Introducing micropores into carbon nanoparticles synthesized via a solution plasma process by thermal treatment and their charge storage properties in supercapacitors.

Carbon materials synthesized via a solution plasma process (SPP) have recently shown great potential for various applications. However, they mainly possess a meso-macroporous structure with a lack of micropores, which limits their applications for supercapacitors. Herein, carbon nanoparticles (CNPs) were synthesized from benzene via SPP and then subjected to thermal treatment at different temperatures (400, 600, 800, and 1000 °C) in an argon environment. The CNPs exhibited an amorphous phase and were more graphitized at high treatment temperatures. A small content of tungsten carbide particles was also observed, which were encapsulated in CNPs. An increase in treatment temperature led to an increase in the specific surface area of CNPs from 184 to 260 m2 g-1 through the development of micropores, while their meso-macropore structure remained unchanged. The oxygen content of CNPs decreased from 14.72 to 1.20 atom% as the treatment temperature increased due to the degradation of oxygen functionality. The charge storage properties of CNPs were evaluated for supercapacitor applications by electrochemical measurements using a three-electrode system in 1 M H2SO4 electrolyte. The CNPs treated at low temperatures exhibited an electric double layer and pseudocapacitive behavior due to the presence of quinone groups on the carbon surface. With increasing treatment temperature, the electric double layer behavior became more dominant, while pseudocapacitive behavior was suppressed due to the quinone degradation. Regarding cycling stability, the CNPs treated at high temperatures (with a lack of oxygen functionality) were more stable than those treated at low temperatures. This work highlights a way of introducing micropores into CNPs derived from SPP via thermal treatment, which could be helpful for controlling and adjusting their pore structure for supercapacitor applications.

Highly Efficient and Stable 2D/3D Heterojunction Perovskite Solar Cells by In Situ Interface Modification with [(p-Fluorophenyl)ethyl]ammonium Acetate.

2D/3D heterojunction perovskites, meaning a rationally prepared 2D capping layer on 3D perovskite films, have been demonstrated as an effective avenue for simultaneously enhancing the efficiency and stability in perovskite solar cells (PSCs). However, the mechanism of the 2D perovskite induced by organic agents is still not extensively studied. Here, we report 2D/3D heterojunction PSCs by in situ fabricating a 2D modified layer on 3D perovskite films with [(p-fluorophenyl)ethyl]ammonium acetate (FPEAAc). During the annealing process, FPEAAc melts and uniformly covers the 3D perovskite films. Then, the excess acetate salt is volatilized, eventually forming a compact 2D perovskite thin layer. On the one hand, the organic agents can effectively rivet onto the 3D perovskite surface, ensuring formation of the necessary 2D perovskites with hydrophobic FPEA+ ions. On the other hand, the reaction generates some PbI2, which passivates the defects on 3D perovskite films and improves the interface contact, significantly enhancing the open-circuit voltage (VOC) and fill factor (FF) in 2D/3D PSCs. The highest power conversion efficiency of 22.53% is achieved compared with 20.16% in 3D PSCs. The 2D/3D-heterojunction-structured PSCs modified by FPEAAc exhibit high stability, retaining about 90% of the initial device efficiency after 500 h at 85 °C and 40 ± 5% relative humidity. Our research provides a simple method to control the 2D perovskite layer formation and effectively enhance the performance and stability in 2D/3D heterojunction perovskite cells.

Diagnosis and management of adrenal insufficiency.

Adrenal insufficiency is the inadequate secretion of glucocorticoid and/or mineralocorticoid secretion from the adrenal cortex. Primary adrenal insufficiency is the result of failure of the adrenal gland and secondary adrenal insufficiency is due to a lack of stimulation via pituitary adrenocorticotropic hormone or hypothalamic corticotropin-releasing hormone. Adrenal insufficiency may cause non-specific symptoms. Early detection and testing based on clinical suspicion may prevent subsequent presentation with adrenal crisis. Once identified, a low baseline cortisol (often <100 nmol/L) alongside raised adrenocorticotropic hormone (ACTH) can be enough to diagnose primary adrenal insufficiency. However, confirmatory testing can be done using the cosyntopin (Synacthen®) stimulation test or the insulin tolerance test, which is the gold standard for secondary adrenal insufficiency. The underlying cause of adrenal insufficiency can often be identified via a strategic approach to investigation. Adrenal crisis is a life-threatening medical emergency which must be treated immediately if there is strong clinical suspicion with fluids and corticosteroids otherwise can be fatal. Patients must be educated and empowered to take control of their own medical management.

Characterization of a bioscaffold containing polysaccharide acemannan and native collagen for pulp tissue regeneration.

Dental pulp regeneration exploits tissue engineering concepts using stem cells/scaffolds/growth-factors. Extracted collagen is commonly used as a biomaterial-scaffold due to its biocompatibility/biodegradability and mimics the natural extracellular matrix. Adding biomolecules into a collagen-scaffold enhanced pulp regeneration. Acemannan, ß-(1-4)-acetylated-polymannose, is a polysaccharide extracted from aloe vera. Acemannan is a regenerative biomaterial. Therefore, acemannan could be a biomolecule in a collagen-scaffold. Here, acemannan and native collagen were obtained and characterized. The AceCol-scaffold's physical properties were investigated using FTIR, SEM, contact angle, swelling, pore size, porosity, compressive modulus, and degradation assays. The AceCol-scaffold's biocompatibility, growth factor secretion, osteogenic protein expression, and calcification were evaluated in vitro. The AceCol-scaffolds demonstrated higher hydrophilicity, swelling, porosity, and larger pore size than the collagen scaffolds (p < 0.05). Better cell-cell and cell-scaffold adhesion, and dentin extracellular matrix protein (BSP/OPN/DSPP) expression were observed in the AceCol-scaffold, however, DSPP expression was not detected in the collagen group. Significantly increased cellular proliferation, VEGF and BMP2 expression, and mineralization were detected in the AceCol-scaffold compared with the collagen-scaffold (p < 0.05). Computer simulation revealed that acemannan's 3D structure changes to bind with collagen. In conclusion, the AceCol-scaffold synergistically provides better physical and biological properties than collagen. The AceCol-scaffold is a promising material for tissue regeneration.

Genetic Diversity and Population Structure of Myanmar Rice (Oryza sativa L.) Varieties Using DArTseq-Based SNP and SilicoDArT Markers.

Myanmar is well known as a primary center of plant genetic resources for rice. A considerable number of genetic diversity studies have been conducted in Myanmar using various DNA markers. However, this is the first report using DArTseq technology for exploring the genetic diversity of Myanmar rice. In our study, two ultra-high-throughput diversity array technology markers were employed to investigate the genetic diversity and population structure of local rice varieties in the Ayeyarwady delta, the major region of rice cultivation. The study was performed using 117 rice genotypes with 7643 SNP and 4064 silicoDArT markers derived from the DArT platform. Genetic variance among the genotypes ranged from 0 to 0.753 in SNPs, and from 0.001 to 0.954 in silicoDArT. Two distinct population groups were identified from SNP data analysis. Cluster analysis with both markers clearly separated traditional Pawsan varieties and modern high-yielding varieties. A significant divergence was found between populations according to the Fst values (0.737) obtained from the analysis of molecular variance, which revealed 74% genetic variation at the population level. These findings support rice researchers in identifying useful DNA polymorphisms in genes and pinpointing specific genes conferring desirable phenotypic traits for further genome-wide association studies and parental selection for recombination breeding to enhance rice varietal development and release.

Effects of task-oriented training on upper extremity functional performance in patients with sub-acute stroke: a randomized controlled trial.

[Purpose] The present study aimed to determine the effects of a task-oriented training on paretic upper extremity functional performance in patients with subacute stroke. [Participants and Methods] Twenty-eight subacute stroke sufferers (mean age: 50.07, standard deviation 9.31 years; mean time since stroke 11.11, standard deviation 6.73 weeks) were randomly allocated to task-oriented training (n=14) or conventional exercise program (n=14) group. They were trained as a hospital-based, individualized training 1 hour a session, 5 sessions a week for 4 weeks. Wolf Motor Function Test (primary outcome), motor portion of Fugl-Meyer assessment upper extremity, and hand function domain of Stroke Impact Scale were assessed at baseline, after 2 and 4 weeks of training. [Results] All participants completed their training programs. At all post-training assessments, the task-oriented training group showed significantly more improvements in all outcomes than the conventional exercise program group. No serious adverse effects were observed during or after the training. [Conclusion] Task-oriented training produced statistically significant and clinically meaningful improvements of paretic upper extremity functional performance in patients with subacute stroke. These beneficial effects were observed after 2 weeks (10 hours) of training. Future investigation is warranted to confirm and expand these findings.

Post-stroke seizure-Do the locations, types and managements of stroke matter?

OBJECTIVE: To determine the incidence of post-stroke seizures and the associated risk factors in a government-restructured hospital in Singapore. METHODS: This retrospective study included consecutive patients (age ≥21 years) admitted to the stroke rehabilitation facility at Changi General Hospital, Singapore, between June 2008 and May 2017, with a minimum post-discharge follow-up of 6 months. Patients with known epilepsy central nervous system infection or tumor, a history of neurosurgery and or missing data were excluded from study. To determine the incidence of seizures, the patients' hospital records, including those for all initial and subsequent admissions and outpatient follow-ups, were reviewed. All prescribed medications were checked and documented. Seizures were diagnosed on the basis of clinical examination with or without electroencephalography. RESULTS: In total, 722 patients (women, 38%) with a mean age of 64 years were included. Of these, 48 (6.64%) experienced post-stroke seizures during a follow-up period of 6-108 months. The incidence of seizures was significantly higher in patients with hemorrhagic stroke (42%, p = 0.010), those with ischemic partial anterior circulation stroke (PACS) (27%, p = 0.025), those who underwent a neurosurgical procedure after stroke (p < 0.001), those with a low activated partial thromboplastin time (APTT) at admission (mean, 25.6; p = 0.015), and those using levodopa (21%, p < 0.001). Neurosurgical intervention after stroke (odds ratio [OR] 6.2, 95% confidence interval [CI] 2.9-13.1; p < 0.001), APTT (per-unit increase; OR 0.86, 95% CI 0.76-0.98; p = 0.028), and underlying ischemic heart disease (IHD; OR 2.2, 95% CI 1.08-4.60; p = 0.029) were found to be independent predictors of seizure occurrence after stroke. SIGNIFICANCE: Post-stroke seizure incidence from our study is 6.64%, with a median follow-up of 49 months. Among patients with stroke, those with underlying IHD, those who undergo a neurosurgical procedure, and those with a low APTT at admission need careful monitoring. Levodopa should be used with caution and withdrawn as soon as possible.

Role of caspases in 5-FU and selenium-induced growth inhibition of colorectal cancer cells.

BACKGROUND: The mechanisms that could explain the poor sensitivity to 5-FU in certain colorectal cancer (CRC) cells were investigated and whether or not cotreatment with low doses of selenium would offer a therapeutic benefit was explored. MATERIALS AND METHODS: Four CRC cell lines (Caco2, RKO, DLD1 and HT-29) with defined tumor signatures and seven different chemical forms of selenium were tested. RESULTS: 5-FU partially inhibited the HT-29 and RKO cells, but had a weak effect on the DLD1 and almost none on the Caco2 cells. Selenous acid and sodium selenite induced growth inhibition of the DLD1, RKO and HT-29 cells, with a marginal effect on the Caco2 cells. The Caco2 cells with mutant p53, failure to activate caspase-8, -9, -7 and -3 and with hypermethylated caspase-8 were resistant to 5-FU. Conversely, RKO cells expressing wildtype p53, proteolytically activated caspase-8, -9, -7 and -3 and unmethylated caspase-8 were more responsive to 5-FU and selenous acid-induced apoptosis. CONCLUSION: Combination treatment with selenous acid may offer an efficacious strategy to overcome 5-FU resistance in certain CRC cells.

A role for focal adhesion kinase signaling in tumor necrosis factor-alpha-dependent matrix metalloproteinase-9 production in a cholangiocarcinoma cell line, CCKS1.

We have previously reported that tumor necrosis factor-alpha (TNF-alpha) stimulation of CCKS1, a cell line established from cholangiocarcinoma with i.p. dissemination, dramatically increased matrix metalloproteinase-9 (MMP-9) production and tumor invasion. We investigated the role of focal adhesion kinase (FAK) in TNF-alpha-dependent production of MMP-9 in CCKS1 and FAK-null mouse fibroblast cells. TNF-alpha stimulation of CCKS1 or wild-type fibroblasts substantially activated FAK phosphorylation and increased MMP-9 production. In contrast, FAK-null fibroblasts could not respond well to TNF-alpha stimulation. Conditional expression of wild-type FAK in FAK-null cells restored the TNF-alpha-dependent production of MMP-9. TNF-alpha treatment activated the kinase activity of FAK and its phosphorylation especially at Y397 and Y925. Phosphorylated FAK accumulated at focal adhesions and formed a complex with growth factor receptor binding protein 2 and SOS. In contrast, Y397F FAK and Y925F FAK, whose Y397 and Y925 were replaced with phenylalanine, respectively, as well as KD FAK, whose kinase was inactivated, could not restore the MMP-9 production. In addition, small interfering RNA against FAK drastically suppressed the TNF-alpha-dependent production of MMP-9 and inhibited the TNF-alpha-dependent invasion of CCKS1. Taken together, our results suggest the pivotal role of FAK in TNF-alpha-dependent production of MMP-9 and subsequent activation of tumor invasion.

Secretion of matrix metalloproteinase-9 by the proinflammatory cytokine, IL-1beta: a role for the dual signalling pathways, Akt and Erk.

BACKGROUND: Matrix metalloproteinases including MMP-9 mediate matrix destruction during chronic inflammatory diseases such as arthritis and atherosclerosis. MMP-9 up-regulation by inflammatory cytokines involve interactions between several transcription factors including activator protein-1 and NFkappaB. The upstream regulatory pathways are less well understood. RESULTS: To search for the mechanism of tissue destruction in the process of inflammatory disorders, we investigated the signalling pathway critical for the activation of MMP-9 expression and secretion by IL-1beta. Treatment of Balb 3T3 cells with IL-1beta activated MMP-9 transcription and subsequent secretion in a time- and dose-dependent manner. Concomitantly, IL-1beta treatment of cells activated phosphorylation of Akt, Erk and p38. Treatment of cells with either LY294002, a PI3K inhibitor, or expression of a dominant negative form of Akt drastically suppressed the IL-1beta-dependent secretion of MMP-9. Pretreatment of cells with a MEK1 inhibitor, U0126, also strongly inhibited IL-1beta-dependent secretion of MMP-9. In contrast, pre-treatment with a specific p38 kinase inhibitor, SB203580, had no effect on IL-1beta-dependent secretion of MMP-9. In addition, cells expressing constitutively active form of Akt or MEK1 showed no clear activation of MMP-9 secretion, whereas these cells responded well to IL-1beta treatment. However, co-transfection of cells with both active Akt and MEK1 was sufficient to induce MMP-9 secretion without stimulation with IL-1beta. CONCLUSION: Taken together, our results suggest that IL-1beta stimulation of cells activates MMP-9 secretion by the activation of the dual signalling pathways, the PI3K-Akt and MEK1-Erk and constitutive activation of these pathways were sufficient to induce MMP-9 secretion.

Cysteine residues in the C-terminal lobe of Src: their role in the suppression of the Src kinase.

To evaluate the function of cysteine residues of the Src kinase, we constructed a series of Src mutants in which some of cysteines were replaced to alanines. With these mutants, we studied the effect of SH-alkylating agents, N-[p-(2-benzimidazolyl)phenyl] maleimide (BIPM) and N-(9-acridinyl) maleimide (NAM), on their kinase activity. Of 10 cysteine residues scattered over v-Src, either a single mutation at Cys520 or multiple mutations at the four clustered cyteines, Cys483, Cys487, Cys496 and Cys498, yielded clear resistance to the treatment with 10 microM BIPM or 1 microM NAM. In contrast, other cysteines including those in the SH2 domain and those in the catalytic cleft of the kinase domain were dispensable for the inactivation by BIPM and NAM. Similarly, deletion of SH2 and SH3 did not confer the resistance to v-Src, suggesting the inactivation by the SH-alkylating agents is SH2/SH3-independent. Although Cys520-mutated v-Src was resistant to 1 microM NAM, it was inactivated by 5 microM NAM. However, combined mutation including all of Cys483, Cys487, Cys496, Cys498 and Cys520 yielded clear resistance to 5 microM NAM. Among these mutants, those with double mutations in the four clustered cysteines yielded a temperature sensitive phenotype in the transfected cells, whereas Cys520 did not, suggesting that Cys520 has, at least in part, a discrete function. In contrast to v-Src, c-Src, which lacks cysteine at position 520, was resistant to 1 microM NAM but sensitive to 5 microM NAM. While replacement of Phe520 of c-Src to cysteine made it sensitive to 1 microM NAM, double mutation in clustered cysteines again yielded resistance to 5 microM NAM. Taken together, our results strongly suggest that the multiple cysteine residues clustered at the end of the C-terminal lobe are critical for the inhibition by the SH-alkylating agents and, thereby, have an allosteric repressor effect on the catalytic activity of Src in a SH2-phosphoTyr527 independent manner.

A role for SHPS-1/SIRPalpha1 in IL-1beta- and TNFalpha-dependent signaling.

We investigated the role of SHPS-1/SIRPalpha1 in IL-1beta- and TNFalpha-dependent signaling that leads to the activation of Erk 1/2 and Akt. Treatment of Balb3T3 cells with IL-1beta or TNFalpha activated tyrosine phosphorylation of SHPS-1, its association with SHP-2 and the phosphorylation of Erk 1/2 and Akt. PP1, a specific inhibitor for the Src family protein tyrosine kinases, strongly inhibited tyrosine phosphorylation of SHPS-1 and complex formation of SHPS-1 with SHP-2 by IL-1beta. In addition, PP1 substantially inhibited the IL-2beta- and TNFalpha-dependent activation of Erk 1/2 and Akt. Exogenous expression of either SHPS-1 mutants that lack SHP-2 binding function or a dominant negative mutant of SHP-2 markedly inhibited the activation of Erk 1/2 and Akt by IL-1beta, whereas wild type SHPS-1 did not. Moreover, IL-1beta-stimulation induced association of SHPS-1 with IL-1RAcP, a second subunit of IL-1 receptor, whereas expression of SHPS-1 mutant that lack SHP-2 binding function clearly blocked the association and tyrosine phosphorylation of endogenous SHPS-1. Taken together, our results strongly suggest that activation of Erk 1/2 and Akt by proinflammatory cytokines requires tyrosine phosphorylation of SHPS-1 and subsequent association of SHPS-1 with SHP-2.

Hyaluronan-CD44s signaling regulates matrix metalloproteinase-2 secretion in a human lung carcinoma cell line QG90.

We investigated the production of matrix metalloproteinase (MMP) by hyaluronan(HA) stimulation in a human cancer cell line, QG90, that expresses a large amount of CD44s, a HA receptor. Treatment of QG90 with HA strongly activated MMP-2 secretion in a time- and dose-dependent manner. We found that expression of antisense CD44s in QG90 cells substantially inhibited the HA-dependent secretion of MMP-2, whereas overexpression of full-length CD44s augmented the HA-dependent secretion of MMP-2. In addition, pretreatment of cells with the neutralizing anti-CD44 antibody significantly inhibited both the HA-dependent MMP-2 secretion and the HA-dependent activation of mitogen-activated protein kinase in a dose-dependent manner. Similarly, treatment of cells with a Ras farnesyltransferase inhibitor, manumycin A, strongly inhibited the HA-dependent MMP-2 secretion. Moreover, in vitro invasiveness of QG90 and its activation by HA were clearly suppressed by the expression of antisense CD44s. In addition, treatment of cells with anti-CD44, a mitogen-activated protein/extracellular signal-regulated kinase kinase 1 inhibitor, PD98059, or phosphatidylinositol 3'-kinase inhibitors, wortmannin and LY294002, effectively blocked the HA-dependent activation of the invasiveness. In contrast, overexpression of full-length CD44 substantially activated the invasiveness of QG90. Taken together, HA-CD44s signaling plays a key role in the HA-dependent secretion of MMP-2 and, hence, in the invasiveness of QG90 cells.

A role for focal adhesion kinase in hyluronan-dependent MMP-2 secretion in a human small-cell lung carcinoma cell line, QG90.

Hyluronan (HA), a nonsulfated high-molecular mass glycoaminoglycan, has been assigned as a clinical marker for the progression of various tumors. We found that HA stimulation of QG90, a cell line derived from human small-cell lung carcinoma, activates the secretion of matrix metalloproteinase-2 (MMP-2) in a focal adhesion kinase (FAK)-dependent manner. HA stimulation of QG90 cells activated MMP-2 secretion in a time-dependent manner. Larger sizes of HA seemed to have higher activities than smaller size one in MMP-2 secretion. Under HA stimulation, tyrosine phosphorylation of cellular proteins including FAK was activated. By use of antisense oligonucleotide to FAK, we found that FAK signaling was required for the activation of MMP-2 secretion and for the sustained activation of MAP kinase by HA treatment. These results strongly suggest that FAK-MAPK signaling is involved, at least in part, in HA-dependent activation of MMP-2 secretion in QG90 cells.