CXCR4-Mediated Codelivery of FLT3 and BCL-2 Inhibitors for Enhanced Targeted Combination Therapy of FLT3-ITD Acute Myeloid Leukemia.

Acute myeloid leukemia (AML) is often associated with poor prognosis and survival. Small molecule inhibitors, though widening the treatment landscape, have limited monotherapy efficacy. The combination therapy, however, shows suboptimal clinical outcomes due to low bioavailability, overlapping systemic toxicity and drug resistance. Here, we report that CXCR4-mediated codelivery of the BCL-2 inhibitor venetoclax (VEN) and the FLT3 inhibitor sorafenib (SOR) via T22 peptide-tagged disulfide cross-linked polymeric micelles (TM) achieves synergistic treatment of FLT3-ITD AML. TM-VS with a VEN/SOR weight ratio of 1/4 and T22 peptide density of 20% exhibited an extraordinary inhibitory effect on CXCR4-overexpressing MV4-11 AML cells. TM-VS at a VEN/SOR dosage of 2.5/10 mg/kg remarkably reduced leukemia burden, prolonged mouse survival, and impeded bone loss in orthotopic MV4-11-bearing mice, outperforming the nontargeted M-VS and oral administration of free VEN/SOR. CXCR4-mediated codelivery of BCL-2 and FLT3 inhibitors has emerged as a prospective clinical treatment for FLT3-ITD AML.

Antibody-Mediated Nanodrug of Proteasome Inhibitor Carfilzomib Boosts the Treatment of Multiple Myeloma.

Multiple myeloma (MM) is the second most common hematological malignancy. For relapsed and refractory MM, a proteasome inhibitor, carfilzomib (CFZ), has become one of the few clinical options. CFZ suffers, nevertheless, metabolic instability and poor bioavailability and may induce severe cardiovascular and renal adverse events. Here, we report that daratumumab (Dar)-decorated polypeptide micelles (Dar-PMs) mediate the targeted delivery of CFZ to CD38-positive MM, effectively boosting its anti-MM efficacy. CFZ-loaded Dar-PMs (Dar-PMs-CFZ) exhibited an average diameter of ca. 80 nm and Dar density-dependent cell endocytosis and anti-MM activity, in which over 6-fold greater inhibitory effect to LP-1 and MM.1S MM cells than nontargeted PMs-CFZ control was achieved at a Dar density of 3.2 (Dar3.2-PMs-CFZ). Interestingly, Dar3.2-PMs-CFZ markedly enhanced the growth inhibition of orthotopic LP-1 MM in mice and significantly extended the median survival time compared with PMs-CFZ and free CFZ (95 days vs 60 and 54 days, respectively). In line with its high MM targetability and anti-MM efficacy, Dar3.2-PMs-CFZ revealed little toxic effects and effectively prevented osteolytic lesions. The antibody-targeted nanodelivery of a proteasome inhibitor appears to be an appealing strategy to treat multiple myeloma.

Removal and Recovery of Gaseous Elemental Mercury Using a Cl-Doped Protonated Polypyrrole@MWCNTs Composite Membrane.

Due to the restrictions on mercury mining, recovering the mercury from mercury-containing waste is attracting increasing attention. This study successfully achieved the removal and recovery of gaseous elemental mercury (Hg0) by using membrane technology. A novel composite membrane of Cl-doped protonated polypyrrole-coated multiwall carbon nanotubes (Cl-PPy@MWCNTs) was fabricated in which MWCNTs acted as the framework to support the active component Cl-PPy. The morphology, structure, and composition of the prepared membranes were determined by field emission scanning electron microcopy, energy-dispersive spectroscopy, X-ray photoelectron spectroscopy, Fourier-transform infrared spectroscopy, etc. The composite membrane exhibited an excellent performance in Hg0 removal (97.3%) at a high space velocity of 200,000 h-1. The dynamical adsorption capacity of Hg0 was 3.87 mg/g when the Hg0 breakthrough reached 10%. The adsorbed Hg0 could be recovered/enriched via a leaching process using acidic NaCl solution; meanwhile, the membrane was regenerated. The recovered mercury was identified in the form of Hg2+, with a recovery efficiency of over 99%. Density functional theory calculations and mechanism analysis clarified that the electrons of Hg0 transported to the delocalized electron orbits of protonated PPy and then combined with Cl- to form Hg2Cl2/HgCl2. Finally, we first demonstrated that the analogous protonated conductive polymers (e.g., polyaniline) also possessed good Hg0 removal ability, implying that such species may offer more outstanding answers and attract attention in future.

Two occurrences of delayed epidural hematoma in different areas following decompressive craniectomy for acute subdural hematoma in a single patient: a case report.

BACKGROUND: Delayed epidural hematoma (DEH) following evacuation of traumatic acute subdural hematoma (ASDH) or acute epidural hematoma (EDH) is a rare but devastating complication, especially when it occurs sequentially in a single patient. CASE PRESENTATION: A 19-year-old man who developed contralateral DEH following craniotomy for evacuation of a traumatic right-side ASDH and then developed a left-side DEH of the posterior cranial fossa after craniotomy for evacuation of the contralateral DEH. He was immediately returned to the operating room for additional surgeries and his neurological outcome was satisfactory. CONCLUSIONS: Although DEH occurring after evacuation of ASDH or acute EDH is a rare event, timely recognition is critical to prognosis.

Management of screwdriver-induced penetrating brain injury: a case report.

BACKGROUND: Penetrating brain injury (PBI) can be caused by several objects ranging from knives to chopsticks. However, an assault with long and electric screwdriver is a peculiar accident and is relatively rare. Because of its rarity, the treatments of such injury are complex and nonstandardized. CASE PRESENTATION: We presented a case of a 54-year-old female who was stabbed with a screwdriver in her head and accompanied by loss of consciousness for 1 h. Computer tomography (CT) demonstrated that the screwdriver passed through the right zygomatic bone to posterior cranial fossa. Early foreign body removal and hematoma evacuation were performed and the patient had a good postoperative recovery. CONCLUSIONS: In this study, we discussed the clinical presentation and successful management of such a unique injury caused by a screwdriver. Our goal is to demonstrate certain general management principles which can improve patient outcomes.

A theoretical study on toluene oxidization by OH radical.

Toluene, a prominent member of volatile organic compounds (VOCs), exerts a substantial adverse influence on both human life and the environment. In the context of advanced oxidation processes, the ·OH radical emerges as a highly efficient oxidant, pivotal in the elimination of VOCs. This study employs computational quantum chemistry methods (G4MP2//B3LYP/6-311++G(d,p)) to systematically investigate the degradation of toluene by ·OH radicals in an implicit solvent model, and validates the rationale of choosing a single-reference method using T1 diagnostics. Our results suggest three possible reaction mechanisms for the oxidation of toluene by ·OH: firstly, the phenyl ring undergoes a hydrogen abstraction reaction followed by direct combination with ·OH to form cresol; secondly, ·OH directly adds to the phenyl ring, leading to ring opening; thirdly, oxidation of sidechain to benzoic acid followed by further addition and ring opening. The last two oxidation pathways involve the ring opening of toluene via the addition of ·OH, significantly facilitating the process. Therefore, both pathways are considered feasible for the degradation of toluene. Subsequently, the UV-H2O2 system was designed to induce the formation of ·OH for toluene degradation and to identify the optimal reaction conditions. It was demonstrated that ·OH and 1O2 are the primary active species for degrading toluene, with their contribution ranking as ·OH > 1O2. The intermediates in the mixture solution after reactions were characterized using GC-MS, demonstrating the validity of theoretical predictions. A comparative study of the toluene consumption rate revealed an experimental comprehensive activation energy of 10.33 kJ/mol, which is consistent with the preliminary activation energies obtained via theoretical analysis of these three mechanisms (0.56 kJ/mol to 13.66 kJ/mol), indicating that this theoretical method can provide a theoretical basis for experimental studies on the oxidation of toluene by ·OH.

Pathological features and molecular signatures of early olfactory dysfunction in 3xTg-AD model mice.

BACKGROUND: Olfactory dysfunction is known to be an early manifestation of Alzheimer's disease (AD). However, the underlying mechanism, particularly the specific molecular events that occur during the early stages of olfactory disorders, remains unclear. METHODS: In this study, we utilized transcriptomic sequencing, bioinformatics analysis, and biochemical detection to investigate the specific pathological and molecular characteristics of the olfactory bulb (OB) in 4-month-old male triple transgenic 3xTg-AD mice (PS1M146V/APPSwe/TauP301L). RESULTS: Initially, during the early stages of olfactory impairment, no significant learning and memory deficits were observed. Correspondingly, we observed significant accumulation of amyloid-beta (Aß) and Tau pathology specifically in the OB, but not in the hippocampus. In addition, significant axonal morphological defects were detected in the olfactory bulb, cortex, and hippocampal brain regions of 3xTg-AD mice. Transcriptomic analysis revealed a significant increase in the expression of neuroinflammation-related genes, accompanied by a significant decrease in neuronal activity-related genes in the OB. Moreover, immunofluorescence and immunoblotting demonstrated an activation of glial cell biomarkers Iba1 and GFAP, along with a reduction in the expression levels of neuronal activity-related molecules Nr4a2 and FosB, as well as olfaction-related marker OMP. CONCLUSION: In sum, the early accumulation of Aß and Tau pathology induces neuroinflammation, which subsequently leads to a decrease in neuronal activity within the OB, causing axonal transport deficits that contribute to olfactory disorders. Nr4a2 and FosB appear to be promising targets for intervention aimed at improving early olfactory impairment in AD.

Integrated transcriptomics reveals the brain and blood biomarkers in Alzheimer's disease.

BACKGROUND: The systematic molecular associations between the peripheral blood cells and brain in Alzheimer's disease (AD) remains unclear, which hinders our understanding of AD pathological mechanisms and the exploration of new diagnostic biomarkers. METHODS: Here, we performed an integrated analysis of the brain and peripheral blood cells transcriptomics to establish peripheral biomarkers of AD. By employing multiple statistical analyses plus machine learning, we identified and validated multiple regulated central and peripheral network in patients with AD. RESULTS: By bioinformatics analysis, a total of 243 genes were differentially expressed in the central and peripheral systems, mainly enriched in three modules: immune response, glucose metabolism and lysosome. In addition, lysosome related gene ATP6V1E1 and immune response related genes (IL2RG, OSM, EVI2B TNFRSF1A, CXCR4, STAT5A) were significantly correlated with Aß or Tau pathology. Finally, receiver operating characteristic (ROC) analysis revealed that ATP6V1E1 showed high-diagnostic potential for AD. CONCLUSION: Taken together, our data identified the main pathological pathways in AD progression, particularly the systemic dysregulation of the immune response, and provided peripheral biomarkers for AD diagnosis.

A global genomic view on LNX siRNA-mediated cell cycle arrest.

LNX protein is the first described PDZ domain-containing member of the RING finger-type E3 ubiquitin ligase family. Studies have approved that LNX could participate in signal transduction, such as Notch pathway, and play an important role in tumorigenesis. In this study, we found that down-regulation of LNX resulted in G0/G1 cell cycle arrest in G0/G1 phase in HEK293 cells. To explore the molecular mechanism of this phenomenon, we employed expression microarray to comparatively analyze the genome-wide expression between the LNX-knockdown cells and the normal cells. We also used quantitative real-time PCR to further confirm the differential expression patterns of 25 transcripts involved in cell cycle. Combined with known information about genic functions, signal pathways and cell cycle machinery, we analyzed the role of endogenous LNX in cell cycle. The results suggest that down-regulation of LNX could result in cell cycle arrest in G0/G1 phase through inhibition of ß-catenin, MAPK, NFκB, c-Myc-dependent pathway and activation of p53, TGF-ß-dependent pathway. This study provides new perspectives on LNX's pleiotropic activities, especially its essential role in cell proliferation and cell cycle.

Cellular and molecular mechanisms of photodynamic hypericin therapy for nasopharyngeal carcinoma cells.

Hypericin-mediated photodynamic therapy (HY-PDT) has become a potential treatment for tumors and nonmalignant disorders. Some studies reported that HY-PDT could lead to apoptosis in some carcinoma cells. However, the molecular mechanism of HY-PDT remains unknown. In this study, we evaluated the molecular mechanisms of hypericin associated with light-emitting diode irradiation on the poorly differentiated human nasopharyngeal carcinoma cell line CNE-2 in vitro. To comprehensively understand the effects of HY-PDT on CNE-2 cells, we detected cell viability, cell cycle, apoptosis, intracellular glutathione content, and intracellular caspase (caspase-9, caspase-3, and caspase-8) activity. Furthermore, we performed genome-wide expression analysis via microarrays at different time points in response to HY-PDT, and we found that differentially expressed genes were highly enriched in the pathways related to reactive oxygen species generation, mitochondrial activity, DNA replication and repair, cell cycle/proliferation, and apoptosis. These results were consistent with our cytology test results and demonstrated that caspase-dependent apoptosis occurred after HY-PDT. Taken together, both cellular and molecular data revealed that HY-PDT could inhibit the growth of CNE-2 cells and induce their apoptosis.

LNX (Ligand of Numb-protein X) interacts with RhoC, both of which regulate AP-1-mediated transcriptional activation.

LNX (Ligand of Numb-protein X) was originally isolated as a binding partner to the cell-fate Determinant Numb during development, and then identified to act as a RING finger-type E3 ubiquitin ligase for the ubiquitylation and degradation of Numb. LNX contains 4 PDZ domains which are proved to play a central role in organizing diverse cell signaling assemblies. A yeast two-hybrid screening was used to identify LNX as a potential binding partner for RhoC. RhoC, a member of the Ras family of small GTPases, promotes reorganization of the actin cytoskeleton and regulation of cell shape, attachment, and motility. The interaction between LNX and RhoC in mammalian cells was identified by co-immunoprecipitation assays, and the efficient binding required the first PDZ domain of LNX. LNX and RhoC were further colocalized with each other in mammalian cells, in which RhoC changed its sublocalization from cytoplasm to nucleus when co-transferred with LNX. Furthermore, co-expression of RhoC reduced the transcriptional activity of AP-1, which was up-regulated by over-expression of LNX alone. These results suggest that LNX and RhoC might be part of a larger protein complex that would have important functions in signaling transduction about regulating the transcriptional activities of AP-1.

Grb10 interacts with Bim L and inhibits apoptosis.

Bim is a proapoptotic member of the Bcl-2 family and is primarily involved in the regulation of the intrinsic apoptotic pathway. However, the detail of regulation of Bim's proapoptotic activity has not been clarified yet. Using Bim L as bait, we screened a human fetal cDNA library for interacting proteins and identified Grb10 as an interactor. This interaction was verified by co-immunoprecipitation and intracellular co-localization studies. The potential segment of Bim L that binds Grb10 was identified via a yeast mating test. Grb10 interacted with the DBD (dynein binding domain) of Bim and inhibited apoptosis triggered by overexpression of DBD containing Bim isoforms. The putative phosphorylation sites on DBD of Bim play a role for the anti-proapoptotic activity of Grb10. Our results suggest that Grb10 interacts with Bim L and inhibits its proapoptotic activity in a phosphorylation-dependant manner.

Expression, purification and characterization of human ubiquitin-activating enzyme, UBE1.

UBE1 plays an important role in the first step of ubiquitin-proteasome pathway to activate ubiquitin. Both the structure and biochemical property research of human UBE1 protein, and the activity analysis of those enzymes which are related with ubiquitination pathway, are based on high purity of UBE1 protein. To obtain human UBE1 protein, the full length of human UBE1 was expressed in E. coli and purified by Ni-NTA superflow sepharose and strep-tactin sepharose which based on UB-UBE1 high-energy thioester bonded intermediate complex. It was demonstrated that purified UBE1 could activate and conjugate UB to ubiquitin-conjugating enzyme E2s. The purified large amount of UBE1 could be used for in vitro studies of ubiquitin pathway and structural studies.

Selection of reliable reference genes for gene expression study in nasopharyngeal carcinoma.

AIM: To construct a system for selecting reference genes (RGs) and to select the most optimal RGs for gene expression studies in nasopharyngeal carcinoma (NPC). METHODS: The total RNAs from 20 NPC samples were each labeled with Cy5-dUTP. To create a common control, the total RNA from 15 nasopharyngeal phlogistic (NP) tissues was mixed and labeled via reverse transcription with Cy3-dUTP. cDNA microarrays containing 14 112 genes were then performed. A mathematical approach was constructed to screen stably expressed genes from the microarray data. Using this method, three genes (YARS, EIF3S7, and PFDN1) were selected as candidate RGs. Furthermore, 7 commonly used RGs (HPRT1, GAPDH, TBP, ACTB, B2M, G6PDH, and HBB) were selected as additional potential RGs. Real-time PCR was used to detect these 10 candidate genes' expression levels and the geNorm program was used to find the optimal RGs for NPC studies. RESULTS: On the basis of the 10 candidate genes' expression stability level, geNorm analysis identified the optimal single RG (YARS or HPRT1) and the most suitable set of RGs (HPRT1, YARS, and EIF3S7) for NPC gene expression studies. In addition, this analysis determined that B2M, G6PDH, and HBB were not appropriate for use as RGs. Interestingly, ACTB was the least stable RG in our study, even though previous studies had indicated that it was one of the most stable RGs. Three novel candidate genes (YARS, EIF3S7, and PFDN1), which were selected from microarray data, were all identified as suitable RGs for NPC research. A RG-selecting system was then constructed, which combines microarray data analysis, a literature screen, real-time PCR, and bioinformatic analysis. CONCLUSION: We construct a RG-selecting system that helps find the optimal RGs. This process, applied to NPC research, determined the single RG (YARS or HPRT1) and the set of RGs (HPRT1, YARS, and EIF3S7) that are the most suitable internal controls.

Risk Factors for Outcomes After Microvascular Decompression for Trigeminal Neuralgia.

BACKGROUND: Microvascular decompression (MVD) has been the most effective long-term surgical treatment of trigeminal neuralgia (TN). However, the risk factors for poor pain control after MVD are not fully understood. METHODS: A total of 184 patients with typical TN who had undergone MVD at our institution from January 3, 2008 to January 3, 2016 were enrolled in the present study. The data were collected from the electronic operative records and case notes and retrospectively analyzed. Patients were followed up at the outpatient department or by telephone at a minimum of 3 months and a maximum of 48 months postoperatively. RESULTS: Of the 184 patients enrolled in the present study, 72.3% had had freedom from pain after MVD and 27.7% had experienced poor pain control at the follow-up examinations (minimum, 3 months; maximum, 48 months). The risk factors for poor pain control after MVD using binary logistic regression and receiver operating characteristic curve analysis included younger age (odds ratio [OR], 0.90; 95% confidence interval [CI], 0.82-0.99; P = 0.028; area under the curve [AUC], 0.774), poor preoperative pain control (Barrow Neurological Institute score >IV; OR, 52.03; 95% CI, 6.44-420.16; P < 0.001; AUC, 0.858), intraoperatively detected multivessel compression (OR, 2.49; 95% CI, 3.10-46.59, P < 0.001; AUC, 0.871). Furthermore, combined compression of the superior cerebellar artery and petrosal vein was an independent risk factor predicting a poor outcome after MVD (OR, 5.69; 95% CI, 33.78-2579.03; P < 0.001; AUC, 0.812). CONCLUSIONS: Younger patients with TN had worse long-term pain outcomes after MVD. The additional factors associated with postoperative recurrence included poor preoperative pain control (Barrow Neurological Institute score >IV) and multivessel compression. Furthermore, combined compression of the superior cerebellar artery and petrosal vein was associated with worse outcomes.

Global gene expression analysis reveals reduced abundance of putative microRNA targets in human prostate tumours.

BACKGROUND: Recently, microRNAs (miRNAs) have taken centre stage in the field of human molecular oncology. Several studies have shown that miRNA profiling analyses offer new possibilities in cancer classification, diagnosis and prognosis. However, the function of miRNAs that are dysregulated in tumours remains largely a mystery. Global analysis of miRNA-target gene expression has helped illuminate the role of miRNAs in developmental gene expression programs, but such an approach has not been reported in cancer transcriptomics. RESULTS: In this study, we globally analysed the expression patterns of miRNA target genes in prostate cancer by using several public microarray datasets. Intriguingly, we found that, in contrast to global mRNA transcript levels, putative miRNA targets showed a reduced abundance in prostate tumours relative to benign prostate tissue. Additionally, the down-regulation of these miRNA targets positively correlated with the number of types of miRNA target-sites in the 3' untranslated regions of these targets. Further investigation revealed that the globally low expression was mainly driven by the targets of 36 specific miRNAs that were reported to be up-regulated in prostate cancer by a miRNA expression profiling study. We also found that the transcript levels of miRNA targets were lower in androgen-independent prostate cancer than in androgen-dependent prostate cancer. Moreover, when the global analysis was extended to four other cancers, significant differences in transcript levels between miRNA targets and total mRNA backgrounds were found. CONCLUSION: Global gene expression analysis, along with further investigation, suggests that miRNA targets have a significantly reduced transcript abundance in prostate cancer, when compared with the combined pool of all mRNAs. The abnormal expression pattern of miRNA targets in human cancer could be a common feature of the human cancer transcriptome. Our study may help to shed new light on the functional roles of miRNAs in cancer transcriptomics.

TP53 Arg72Pro polymorphism and lung cancer risk: a meta-analysis.

No clear consensus has been reached on the TP53 Arg72Pro polymorphism (G12139C) and lung cancer risk. Thus, a meta-analysis was conducted to summarize the possible association. There was no statistical association between 12139C (Pro allele) and lung cancer risk in Caucasians compared with 12139G allele. However, the association was observed in all subjects (9,387 patients and 9,922 controls, p=0.04, OR=1.08, 95% CI 1.00-1.17), as well as in Asians (p=0.0004, OR=1.14, 95% CI 1.06-1.22). The association was also found in Asians under recessive genetic model (p<0.00001, OR=1.37, 95% CI 1.20-1.57) and homozygote comparison (CC vs. GG) (p<0.0001, OR=1.34, 95% CI 1.16-1.56). 12139C allele might increase the lung adenocarcinoma risk compared with 12139G allele (p=0.01, OR=1.11, 95% CI 1.02-1.21), and the effect was also found under recessive genetic model (p=0.003, OR=1.28, 95% CI 1.09-1.50) and homozygote comparison (CC vs. GG) (p=0.007, OR=1.28, 95% CI 1.07-1.52). There was an elevated association between the 12139C and the stage I lung cancer under dominant genetic model (p=0.04, OR=1.48, 95% CI 1.02-2.16), but no association was observed in other stages. No association of smoking was found between 12139C allele and lung cancer under recessive genetic model. Our result indicated that 12139C might increase the risk of lung cancer under recessive genetic model in adenocarcinoma, in Asians, and in lung cancer stage I. More studies stratified for lung cancer stage-genotyping interaction should be performed to clarify the role of TP53 Arg72Pro polymorphism in the development of lung cancer.

Crystallization and preliminary X-ray analysis of the splice variant of human ankyrin repeat and suppressor of cytokine signaling box protein 9 (hASB9-2).

Human ankyrin repeat and suppressor of cytokine signaling box protein 9 (hASB9), a subunit of an Elongin C-cullin-SOCS box (ECS) E3 ubiquitin ligase complex, is believed to be involved in specific substrate-recognition for ubiquitination and degradation. In fact, this specific substrate-recognition is determined by the ankyrin repeats of hASB9 protein. Here, we have cloned and overexpressed the hASB9-2, the splice variant of hASB9 with only one ankyrin repeat domain, as a 6His-tagged recombinant protein in Escherichia coli. The purified hASB9-2 protein was crystallized by the hanging-drop vapor-diffusion technique and diffracted to 2.2A resolution. The data showed that the cubic hASB9-2 crystal belongs to space group P4(3)32 with unit-cell parameters (a=b=c=129.25A, alpha=beta=gamma=90 degrees). An asymmetric unit in the crystal was assumed to contain one protein molecule giving the Matthews Coefficient factor of 2.81 and the solvent content of 56.3%.

Stereotactic Catheter Drainage Versus Conventional Craniotomy for Severe Spontaneous Intracerebral Hemorrhage in the Basal Ganglia.

Intracerebral hemorrhage (ICH) is one of the most devastating forms of cerebrovascular pathology. However, its treatment remains a matter of debate among neurosurgeons and neurologists. The study was to explore the efficacy of minimally invasive surgery (stereotactic catheter drainage, SCD) for patients with severe intracerebral hemorrhage (Glasgow Coma Scale, GCS) score ≤ 8 and hematoma volume ≥ 30 cm3) and to determine predisposing factors for good clinical outcome. A total of 75 patients with severe ICH were included in this retrospective study. Patients were assigned to the SCD group (n=38) or the conventional craniotomy group (n=37). Patients were followed up for 12 months postoperatively, and their clinical parameters were compared. During the operation, the SCD group exhibited a lower bleeding volume (p<0.001) and shorter operating time (p<0.001) than the conventional craniotomy group. For postoperative efficacy, the rates of pneumonia and tracheotomy were lower (p=0.002 and p=0.027, respectively), and the duration of hospital and neurosurgery intensive care unit (NSICU) in days were significantly shorter in the SCD group (p=0.046 and p=0.047, respectively). Furthermore, patients in the SCD group showed improved modified Rankin Scale (mRS) scores at discharge (p<0.018) and at 12-month follow up (p<0.001). Predisposing factors for good clinical outcomes were hematoma volume (<50 cm3, 95% confidence interval (CI): 1.043-1.956, p<0.046), initial GCS score (>6, 95% CI: 3.248-187.466, p<0.001), hypertension (none, 95% CI: 1.440-2.922, p<0.001), and treatment modality (SCD, 95% CI: 1.422-3.226, p<0.001). Taken together, SCD surgery is safe and effective in patients with severe ICH and has fewer complications and better clinical outcomes than conventional craniotomy.

Combustion behavior, emission characteristics of SO2, SO3 and NO, and in situ control of SO2 and NO during the co-combustion of anthracite and dried sawdust sludge.

The combustion behaviors of anthracite and dried sawmill sludge (DSS) were studied using thermogravimetric analysis (TGA) and derivative thermogravimetric analysis (DTG). DSS was found to be a promoter for anthracite combustion, the addition of DSS in anthracite decreased the burnout temperature and time. But DSS caused the rapid releases of SO2 and NO in the initial combustion stage. In overall, the increasing of DSS significantly decreased the emission factor of SO2 from 13.42 ±â€¯1.80 to 0.31 ±â€¯0.08 g/kg; while the emission factor of NO was not obviously changed and stable at 0.7-0.8 g/kg in all cases. The oxygen-rich atmosphere was helpful for the rapid and sufficient combustion of blend; the oxygen-lean atmosphere delayed the combustion process and slowed down the releases of SO2 and NO. The increasing combustion temperature improved the anthracite combustion, and the emission factors of SO2 and NO were all increased with the temperature increasing. 900 °C was found to be the best combustion temperature for NO generation. SO3 was detected in the combustion of anthracite under 21% and 30% of O2. Two promising ways for control of SO2 and NO were provided: 1) urea-fuel mixture combustion combined with the post-combustion wet absorption by Na2CO3; 2) post-combustion wet absorption by NaClO/Na2CO3. The removal efficiencies of SO2 and NO could reach 100% and over 95% respectively. The removal products were determined as sulfate, sulfite and nitrate by IC, with no toxic byproducts being produced.