Role Of OS Research Articles

ANK1 inhibits malignant progression of osteosarcoma by promoting ferroptosis

PurposeOsteosarcoma (OS) is a primary bone tumor with high malignancy and poor prognosis. Ferroptosis plays a crucial role in OS. This study aimed to evaluate the effects of Ankyrin 1 (ANK1) on OS and to investigate its specific mechanisms.MethodsMicroarray datasets related to “osteosarcoma” were selected for this study. Relevant hub genes in OS were identified through bioinformatics analysis. Transfected U-2OS and MG-63 cells were used for in vitro experiments. The effects of ANK1 overexpression on cell viability, migration, and invasion were determined through CCK-8, wound healing, and transwell assays. An OS mouse model was established for the in vivo experiments. Hematoxylin-eosin staining and immunohistochemistry were conducted to observe the histological effects of ANK1 overexpression on mouse tumors. TUNEL staining was performed to evaluate apoptosis in mouse.ResultsThere were 159 common differentially expressed genes in the GSE16088 and GSE19276 datasets. The hub genes ANK1, AHSP, GYPB, GYPA, KEL, and ALAS2 were identified. Pan-cancer analysis verified that ANK1 was closely associated with cancer prognosis and immune infiltration. Furthermore, ANK1 overexpression inhibited the proliferation, migration, and invasion of OS cells and promoted ferroptosis, while ferroptosis inhibitor (fer-1) weakened these effects. Moreover, ANK1 overexpression suppressed tumor growth, promoted apoptosis, reduced the number of Ki67 positive cells, and elevated the number of caspase-3 positive cells in vivo.ConclusionsANK1 is a prognosis biomarker of OS that can alleviate the progression of OS by promoting ferroptosis.

HGG-13. INFANT-TYPE HEMISPHERIC GLIOMA (IHG): AN INDIVIDUAL PATIENT DATA META-ANALYSIS

Abstract BACKGROUND Infant-type hemispheric gliomas (IHG) are epigenetically distinct pediatric high-grade gliomas characterized by fusions in receptor tyrosine kinase (RTK) genes. METHODS We performed a methodical literature search, including 30 publications (22 case reports), to identify patients who met the diagnostic criteria of IHG based on the 2021 WHO Classification of CNS Tumors. Individual patient data were obtained from published literature and/or via the authors of the publications. Survival analysis was conducted using the Kaplan-Meier method, and multivariate analysis was performed to investigate the effect of clinical and molecular variables on outcomes. RESULTS Hundred-fifty-five previously reported and one unpublished IHG were identified: 131 (84%) had fusions in RTK genes, of which ALK was most prevalent (62/131), followed by NTRK1/2/3 (30/131), ROS1 (30/131), and MET (9/131). Twenty-five patients, with either no identified RTK fusion (6/156) or not assessable fusion (19/156), had methylation scores ≥ 0.9 for IHG (using the Molecular Neuropathology brain tumor classifier versions ≥ 11b4). Surgery followed by adjuvant chemotherapy in 69% (67/97) was the most common primary treatment used in our cohort. The 3-year EFS and OS were 55% (95%CI: 45-67) and 81 % (95%CI: 73-89). 41 patients with relapsed or progressive tumors received various second-line treatments including surgery, chemotherapy, radiotherapy, and targeted therapy. Based on multivariate analysis, complete resection resulted in better EFS (p = 0.05) and OS (p = 0.009), and the presence and type of RTK gene fusion were not associated with clinical outcomes. CONCLUSION Our results show that despite favorable OS, patients with IHG often show early progression, indicating that the primary optimal treatment for IHG is yet to be established. Our analysis further indicates that achieving a safe, complete resection may play an important role in treating these patients. A comprehensive analysis of the salvage regimen is required to understand their role in OS.

INHBA gene silencing inhibits proliferation, migration, and invasion of osteosarcoma cells by repressing TGF-β signaling pathway activation

BackgroundOsteosarcoma (OS) is a refractory malignancy. This study aimed to explore the roles and mechanisms of Inhibin subunit beta A (INHBA) in OS.MethodsINHBA expression levels in OS tissues and cells were assessed using RT-qPCR and western blotting. The impact of INHBA silencing on OS development was then explored by transfecting the OS cell lines U2OS and MG63 with INHBA-small interfering RNA (siRNA). The influence of INHBA silencing on U2OS and MG63 cell proliferation, migration, and invasion was examined using MTT and Transwell assays. Epithelial–mesenchymal transition (EMT) markers (E-cadherin and N-cadherin) were analyzed by RT-qPCR. The expression of genes involved in cell proliferation, migration, invasion, and the TGF-β signaling pathway was evaluated by western blotting and RT-qPCR.ResultsINHBA levels were elevated in the OS tissues and cells. Furthermore, the transforming growth factor-β (TGF-β) signaling pathway of OS cells was suppressed in response to INHBA-siRNA, whereas proliferation, migration, and invasion of OS cells were inhibited. Besides, INHBA-siRNA significantly inhibited OS cell EMT, evidenced by enhanced E-cadherin mRNA expression and reduced N-cadherin mRNA expression. Further mechanistic studies revealed that the TGF-β1 agonist SRI-011381 hydrochloride increased OS cell proliferation, migration, and invasion after INHBA downregulation.ConclusionWe found that INHBA silencing could play a vital role in OS via TGF-β1-regulated proliferation, migration, and invasion.

Oxidative stress gene expression, DNA methylation, and gut microbiota interaction trigger Crohn’s disease: a multi-omics Mendelian randomization study

BackgroundOxidative stress (OS) is a key pathophysiological mechanism in Crohn’s disease (CD). OS-related genes can be affected by environmental factors, intestinal inflammation, gut microbiota, and epigenetic changes. However, the role of OS as a potential CD etiological factor or triggering factor is unknown, as differentially expressed OS genes in CD can be either a cause or a subsequent change of intestinal inflammation. Herein, we used a multi-omics summary data-based Mendelian randomization (SMR) approach to identify putative causal effects and underlying mechanisms of OS genes in CD.MethodsOS-related genes were extracted from the GeneCards database. Intestinal transcriptome datasets were collected from the Gene Expression Omnibus (GEO) database and meta-analyzed to identify differentially expressed genes (DEGs) related to OS in CD. Integration analyses of the largest CD genome-wide association study (GWAS) summaries with expression quantitative trait loci (eQTLs) and DNA methylation QTLs (mQTLs) from the blood were performed using SMR methods to prioritize putative blood OS genes and their regulatory elements associated with CD risk. Up-to-date intestinal eQTLs and fecal microbial QTLs (mbQTLs) were integrated to uncover potential interactions between host OS gene expression and gut microbiota through SMR and colocalization analysis. Two additional Mendelian randomization (MR) methods were used as sensitivity analyses. Putative results were validated in an independent multi-omics cohort from the First Affiliated Hospital of Sun Yat-sen University (FAH-SYS).ResultsA meta-analysis from six datasets identified 438 OS-related DEGs enriched in intestinal enterocytes in CD from 817 OS-related genes. Five genes from blood tissue were prioritized as candidate CD-causal genes using three-step SMR methods: BAD, SHC1, STAT3, MUC1, and GPX3. Furthermore, SMR analysis also identified five putative intestinal genes, three of which were involved in gene–microbiota interactions through colocalization analysis: MUC1, CD40, and PRKAB1. Validation results showed that 88.79% of DEGs were replicated in the FAH-SYS cohort. Associations between pairs of MUC1–Bacillus aciditolerans and PRKAB1–Escherichia coli in the FAH-SYS cohort were consistent with eQTL–mbQTL colocalization.ConclusionsThis multi-omics integration study highlighted that OS genes causal to CD are regulated by DNA methylation and host-microbiota interactions. This provides evidence for future targeted functional research aimed at developing suitable therapeutic interventions and disease prevention.

Adiposity in resectable colorectal cancer.

3614 Background: Sarcopenia and myosteatosis affect survival in colorectal cancer (CRC). The role of adiposity is not yet fully elucidated. This study explores visceral and subcutaneous adipose tissue (VAT/SAT) distributions, and how they affect overall (OS), disease-free (DFS) and cancer specific survival (CSS). Methods: This retrospective cohort study, included resected stage I-III CRC in Alberta from January 2007 to December 2009. We excluded recurrent/metastatic disease or no CT scan. This study was approved by the Health Research Ethics Board at the University of Alberta. Body composition parameters were measured from CT scans. Sarcopenia and myosteatosis were defined by cohort-specific cut-off values. Total and visceral fat areas were indexed by height, and cohort-specific cut-offs defined total and visceral obesity (VO). SAT (SC:TFR) and VAT (V:TFR) to total adipose ratios were compared by gender, as described by Fleming. SAT and VAT fat radiodensity (Hounsfield units, HU) was measured and divided into quartiles. Differences between groups were compared with student’s t-test and Fisher Exact test. Cox proportional hazard models were created, adjusting for important covariates, to assess adiposity effects on OS, DFS and CSS. Results: Our cohort included 968 patients with a median follow up of 63.5 months. The majority were stage II (38.6%) and III (51.0%). In total, 67.9% had total obesity and 51.0% had visceral obesity. In males, there was no difference in the incidence of myosteatosis or sarcopenia, regardless of V:TFR or SC:TFR. In women, those with a high V:TFR or SC:TFR had significantly higher incidence of myosteatosis, but not sarcopenia. Men and women with elevated V:TFR had significantly lower VAT and SAT HU (p<0.001, p=0.0113). Those with elevated SC:TFR had significantly higher VAT and SAT HU (p<0.001). VAT and SAT HU was lowest in those with myosteatosis alone (p<0.001; p=0.005). In survival analysis, VO and VAT HU quartiles predicted worse OS in uni-, but not multivariate analysis. SAT HU quartiles predicted worse survival in uni- and multivariate analysis, with the highest quartile of SAT HU predicting increased risk of death (HR 1.35, p=0.037). Adiposity was not predictive of CSS or DFS in uni- or multivariate analysis. Conclusions: This study demonstrated changes in VAT/SAT in relation to well described body composition parameters. SAT HU may have a more important role in OS than visceral adipose characteristics, despite known metabolic characteristics of VAT. True roles of adipose tissue in CRC outcomes remains unclear. VAT/SAT measurements using cross-sectional imaging allows for a detailed analysis and understanding of how adiposity may affect survival. [Table: see text]

LncRNA HCG18 promotes osteosarcoma growth by enhanced aerobic glycolysis via the miR-365a-3p/PGK1 axis

BackgroundOsteosarcoma (OS) is a common primary bone malignancy. Long noncoding RNA HCG18 is known to play an important role in a variety of cancers. However, its role in OS and relevant molecular mechanisms are unclear.MethodsReal-time quantitative PCR was performed to determine the expression of target genes. Function experiments showed the effects of HCG18 and miR-365a-3p on OS cell growth.ResultsHCG18 expression was increased in OS cell lines. Moreover, in vitro and in vivo experiments demonstrated that HCG18 knockdown inhibited OS cell proliferation. Mechanistically, HCG18 was defined as a competing endogenous RNA by sponging miR-365a-3p, thus elevating phosphoglycerate kinase 1 (PGK1) expression by directly targeting its 3ʹUTR to increase aerobic glycolysis.ConclusionHCG18 promoted OS cell proliferation via enhancing aerobic glycolysis by regulating the miR-365a-3p/PGK1 axis. Therefore, HCG18 may be a potential target for OS treatment.

The Influence of Cross-Linguistic Similarity and Language Background on Writing to Dictation.

This study used a word dictation task to examine the influence of a variety of factors on word writing production: cognate status (cognate vs. non-cognate words), orthographic (OS) and phonological similarity (PS) within the set of cognate words, and language learning background [late bilinguals (LBs) with academic literacy and formal instruction in English and Spanish, and heritage speakers (HSs) with academic literacy and formal instruction only in English]. Both accuracy and reaction times for the first key pressed by participants (indicating lexical access), and the time required to type the rest of the word after the first keypress (indicating sublexical processing) was assessed. The results revealed an effect of PS on the dictation task particularly for the first keypress. That is, cognates with high PS were processed faster than cognates with low PS. In contrast to reading studies in which PS only revealed a significant effect when the OS between languages was high (O+P+ vs. O+P−), in the dictation to writing task, the phonology had a more general effect across all conditions, regardless of the level of OS. On the other hand, OS tended to be more influential for typing the rest of the word. This pattern is interpreted as indicating the importance of phonology (and PS in cognates) for initial lexical retrieval when the input is aural. In addition, the role of OS and PS during co-activation was different between groups probably due to the participants’ linguistic learning environment. Concretely, HSs were found to show relatively lower OS effects, which is attributed to the greater emphasis on spoken language in their Spanish language learning experiences, compared to the formal education received by the LBs. Thus, the study demonstrates that PS can influence lexical processing of cognates, as long as the task demands specifically require phonological processing, and that variations in language learning experiences also modulate lexical processing in bilinguals.

Phosphotyrosine picked threonine kinase stimulates proliferation of human osteosarcoma cells in vitro and in vivo.

IntroductionOsteosarcoma (OS) is the most common primary bone tumor, and the main affected population is adolescents. The survival of OS patients was 10–20% when surgery was used as a single treatment. There is less basic research on OS than other tumors, and we need more ways to improve the survival rate. Phosphotyrosine picked threonine kinase (TTK) has been widely reported as an oncogene in multiple types of cancers, and it is also known as a clinical therapeutic target. This study aims to assess TTK expression levels in human OS tissues and its link with the clinical characteristics of OS patients, and to evaluate the potential role in OS development.Material and methodsImmunohistochemical (IHC) assays were conducted to detect the expression levels of TTK in a total of 74 OS tissues and the corresponding adjacent tissues. Furthermore, according to the staining intensity of TTK in tumor tissues, patients were divided into TTK high and low expression groups. The possible correlation between TTK expression levels and clinical features were analyzed, and the effects of TTK on OS cell proliferation were detected through colony formation and cell counting kit-8 (CCK8) assays. The effects of TTK on tumor growth were detected using an animal model.ResultsPhosphotyrosine picked threonine kinase was abnormally highly expressed in human OS tissues. Meanwhile, TTK was significantly correlated with the clinical characteristics such as tumor size (p = 0.004*) and clinical stage (p = 0.014*) of OS patients. Our results also revealed that the inhibition of TTK dramatically suppressed the proliferation of OS cells in vitro and blocked tumor growth in mice.ConclusionsWe demonstrated the involvement of TTK in the development of OS, and therefore we suggest that TTK should be considered as a promising therapy target for OS.

Long non-coding RNA LINC01419 mediates miR-519a-3p/PDRG1 axis to promote cell progression in osteosarcoma

BackgroundOsteosarcoma (OS) is one of the most aggressive malignancies with mortality rate worldwide. Accumulating evidence has revealed that long noncoding RNAs (lncRNAs) exert important functions in regulation of cancer initiation and progression. Recently, long intergenic non-protein coding RNA 1419 (LINC01419) has been reported to function as an oncogene in several cancers. However, its role in OS has not been explored yet.MethodsqRT-PCR and western blot analyses were implemented to determine the expression of genes. The function of OS cells was assessed through colony formation, EdU, JC-1, TUNEL, transwell, and immunofluorescence (IF) assays. FISH and subcellular fractionation assays were conducted to estimate the localization of LINC01419 in OS cells. The interaction between genes was validated through luciferase reporter and RNA pull down assays.ResultsLINC01419 expression was elevated in OS tissues and cells. Functionally, LINC01419 accelerated OS cell proliferation, motility and EMT. In vivo assay showed that silencing LINC01419 hindered the growth of OS tumors. Mechanistic investigation unveiled that LINC01419 acted as a competing endogenous RNA (ceRNA) to augment PDRG1 expression by miR-519a-3p sequestration. Rescue assays verified the oncogenic effect of LINC01419/miR-519a-3p/PDRG1 axis on OS development.ConclusionLINC01419 mediates malignant phenotypes in OS by targeting miR-519a-3p/PDRG1 axis.

RETRACTED ARTICLE: Down-regulation of LINC00472 promotes osteosarcoma tumorigenesis by reducing FOXO1 expressions via miR-300

BackgroundOsteosarcoma (OS) is one of the most common types of primary bone tumors which poses negative effects on the bones of both young children and adolescents. LncRNA LINC00472 has been reported to be involved with poor prognostics in breast cancer and ovarian cancer. As a new lncRNA, its role in OS remains to be elusive. Herein, we are focused to explore its regulatory mechanism in the development of OS.MethodsqRT-PCR was utilized to examine the expressions of LINC00472 and miR-300 in OS tissues and cell lines. OS cell lines of U2OS and MG63 were used to investigate the biological function of LINC00472. Xenograft tumor model was built in nude mice with MG63 cells.ResultsThe expressions of LINC00472 were inhibited in OS tissues and cells, and were negatively related to the expressions of miR-300. LINC00472 directly targeted miR-300. FOXO1 was inhibited in OS tissues and its expressions were negatively related to the expressions of miR-300. LINC00472 over-expressions decreased cell proliferation abilities and colony formation abilities. These effects were mediated by miR-300. The silence of LINC00472 and over-expressions of miR-300 suppressed FOXO1 expressions. LINC00472 greatly reduced tumor growth in vivo and this effect was attenuated by miR-300 mimic.ConclusionsFrom all the experiments and observations, we demonstrated that LINC00472 could be a potential tumor suppressor in OS through interacting with miR-300 and FOXO1.

Oxidative Stress-Related Endothelial Damage in Vascular Depression and Vascular Cognitive Impairment: Beneficial Effects of Aerobic Physical Exercise.

Oxidative stress- (OS-) related endothelial damage is involved in the occurrence and progression of several disorders, such as vascular depression and dementia. It has been reported that moderate, aerobic, physical exercise could reduce OS and inflammation, thus limiting the cardiovascular risk factors while improving endothelial homeostasis, mood, and cognition. In this review, we will discuss about the role of OS and OS-related endothelial damage in vascular depression and vascular cognitive impairment. Then, we will comment on the effects of physical exercise on both disorders.

Patterns of metastasis and second primary malignancies (SPM) in colorectal cancer: A perspective from Peru.

e15068 Background: The incidence of colorectal cancer (CRC) in Peru has increased in the last decades. Approximately 20% of patients with CRC already have metastases at diagnosis, and this figure has been stable over the last two decades. The lack of data makes it more difficult to manage our patients. The metastatic setting and patients with second primary malignancies are complicated scenarios. The objective of our study was to explore and describe the metastasis patterns and the second primary malignancies’ frequency in CRC patients. Methods: We retrospectively reviewed the electronic medical records of 609 patients with CRC from one specialized Peruvian cancer center between 2006 and 2016. For the evaluation of the metastasis pattern, we selected 198 patients with metastasis at debut and the patients who had relapse of the disease. Descriptive results for numeric variables were presented as means with standard deviation (SD) or medians with interquartile range (IQR), depending on their distributions; otherwise, we expressed the qualitative variables as numbers with percentages. We evaluated the metastasis pattern according to primary tumour sidedness, age, CEA, histological grade, histological type. A survival analysis was performed with Kaplan Meier method, comparing the curves with Log Rank test for metastasectomy, biological therapy and number of sites with metastatic disease. A multivariate analysis was performed using the Cox regression model with the statistically significant variables found in the univariate analysis. Results: At the time of diagnosis, stage IV disease accounted for 15.3% (93) of all CRC cases. 105 (stage I-III) pts had relapse disease. Regardless of the primary tumor site, the most common site for metastatic spread was the liver (42.9%), lung (12.6%), carcinomatosis (18.2%). Pts who underwent metastasectomy presented a better OS [HR, 0.284; 95% CI, 0.123-0.657; p < 0.05], as well as pts who received biologic therapy [HR, 0.641; 95% CI, 0.416-0.990; p < 0.05] and a greater number of sites with metastatic disease had worst OS [HR, 1.878; 95% CI, 1.181-2.985; p < 0.05] The incidence of SPM following CRC was 48/609 (7.8%), the more frequent localizations were: breast, prostate and lung with 14.6% each, then kidney 10.4%, bladder 8.3%. Conclusions: In mCRC metastasectomy, biological therapy and number of sites with metastatic disease play an important role in OS. The more frequent localizations with SPM were breast, prostate and lung.

Role of OS "Technical education / engineering education" at department lecture and its achievements

Role of OS "Technical education / engineering education" at department lecture and its achievements

Role of OS " Technical education and engineering education" in the annual meeting and the result.

Role of OS " Technical education and engineering education" in the annual meeting and the result.

Abstract A54: PTHR1 signaling regulates the invasion and differentiation stage of osteosarcoma

Abstract Osteosarcoma (OS) is the most common tumor of bone. Parathyroid hormone (PTH) is a major endocrine regulator of skeletal development and homeostasis. We have sought to understand the contribution of PTH and parathyroid hormone related protein (PTHrP) in the regulation of osteosarcoma behaviour. In the present study we have used shRNA to knock-down the PTH receptor (PTHR1) to understand the role of PTH/PTHrP signaling in OS. Methods: shRNA to PTHR1 were designed and screened for activity using cyclic AMP (cAMP) radioimmunoassay following stimulation with PTH(1-34) (1). The most effective shRNA was designated PTHR1.358. OS cell lines derived from Osx-Cre p53fl/flpRbfl/fl mice (2) were stably infected with PTHR1.358 or Ren.1309 (negative control) and tested for gene expression changes, cellular invasion and cell cycle parameters. Cells were tagged with luciferase and grafted subcutaneously to determine the in vivo effects of PTHR1 signaling. Results: We have made use of an engineered murine model in which p53 and Rb have been deleted in an osteoblast-specific manner using Osx-Cre. Tumors in the mouse model share the cardinal features of human OS including histology, metastatic behavior and gene expression profiles. PTHR1 and PTHrP are expressed in the primary and metastatic lesions, and OS cell cultures derived from the tumors show cAMP induction in response to PTH or PTHrP treatment. Expression analysis confirmed PTHR1 expression in human OS. PTHR1 knock-down did not affect viability, but impaired the invasive capacity of the cells and altered gene expression, notably a reduction in RANKL RNA, an increase in OPG, and increased mRNA for Phex and matrix gla protein (MGP), with the latter effects likely related to the increased mineralization in knockdown cells. Strikingly, PTHR1.358 expressing cells showed a dramatically reduced proliferation in vivo which did not appear due to profound death of the cells but rather, as revealed by microCT, the acquisition of a more differentiated phenotype in the tumors. The Pthr1.358 tumors were smaller and more highly mineralized. PTH treatment did not influence tumor growth in vivo, nor did treatment with neutralizing antibody against PTHrP (3), the likely in vivo ligand for PTHR1 in OS cells. These results together establish clearly the importance of signaling through the PTHR1 in maintaining OS proliferation, but indicate that extracellular PTHrP is not significantly contributing to this effect, making it likely that an intracrine action of PTHrP contributes to this aspect of OS biology. Conclusions: Collectively these studies demonstrate that PTHR1 signaling plays a cell autonomous role in OS, acting in an intracrine manner. Inhibition of PTHR1 signaling reduced in vitro cell invasion but most notably profoundly reduces OS proliferation in vivo and drives the acquisition of a mineralized phenotype. Therapeutic inhibition of PTHR1 may be useful at impairing OS proliferation and/or increasing differentiation. 1. R. A. Dickins et al., Nat Genet 37, 1289 (Nov, 2005). 2. C. R. Walkley et al., Genes Dev 22, 1662 (Jun 15, 2008). 3. E. Onuma et al., Anticancer Res 24, 2665 (Sep-Oct, 2004). Citation Format: Patricia WM Ho, Megan Russell, Ankita Goradia, Alistair Chalk, John Slavin, Ross Dickins, T. John Martin, Carl Walkley. PTHR1 signaling regulates the invasion and differentiation stage of osteosarcoma. [abstract]. In: Proceedings of the AACR Special Conference on Pediatric Cancer at the Crossroads: Translating Discovery into Improved Outcomes; Nov 3-6, 2013; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2013;74(20 Suppl):Abstract nr A54.

Response of Rice to Insect Elicitors and the Role of OsJAR1 in Wound and Herbivory‐Induced JA‐Ile Accumulation

Plants produce jasmonic acid (JA) and its amino acid conjugate, jasmonoyl-L-isoleucine (JA-Ile) as major defense signals in response to wounding and herbivory. In rice (Oryza sativa), JA and JA-Ile rapidly increased after mechanical damage, and this increase was further amplified when the wounds were treated with oral secretions from generalist herbivore larvae, lawn armyworms (Spodoptera mauritia), revealing for the first time active perception mechanisms of herbivore-associated elicitor(s) in rice. In the rice genome, two OsJAR genes can conjugate JA and Ile and form JA-Ile in vitro; however, their function in herbivory-induced accumulation of JA-Ile has not been investigated. By functional characterization of TOS17 retrotransposon-tagged Osjar1 plants and their response to simulated herbivory, we show that OsJAR1 is essential for JA-Ile production in herbivore-attacked, field-grown plants. In addition, OsJAR1 was required for normal seed development in rice under field conditions. Our results suggest that OsJAR1 possesses at least two major functions in rice defense and development that cannot be complemented by the additional OsJAR2 gene function, although this gene previously showed overlapping enzyme activity in vitro.

Antiapoptotic and Antioxidant Properties of Orthosiphon stamineus Benth (Cat′s Whiskers): Intervention in the Bcl‐2‐Mediated Apoptotic Pathway

Antiapoptotic and antioxidant activities of aqueous-methanolic extract (CAME) of Orthosiphonstamineus Benth(OS), and its hexane (HF), chloroform (CF), n-butanol (NBF), ethyl acetate (EAF) and water (WF) fractions were investigated. Antioxidant properties were evaluated using the assays of Folin-Ciocalteu, aluminiumtrichloride, β-carotene bleaching and DPPH. The role of OS against hydrogen peroxide induced apoptosis on MDA-M231 epithelial cells was examined using MTT assay, phase contrast microscope, colorimetric assay of caspase-3, western blot and quantitative real-time PCR. Results showed that EAF showed the highest total phenolic content followed by CAME, NBF, WF, CF and HF, respectively. Flavonoid content was in the order of the CF > EAF > HF > CAME > NBF > WF. The IC50 values on DPPH assay for different extract/fractions were 126.2 ± 23, 31.25 ± 1.2, 15.25 ± 2.3, 13.56 ± 1.9, 23.0 ± 3.2, and 16.66 ± 1.5 μg/ml for HF, CF, EAF, NBF, WF and CAME, respectively. OSreduced the oxidation of β-carotene by hydroperoxides. Cell death was dose-dependently inhibited by pretreatment with OS. Caspase-3 and distinct morphological features suggest the anti-apoptotic activities of OS. This plant not only increased the expression of Bcl-2, but also decreased Bax expression, and ultimately reduced H2O2-induced apoptosis. The current results showed that phenolics may provide health and nutritional benefits.

Role of Os−H- - -H−N Interactions in Directing the Stereochemistry of Carbonyl Cluster Hydride Derivatives

Unconventional hydrogen-bond interactions involving metal hydrides as proton acceptors from N−H bonds have been recently discovered in mononuclear organometallic systems. The work herein reported on H2Os3(CO)10L (L= NH2Et, NHEt2) suggests that this type of interaction may be even more important in cluster chemistry in directing the stereochemistry of the products as well as affecting the intramolecular ligand exchange processes.

A module structure real-time operating system for microcomputers

With the advent of large-scale and complicated microcomputer application systems, the role of OS is becoming more important. An OS which can cope with various application requirements is strongly desired. This paper aims at the construction of OS which can be made optimum for various real-time applications. A construction of real-time modular structure OS using the microcomputer 68000 is proposed. The message-passing and procedure-call schemes are combined to connect the modules. A two-layered hierarchy module structure is proposed, suppressing the increase of the overhead due to modular implementation, and also providing the flexibility for replacing modules. By this scheme, operating systems with capacity from 10 KB to 150 KB can be constructed, covering a wide range of applications from a small-scale system with hardware built-in structure to the relatively large-scale system requiring programming functions, by simply modifying the combination of modules. To utilize commercial softwares or general-purpose OS in the real-time environment, a scheme is proposed in which the general-purpose OS is executed as the secondary OS with the real-time kernel. As a result of evaluation, when a general-purpose OS, CP/M-68K, is executed as the secondary OS, the processing time is increased by 12.7% compared with CP/M-68K directly implemented on the 68000.