transformation from an icosahedron to a plane happens when 5 to 7 iodine atoms are remained [P. Farràs et al., Chem. - Eur. J. 18, 13208-13212 (2012)]. Later, the transition was confirmed to be seven iodine atoms based on an infrared spectroscopy study [M. R. Fagiania et al., Chem. Phys. Lett. 625, 48-52 (2015)]. In this study, we investigated the effects of different halogen atoms on the opening of the B12 icosahedral cage by means of density functional theory calculations. We found that the halogen elements do not have significant effects on the geometries of the clusters. The computed infrared (IR) spectra show similar representative peaks for all halogen doped clusters. Interestingly, we found a blue-shift in the IR spectra with the increase in the mass of the halogen atoms. Further, we compared the Gibbs free energies at different temperatures for different halogen atoms. The results show that the Gibbs free energy differences between open and close structures of B12X7- become larger when heavier halogen atoms are presented. This interesting finding was subsequently investigated by the energy decomposition analysis.

Up-Regulation of Corticocerebral NKD2 in Lipopolysaccharide-Induced Neuroinflammation.

Naked2 (NKD2), one member of Naked family, has been shown to negatively regulate Wnt/ß-catenin signaling pathway. It has been recognized that NKD2 plays a vital role in cell homeostasis and prevention of tumorigenesis. However, NKD2 expression and its functional role in the brain in neuroinflammatory processes remain unclear. In our study, we investigated NKD2 distribution and role in lipopolysaccharide (LPS)-induced neuroinflammation rat model. The data indicated that NKD2 was up-regulated in LPS-injected brain, and the cellular localization of NKD2 was predominantly in cerebral cortical neurons. Furthermore, we treated primary neurons with conditioned media (CM) collected from LPS-stimulated mixed glial cultures (MGC). We detected that the up-regulation of NKD2 might be associated with the subsequent apoptosis in neurons. We also found knockdown NKD2 partially depressed the increase of cleaved caspase-3 and increased the reduction of ß-catenin stimulated by MGC-CM. Taken together, these results suggested that NKD2 might be involved in neuronal apoptosis via the Wnt/ß-catenin pathway during neuroinflammation in CNS. Our findings might provide a new therapeutic target for the prevention of neuroinflammation-involved neurological disorders.

The role of Homer1b/c in neuronal apoptosis following LPS-induced neuroinflammation.

Homer, also designated Vesl, is one member of the newly found postsynaptic density scaffold proteins, playing a vital role in maintaining synaptic integrity, regulating intracellular calcium mobilization, and being critical for the regulation of cellular apoptosis. However, its function in the inflamed central nervous system (CNS) is not fully elucidated. Here, we investigated the role of Homer1b/c, a long form of Homer1, in lipopolysaccharide (LPS) induced neuroinflammation in CNS. Western blot analysis indicated that LPS administration significantly increased the expression of Homer1b/c in rat brain. Moreover, double immunofluorescent staining suggested Homer1b/c was mainly distributed in the cytoplasm of neurons and had a close association with cleaved caspase-3 level in neurons in rat brain after LPS injection. In vitro studies indicated that up-regulation of Homer1b/c might be related to the subsequent apoptosis in neurons treated by conditioned media (CM), collected from LPS-stimulated mixed glial cultures (MGC). We also found down-regulation of Homer1b/c partly blocked the increase of cleaved caspase-3 and the proportion of Bax/Bcl-2 in neurons induced by MGC-CM. Taken together, these findings suggested that Homer1b/c might promote neuronal apoptosis via the Bax/Bcl-2 dependent pathway during neuroinflammation in CNS, and inhibiting Homer1b/c expression might provide a novel neuroprotective strategy against the inflammation-related neuronal apoptosis.

Up-Regulation of CCT8 Related to Neuronal Apoptosis after Traumatic Brain Injury in Adult Rats.

Traumatic brain injury (TBI) initiates a series of neurochemical and signaling changes that could eventually lead to neuronal apoptosis. Recent studies indicated that mature neurons cell cycle re-enter played a crucial role in neuronal apoptosis. In this study, we identified that the chaperonin containing TCP-1, subunit 8 (CCT8), as a member of class II chaperonins, was significantly upregulated following TBI. Moreover, double immunofluorescence staining revealed that CCT8 was co-expressed with neuronal nuclei (NeuN). Besides, co-localization of CCT8/active caspase 3 was detected in NeuN. We also examined the expression profiles of active caspase 3 whose changes were correlated with the expression of CCT8. All our findings suggested that CCT8 might be involved in the pathophysiology of brain after TBI.

Upregulated expression of SSTR1 is involved in neuronal apoptosis and is coupled to the reduction of bcl-2 following intracerebral hemorrhage in adult rats.

Somatostatins are peptide hormones that regulate diverse cellular processes, such as neurotransmission, cell proliferation, apoptosis, and endocrine signaling as well as inhibiting the release of many hormones and other secretory proteins. SSTR1 is a member of the superfamily of somatostatin receptors possessing seven-transmembrane segments. Aberrant expression of SSTR1 has been implicated in several human diseases, including pseudotumor cerebri, and oncogenic osteomalacia. In this study, we investigated a potential role of SSTR1 in the regulation of neuronal apoptosis in the course of intracerebral hemorrhage (ICH). A rat ICH model in the caudate putamen was established and subjected to behavioral tests. Western blot and immunohistochemistry indicated a remarkable up-regulation of SSTR1 expression surrounding the hematoma after ICH. Double-labeled immunofluorescence showed that SSTR1 was mostly co-localized with neurons, and was rarely distributed in activated astrocytes and microglia. Additionally, SSTR1 co-localized with active-caspase-3 and bcl-2 around the hematoma. The expression of active-caspase-3 was parallel with that of SSTR1 in a time-dependent manner. In addition, SSTR1 knockdown specifically resulted in reduced neuronal apoptosis in PC12 cells. All our findings suggested that up-regulated SSTR1 contributed to neuronal apoptosis after ICH, which was accompanied with reduced expression of bcl-2.

Rocuronium blockade reversal with sugammadex vs. neostigmine: randomized study in Chinese and Caucasian subjects.

BACKGROUND: This study compared efficacy and safety of the selective relaxant binding agent sugammadex (2 mg/kg) with neostigmine (50 µg/kg) for neuromuscular blockade (NMB) reversal in Chinese and Caucasian subjects. METHODS: This was a randomized, active-controlled, multicenter, safety-assessor-blinded study (NCT00825812) in American Society of Anesthesiologists Class 1-3 subjects undergoing surgery with propofol anesthesia. Rocuronium 0.6 mg/kg was administered for endotracheal intubation, with 0.1-0.2 mg/kg maintenance doses given as required. NMB was monitored using TOF-Watch(®) SX. At second twitch reappearance, after last rocuronium dose, subjects received sugammadex 2 mg/kg or neostigmine 50 µg/kg plus atropine 10-20 µg/kg, according to randomization. Primary efficacy variable was time from sugammadex/neostigmine to recovery of the train-of-four (TOF) ratio to 0.9. RESULTS: Overall, 230 Chinese subjects (sugammadex, n = 119, neostigmine, n = 111); and 59 Caucasian subjects (sugammadex, n = 29, neostigmine, n = 30) had evaluable data. Geometric mean (95% CI) time to recovery to TOF ratio 0.9 was 1.6 (1.5-1.7) min with sugammadex vs 9.1 (8.0-10.3) min with neostigmine in Chinese subjects. Corresponding times for Caucasian subjects were 1.4 (1.3-1.5) min and 6.7 (5.5-8.0) min, respectively. Sugammadex 2 mg/kg was generally well tolerated, with no serious adverse events reported. There was no residual NMB or recurrence of NMB. CONCLUSION: Both Chinese and Caucasian subjects recovered from NMB significantly faster after sugammadex 2 mg/kg vs neostigmine 50 µg/kg, with a ~5.7 times (p < 0.0001) faster recovery with sugammadex vs neostigmine in Chinese subjects. Sugammadex was generally well tolerated. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT00825812.

[Neuromuscular effects of cisatracurium besylate in obese patients].

OBJECTIVE: To explore the neuromuscular effects of cisatracurium besylate in morbidly obese patients when dosed according to real body weight under total intravenous anesthesia with propofol. METHODS: Thirty-six ASA I-II patients aged 18-65 years scheduled for elective procedures at our hospital during July 2012 to December 2012 were allocated into 2 groups according to body mass index (normal weight: body mass index: <24, overweight: body mass index >28). Anesthesia was induced with target-controlled infusion of propofol (Cp 3 µg/ml) and remifentanil (Ce 3-5 ng/ml). A bolus of cisatracurium 0.2 mg/kg was administered intravenously over 5-10 s as soon as a patient lost consciousness. Neuromuscular block was monitored with TOF-Watch SX (Oaganon, the Netherlands). Single stimulation (0.1 Hz) was applied to ulnar nerve at wrist. The maximal degree of neuromuscular block, onset time, clinical duration and recovery index were recorded. They were intubated and mechanically ventilated when neuromuscular block reached the maximal degree. The intubation condition was evaluated. RESULTS: The average onset time was (164 ± 25) s in obese group versus (201 ± 48) s in normal weight group. And there was significant difference between groups (t = 2.83, P < 0.05) . The clinical duration was (68.4 ± 9.6) min in obese group versus (62.0 ± 6.5) min in normal weight group. And there was significant difference between groups (t = 2.33, P < 0.05). The recovery index was (15.6 ± 4.7) min in obese group versus (10.8 ± 4.2) min in normal weight group. And there was significant difference between groups (t = 3.03, P < 0.05) . Also 75% recovery time was (83.9 ± 11.5) min in obese group versus (73.0 ± 9.2) min in normal weight group. And there was significant difference between groups (t = 2.94, P < 0.05). But no differences existed in intubation conditions. CONCLUSION: When dosed according to real body weight, onset time of cisatracurium is shorter while clinical duration and recovery index are prolonged in morbidly obese patients compared with normal weight counterparts.

Review on active components and mechanism of natural product polysaccharides against gastric carcinoma.

One of the malignant tumors with a high occurrence rate worldwide is gastric carcinoma, which is an epithelial malignant tumor emerging from the stomach. Natural product polysaccharides are a kind of natural macromolecular polymers, which have the functions of regulating immunity, anti-oxidation, anti-fatigue, hypoglycemia, etc. Natural polysaccharides have remarkable effectiveness in preventing the onset, according to studies, and development of gastric cancer at both cellular and animal levels. This paper summarizes the inhibitory mechanisms and therapeutic significance of plant polysaccharides, fungi polysaccharides, and algal polysaccharides in natural product polysaccharides on the occurrence and development of gastric cancer in recent years, providing a theoretical basis for the research, development, and medicinal value of polysaccharides.

Ginsenoside Rd reduces cell proliferation of non-small cell lung cancer cells by p53-mitochondrial apoptotic pathway.

Ginsenoside Rd is a tetracyclic triterpenoid derivative, widely existing in Panax ginseng, Panax notoginseng and other traditional Chinese medicines. Many studies have proved that ginsenoside Rd have a variety of significant biological activities on certain types of cancer. However, the mechanism of ginsenoside Rd remains unclear in lung cancer. The findings of this study reveal that GS-Rd inhibits the proliferation of NSCLC cells, induces apoptosis, and suppresses migration and invasion. The results showed Ginsenoside Rd inhibited the cell proliferation (∼99.52 %) by S phase arrest in cell cycle and promoted the apoptosis (∼54.85 %) of NSCLC cells. It also inhibited the migration and invasion of cells (p < 0.001). The expression levels of related mitochondrial apoptosis proteins (Bax/Bcl-2/Cytochrome C) and matrix metalloproteinases (MMP-2/-9) were significantly changed. The results showed that ginsenoside Rd inhibited the proliferation of tumor cells by activating p53/bax-mediated mitochondrial apoptosis and the expression of key enzymes for cell apoptosis caspase-3/cleaved-caspase-3 were significantly increased. This research contributes to a better understanding of the anti-tumor effects and molecular mechanisms of GS-Rd, paving the way for its potential development and clinical application in NSCLC therapy.

Up-regulation of Che-1 relates to neuronal apoptosis after traumatic brain injury in adult rats.

Che-1, a recently identified apoptosis related protein, affects the fate of various cell types when under stress. One attractive biological function of Che-1 is promoting the transcription of p53 after DNA damage; besides, it can also regulate cell cycle via interacting with retinoblastoma protein. Although previous evidence has showed its anti-apoptotic role in cancer cells, some studies point out that Che-1 might play an opposite role in central nervous system (CNS). However, the function of Che-1 in CNS is still with limited acquaintance. To investigate whether Che-1 is involved in CNS lesion, we performed a traumatic brain injury model in adult rats. Up-regulation of Che-1 was observed in the peritrauma brain cortex by performing western blotting and immunohistochemistry. Terminal deoxynucleotidyl transferase deoxy-UTP nick-end labeling and 4',6-diamidino-2-phenylindole staining suggested that Che-1 was involved in neuronal apoptosis after brain injury. We also investigated co-localization of Che-1 and active-caspase-3 in the ipsilateral brain cortex. In addition, the expression patterns of p53, Bax and PCNA were parallel with that of Che-1. Besides this, neurotrophin receptor-interacting MAGE homolog was found to be associated with Che-1 after brain trauma. Based on our data, we suggested that Che-1 might play an important role in neuronal apoptosis following TBI; and might provide a basis for the further study on its role in regulating the expression of p53 and cell cycle re-entry in traumatic brain injury.

The role of HSPA12B in regulating neuronal apoptosis.

Heat shock protein A12B (HSPA12B) is the newest member of a recently defined subfamily of proteins distantly related to the 70-kDa family of heat shock proteins (HSP70) family. HSP70s play a crucial role in protecting cells, tissues, organs and animals from various noxious conditions. Here we studied the dynamic expression changes and localization of HSPA12B after middle cerebral artery occlusion (MCAO) with reperfusion induced ischemic insult processes in adult rats. Apoptosis, as indicated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, was also increased in the peri-ischemic cortex compared to non-ischemic hemisphere. The expression of HSPA12B was strongly induced in the ischemic hemisphere of MCAO reperfusion rats in vivo. In vitro studies indicated that the up-regulation of HSPA12B may be involved in oxygen-glucose deprivation-induced PC12 cell death. And knockdown of HSPA12B in cultured differentiated PC12 cells by siRNA showed that HSPA12B inhibited the expression of active caspase-3. Collectively, these results suggested that HSPA12B may be required for protecting neurons from ischemic insults.

The expression pattern of Nischarin after lipopolysaccharides (LPS)-induced neuroinflammation in rats brain cortex.

OBJECTIVE: To investigate whether Nischarin participated in neuronal apoptosis induced by neuroinflammation and via the phosphatidylinositol 3-kinase (PI3K) and PKB-dependent pathway. MATERIAL: Use of male Sprague-Dawley rats, rat pheochromocytoma (PC12), and murine microglial cells (BV-2). Treatment lipopolysaccharides (LPS) were injected into the brain lateral ventricle of the rat. The BV-2 cells were treated by LPS. The PC12 cells were pretreated by or not pretreated by conditioned media and siRNA. METHODS: Western blotting was used for analyzing the expression level of Nischarin, pAKT, BAD and Bcl-2. Immunohistochemistry and immunofluorescence were used to perform the morphology and localization of Nischarin. The siRNA could down-regulate the protein level of endogenous Nischarin. RESULTS: The expression level of Nischarin was elevated after LPS injection; meanwhile, Nischarin was located in the neuron. Nischarin was involved in regulating the PI3K/PKB patway. CONCLUSION: Nischarin might be involved in mediating the process of PI3K/PKB pathway-dependent neuronal apoptosis. After the silencing of Nischarin in cultured PC12 (pheochromocytoma) by siRNA, these results showed that it would induce a reduction of pAKT and Bcl-2 proteins expression; meanwhile, it induces an increase of BAD and active caspase-3.

Perioperative acute myocardial infarction increases mortality following noncardiac surgery.

OBJECTIVE: To provide insight into diagnosis, treatment, and prevention of perioperative myocardial infarction (PMI). DESIGN: The authors retrospectively analyzed PMI characteristics in patients undergoing noncardiac surgery and identified risk factors for death. SETTING: An affiliated teaching hospital with about 1500 beds. PARTICIPANTS: The authors screened electronic medical records and retrospectively analyzed clinical data from 117,856 patients who underwent noncardiac surgery during the period from August 2003 through June 2011. INTERVENTIONS: Patients were divided into two groups based on survival at 30 days after PMI. MEASUREMENTS AND MAIN RESULTS: PMI was reported in 61 patients, for an overall incidence rate of 5.2 per 10,000. PMI incidence increased significantly with age, with a rate of 0.97 per 10,000 for the 45- to 60-year-old group, and increasing to a rate of 40.4 per 10,000 for the>75-year-old group (p<0.001). The mortality rate of non-PMI patients (n = 117,795) was 0.32%, whereas the mortality rate for the 61 PMI patients was 36.1% (p<0.001). PMI occurred acutely (within 48 to 72 hours of surgery) in the majority of patients (78.7%), and only 18% of these patients complained of chest pain. The majority of patients who suffered PMI had non-ST segment elevation acute myocardial infarction (78.7%). By multiple logistic regression analysis, lack of anticoagulation/antiplatelet therapy and cardiogenic shock were independent risk factors for death in PMI patients (p = 0.001 for both). CONCLUSIONS: PMI incidence increased significantly with advanced age. PMI increased mortality following non-cardiac surgery. The independent risk factors for death in PMI patients following noncardiac surgery were lack of anticoagulation/antiplatelet therapy and cardiogenic shock.

[Study of blood oxygen saturation, heart rate changes and plateau reaction of the Antarctic Kunlun station investigation team in different plateau environments].

OBJECTIVE: To explore the blood oxygen saturation and heart rate changes of the Antarctic explorers. METHODS: During August 2010 to April 2011, the changes in blood oxygen saturation, heart rate and plateau reaction of 16 Antarctic expedition team in different plateau environments (Tibetan plateau versus Antarctic plateau) were monitored with the noninvasive pulse oximeter MD300-C. The extent of acute mountain sickness was determined according to the Lake Louise Consensus acute mountain reaction symptom scores and judgment method. RESULTS: The changes of blood oxygen saturation, heart rate at different altitudes of 110, 3650, 4300 m (96.8% ± 1.2%,89.1% ± 1.2%, 86.1% ± 2.0%, (75.0 ± 5.4) times/min, (104.0 ± 4.3) times/min, (113.0 ± 5.2) times/min,F = 214.155, 240.088,both P < 0.05). With rising latitude and elevation gradient in Antarctic plateau, the changes of blood oxygen saturation, heart rate at different altitudes of 2000, 2500, 3000, 3500 and 4087 m(91.9% ± 1.3%,90.5% ± 1.3%,87.6% ± 1.4%,85.0% ± 1.8%,81.5% ± 2.2%, (85.9 ± 3.2) times/min, (90.6 ± 2.8) times/min, (97.8 ± 4.1) times/min, (102.0 ± 3.4) times/min, (106.3 ± 3.9) times/min, F = 105.418, 90.174, both P < 0.05). Levels of blood oxygen saturation and heart rate were both correlated with the risk of altitude sickness (r = -0.446 and 0.565, both P < 0.05). CONCLUSIONS: As the increases of altitude, there are significant changes in oxygen saturation, heart rate of the Antarctic explorers. And with the increases of altitude, the risk of altitude sickness gradually increases.

Involvement of CLEC16A in activation of astrocytes after LPS treated.

CLEC16A, C-type lectin domain family 16, member A was recently found to be associated with inflation process in the autoimmune diseases. In this study, we elucidated the dynamic expression changes and localization of CLEC16A in lipopolysaccharide (LPS)-induced neuroinflammatory processes in adult rats. CLEC16A expression was strongly induced in active astrocytes in inflamed cerebral cortex. In vitro studies indicated that the up-regulation of CLEC16A may be involved in the subsequent astrocyte activation following LPS challenge. And Knock-down of CLEC16A in cultured primary astrocytes by siRNA showed that CLEC16A was required for the activation of astrocytes induced by LPS. Collectively, these results suggested CLEC16A may be important in host defense in astrocyte-mediated immune response. Understanding the cell signal pathway may provide a novel strategy against inflammatory and immune reaction in neuroinflammtion in CNS.

Primary intracranial extraskeletal myxoid chondrosarcoma: A case report and review of literature.

BACKGROUND: Primary intracranial extraskeletal myxoid chondrosarcoma (EMC) is an extremely rare low- to intermediate-grade malignant soft tissue sarcoma, and only 15 cases have been reported in the literature. Due to its rarity, clinical data and research on this tumor type are extremely limited, the pathogenesis and histological origin are still unclear, and the diagnostic and standard clinical treatment strategies for intracranial EMC remain controversial and undefined. CASE SUMMARY: We reported a case of a 52-year-old male who was admitted to the hospital with headache and dizziness for 1 mo, and his health status deteriorated during the last week. CT of the head showed a well-defined low-density lesion situated in the left cavernous sinus. Brain magnetic resonance imaging (MRI) showed a 3.4 cm × 3.0 cm sized, well-defined, round-shaped and heterogeneously enhanced lesion located in the left cavernous sinus. The entire lesion was removed via supratentorial craniotomy and microsurgery. Postoperative pathological diagnosis indicated primary intracranial EMC. Subsequently, the patient underwent 45 Gy/15 F stereotactic radiotherapy after discharge. At present, it is 12 mo after surgery, with regular postoperative follow-up and regular MRI examinations, that there are no clinical symptoms and radiographic evidence indicating the recurrence of the tumor, and the patient has returned to normal life. CONCLUSION: Currently, the most beneficial treatment for primary intracranial EMC is gross total resection combined with postoperative radiotherapy. Long-term follow-up is also necessary for patients.

Structural characterisation and antitumor activity against non-small cell lung cancer of polysaccharides from Sanghuangporus vaninii.

The medicinal fungus Sanghuangporus vaninii can be cultivated in large scale and has outstanding antitumour activity. In this study, water-soluble S. vaninii polysaccharides (SVPs) were extracted from fruiting bodies. Four polysaccharide sub-fractions (SVP-W, SVP-1, SVP-2 and SVP-3) were isolated, with molecular weights from 90.50 kDa to 261.70 kDa, and all inhibited the proliferation of non-small cell lung cancer cell lines A549, 95-D and NCI-H460, especially the acidic SVP-1. SVP-1 affected cell morphology and colony formation in NCI-H460 cells. It also promoted cell apoptosis following nuclear fluorescence staining and flow cytometry. Methylation and nuclear magnetic resonance analyses revealed that SVP-1 is a heteroglycan with the main chain →4)-ß-D-Glcp-(1 â†’ 6)-ß-D-Glcp-(1 â†’ 6)-α-D-Galp-(1 â†’ 6)-ß-D-Glcp-(1→, and the branched chain α-D-Manp-(1 â†’ 2)-α-D-Manp-(1 â†’ 3)-ß-D-Glcp-(1 â†’ 3,6)-ß-D-Glcp-(1→. The findings indicate that this natural acidic polysaccharide has potential for non-small cell lung cancer therapy.

[A comparison of remifentanil versus sufentanil with target-controlled infusion in combined inhalation anesthesia for surgical patients: effects on hemodynamics and postoperative recovery].

OBJECTIVE: To compare the effect of remifentanil versus sufentanil with target-controlled infusion in combination with inhalation anesthesia for surgical patients on the parameters of hemodynamics and postoperative recovery. METHODS: Forty ASA I-II patients aged 18 - 65 years old with BMI (body mass index) < 30, undergoing colectomy or pedical screw interfix were enrolled. Upon the approval of institutional Ethics Committee, they were randomized to receive remifentanil or sufentanil at a target plasma concentration of 3 ng/ml and 0.3 ng/ml respectively in combination of inhalated anesthesia at 0.9 MAC (minimal alveolar concentration). The infusion of remifentanil was discontinued at the end of surgery while the infusion of sufentanil at 40 - 60 minutes before the end of surgery. The arterial blood pressure (ABP), heart rate (HR), electrocardiogram (ECG) and pulse blood oxygen saturation during anesthesia were monitored. The time between the termination of anesthetic use and recovery of spontaneous breathing and extubation were observed. And the incidence of postoperative pain and respiratory depression were recorded. RESULTS: As compared with the baseline values, BP and HR decreased significantly in both groups. BP was similar in both groups whereas HR was lower in Group R than that in Group S at post-induction, post-intubation, incision, the end of surgery and extubation (P < 0.05). The time from termination of anesthesia to recovery of spontaneous breathing was 1.8 ± 1.4 min in Group R. And it was significantly shorter than that in Group S (2.9 ± 1.5 min) (P < 0.05). The time from termination of anesthetic use to extubation was 6.8 ± 3.9 min in Group R. And it was also significantly shorter than that in Group S (9.1 ± 2.8 min) (P < 0.05). Seven patients experienced postoperative pain with visual analogue scale (VAS) > 4. And morphine was used for rescue analgesia in recovery room. CONCLUSION: When combined with inhalation anesthesia, the effects on hemodynamics are similar between the patients receiving the target-controlled infusions of remifentanil and sufentanil. Remifentanil offers a shorter time to recovery of spontaneous breathing and tracheal extubation.