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Subarachnoid hemorrhage (SAH) causes significant long-term neurocognitive dysfunction, which is associated with neuronal death in the hippocampus. Microglia can activate A1 astrocytes by secreting toxins. However, whether NeuroD1 application ameliorates M1microglial polarization through the reduction of A1 astrocyte remains unknown. Methods: 80 adult male C57BL/6 mice were used in this study. SAH was established by pre-chiasmatic injection of 100µl blood. AAV-NeuroD1-GFP virus was injected to the hippocampus 3 days post-SAH. Neurocognitive function, brain water content, In vivo electrophysiology, Golgi staining, western blot and immunofluorescent staining were assessed at day 14 post virus injection. Results: NeuroD1 application dramatically attenuated SAH-induced neuroinflammation by reducing the number of reactive astrocytes and microglia, reversing the transformation of neurotoxic A1 astrocytes and decreasing the secretion of neuroinflammatory cytokines. Interestingly, NeuroD1 significantly boosted the endogenous neurogenesis at the late phase of SAH, likely benefited from the improvement of microenvironment by NeuroD1 treatment after SAH. Notably, hippocampus subgranular zone was one of the brain regions most severely affected by SAH and also the region benefited significantly from NeuroD1 treatment. Above all, NeuroD1 treatment significantly alleviated neurocognitive dysfunction by directly reduction A1astrocytes, followed by the amelioration of M1micorglia, and then restoring endogenous neurogenesis impaired by SAH. Conclusions: NeuroD1 efficiently improved neurocognitive function after SAH by modulating astrocytic and microglial polarization. Moreover, NeuroD1 boosted endogenous neurogenesis at the late phase of SAH, likely thanks to the alleviation of neuroinflammatory microenvironment.

Depression is a prevalent psychiatric disorder. Mitogen-activated protein kinase phosphatase-1 (MKP-1) is considered as a key factor in depression. The cerebrospinal fluid-contacting nucleus (CSF-CN) is localized in the periaqueductal gray in the midbrain and functions in signal transmission and substance transportation between the brain and cerebrospinal fluid (CSF). Here, we aimed to determine whether the CSF-CN contributes to depression via MKP-1 in rats.Male Sprague-Dawley rats were subjected to chronic forced swimming stress (CFSS) to induce depression-like behavior. Cholera toxin subunit B-saporin (CB-SAP) was administered via intracerebroventricular injection 7 days before CFSS intervention. CFSS-induced depression-like behavior was blocked with chronic antidepressant treatment with fluoxetine. Depression-like behaviors assessment, western blot and double immunofluorescence staining were performed at 28 days after CFSS exposure.CFSS induced significant depression-like behaviors by decreasing body weight gains, reducing sucrose preference and decreasing scores in the open field test. The CSF-CN was activated after CFSS treatment, and targeted-ablation of the CSF-CN partially mitigated depression-like behaviors, mainly by ameliorating anxiety-like behavior. MKP-1 was colocalized and expressed in the CSF-CN after CFSS treatment. Moreover, pharmacological intervention with fluoxetine dramatically alleviated depression-like behaviors and downregulated the expression of MKP-1 in the CSF-CN after CFSS treatment.The CSF-CN may contribute to the pathogenesis of CFSS-induced depression-like behaviors via MKP-1. Future therapy targeting the MKP-1 in the CSF-CN may be a promising new choice.

Pain is a major complication of cancer and significantly affects the quality of life. Cerebrospinal fluid-contacting nucleus (CSF-CN) has been reported to be involved in the development of neuropathic pain and inflammatory pain. However, whether CSF-CN contributes to cancer-induced bone pain (CIBP) remains unknown. In this study, we aimed to illustrate the role of CSF-CN in the pathogenesis of CIBP and identify its potential mechanism via the MKP-1-mediated MAPK pathway. The Walker 256 cancer cells were injected into the tibia cavity of female Sprague-Dawley rats to induce CIBP models. Intracerebroventricular injection of cholera toxin subunit B- saporin (CB-SAP) was performed to "knockout" the CSF-CN. Morphine and LV-MKP-1 were applied. Mechanical and thermal hyperalgesia behaviors, double immunofluorescence staining and Western blot were conducted after CIBP induction. The results revealed that CIBP significantly reduced the mechanical withdrawal threshold and the thermal threshold. Double immunofluorescence staining revealed that c-Fos-positive neurons in CSF-CN were significantly higher in the CIBP group than that in the sham group. Targeted ablation of CSF-CN dramatically aggravated pain sensitivity. Moreover, MKP-1 was down-regulated in the CSF-CN after CIBP induction. Pharmacological intervention with morphine significantly ameliorated the mechanical and thermal hyperalgesia through reversing the down-expression of MKP-1 in the CSF-CN on day 14 after CIBP induction. Mechanically, overexpression of MKP-1 by LV-MKP-1 injection significantly relieved CIBP via inhibiting the expression of phosphorylated p38, which subsequently decreased the protein levels of Bax, cleaved caspase-3 and Iba-1, and reduced the mRNA levels of IL-1β, TNF-α and IL-6 in CSF-CN. In conclusion, CSF-CN contributed to CIBP via regulating the MKP-1-mediated p38-MAPK pathway. Future therapy targeting the expression of MKP-1 in the CSF-CN may be a promising new choice.

Background Pseudomonas aeruginosa (PA) bloodstream infection (BSI) is a common complication in patients with acute leukemia (AL), and the prevalence of antibiotic-resistant strains poses a serious problem. However, there is limited information regarding antibiotic resistance, clinical characteristics, and outcomes of PA BSI in AL patients. This study explored characteristics associated with the clinical outcomes of AL patients with PA BSI and analyzed factors associated with BSI caused by multidrug-resistant (MDR) or carbapenem-resistant strains. Methods This single-center retrospective study enrolled hospitalized AL patients who developed PA BSI during January 2014–December 2019. The Kaplan-Meier method was used to plot survival curves. Multivariate logistic regression analyses were also performed. Results Of 293 eligible patients with PA BSI, 55 (18.8%) received inappropriate empirical antibiotic therapy within 48 hours of BSI onset, whereas up to 65.8% MDR-PA BSI patients received inappropriate empirical treatment. The 30-day mortality rate was 8.5% for all patients. However, the 30-day mortality rates were 28.9% and 5.5% in MDR-PA BSI and non–MDR-PA BSI patients, respectively (P Conclusions MDR increases mortality risk in PA BSI patients, and previous antibiotic exposure is important in MDR-PA BSI development. Rational antibiotic use based on local antimicrobial susceptibility and clinical characteristics can help reduce antibiotic resistance and mortality.

Parkinson's disease (PD) is the second most common neurodegenerative disorder and is characterized by severe neuronal loss. Necroptosis, or programmed cell necrosis, is mediated by the receptor interacting protein kinase-1 and -3/mixed lineage kinase domain-like protein (RIP1/RIP3/MLKL) pathway, and is involved in several neurodegenerative diseases. Here we aimed to explore the involvement of necroptosis in 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine hydrochloride (MPTP)-induced PD and determine the potential mechanisms. We found that the protein levels of RIP1, RIP3, and MLKL increased significantly in a MPTP-induced mouse PD model. High expression of RIP1/RIP3/MLKL was associated with severe loss of dopaminergic neurons. Pretreatment with necrostatin-1 or the knockout of the RIP3/MLKL gene to block necroptosis pathway dramatically ameliorated PD by increasing dopamine levels and rescuing the loss of dopaminergic neurons, independent of the apoptotic pathway. Moreover, upregulation of inflammatory cytokines in MPTP-treated mice was partially inhibited by deletion of RIP3 or MLKL gene, indicating that a positive feedback loop exists between these genes and inflammatory cytokines. Our data indicate that RIP1/RIP3/MLKL-mediated necroptosis is involved in the pathogenesis of MPTP-induced PD. Downregulating the expression of RIP1, RIP3, or MLKL can significantly attenuate MPTP-induced PD. Future therapy targeting necroptosis may be a promising new option.

Enhancing phagocytosis can facilitate the removal of inflammatory molecules, limit the toxicity of dead cells and debris, and promote recovery after brain injury. In this study, we aimed to explore the role of bexarotene (Bex), a retinoid X receptor (RXR) agonist, in promoting astrocyte phagocytosis and neurobehavioral recovery after subarachnoid hemorrhage (SAH).Mice SAH model was induced by pre-chiasmatic injection of blood. Modified Garcia score, novel object recognition, rotarod test, and Morris water maze were performed to assess neurological function. Immunofluorescence and electron microscopy were used to evaluate astrocyte phagocytosis in vivo. In addition， ABCA1/MEGF10GULP1, the primary astrocyte phagocytosis pathway, were stimulated by Bex or suppressed by HX531 (a RXR antagonist) to evaluate their impacts on astrocyte phagocytosis and neurological recovery.Astrocytes phagocytosis of blood components were observed in mice after SAH induction, which is further increased by Bex treatment. Bex dramatically attenuated neuroinflammation, reduced brain edema, improved early neurological performance and promoted neurocognitive recovery. Meanwhile, Bex decreased neurotoxic reactive astrocytes and preserved neurogenesis after SAH. Bex increased the expression of astrocyte phagocytosis-related proteins ABCA1, MEGF10, and GULP1. Bex also increased the lysosomal processing of engulfed blood components in astrocytes. Moreover, Bex significantly promoted astrocytes to phagocytize debris in vitro by increasing the expression of ABCA1, MEGF10 and GULP1, while HX531 inhibited astrocyte phagocytosis and decreased these protein levels.Bex enhanced astrocyte phagocytosis through the ABCA1-mediated pathways, and promoted neurobehavior recovery in mice after SAH induction.

WW domain binding protein 2 (WBP2), a transcriptional coactivator, plays a vital role in breast tumorigenesis. It positively regulates estrogen receptor, Hippo, and Wnt pathways, which subsequently enhance the transcription of downstream target genes contributing to cancer. Understanding the regulation of the expression and activity of WBP2 oncoprotein has implication in cancer therapy. We have previously reported that WBP2 is regulated at the post-translational and post-transcriptional levels. However, its regulation at the transcriptional level is not known. In this study, the minimal promoter region of WBP2 that is critical for its transcription was identified. The E-box motif in the WBP2 promoter was demonstrated to be essential for its transcription. The E-box binding protein upstream stimulatory factor 1 (USF-1) was discovered to be a key transcription factor for WBP2 by yeast one-hybrid analysis and was validated through reporter and chromatin immunoprecipitation assays and tandem mass spectrometry, which also suggested that USF-1 acts by regulating a network of genes, in addition to WBP2, associated with cell movement, proliferation, cell-cycle, and survival cellular processes. USF-1 is overexpressed in majority of the breast cancer cell lines and tissues tested, and has profound effects on cancer cell proliferation. USF-1-mediated transcription of WBP2 was demonstrated to be inducible by insulin, which led to AKT-mediated phosphorylation of USF-1 that modulated its ability to bind to the WBP2 promoter and activate its transcription. This study sheds new light onto the regulation of the WBP2 oncogene at the transcriptional level by a novel oncogenic transcription factor, USF-1. USF-1 is a potential drug target for treatment of WBP2-positive breast cancer.-Ramos, A., Miow, Q. H., Liang, X., Lin, Q. S., Putti, T. C., Lim, Y. P. Phosphorylation of E-box binding USF-1 by PI3K/AKT enhances its transcriptional activation of the WBP2 oncogene in breast cancer cells.

To investigate the value of 3-dimensional (3D)-printed models with pathologic entities in enhancing the learning curve of surgery of tuberculum sellae meningioma.We printed 4 models of tuberculum sellae meningiomas based on radiologic data using a 3D printer. Participants were allocated to the 3D group and the atlas group. In the 3D group, participants learned surgery with the assistance of 3D models. In the atlas group, participants used only 2-dimensional materials to assist their learning. All participants undertook a pre-test and post-test. The scores were used to identify the difference in learning efficiency between the 2 groups.A total of 42 new trainees were recruited, of whom 22 were in the 3D group and 20 in the atlas group. The baseline data were not significantly different. The difference of pre-test score was not significant, either. However, the post-test score was significantly greater in the 3D group (P = 0.005), and the change in score was also significantly greater in the 3D group (P0.001). In accordance with the objective test, the subjective survey through a questionnaire from participants in the 3D group showed that 3D models significantly promoted the learning curve of this kind of complex skull base surgery.3D-printed models can assist in improving the learning curve of surgery of tuberculum sellae meningiomas. It particularly aids in memorization and spatial construction, improves understanding of surgical view, and arouses interest on the part of the trainee. We recommend using it in the education of complex skull base surgery.

Objective The transversus abdominis plane (TAP) block ameliorates visual analogue scale scores and decreases morphine requirements, but its role remains unclear. Patients of advanced age are susceptible to local anesthetic intoxication. We aimed to identify an optimal concentration that can be used in enhanced recovery after surgery (ERAS) without compromising analgesic efficacy. Methods In total, 120 patients aged ≥65 years undergoing laparoscopic rectal cancer surgery received general anesthesia combined with a TAP block using 0.25% ropivacaine (Group A), 0.50% ropivacaine (Group B), or 0.75% ropivacaine (Group C) in a 40-mL volume. Group D only received general anesthesia. Epinephrine, plasma cortisol, interleukin-6, and tumor necrosis factor-α were measured at baseline, skin incision, celiac exploration, and tracheal extubation. The proportions of CD4+ and CD4+/CD8+ cells were measured at baseline and postoperative days 1 and 3. Results The TAP block relieved the stress response and accelerated intestinal functional recovery as shown by significant reductions in VAS scores and anesthetic requirements. However, there was no significant difference between Groups B and C. Conclusion The TAP block plays an important role in ERAS in older patients undergoing laparoscopic rectal cancer surgery, and 0.5% ropivacaine is an optimal concentration that can reduce toxicity without undermining analgesia.

OBJECTIVEGlutamate excitotoxicity and neuronal apoptosis are suggested to contribute to early brain injury after subarachnoid hemorrhage (SAH). Annexin A7 (ANXA7) has been shown to regulate glutamate release. However, the role of ANXA7 in early brain injury after SAH has not been illustrated. In this study, we aimed to investigate the effect of ANXA7 knockdown in reducing the severity of early brain injury after SAH, and determine the underlying mechanisms.METHODSEndovascular perforation was performed to induce SAH in male Sprague-Dawley rats. ANXA7-siRNA was administered via intraventricular injection 5 days before SAH induction. Neurological test, evaluation of SAH grade, assessment of blood-brain barrier (BBB) permeability, measurement of brain water content, Western blot, double immunofluorescence staining, TUNEL staining, and enzyme-linked immunosorbent assay (ELISA) were performed at 24 hours of SAH induction.RESULTSANXA7 protein expression increased significantly after SAH induction and was seen mainly in neurons. High expression of ANXA7 was associated with poor neurological status. ANXA7 knockdown dramatically ameliorated early brain injury through alleviating BBB disruption and brain edema. Further investigation of the mechanism showed that inhibiting ANXA7 expression can rescue neuronal apoptosis. In addition, ANXA7 knockdown also significantly reduced glutamate release, which was consistent with a significant increase of Bcl-2 expression and decreases of Bax and cleaved caspase-3 expression.CONCLUSIONSANXA7 can induce neuronal apoptosis by affecting glutamate release in rats with SAH. Downregulating the expression of ANXA7 can significantly attenuate early brain injury after SAH. Future therapy targeting ANXA7 may be a promising new choice.

To investigate the effects of serum procalcitonin(PCT) levels for predicting the outcome of bacteria bloodstream infection in acute leukemia patients.Clinical data from 236 patients with acute leukemia accompanied by bacterial bloodstream infection during July 2014 to November 2017 were retrospectively analyzed, 236 patients were divided into 5 groups (0.05 ng/ml, 0.05-0.5 ng/ml, 0.5-2.0 ng/ml, 2.0-10.0 ng/ml and10.0 ng/ml) according to PCT concentrations.The median age of patients was 40(13-73) years old. The male 123 cases(52.1%) and female 113 cases(47.9%) in 236 patients. The incidence of infection-related dealth in 5 groups was 0%, 1.4%, 13.8%, 25.0% and 33.3%, respectively; the incidence of septic shock and other serious complications in 5 groups was 0%, 2.1%, 13.8%, 25.0%, 33.3% and 6.4%, 7.0%, 24.1%, 41.7%, 50.0%, respectively, showing the concentration dependent manner and statistically significant difference (u=2127, P=0.000; u=2234, P=0.000; u=4102, P=0.000). Further analysis showed that with the increase of PCT concentration, the cumulative incidence of septic shock, infection-related death and other serious complications was gradually increased with statistically significance (HR=2.887, P=0.000, 95%CI:1.960-4.260; HR=3.158, P=0.000, 95%CI: 2.100-4.740; HR=2.158, P=0.000, 95%CI:1.550-3.000) respectively. Increased procalcitonin level is an independent risk factor for septic shock and infection-related death (HR=2.517, P=0.000, 95%CI: 1.520-4.168; HR=2.881, P=0.000, 95%CI: 1.692-4.904)respectively.Serum procalcitonin level positively correlates with the incidence of serious bacteria bloodstream infection complications in the patients with acute leukemia. Increased procalcitonin level is an independent risk factor for septic shock and infection-related death, indicating that procalcitonin may be an important prognostic factor for infection outcome in acute leukemia patients with bacteremia.

Pro-inflammatory cytokine-induced chondrocyte apoptosis is a primary cause of cartilage destruction in the progression of rheumatoid arthritis (RA). Advanced oxidation protein products (AOPPs), a novel pro-inflammatory mediator, have been confirmed to accumulate in patients with RA. However, the effect of AOPPs accumulation on chondrocyte apoptosis and the associated cellular mechanisms remains unclear. The present study demonstrated that the plasma formation of AOPPs was enhanced in RA rats compared with normal. Then, chondrocyte were treated with AOPPs-modified rat serum albumin (AOPPs-RSA) in vitro. Exposure of chondrocyte to AOPPs activated nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and increased expression of NADPH oxidase subunits, which was mediated by receptor for advanced glycation end products (RAGE), but not scavenger receptor CD36. Moreover, AOPPs challenge triggered NADPH oxidase-dependent ROS generation which induced mitochondrial dysfunction and endoplasmic reticulum stress resulted in activation of caspase family that eventually lead to apoptosis. Lastly, blockade of RAGE, instead of CD36, largely attenuated these signals. Our study demonstrated first time that AOPPs induce chondrocyte apoptosis via RAGE-mediated and redox-dependent intrinsic apoptosis pathway in vitro. These data implicates that AOPPs may represent a novel pathogenic factor that contributes to RA progression. Targeting AOPPs-triggered cellular mechanisms might emerge as a promising therapeutic option for patients with RA.

Two-step method is used to research stress and its distribution in 64×64 InSb infrared focal plane array (IRFPA) employing finite element method. First, a small 8×8 InSb IRFPA is studied by changing indium bump diameters from 24μm to 36μm, with indium bump thickness 20μm and InSb thickness 10μm, the simulated results show that von Mises stress in InSb chip is dependent on indium bump diameters, the varying tendency is just like the letter V, here when indium bump diameters is set to 30μm, the smallest von Mises stress is achieved and its distribution in InSb chip is uniform at contacting areas. Then, InSb IRFPA array scale is doubled once again from 8×8 to 64×64 to learn the effect from array size, thus, the stress and its distribution of 64×64 InSb IRFPA is obtained in a short time. Simulation results show that von Mises stress maximum in InSb chip and Si readout integrated circuit almost do not increases with array scale, and the largest von Mises stress is located in InSb chips. Besides, stress distribution on the bottom surface of InSb chip is radiating, and decreases from core to four corners, and stress value at contacting area is smaller than those on its surrounding areas, contrary to stress distribution on top surface of InSb chip.

The purpose of this research is to explore the distribution and expression of MAP kinase phosphatase-1 (MKP-1) in cerebrospinal fluid (CSF)-contacting nucleus in depression, and provide experimental evidence to reveal the biological function and regulatory mechanisms of CSF-contacting nucleus in depression. Depression model was produced by chronic forced swimming stress (CFSS) in Sprague-Dawley (SD) rats. Intracerebroventricular injection of cholera toxin subunit B (CTb) labeled with horseradish peroxidase (CB-HRP) was used to specifically mark distal CSF-contacting nucleus. The rate of animal growth and behavioral tests including sucrose preference test (SPT) and open field test (OFT) were used to validate the model of depression. The expressions of MKP-1 and fos proteins in CSF-contacting nucleus were detected by immunofluorescence. Software Image-Pro Plus version 6.0 was used to count the positive neurons. The results showed that, the distributions of MKP-1 were found in the CSF-contacting nucleus. After 28 days of swimming, the rats in stress group had a lower growth rate, a less consumption of sucrose and lower scores of OFT compared to control group. The number of neurons double labeled with CB-HRP/fos or CB-HRP/MKP-1 in stress group was significantly higher than that in control group (P0.01). These results suggest that the CSF-contacting nucleus may be involved in the process of depression via the MKP-1.

Rationale:Intracranial ganglioneuroblastoma represents a rare subtype of primitive neuroectodermal tumor. Here, we report a hippocampal ganglioneuroblastoma and a literature review of cerebral anglioneuroblastoma is carried out.Patient concerns:We report a 16-year-old male patient presenting

Palm oil is a highly versatile commodity with wide applications in the food, cosmetics, and biofuel industries. Storage oil in the oil palm mesocarp can make up a remarkable 80% of its dry mass, making it the oil crop with the richest oil content in the world. As such, there has been an ongoing interest in understanding the mechanism of oil production in oil palm fruits. To identify the proteome changes during oil palm fruit maturation and factors affecting oil yield in oil palm fruits, we examined the proteomic profiles of oil palm mesocarps at four developing stages--12, 16, 18, and 22 weeks after pollination--by 8-plex iTRAQ labeling coupled to 2D-LC and MALDI-TOF/TOF MS. It was found that proteins from several important metabolic processes, including starch and sucrose metabolism, glycolysis, pentose phosphate shunt, fatty acid biosynthesis, and oxidative phosphorylation, were differentially expressed in a concerted manner. These increases led to an increase in carbon flux and a diversion of resources such as ATP and NADH that are required for lipid biosynthesis. The temporal proteome profiles between the high-oil-yielding (HY) and low-oil-yielding (LY) fruits also showed significant differences in the levels of proteins involved in the regulation of the TCA cycle and oxidative phosphorylation. In particular, the expression level of the β subunit of the ATP synthase complex (complex IV of the electron transport chain) was found to be increased during fruit maturation in HY but decreased in the LY during the fruit maturation. These results suggested that increased energy supply is necessary for augmented oil yield in the HY oil palm trees.

Due to greater flexibility and wider adaptability, the fractional order PIλDμ controller has been drawn more attention by more researchers. However, there is less research of improving specific dynamic performance of servo system by far. For a typical DC servo system, the fractional order PIλDμ is designed in this paper, and the improved chaotic particle swarm optimization algorithm is also used to set the parameters. At the same time, under the requirements of dual-ten index, the bandwidth of the feed forward controller and the PID controller of the DC servo system are compared, of course the comparison and analysis of the velocity and acceleration at the same bandwidth. The simulation results show that, the DC servo system of fractional order PIλDμ controller has better dynamic performance.

Rebleeding of an aneurysm is a major cause of morbidity and mortality after subarachnoid hemorrhage (SAH). Whereas numerous studies have demonstrated predictors of rebleeding and effect of systolic blood pressure variability (SBPV) on stroke, few data on the association between SBPV and rebleeding. Here, we sought to identify the effect of SBPV on rebleeding in acute aneurysmal SAH. Case–control study. From January 2010 to June 2015, 612 patients with aneurysmal SAH were enrolled in our tertiary care medical center. Main outcome measures: Consecutive patients with acute (

Integrating repetitive control and RBF neural network PID control , a novel control scheme for DC servo system is proposed for the high accuracy of Oscillating Mirrorsystem . The repetitive control is used to improve the steady-state characteristi of the control serosystem and enhance its ability to withstand the disturbance with same frequency; the RBF neural network PID control is used to enhance the ability of the control system to withstand the parameter variations and nonlinear uncertain disturbances, so the dynamic characteristic of the system can be improved. the result of Experiments show that the proposed control scheme can endow the servo system with good dynamic and static characteristics and tracking accuracy was improved,the servosystem can efficiently improve the velocity stability of Oscillating Mirror,and decrease the shocking of motor.

It is difficult for the control system to get expected effect because of factors such as time-varying and non-linear. Considering the fact, a new algorithm is put forward, in which parameters of the PID control parameters are optimized by BP and RBF nets. By using MATLAB as the simulation tool, this new PID auto-tuning algorithm is simulated and researched. The simulation results show that this algorithm has enhanced response speed and robustness.

The objective of this study was to explore the useful value of circulating galactomannan (GM) for early diagnosis of invasive aspergillosis. All 141 patients were classified as 103 patients of clinical and possible diagnosis, and 38 non-Aspergillus patients. 209 serum samples for the detection of GM by Platelia Aspergillus were collected before anti-fungal vaccine therapy. ELISA method was used in detection of GM. The results showed that (1) the sensitivity of 87.5%, specificity of 81.6%, positive prediction of 66.7% and negative prediction of 93.9% were determined by using cut-off value. According to the result of ELISA, the clinical diagnosed patients was up to 48, while the possible diagnosed patients were 55. (2) Among 62 patients with consecutive examinations of serum samples, 50 patients were successfully diagnosed and treated, while 12 patients died. A progressive reduction of GM level was found in survivors, however, the patients of poor prognosis showed higher antigen titres. It is concluded that GM test has more significance for earlier diagnosis of aspergillosis, the concentration of GM is related to prognosis of disease.

In the past, the method of reconstitution was used to investigate the interaction between metalloenzymes (containing Zn(II)) and metal ions. In this paper, electron paramagnetic resonance (EPR) has been employed to firstly study the direct interactions between Bacillus subtilis neutral proteinase (BSNP), nuclease P1 and Cu(II) ions added in aqueous solution, respectively. These results show that a dynamic equilibrium exists between the Zn(II) in the active site of native enzymes and the added Cu(II), the added Cu(II) partly replaces the Zn(II), forming Cu(II)-enzyme derivatives. As a result, the activity of the native enzymes is influenced. The influences of pH value on this kind of interaction have also been investigated, and the results demonstrate that the change of pH value has little influence on the system of nuclease P1, but has remarkable influence on BSNP. We firstly obtained the EPR spectra for Cu(II)-enzyme derivatives. In addition, the derivative of Cu(II)-BSNP exists in the solution with two different conformations (I type g(parallel)=2.34, A(parallel) (mT)=13.4; II type g(parallel)=2.25, A(parallel) (mT)=16.1), and this two conformations exchanged each other depending on pH.

A series of deletion mutants were constructed using polymerase chain reaction (PCR) to investigate the roles of luciferase N-terminal residues. The coding sequences of the first 0 (Luc0), 6 (Luc6), 7 (Luc7), 8 (Luc8), 9 (Luc9), 10 (Luc10) and 20 (Luc20) amino acids of the N-terminus were deleted and inserted into the prokaryotic expression vector pBV220. The results showed that the enzymes were completely inactivated when the first eight or more N-terminal amino acids were removed. The recombinant Luc0 and mutants Luc6 and Luc7 were purified to homogeneity by ammonium sulfate precipitation and liquid chromatography for determination of their activity and conformational changes. The activity assay showed that removal of the first six amino acids resulted in 29% loss of enzymatic activity while removal of the first seven amino acids resulted in nearly complete inactivation (with remaining activity

Sellar plasmacytoma is a rare cause of sellar lesions. Preoperative diagnosis remains a challenge. We present a 34-year-old Chinese woman with a 25-day history of headache and diplopia. A physical examination revealed incomplete left abducens nerve palsy. The initial diagnosis was invasive pituitary adenoma. The patient’s condition deteriorated suddenly the day before the arranged operating date, with the hemoglobin level declining from 113 to 70 g/L. The operation was cancelled and further studies confirmed the diagnosis of sellar solitary plasmacytoma that progressed to multiple myeloma. After undergoing radiotherapy, high-dose chemotherapy, and autologous peripheral blood stem cell transplantation, complete remission was achieved on 4 years follow-up. We reviewed the pertinent literature and reached the following conclusions: sellar plasmacytomas with development of multiple myeloma on follow-up more likely happened in men than in women; and if the sellar plasmacytoma does not compress the cranial nerve, transsphenoidal resection should be cautious because the systemic treatment with radiotherapy, chemotherapy, and autologous peripheral blood stem cell transplantation may be more effective with little invasion.

Alternating copolymers of vinyl acetate (VAC) and acrylic acid (AA) were obtained by free radical polymerization in the presence of GeCl4 and BCl3. For the GeCl4 system, the reaction rate was proportional to [initiator]1/2. Optimum rate was obtained when the molar ratio of the monomers was 1:1. The chain transfer agent CCl4 had no effect on the reaction. By means of ultra-violet spectra analysis, it was concluded that both VAC and AA formed complexes with GeCl4. ESR analysis gave us the information that salt complexed acrylic acid radical had greater cationic characteristics than uncomplexed radical. Thus the nature of alternation may be due to both complexed AA radical and activated monomer complexes.