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text:
Q: When view is removed from superview all animations are removed or not?
*

*I add an endlessly repeating animation to view_A.

*The animation starts.

*I swap view_A out of its superview for view_B.

*The animation on view_A stops — I can tell that in my animationDidStop:finished: delegate method — and I can see [view_A.layer animationForKey:theAnimationKey] is nil, view_A.layer.animationKeys is nil and view_A.layer.animations(print view_A.layer in GDB can reveal that) is empty. (Question 1: Are all animations removed automatically when view is removed from its superview?)

*I swap view_A back. Here comes the odd thing: I see the animation is still going. (Question 2: how could the animation keep going after it is stopped and removed from its view?)

*The even more bizarre thing is that I can stop the animation after step 5 by calling [view_A.layer removeAnimationForKey:theAnimationKey]!

A: I believe it is a bug of Core Animation. Here is my radar: http://openradar.appspot.com/radar?id=6165852231565312.

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text:
Myron Tribus (-) est un mathématicien et scientifique américain. Il est à l'origine ou a contribué à la diffusion de plusieurs concepts scientifiques qui ont eu un succès inégal. En France, il est surtout connu pour son livre Décisions rationnelles dans l'incertain (Rational descriptions, decisions and designs) qui y a popularisé à partir de 1974 les méthodes bayésiennes.

Diplômé de l'Université de Californie à Los Angeles (UCLA), il a été professeur à Dartmouth, et de 1974 à 1986 directeur du Center for Advanced Engineering Study au Massachusetts Institute of Technology, après avoir été directeur scientifique de la compagnie Xerox à l'époque du PARC.

Il a publié beaucoup de travaux en théorie de l'information, théorie de la décision et thermodynamique, ainsi que créé le concept d'essergie (exergy) autour desquels il avait fondé sa compagnie Exergy.

Il a eu une action militante concernant les domaines de la qualité industrielle, de l'ergonomie et de l'éducation, en participant aux travaux de Deming. C'est sous son impulsion que le Massachusetts Institute of Technology a publié en 1986 le livre de Deming Out of the Crisis.

À partir sa rencontre avec Deming en 1980, son principal centre d'intérêt était le management. Il écrivait notamment : « Les individus travaillent dans un système. La mission du manager est de travailler sur le système pour l'améliorer, avec leur aide. Si vous acceptez cette définition, vous devez admettre que les opérateurs ne contrôlent pas les résultats de leur travail. Diriger une équipe en disant aux gens que vous les tenez pour personnellement responsables des résultats est un défi à ce que vous savez réellement. Quand vous dites cela, vous n'êtes pas cohérent avec vous-même. »

Dans le domaine de l'éducation, il a introduit dans plusieurs établissements d'enseignement des États-unis une méthode pédagogique inspirée de la méthode de management de la qualité appliquée au Mount Edgecumbe High School en Alaska.

Citations
 « Nous devons éviter que nos objectifs (goals) ne deviennent les geôles (gaols) de nos enfants ». Cette phrase avertissait des dangers d'une spécialisation prématurée dans l'enseignement, toute spécialisation excessive devenant tôt ou tard un obstacle au recyclage professionnel entraîné par l'obsolescence des techniques.

 « La quantité de photons nécessaire pour que nous puissions photocopier une page est maintenant inférieure à celle qu'il nous faut pour la lire ».
 La seule façon de survivre est d'apprendre comment mieux gérer les ressources. Telle est votre mission : vous devez apprendre comment faire un management correct, pour la qualité.

Notes et références

Liens externes

  Rational Description, Decisions and Designs sur Google Books (extraits)
  Systems, probability, entropy and management (PDF)

Tribus, Myron
Personnalité américaine de l'informatique
Naissance en octobre 1921
Naissance à San Francisco
Décès à 94 ans
Décès en août 2016
Décès à Pensacola

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We are currently recruiting for a National Operations Manager to join our expanding management team. You would be responsible for the proactive management and supervision of the daily operational aspect of the business reporting directly to the Group General Manager.
The day to day management and supervision of all operative activity.
Operative recruitment, development, support, performance and attendance in line with company subcontractor policies.
Working with and providing supervision of operatives while managing all other company cleaning activities.
Monitor company performance according to agreed standards and take appropriate action to maintain and improve those standards to meet clients requirements.
Develop and maintain a positive and constructive working relationship within our client portfolio.
Manage operative's attendance, appearance, timekeeping and work performance, taking appropriate action where required under the relevant company policies and procedures.
Carry out weekly quality audits with office administration team, ensuring all company reporting procedures are being met.
Produce oral and written reports, as required, for the office administration team.
Attend all new or major contracts.
Manage transfer, repair or replacement of machinery and equipment, maintaining asset register accordingly.
Ensure all company vehicles/fuel cards are used according to company and legal requirements. Carry out weekly vehicle audits and manage correct frequency of service while ensuring continuity of cleaning delivery.
Contribute towards continued growth and development of company.
Identify, manage and deliver practical training and co-ordination of all training needs of operatives.
Develop and maintain effective two-way communications with the client, operatives, office, subcontractors and associated service providers.
Recruit the highest possible calibre operatives to fill vacancies, personally monitor all applications for authenticity and seek and obtain references. Ensure all employee documentation is processed correctly.
Previous experience within a similar service environment.
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Experience of working with a range of computer packages eg excel, word.
Able to be flexible to with working hours to meet the needs of the business including working away nationally.
Self motivated and enthusiastic-with the ability to motivate your team.


text:
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Mesial Temporal Sclerosis
The condition called mesial temporal sclerosis is closely related to temporal lobe epilepsy, a type of partial (focal) epilepsy in which the seizure initiation point can be identified within the temporal lobe of the brain.
Mesial temporal sclerosis is the loss of neurons and scarring of the deepest portion of the temporal lobe and is associated with certain brain injuries.
Brain damage from traumatic injury, infection, a brain tumor, a lack of oxygen to the brain, or uncontrolled seizures is thought to cause the scar tissue to form, particularly in the hippocampus, a region of the temporal lobe. The region begins to atrophy; neurons die and scar tissue forms.
This damage is thought to be a significant cause of temporal lobe epilepsy. In fact, 70 percent of temporal lobe epilepsy patients have some degree of mesial temporal sclerosis. It also appears that the mesial temporal sclerosis can be worsened by additional seizures.
Mesial temporal sclerosis usually results in partial (focal) epilepsy. This seizure disorder can cause a variety of symptoms such as strange sensations, changes in behavior or emotions, muscle spasms, or convulsions.
The seizures usually are localized in the brain, but they may spread to become generalized seizures, which involve the entire brain and may cause a sudden loss of awareness or consciousness.
The changes associated with mesial temporal sclerosis are usually identifiable on a magnetic resonance imaging (MRI) scan.
The assessment of the extent of mesial temporal sclerosis is important because it can be a good indicator of the outcome for patients undergoing temporal lobectomy to climate seizures. For this procedure, the part of the brain containing the point at which the seizures start is removed.
The best outcomes for the surgery are in patients with mesial temporal sclerosis on only one side of the brain. Also, the best outcomes are achieved with complete removal of the sclerotic medial temporal structures. This is the single most common surgery for patients with medically refractory epilepsy, as it has a high rate of eliminating seizures and is associated with a low incidence of significant new neurological impairments.
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In addition, nega tive RKIP and positive p ERK expression was observed in 18 of 26 metastatic lymph nodes obtained from patients with recurrent disorder. Our findings recommend that mixed expression may be an independent prognostic component. ERK or MEK activation success in the sequential activation of the series of protein kinases, such as Raf one, plus the up regulating protein RAS. Somewhere around 30% of all human tumours have an activating mutation in the RAS gene. Specifically, KRAS mutations are amid the most common genetic abnormalities in many kinds of human cancer, which include pancreatic cancer, colon can cer, and lung cancer. In contrast, RAS mutations have already been observed in only a smaller proportion of human gastric cancers,implicating other mechanisms during the activation of RAS signaling in gastric tumourigen esis.
B RAF mutations are additional narrowly distributed and are prevalent within a couple of specific malignancies, includ ing melanoma, papillary thyroid cancer, and very low grade ovarian cancer, but are certainly not found in gastric cancer. During the existing study, we focused on extra down stream proteins this kind of as MEK, ERK, and RAF inhibitors this kind of as RKIP, and did not measure RAS or RAF expres sion. We previously showed that substantial expression of HER1 or HER3, which are upstream selleck chemicals elements of your RAS RAF MAPK along with other tyrosine kinase pathways, was linked with bad survival in gastric cancer. Moreover, we reported that the expression of m TOR in a further pathway involving HER was linked to survi val in gastric cancer. Signaling pathways involving tyrosine kinase receptors appear to be intimately related to invasion, metastasis, and outcomes in gastric cancer. However, anticancer agents that inhibit these pathways usually are not utilized clinically, together with the exception of trastuzu mab, an HER2 antagonist.
Molecules implicated in downstream signaling pathways, such as ERK, could be targets for chemotherapy in superior or metastatic gasoline tric cancer. Smaller molecule inhibitors of your MAPK cas cade which can be created to target a variety of techniques of this pathway, this kind of as MEK inhibitor and Raf inhibitor, have entered clinical trials, but direct ERK inhibitors have however for being evaluated. Lots of pathological and molecular assays suggest that the full details gastric cancer is often a heterogeneous ailment. Nonetheless, in spite of evidence indicating that gastric cancer is charac terized by interindividual differences in tumour progres sion, histopathological features, and treatment response, a one particular dimension fits all technique to evaluation has become utilized in many studies of gastric cancer, resulting in inconsis tent outcomes. The procurement of specimens from multiple internet sites can be vital when assessing het erogeneous tumours.
We uncovered that E2F variables had been linked to Cluster 3 expression sug gesting the acknowledged ethanol dependent reduction of ionized calcium levels is acting with the transcription level to inhibit, then release entry into the cell cycle. NFB as central regulator NFB is a central regulator appearing in all but certainly one of the cluster perform analyses,indicating a amount of co regulation linking ethanol ingestion to in nate immunity and the inflammatory response. Combin ing temporal expression patterns with direct and indirect molecular interactions defined by pathway analysis, we hypothesize that NFB regulated inflammation is down regulated early and moderates as blood ethanol amounts reduce. The reducing inflammatory response outcomes from decrease levels of S100A proteins and their impact on RAGE induction of NFB, and RORA activation of NFKBIA. BMI1 is induced in an quick early res ponse and could counter the decreased inflammatory response.
Proof for that return to ordinary amounts of NFB exercise is while in the late enhance in expression PD184352 MEK inhibitor of S100A8 and Cluster one genes KLF3, UBE2D3, and PF4V1, and might be a end result of improved expression of Cluster seven gene, HMGB1 and subsequent activation of RAGE. Modulating the late maximize in NFB exercise is BAX, a further Cluster 1 gene. NFB acts as the two an enhancer and suppressor inside the MHC CII promoter,suggesting NFB regulation of the expression spike during the two Cluster six MHC CII components. BIOBASE is known as a impressive tool that complements the IPA analysis by on the lookout for conserved transcription component binding web-sites inside the GOIs and moving upstream to iden tify vital signaling pathways. Inside a 1200 bp window, various transcription things had been uncovered to bind to GOI promoters across over a single cluster.
SPI 1, ATF2, and CREB1 are just about every binding inside of genes in mul tiple but not precisely the same clusters,. ATF2 and Dovitinib JUN are both found in Clusters three and four, which have differing expression patterns general, but share a marked lower in expression from BAC1 to BAC2. The shared ATF2 CREB binding internet site is observed in Clusters two and 3 which have equivalent expression patterns, specially from BAC2 to BAC5. The p38 MAPK pathway was recognized being a central regulatory pathway for clusters one, 2, three, four, and 5. These clusters have varied expression patterns very likely reflecting the heterogeneity of cells in entire blood, interac tions with diverse other signaling molecules or tran scription elements, and also the variability of post translational modification, none of which can be detected by BIOBASE. The p38 regulated practical classes predicted by BIOBASE comprise of the innate and inflammatory immune re sponses, ubiquitination, apoptosis, and power metabolic process. One of a kind signaling pathways that may modulate p38 MAPK were predicted by BIOBASE within three clusters.
In this format, 1133 exceptional transcripts have been overexpressed in resting NK cells. Comparison of the NK cell signatures from your two platforms resulted in the widespread set of 164 genes. The genes included inhibitory NK cell surface molecules, activating NK cell surface molecules also as cytotoxic mediators. Quite a few genes encoding chemokines, cytokines and their receptors and genes involved in secretory functions were also expressed at high ranges in resting cells. We also examined a curated resting NK signature in the literature derived through the Affymetrix platform. Thirty 3 of sixty genes have been noticed in our Affymetrix derived signature. demon strating consistency inside of the individual platform. Temporal evaluation on the IL2 stimulated NK cells Self organizing maps created from spotted microarray information identified the differentially expressed genes that had at the least a 2 fold alteration in expression degree between the time factors analyzed.
The expression of your selected pathways was examined and cross validated on both platforms. Additional genes on Affymetrix microarray small molecule inhibitors platform belonging to practical groups that had been established for being differentially expressed have been integrated for much more extensive interpretation. Countless members on the TNFSF and TNFRSF were upregu lated early. Some affecting the death receptor apoptotic pathway and TNFSF10 and other folks in all probability activating the NFB pathway. TNFRSF14, TNFRSF4, TNF and TRADD. Of curiosity was TNFSRF14, which may interact with a few members of TRAFs to activate innate immune response in concordance with improved expression of several members of your TRAF household. Moreover, a group of of dipeptidylpeptidases the vast majority of that are serine proteases concerned in cleaving proline adjacent bonds, showed greater expression mainly at eight 24 hrs.
read this post here The effectively characterized DPPs impli cated in cytolysis are DPP1. involved in processing of GZMA, B and DPP4. a serine protease concerned in CD16 mediated cytolysis by NK cells. Cytokines, chemokines and their receptors A few chemokine ligands and receptors showed higher expression in resting cells very likely associated on the instant immune response of NK cells. A group of chemokine receptors and CX3CR1 showed an early improved expression just after IL2 stimulation. Later on a substantial variety of chemokines in addition to a number of chemokine recep tors. CCR5, CCR6 and CXCR6 showed elevated expression at eight 24 hours. The elevated expression of these genes is probably responsible for that proinflammatory response of NK cells, such as the recruitment of NK cells as well as other immune cells to web sites of irritation. A lot of interferons and interferon induced genes were upregulated. IFN inducible protein 16, IFN regulatory issue 6. 2, 7, IFNA16, 4, IFNAR1, two, IFN induced protein 35.
Macroscopically incomplete resection was thanks to an internal spot with huge tumor size. The 8 patients with R2 status right after surgical procedure obtained submit operative pal liative chemotherapy. Five also obtained radiotherapy that delivered a total dose of 50 Gy or thirty Gy before or just after the end on the initial line chemotherapy. Four with the eight individuals showed rapid dis ease progression with chemotherapy. Five patients did not undergo surgery and acquired only palliative chemotherapy. They showed progressive disease following 2, 5, five, 7 and 9 months, respectively. All 21 patients showed treatment failure, with median time to therapy failure 7. eight months. On the time from the last stick to up,19 patients were dead, all as a result of cancer. two were still alive at 138 and 167 months, respectively, of observe up. The 1st patient knowledgeable two other MPNSTs as well as second community recurrence, which was handled with sur gery and radiotherapy.
The two had localized grade 3 tu mors with R0 resection followed by chemotherapy early right after surgery. The chemotherapy regimen was ifosfamide and doxorubicin and was not associated selleckchem GDC-0068 with radiotherapy. Survival at 12, 18 and 24 months was 81%,47. 6% and 38%,respect ively. The median general survival for that whole cohort was 17 months. The median time for you to survival for sufferers with peripheral MPNSTs was 21. four months and for sufferers with axial MPNSTs, 12. 6 months. Univariate examination uncovered no association of variables examined and time for you to therapy failure or total survival. Improved tumor dimension at diagnosis was as sociated using a brief time for you to treatment failure and total survival. As in contrast with locally superior or metastatic dis ease, R0 and R1 status was related with lowered danger of death. Because of the little amount of patients, we could not determine aspects associ ated using the 2 amputation failures.
Discussion In our working experience managing NF1 with MPNSTs by chemotherapy, general survival was bad, by using a median time of 17 months and five yr survival of 14%. BMS387032 While a big difference in survival among sporadic and NF1 relevant MPNSTs continues to be a matter of debate, sev eral research showed the prognosis of patients with NF1 is bad. This bad final result may be explained by many points. For most of our patients, MPNSTs had a deep place, with significant dimensions and large histological grade,as previously shown. We reveal a reduced charge of comprehensive surgery in accordance to your localization and size of lesions at diagnosis. only 6 from the 21 patients had R0 resection, and regional control rate was reduced. Certainly, the majority of the MPNSTs have been internal as previously proven. In contrast, for sufferers with per ipheral MPNSTs, survival was much better, even though not signifi cantly, than with axial MPNSTs.
NF ?B is activated by phosphorylation of I?B through activation of MAPKs including ERK1 two, JNK and p38 subfamilies, and after that migrates to the nucleus and activates the expression of inflammatory cytokines and mediators. The activation of NF ?B in response to professional inflammatory stimuli for instance TNF as a result of phosphorylation of I?B success in the NF ?B Raw 264. 7 cell line was obtained from cell financial institution, Insti tute of Biochemistry and Cell Biology. Raw 264. seven cells have been cultured in DMEM with 10% fetal bovine serum, in an incubator at 37 C, 5% CO2 and 95% humidity. The cyctotoxic effects of WEL had been evaluated in absence or presence of LPS by MTT assay. WEL was dissolved in 10% dimethyl sulfoxide and additional right to culture media before the addition of LPS. The last concentration of DMSO under no circumstances exceeded 0. 1%. Measurement of NO levels The nitrite concentration within the culture medium was measured by a Griess reaction check.
Cells had been plated like a density of two ? 106 cells properly in 24 nicely culture plates and pretreated with or with no indicated concentrations of WEL or N nitro L arginine methyl ester for twelve h, then incubated with LPS. one hundred uM L Title, an inhibitor of NO, was applied like a constructive manage. Just after twenty h incubation, cells selleck chemical Serdemetan were washed three times to clear away non adherent cells. Then, one hundred ul of your Griess reagent was mixed with an equal volume of cell supernatant, the optical density at 540 nm was measured plus the concentration of nitrite was calculated in accordance to your standard curve created from acknowledged concentrations of sodium nitrite. Measurement of PGE2 ranges RAW 264. 7 macrophages have been subcultured in 24 well plates and pretreated with or without having indicated concen trations of WEL for twelve h or DX for 1 h, then incubated with LPS for twenty h.
The accumulated PGE2 inside the culture medium was measured working with ELISA Kit in accordance on the makers directions. 0. one uM DX was applied as being a favourable control. Measurement of TNF levels The effects of WEL within the manufacturing of TNF have been measured by ELISA. 2 ? 106 RAW 264. 7 cells had been seeded on 24 very well plate at a density selelck kinase inhibitor of 2 ? 106 per well for more than evening. Cells were pre incubated with WEL or DX for 1 h, then stimulated with one ug ml LPS for yet another 20 h. The cytokine concentrations have been calculated in accordance to your conventional curve working with recombinant cytokines in each and every ELISA kits. All measurements over were carried out in triplicate. Transient transfection and luciferase reporter assay NF ?B reporter constructs had been obtained from Clon tech Laboratories, Inc. For that reporter assay, cells have been seeded into 24 very well plates at a density of 5 ? 105 cells per very well in 500 ul of DMEM without having antibiotics and incubated overnight. The cells in each well have been transiently transfected with 200 ng of luciferase reporter construct and 50 ng of internal control plasmid of your pCMV B galactosidase reporter plasmid or empty expression vector pcDNA3 using li pofectamine TM 2000 reagent according to your manu facturers procedures.
Growth inhibition results of salirasib are p53 indepen dent as salirasib have an effect on in a comparable trend HepG2 and Hep3B cells. This really is additional sub stantiated from the lessen in p53 expression observed after 2 days of treatment in HepG2 cells. This factor could possibly be clinically appropriate, for the reason that most human HCC harbor defective p53 function, A treatment strongly based upon p53 activation could thus be much less effec tive in these tumors. Our results contrast using a prior report of enhanced p53 perform in colon cancer cells in response to salirasib, Having said that, p53 downregulation is compatible with ras inhibition, since K ras activation is regarded to induce p53 up regulation, This lack of p53 upregulation in our examine may be linked to the absence of ERK inhibition upon therapy.
Without a doubt, in HepG2 cells, ERK is often a important activator of Mdm2, that is responsible for p53 degradation, Complete Ras protein expression was diminished inside the 3 examined cell lines after two days of therapy, even though Ras mRNA amounts remained steady. Also, salirasib reduced the expression of active GTP bound Ras in HepG2 cells purchase VX-809 stimulated with EGF. These observations indicate an increase in ras protein degradation, which is consistent using the postulated mechanism of action of salirasib, involving the dislodgement of ras from your cell membrane followed by a cytosolic degradation, Sur prisingly, salirasib was not able to inhibit neither ERK nor Akt phosphorylation. To the contrary, it even tended to boost their phosphorylation levels, which might be because of a powerful inhibition of p70 and also to the consequent relief of the detrimental suggestions loop affecting ERK and Akt, Importantly, p70 phosphorylation was abrogated on treatment method in all cell lines when stimulated with EGF, which occurred devoid of concomitant inhibition of ERK or Akt, each of that are recognized to activate mTOR.
Furthermore, salirasib also effectively diminished MK-2461 p70 phos phorylation in all cell lines upon IGF2 stimulation, a condition where stimulation with the Akt mTOR axis is independent of ras activation, Indeed, no ras activa tion above baseline amounts was observed in HepG2 cells stimulated with IGF2, and IGF2 did not induce ERK phosphorylation in any with the examined cell lines. Alto gether, these information recommend that salirasib induced inhibi tion of mTOR in HCC cells occurs, no less than in aspect, independently of ras, and thus level to a direct inhibi tory effect about the mTOR complicated one, confirming earlier observations, Nevertheless, it should not be concluded the development inhibitory effect that is observed in HCC cell lines solely relies on mTOR inhibition, as other unex plored ras mediators may very well be impacted. Even though, each ras and mTOR inhibition taken separately could make clear the lower in cyclin A plus the raise in p27 amounts, it truly is really worth to note that these alterations parallel the down regulation of ras in HepG2 and Hep3B cells.
Nevertheless, our acquiring signifies that none from the AKT isofoms had been able to advertise mesenchymal properties nor increase cell mobility in nonmalignant MCF10A cells, im plicating a likely tumor repressing in lieu of tumor selling part as indicated in earlier reports, Furthermore, to exclude the probability that our obser vation is due to the truth that MCF10A cells are immorta lized, this discovery was even more substantiated through the use of non immortalized major normal human mammary epithelial cells isolated from 3 various gals. Just like the outcomes obtained applying the MCF10A cells, activation of Akt inhibited the expression of mesenchymal linked transcripts selleck chemical and lowered cell motility in HMECs from all 3 donors. These effects weren't linked with any distinct Akt iso form, together with the exception that expression of E cad was marginally repressed in HMEC 2 overexpressing Akt3 too as in HMEC three expressing all 3 isoforms, Likewise, N cad was largely inhibited in HMEC one and 2, but activated in HMEC three.
We view outliers as staying in all probability ascribed to an induction of one more unreported adhesion molecule which can trig ger an epithelial phenotype in lieu of E cad activation or N cad repression. The variability could possibly be because of the undeniable fact that commercial main breast epithelia are rather hetero geneous compared to MCF10A cells. Nonetheless, migra tion was prominently inhibited by activated Akt signaling, Taken with each other, for selelck kinase inhibitor the 1st time by studying all three Akt isoforms, our data recommend that overly activated Akt signaling can lead to a noticeable reduction of mesenchymal related transcripts at the same time as a lower in cell motility and they are observed in non malignant breast epithelial cells such as not simply immor talized MCF10A but also primary breast epithelial cultures HMEC, E cad Activated Akt signaling hinders IGF I and TGFB induced EMT in an isoform independent method The Akt pathway axis has been reported to get modulated by distinct isoforms, Most practical scientific studies of Akt isoforms have already been carried out through gene unique xknockdown of unique Akt isoforms in genetically modified mice.
However, the latter is constrained by species conservation and possibly biased from the proven fact that tumor microenvironment within the mouse might not normally reflect the that in humans, The discrep ancy of information evolved through the two method may well be ascribed to ectopic expression versus knocking down endogenous Akt, On the other hand, knocking down specific Akt isoforms appears to be much less relevant than overexpression techniques given that human car cinomas usually display aberrant activation and amp lification in lieu of suppression of Akt signaling, To decipher how unique Akt isoforms influence IGF I mediated EMT, MCF10A cells were retrovirally transduced to express IGF IR that subsequently grew to become phosphorylated and activated, which in turn induces EMT in response to ligand stimulation.
However, our acquiring signifies that none with the AKT isofoms were in a position to promote mesenchymal properties nor enhance cell mobility in nonmalignant MCF10A cells, im plicating a likely tumor repressing in lieu of tumor promoting position as indicated in past reports, Moreover, to exclude the probability that our obser vation is because of the truth that MCF10A cells are immorta lized, this discovery was additional substantiated through the use of non immortalized main regular human mammary epithelial cells isolated from 3 diverse gals. Much like the outcomes obtained using the MCF10A cells, activation of Akt inhibited the expression of mesenchymal connected transcripts selleck inhibitor and diminished cell motility in HMECs from all 3 donors. These effects were not related with any unique Akt iso type, with the exception that expression of E cad was marginally repressed in HMEC 2 overexpressing Akt3 also as in HMEC three expressing all three isoforms, Likewise, N cad was largely inhibited in HMEC 1 and 2, but activated in HMEC 3.
We see outliers as staying most likely ascribed to an induction of an additional unreported adhesion molecule which can trig ger an epithelial phenotype in lieu of E cad activation or N cad repression. The variability may be because of the proven fact that industrial key breast epithelia are rather hetero geneous compared to MCF10A cells. Nevertheless, migra tion was prominently inhibited by activated Akt signaling, Taken together, for selleck chemicals tgf beta receptor inhibitor the very first time by learning all 3 Akt isoforms, our information recommend that overly activated Akt signaling can lead to a obvious reduction of mesenchymal associated transcripts as well as a decrease in cell motility and they are observed in non malignant breast epithelial cells which include not merely immor talized MCF10A but additionally primary breast epithelial cultures HMEC, E cad Activated Akt signaling hinders IGF I and TGFB induced EMT in an isoform independent manner The Akt pathway axis continues to be reported to get modulated by distinct isoforms, Most functional research of Akt isoforms happen to be carried out via gene precise xknockdown of precise Akt isoforms in genetically modified mice.
Nevertheless, the latter is restricted by species conservation and possibly biased by the proven fact that tumor microenvironment in the mouse might not normally reflect the that in humans, The discrep ancy of information evolved from the two system may well be ascribed to ectopic expression versus knocking down endogenous Akt, However, knocking down distinct Akt isoforms seems to be much less pertinent than overexpression techniques due to the fact human car cinomas often display aberrant activation and amp lification as opposed to suppression of Akt signaling, To decipher how diverse Akt isoforms influence IGF I mediated EMT, MCF10A cells were retrovirally transduced to express IGF IR that subsequently became phosphorylated and activated, which in flip induces EMT in response to ligand stimulation.
The information, even so, recommend that other genetic adjustments could influence the standing of pAKT, rendering it unregulatable by HSP27. For example, the reduction of PTEN, a common aberration in gliomas, results in elevated pAKT. It is less clear as to no matter whether PTEN standing influences the outcome of TMZ treatment, as you will find reviews that wildtype PTEN correlates with elevated survival during the drug treated sufferers and people demonstrating no benefit, Moreover, the outcome could possibly be influenced by MGMT promoter methylation standing. Sufferers acquiring tumors with PTEN favourable tumors with methylated MGMT had a survival benefit when handled with TMZ plus erlotinib and RT, Even more studies are wanted. The combined information working with established cell lines indi cate that blocking HSP27 is surely an productive treatment strategy, but is a lot more effective if SPARC expression is forced and promotes death signaling.
A serious query is whether key selleck inhibitor gliomas have forced or non forced SPARC expression. Two pri mary human glioma cell lines have been treated with control or HSP27 siRNA during the absence or presence of TMZ. Treatment method with HSP27 siRNA resulted in decreased col ony forming efficiency for each cell lines, Nonetheless, the results of HSP27 inhibition on signaling had been diverse concerning the cell lines, Inhibition of HSP27 in HF373 cells did not do away with SPARC suggesting a forced SPARC expression profile as observed to the H2 cells. In contrast on the H2 cells where substantial SPARC expression correlated with substantial pAKT, pAKT remained lower in the HF373 cells. As we had previously demonstrated that PTEN reconstitution could suppress SPARC induced activation of AKT, we considered the PTEN status for this cell line. No mutation has nonetheless been described for HF373, suggesting a wildtype status.
This suggests that wildtype PTEN sup presses SPARC induced pAKT in these cells. For HF2303 cells, inhibition of HSP27 only decreased SPARC by 50% and pAKT remained higher, BI-2536 also recommend ing a forced SPARC profile. Also, PTEN is mutant in HF2303. Hence, SPARC expression com bined with loss of PTEN was adequate to advertise ele vated pAKT. Consequently, the 2 cell lines had a forced SPARC expression profile, but the resultant impact on pAKT amounts differed, most likely resulting from variations inside the PTEN standing. As a consequence the loss of HSP27 promoted apop totic signaling in both cell lines. Nevertheless, the HF373 cells demonstrated greater autophagy, whereas the HF2303 cells didn't. During the latter cells, autophagy was induced with all the AKT IV inhibitor. These observations are in agreement with observations that knockdown of AKT exercise increases autophagy, and apoptosis will not be the prevailing response, Thus, we propose that HSP27 inhibition alone will be most efficient in SPARC positive PTEN wildtype tumors, even though mixed inhibition of HSP27 and pAKT will very likely be warranted for tumors which can be SPARC positive PTEN null.
To serve as a control, we first validated the action of your personal LIP and LAP2 constructs on a C EBPb responsive promoter as shown in Figure 2A. C EBPb null mammary epithelial cells were transfected with either LIP, or LAP2 individually or together with a C EBP responsive, firefly luciferase construct and renilla luciferase construct as control. As expected, LAP2 expression led to a rise in C EBP responsive luciferase activity whilst LIP alone reduced promoter exercise, In combination with LAP2, LIP expression antagonized and decreased LAP2 induced promoter exercise and led to a lower in luci ferase activity. To check for IGF 1 induced, endogenous C EBPb exercise, MCF10A cells were transfected by using a C EBP responsive, luciferase construct before stimula tion with IGF 1. To maximize LIP expression for a sig nificant boost the LIP LAP ratio, cells had been stimulated for sixteen hrs with 39 nM IGF 1.
This led to an anticipated lower in C EBP responsive luciferase action as a result of antagonistic effects of elevated LIP expres sion, These information show that IGF 1R induced increases from the LIP LAP ratio are biologically active. Does IGF 1R and Insulin regulate LIP expression via the activation of order Blebbistatin the EGF receptor Due to the fact IGF 1R signaling is observed to cross talk with EGFR signaling, it had been needed to identify no matter if the IGF 1R induced expression of LIP was, in component, mediated by EGFR signaling. We for that reason investi gated no matter whether therapy of MCF10A and MCF7 cells with IGF one leads to phosphorylation of EGFR. As deter mined by Western blot analysis, neither IGF 1 nor insu lin stimulation led to a substantial increase in EGFR phosphorylation as assessed in whole cell protein extracts 10 minutes soon after addition of ligand.
Moreover, neither a 10? maximize in IGF 1 nor insulin activated the EGF receptor, However, immunoprecipitation followed by immunoblot examination did display a modest boost in phosphorylated EGFR immediately after 10 minutes of IGF 1 stimulation, As well as IGF one and insulin receptors, mammary epithelial cells may also express insulin IGF one hybrid receptors, Hybrid receptors have been detected in most tissues that express each insulin over at this website receptor and IGF one receptor. An IGF 1 concentration of two. six nM won't activate the insulin receptor, but could probably result in the activation with the insulin IGF 1 hybrid recep tors. Information presented in Figure 3C supports this hypoth esis and suggests that IGF 1 signaling has led on the formation of insulin IGF 1 hybrid receptors.
Practical research with hybrid receptors show they behave additional like IGF 1 receptors as opposed to insulin receptors due to the fact they bind IGF one which has a much better affinity than insulin, As expected, we did not observe activation of your hybrid receptor with ten nM insulin, Despite the fact that the significance with the hybrid receptors in mammary epithelial cells in unclear, we hypothesize that the insulin IGF 1 hybrids may be far more abundant in MCF10A cells than otherwise anticipated and this hypothesis is supported by reviews that insulin and hybrid insulin IGF one receptors are critical regulators of breast cancer cells, All through this research, we'll refer to your IGF 1R mediated induction in LIP for simplicity, but the reader must recognize that hybrid receptors can also be concerned in regulation of LIP LAP.


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Blacksburg Summer Arts Festival starts June 6 /
Current page: Blacksburg Summer Arts Festival starts June 6
Henderson Lawn provides the venue for Friday Night Out concerts.
A summer of free family fun begins on June 6 when the Blacksburg Summer Arts Festival presents its first of seven outdoor concerts, and continues throughout the summer with music, live theatre, movies, and more.
This is the 23rd year for the festival, which is sponsored by Virginia Tech and the Town of Blacksburg.
Friday Night Out concerts
All concerts will be held on Henderson Lawn at the corner of Main St. and College Ave. in downtown Blacksburg. The music will go on rain or shine, with Squires Old Dominion Ballroom acting as rain site. All concerts begin at 6 p.m.
Rick Strickland Band (beach music and shag) June 6
3 Minute Lovin' (honkytonk/rockabilly/rock) June 13
The Key West Band (Caribbean rock) June 20
Dixie Power Trio (dixieland jazz) June 27
Crossties (bluegrass) July 11
Domino Band (variety) July 18
Gerry Timlin (Irish folk) July 25
"The True Story of the Three Little Pigs" will be performed by the Roanoke Children's Theatre for six performances June 21-23. The show is adapted from the book by Jon Sceiszka and Lane Smith with book and lyrics by Robert Kauzlaric, and music by Paul Gilvary and William Rush. All performances will be held in the Squires Studio Theatre.
"Poverty Creek Journal" and "Down to Breath," both based on local author Tom Gardner's "Poverty Creek Journal," will be performed in Theatre 101 with multiple performances on July 10-12 and 17-19.
Classic Movies at the Lyric
All movies will be shown at 3 p.m. at the Lyric Theatre, 135 College Ave.
The Sting June 21 and 25
The King and I July 19 and 23
On the Waterfront Aug. 9 and 13
"Printmaking Revered: 40 Years of Prints from the Robert Miller Collection" will be on display June 6 through Aug. 16 in the Perspective Gallery in Squires Student Center.
"Senior Studio Show 2014" celebrates the works of students and will be on display June 6-July 11 in the Armory Art Gallery on Draper Road.
"Life in the Trees" art installation opens July 1 in Theatre 101.
"Maryann Harman: Fresh Paint" is one of a series of shows celebrating emeritus faculty of the School of Visual Arts and will be on display Aug. 1-Sept. 13 in the Armory Art Gallery.
Summer Solstice Fest June 20-21
Independence Day Celebration July 4
Art at the Market July 19
Steppin' Out Street Festival Aug. 1-2
All events are free and open to the public. Additional information is available online or by contacting Jane Harrison via email or call 540-231-5921. Sign up to receive weekly email updates here.
Susan Sanders


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Clyburn Brazenly Admits What We Suspected: Dems Using COVID To Change America To Fit Their Vision
By Ben Marquis
Published March 23, 2020 at 3:27pm
On Sunday, House Speaker Nancy Pelosi tossed a purely partisan grenade into the Senate and utterly destroyed a bipartisan legislative package intended to provide desperately needed economic relief to the country amid the coronavirus pandemic.
Both Republican and Democratic senators had spent several days negotiating a nearly $2 trillion package that would provide financial assistance to workers, small businesses, large corporations and certain industries hit particularly hard by the economic shutdown in response to the public health crisis.
Then Pelosi showed up and declared the package not good enough while touting a number of demands that, at best, were only tangentially related to the coronavirus issue, which prompted Senate Democrats to essentially scuttle the whole thing on Sunday afternoon.
In retrospect, however, we all should have seen this coming, based on a rather telling comment days earlier from one of the California Democrat's top allies in the House.
The Hill reported that, on Thursday, House Democrats held a conference call to discuss both the efforts in the Senate to construct a coronavirus fiscal relief package as well as ideas for a package of their own for the same alleged purpose.
Based on what was reportedly discussed during that call, however, it was clear that House Democrats viewed the current moment as an opportunity worth seizing to try and push through some of their preferred policies. Some of those policies had little or no bearing whatsoever on providing economic relief to laid-off workers, small businesses on the brink of closure, or large corporations struggling to avoid bankruptcy.
In fact, it was House Majority Whip James Clyburn, third in line among House Democratic leadership, who gave the whole game away with one single comment.
"This is a tremendous opportunity to restructure things to fit our vision," the South Carolina Democrat reportedly told his fellow Democratic lawmakers during the conference call.
That remark from Clyburn bears a strong resemblance to an infamous quote attributed to former President Barack Obama's chief of staff Rahm Emanuel, who once quipped in 2008, "You never want a serious crisis to go to waste. And what I mean by that is an opportunity to do things that you think you could not do before."
Are you infuriated by Democrats taking political advantage of the coronavirus crisis?
In other words, exploiting the opportunity presented by a crisis — when the political opposition is certainly more inclined to compromise in order to address an emergency — to press forward with certain agenda items and policy prescriptions that otherwise would be non-starters or be bogged down by debate.
Getting back to Clyburn's comment and the report from The Hill, a number of proposals put forward by Democrats in that conference call were mentioned. Some were related to providing economic relief amid the growing financial crisis, while others were merely priority items on the Democratic wish list that had nothing to do with dealing with a global pandemic or saving the nation's economy from an impending depression.
Clyburn himself suggested that the current crisis would be a great time to legislatively provide for 100 percent broadband internet coverage for the entirety of the United States. He used the fact that schools across the nation are currently shut down for weeks, if not months, and students were being forced to continue their schooling online from home as the reasoning behind his suggestion.
Providing broadband coverage and reliable internet access to everyone across the nation is something worthy of consideration — but is it really a crucial item that must be included in an emergency funding bill intended to keep the nation's economy afloat until the current public health crisis subsides?
Other provisions mentioned by other Democrats in the conference call included things like infrastructure spending, expanding Social Security benefits, election security issues, environmental concerns, limits or requirements attached to any "bailouts" of large corporations, unionized labor demands, and other things that weren't directly related to immediate economic stimulus.
RELATED: Hospital in California Administers Hundreds of Vaccinations in 2 Hours After Freezer Failed
Around the same time as the conference call, no doubt aware of what his Democratic colleagues were intending to do, Senate Majority Leader Mitch McConnell had flatly warned, "Anything that doesn't address that pandemic, it seems to me, should not be considered."
For a few days, it seemed like McConnell's Democratic colleagues took the hint and engaged in reportedly productive negotiations that appeared to be on the verge of success on Sunday — until Pelosi showed up and jammed a partisan wrench into the delicate workings of the deal.
Now, as potentially millions of workers are facing unemployment, tens of thousands of small and large businesses are on the brink, and the markets are in free-fall, Congress is at an utter standstill because Democrats like Clyburn and Pelosi wanted to take advantage of the "opportunity" provided by coronavirus to push their partisan agenda on the American people.
Contributor, Commentary
Ben Marquis is a writer who identifies as a constitutional conservative/libertarian. He has written about current events and politics for The Western Journal since 2014. His focus is on protecting the First and Second Amendments.
Ben Marquis has written on current events and politics for The Western Journal since 2014. He reads voraciously and writes about the news of the day from a conservative-libertarian perspective. He is an advocate for a more constitutional government and a staunch defender of the Second Amendment, which protects the rest of our natural rights. He lives in Little Rock, Arkansas, with the love of his life as well as four dogs and four cats.
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Tags: American left, big government, Coronavirus, Democrats, House of Representatives, Nancy Pelosi, Speaker of the House, the economy


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The Fémmena gold company was born, with the brand *1147AR, under the name of "Creazioni 2A", and at that time it was a silver gifts and fancy goods laboratory who made collector's items of scrupulous and popular manufacture.
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Boncompagni gave life to a particular collection where GOLD and STONES contributed to the extraordinary success of Fémmena. A glamour collection, where the concept "simplicity as provocation" was clearly express by "the fish which starts to travel round the world".
Riding the wave of the evolution of this Brand, Creazioni 2A was renewed and decided to surprise again turning the brand into a company!! Fémmena was born and its products have been going on to draw inspiration from the WOMAN as "Fémmena". The woman of yesterday and today who has an important role in everyday life.
Fémmena achieved an important goal: 25 years of activity! From this point FÉMMENA always sets new goals planning and realizing elegant handcrafted collections of very light jewellery of great impact, keeping on to ride the evolution of its brand and its concept that continue to cause a sensation………….


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Q: How do i read and write a float array? I have a float array. Since i deal with big data > 10 GB i want to allocate some space
But how do i write and read into this data ? I have to say, i'm a matlab coder, and have no idea how to do this in c++.
// allocating space
float *buffnew = new float[size_x*size_y*size_z];
// write
**buffnew[x][y][z] = 1.1f;
// read
prediction = **buffnew[x][y][z];

This does not work.The error i get is:
error: subscripted value is not an array, pointer, or vector

edit : I just see my error. I used an 1D array to allocate ( on the heap, because of the big data ) and then used a 3D to access it.

A: C++ doesn't provide convenient syntax for dynamic multi-dimensional arrays. You've allocated a one-dimensional array, so you'll need to do arithmetic to access it, for example:
buffnew[x*size_y*size_z + y*size_z + z] = 1.1f;

It might make sense to wrap the array in a class, with an accessor function to do the arithmetic:
template <typename T>
class array3d {
public:
    array3d(size_t x, size_t y, size_t z) : array(x*y*z) {}

    T & operator()(size_t x, size_t y, size_t z) {
        return array[x*size_y*size_z + y*size_z + z];
    }

    T const & operator()(size_t x, size_t y, size_t z) const {
        return array[x*size_y*size_z + y*size_z + z];
    }

private:
    std::vector<T> array;
};

array3d<float> buffnew(size_x, size_y, size_z);
buffnew(x,y,z) = 1.1f;
prediction = buffnew(x,y,z);

By using std::vector rather than an evil pointer, the class is copyable, and will automatically free the memory on destruction.

A: Assuming you have enough ram, you use a vector
#include <vector>
std::vector<float> values;
values.resize(size_x * size_y * size_z);

values[z + y*size_z + x*size_y*size_z] = 1.1;
prediction = values[z + y*size_z + x*size_y*size_z];

A completely different approach that will give a nice (x,y,z) interface is to use lambda functions and closures.
#include <vector>
#include <functional>

template<typename T>
std::function<T&(std::size_t, std::size_t, std::size_t)>
vector3d(std::size_t size_x, std::size_t size_y, std::size_t size_z) {
    std::vector<T> values(size_x*size_y*size_z);
    return [values, size_x, size_y, size_z](std::size_t x, std::size_t y, std::size_t z) mutable -> T&
    {
    return values.at(z + y*size_z + x*size_y*size_z);
    };
}

Notice that the lambda captures the allocated vector by value.
This function can then be used like this
std::size_t size_x = 10, size_y = 20, size_z = 30;
auto array = vector3d<float>(size_x, size_y, size_z);

std::size_t x = 3, y = 3, z = 3;
f(x,y,z) = 12.12;
auto prediction = f(x,y,z);

A: You do not need to use
**buffnew[x][y][z]

From the read type, i think you want a three dimensional array. For that, declare
float *buffnew = new float[size_x][size_y][size_z];
buffnew[x][y][z] = 1.1f; //write
prediction = buffnew[x][y][z]; //read

This is how it is done in C++

A: I think this is what you want:
float *buffnew = new float[size_x][size_y][size_z];
buffnew[index1][index2][index3] = 1.1f;
[...]
prediction = buffnew[index1][index2][index3];

That is a standard way of handling a 3-dimensional array in C++.
Or you could use std::vector.

A: You can either make a multi dimensional array
float ***buffnew = new float**[size_x];
for(unsigned int i = 0; i < size_x; ++i) {
  buffnew[i] = new float*[size_y];
  for(unsigned int j = 0; j < size_y; ++j) {
    buffnew[i][j] = new float[size_z];
  }
}

Or make a one dimensional array linearly containing all the elements, but then you would have to calculate the right index from the actual x, y and z.


text:
Pålsjön kan syfta på ett antal insjöar i Sverige:

Pålsjön, Uppland, sjö i Heby kommun,  (8,64 ha)
Pålsjön, Gästrikland, sjö i Ockelbo kommun,  (66 ha)
Pålsjön, Hälsingland, sjö i Ovanåkers kommun,  (27,6 ha)
Pålsjön (Björna socken, Ångermanland), sjö i Örnsköldsviks kommun,  (30,6 ha)
Pålsjön (Vibyggerå socken, Ångermanland), sjö i Kramfors kommun,  (16,5 ha)

Listor över Sveriges insjöar baserat på namn


text:
Q: AWS CloudFormation error: Could not create Change Set "change-set-name" due to: Parameters: "[ssm:param-name:167:167710252826] cannot be found I have a CF template (serverless Typescript file to be precise) which creates a container definition in the following way.
Type: "AWS::ECS::TaskDefinition",
Properties: {
  Family: "client",
  RequiresCompatibilities: ["FARGATE"],
  NetworkMode: "awsvpc",
  Memory: 1024,
  CPU: 512,
  TaskRoleArn: { Ref: ECS_TASK_ROLE },
  ExecutionRoleArn: { Ref: ECS_TASK_ROLE },
  ContainerDefinitions: [
    {
      Name: application,
      Essential: true,
      Image: `${ACCOUNT_ID}.dkr.ecr.us-east-1.amazonaws.com/repository:client-{{resolve:ssm:param-name}}`,
      .
      .
      .
    },
  ],
}

Please note the usage of AWS SSM Dynamic Reference.
When I deploy it I get the following error
Could not create Change Set "change-set-name" due to: Parameters: "[ssm:param-name:167:167710252826] cannot be found.

It used to work fine and all of a sudden started breaking. Same code still works in a different env/AWS account.
Seems like it can't find a specific version of param-name for some reason. The latest param-name verion is 400. AWS SSM only keeps last 100 params. This parameter is updated quite often and it's been a long time since I deployed CF template. From the error message it seems like it is looking for version 167 (I could be wrong because I am not sure what is the number trailing 167 i.e. 167:167710252826)
What I tried:
I hardcoded the version number I pass as below and removed all the references to resolve:ssm:param-name.
Image: `${ACCOUNT_ID}.dkr.ecr.us-east-1.amazonaws.com/repository:client-1.6.3`,

It still throws the same error. Which hints that the problem is not related to code. CF is trying to run an old change set from history to create a diff and can't find an old version of the same param.
What could be the solution to this?
I can't delete the old change set. It throws an error on deleting.
I can't go back and create a parameter in SSM with version 167 if it's a version issue.


text:
Research ArticlePHYSICAL SCIENCES
The fate of carbon dioxide in water-rich fluids under extreme conditions
View ORCID ProfileDing Pan1,* and
Giulia Galli1,2
1The Institute for Molecular Engineering, the University of Chicago, Chicago, IL 60637, USA.
2Argonne National Laboratory, Argonne, IL 60439, USA.
↵*Corresponding author. Email: dingpan{at}uchicago.edu
Science Advances 12 Oct 2016:
Vol. 2, no. 10, e1601278
Ding Pan
ORCID record for Ding Pan
For correspondence: dingpan@uchicago.edu
Giulia Galli
Fig. 1 High-pressure and high-temperature conditions reached in experiments on dissolved carbon in supercritical water, together with the conditions simulated in the present work: Frantz (10), Caciagli and Manning (30), Martinez et al. (19), Facq et al. (31, 36), and Schmidt (11).
The melting curve of ice is from the study by Datchi et al. (51). The shaded area shows the P-T conditions of the upper mantle (7).
Fig. 2 Mole percents of CO2 (orange),
(red),
(black), and H2CO3 (blue) as functions of simulation time in first-principles MD simulations.
(A) Na2CO3 solution [0.9 m (molality)] at 0.2 GPa and 823 K. (B) Na2CO3 solution (0.9 m) at 11 GPa and 1000 K. (C) CO2 solution (0.9 m) at 11 GPa and 1000 K. Calculations carried out with two xc functionals: PBE (22) and PBE0 (23) are compared.
Fig. 3 The solvation structures of carbon species and ion pairing distances in the 0.9 m Na2CO3 solutions.
(A) RDFs of carbon atoms (C) versus oxygen atoms of water (Ow). (B) Probability distributions of the distances between carbon atoms and sodium ions. The MD simulations on the 0.9 m Na2CO3 solutions were conducted at 0.2 GPa, 823 K and 11 GPa, 1000 K. Two xc functionals were compared: PBE and PBE0.
Fig. 4 Probability distributions of positions of protons hopping between
and H2O in the Na2CO3 solution at 11 GPa and 1000 K.
The unit is Å−2. The reaction coordinate RO−O is the distance between the two neighboring oxygen atoms, Oc and Ow, in carbonate ions and water molecules, respectively, and δ is the proton displacement ROc−H − RH−Ow. Two xc functionals were compared: PBE and PBE0.
Table 1 Carbon species in the 0.9 m Na2CO3 and 0.9 m CO2 solutions in first-principles MD simulations.
The concentrations are shown as mole percents of the total dissolved carbon. The mole percents of
include those of ion pairs formed by them, respectively. The experimental results (Expt.) are from the Raman data in the study by Frantz (10) (see text). N/A, not applicable.
Solution P (GPa) T (K) Method Carbon species (%)
H2CO3
Na2CO3 0.2 823 PBE 0.6 16.7 82.4 0.1
PBE0 0.2 26.8 72.9 0.1
Expt. N/A 32 68 N/A
11 1000 PBE 0.1 40.8 57.9 1.2
CO2 11 1000 PBE 0.6 8.2 79.8 11.4
PBE0 0.0 1.7 75.0 23.3
Table 2 The ion pairing in the first solvation shells of the carbon species in the 0.9 m Na2CO3 solutions.
The concentrations are shown as mole percents of the total dissolved carbon.
P (GPa) T (K) Method Ion pairing species (%)
0.2 823 PBE 3.7 13.0 59.7 7.5
PBE0 8.4 18.2 40.8 18.2
11 1000 PBE 18.1 5.9 28.9 7.5
PBE0 22.4 10.0 20.4 12.5
Supplementary material for this article is available at http://advances.sciencemag.org/cgi/content/full/2/10/e1601278/DC1
fig. S1. The vibrational density of states of the 0.9 m Na2CO3 solution at ~11 GPa and 1000 K.
fig. S2. Probability distributions of positions of protons hopping between and H2O in the Na2CO3 solution at 0.2 GPa and 823 K.
fig. S2. Probability distributions of positions of protons hopping between CO2−3 and H2O in the Na2CO3 solution at 0.2 GPa and 823 K.
Adobe PDF - 1601278_SM.pdf
Vol 2, No. 10
You are going to email the following The fate of carbon dioxide in water-rich fluids under extreme conditions
By Ding Pan, Giulia Galli
Science Advances 12 Oct 2016 : e1601278
Quantum mechanical simulations predict the fate of CO2 dissolved in water under the conditions of Earth's upper mantle.


text:
Budapest · Hungary · March 24-28, 2014
Conference Final Program
NSF Student Travel Grant
IEEE Student Travel Grant
Presenters' Guide
About Budapest
Home » PerCom 2014 Panel
Panel Topic
"Infrastructure vs. Mobile Sensing - The Evolving Landscape"
Prof. Archan Misra
Singapore Management University, Singapore
Prof. Yutaka Arakawa
Nara Institute of Science and Technology, Japan
Prof. Anish Arora
Ohio State University, USA
Prof. Paul Lukowicz
DFKI and Technical University of Kaiserslautern, Germany
Prof. Mani B. Srivastava
University of California at Los Angeles, USA
4:30 pm - 6:00 pm, Wednesday, March 26th, 2014
There has been a surge of enthusiasm around the paradigm of participatory urban sensing, which views a citizen-centric distributed and mobile sensing substrate as one of the most promising ways to gather various types of urban information, such as environmental parameters & pollution levels, traffic congestion, popularity of events at various public spaces, etc. In parallel, there have also been significant recent deployments, perhaps less heralded, of infrastructure or ambient sensors, especially in public spaces, such as malls, airports and stadiums. The panel seeks to understand the limits of each of these individual sensing paradigms observed in practice, due to challenges such as resource limitations, privacy, user interfaces and data quality. It will also discuss how the combined capabilities of participatory and infrastructure sensing can be effectively harnessed, for novel urban computing applications.
Panelists Bios
Yutaka Arakawa is an associate professor of Nara Institute of Science and Technology since 2013. From 2006 to 2012, he worked as an assistant professor of Keio University and Kyushu University. Previously, from 2012 to 2013, he joined ENSEEIHT (Toulouse, France) and DFKI (Kaiserslautern, Germany) as a visiting researcher. His current research interests are principally around smartphone-based sensing, including social data analysis and crowd sourcing mechanisms.
Anish Arora is Professor of Computer Science and Engineering at The Ohio State University and co-founder/CTO of The Samraksh Company. At OSU, he has built and deployed several large scale wireless sensor networks, including ExScal, KanseiGenie, and ThermoNet, and, at Samraksh, he has engaged in developing products and solutions for WSNs. His recent work is focused on the architecture and networking alternative for large scale MANETs—this is in the context of redressing the problem that mobile networks today fail to scale in the absence of infrastructure. Arora is an IEEE fellow.
DFKI & Technical University of Kaiserslautern, Germany
Paul Lukowicz is a Professor for Artificial Intelligence at the Technical University of Kaiserslautern Germany and Scientific Director for Embedded Intelligence and the German Research Center for Artificial Intelligence (DFKI). He has a MSc in Computer Science, a MSc in Physics and a PhD in Computer Science all from the University of Karlsruhe (KIT) in Germany. Before coming to Kaiserslautern Paul Lukowicz has been a Post Doc at ETH Zurich where he was in charge of building up the Wearable Computing Laboratory; Professor for Computer Engineering at the University of Health Informatics and Technology (UMIT) in Hall in Tirol Austria; and Professor for Embedded Systems at the University of Passau in Germany. Paul Lukowicz's research interests are wearable systems, ubiquitous and crowd sourced sensing, activity and context recognition, socio-technical systems, and self organization. The research is strongly connected to applications in particular in health, well being, production and civil protection. Paul Lukowicz has been Associate Editor in Chief of the IEEE Pervasive Magazine, is currently member of the editorial board of the Hindawi Advances in Human Computer Interaction and IEEE Journal of Biomedical and Health Informatics. He is a co-founder SIS software, a EU SOCIONICAL project spin-off company dedicated to crowd sensing based civil protection solutions.
Mani B. Srivastava is on the faculty at UCLA where he is associated with the Electrical Engineering Department and the Computer Science Department. His research is broadly in the area of networked human-cyber-physical systems, and spans problems across the entire spectrum of applications, architectures, algorithms, and technologies. His current interests include issues of privacy, security, data quality, and variability in the context of applications in mHealth and sustainable buildings.


text:
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text:
Iris minima es una especie de mantis de la familia Tarachodidae.

Distribución geográfica
Se encuentra en Irán.

Referencias

Insectos de Irán
Minima


text:
package co.ikust.daggerinjector.coffemaker;

import co.ikust.daggerinjector.coffemaker.module.DripCoffeeModule;
import dagger.Component;

/**
 * Created by ivan on 04/03/15.
 */
@Component(modules = DripCoffeeModule.class)
public interface CoffeeShop {

    CoffeeMaker maker();
}

redpajama_set_name: RedPajamaGithub


A selection of the best images from day one of this year's Royal Norfolk Show.
Throughout the day we'll be featuring a range of pictures from the first day of Norfolk's annual celebration.
You can see pictures from the huge array of displays, performances and events taking place across the show - and see if you can spot yourself, too!


For three months, Julia Kurnia took her nonprofit through the famed startup accelerator—all while caring for her 2-year-old son, alone.
It was 2014, and Julia Kurnia was discouraged. It wasn't her personal life that was a problem. Far from it: Kurnia was blissfully happy with her husband, Terra, an Indonesian martial-arts instructor, and their two-year-old, Adam. But Kurnia had a nonprofit, Zidisha, which aimed to redefine international microlending. And a few years in from founding, Zidisha was struggling, stuck, plateaued. Worse: Kurnia's bootstraps were about to snap. She'd sent out around 75 grant applications, and all had been turned down.
Then one of her board members (a former Facebook engineer) suggested she apply to a nontraditional funding source for nonprofits. "I had never heard of Y Combinator," recalls Kurnia. She had spent her youth trekking through remotest Africa, administering U.S. government grants; an "accelerator," to her, was the pedal of a jalopy. But in around 2014, Y Combinator began to expand its mission slightly, inviting people like Kurnia to apply. So she tossed off an application, figuring it was as much a long shot as her other 75.
Then, to her surprise . . . she got in.
She and Terra talked it over. Zidisha's problem at this point, they knew, was fundamentally technological—how to scale up international grant-making while preventing fraud. Zidisha simply needed YC's expertise if it was to grow. The decision was gut-wrenching, but Kurnia made it.
She filled a small corner of her suitcase with two outfits and a pair of sandals. The rest she filled with Legos.
The first problem, as any transplant to the Bay Area knows, was housing. Kurnia rapidly booked a stopgap Airbnb. The place was far from ideal: a dorm-like flophouse outside Mountain View, whose rooms of clustered bunkbeds were mostly filled by young would-be entrepreneurs. The place was miles from Y Combinator, a tough walk with Adam in tow (Uber was out of the question, financially).
Kurnia scoured Airbnb and Craigslist for something better, but at the rare places she could afford, she was rejected by people who didn't want to live with a mother and her two-year-old. The flophouse, then, it would be: Kurnia and Adam wound up sharing a single bunk for the full three months of YC, with as many as 15 other roommates at once.
Sometimes, when Kurnia became absorbed in her work, the naturally curious Adam might wander over to another resident to ask what he (the residents were mostly male) was doing on his computer. Some found this cute; most didn't. Finally, someone complained to the landlord, who threatened to throw Kurnia and Adam out unless she agreed to clean the bathrooms. Scrubbing toilets for 15 people seemed too time-consuming, so Kurnia negotiated: she would pay a higher rent, take out the trash, and keep closer watch over Adam. The landlord granted a reprieve.
Time in Y Combinator is largely unstructured, but Kurnia made at least a few visits there each week. To get there, she would carpool or hoist Adam up on her shoulders and walk. Moving quickly, she found she could cut the round-trip hike to about an hour. The only problem was when it rained, which happened several times. In those cases, she'd pass an umbrella up to Adam. He'd stay mostly dry, but Kurnia would be fairly wet by the time they arrived. But things like this don't bother a woman who has spent years living in rural Africa, sometimes sleeping on hot cement rooftops.
But at the smaller YC events, like the "office hours" with the partners, Adam did well. He even struck up a bond with Paul Graham. Most people either talk down to two-year-olds or ignore them. But Graham took the time to figure out that Adam was fascinated with trains, says Kurnia, and the two of them spent 10 minutes drawing trains on a white board. Graham treated Adam like a little founder, interested in his interests.
There were all manner of YC social and networking events in the evening, but Kurnia passed on those. Instead she'd walk home with Adam, and he would help carry groceries from a store a few blocks from where they were staying. Each evening, Kurnia would "have dinner with my husband," she says, each sitting in front of Skype as they ate, thousands of miles apart. Then she'd take Adam up to the bunk bed and read to him as he fell asleep. She'd read a story about baby bears over the muffled shouts ("We've got to get this app out by tomorrow!") of wannabe Zuckerbergs one room over.
Then, once Adam was asleep, she'd work on Zidisha, guided by the advice she'd gleaned at Y Combinator, until she couldn't stay awake any longer.
After Demo Day—Y Combinator's culminating event—the other founders told her, "You can't go home now, this is your opportunity!" It's customary for YC founders to stick around the Bay Area for weeks or months, riding the wave and drumming up funds. But Kurnia had made a promise to her husband, and flew back with Adam. The three traveled to Indonesia for Ramadan to visit Terra's family.
Kurnia did manage to make a few trips back to the Bay Area over the following months, raising hundreds of thousands of dollars. This past May, she went back for a round of meetings, while pregnant with her second child.
Prior to Y Combinator, Zidisha administered $50,000 per month in loans. Last month it did $200,000, and is on track to grow more.
Those three months at Y Combinator were transformative. They were also, in her circumstances, tough. She remembers what it was like, touching down at Washington Dulles Airport after three months of separating her family for the sake of her work.
I did the right thing, she thought. But I'll never do it again.
Editor's note: This story has been updated to include information about the living expenses covered by Y Combinator.


text:
arkansas razorback football history
In the beginning ...
Join us on the 6th of each month for the newest blog in our series on hawg-tales.com. Feel free to make comments and suggestions for subjects that you would enjoy seeing. Be sure and tell your friends about us, so they can also take part. Thanks for your support. Be sure and Like us on Facebook at hawg-tales.
Keep the history alive!
Back in the day, college football had its beginning on November 6, 1869, when Rutgers College and the College of New Jersey (now known as Princeton University) matched up at College Field in New Brunswick, New Jersey to play the first game. Twenty five years later, it found its way to Fayetteville with the formation of the Cardinals under a full time Latin professor and part time coach John Clinton Futrall.
Their first season consisted of playing Fort Smith High School in two games (winning both 42-0 and 38-0) and traveling on Monday, November 26 by train to play the Longhorns of the University of Texas in Austin. Having won their first two games by large margins, the Cardinals surely felt that they would be as lucky in this game. However, their luck had run out as they lost before a crowd of 1,500 who paid a total of $700 to watch Arkansas go down in defeat by a score of 54-0. Luckily there were few Cardinal fans present. Thus was born one of the greatest rivalries in college football.
The Arkansas-Texas rivalry had grown from the beginning season and culminated at its peak on December 6th of the 100th year of college football. When #1 Texas would again play #2 Arkansas in the "Game of the Century" (15-14 loss). No one on that first team would ever imagine a matchup like this one.
This month I received a comment from Paul Campbell who is the great nephew of LeRoy (corrected by Paul to be Lee Roy) Campbell. Campbell was a tackle and one of the original 14 Cardinals in 1894. From this email I decided that this would be a good hawg-tales and so now I'm going to pass along some of the GOLDEN information with you that he shared with me.
Campbell was born in Van Buren on December 6, 1874 (significant month and day in Hog football history) and died 92 years later on July 31, 1966, in Sikeston, MO as the last living member of the 1894 team. Had he lived for three more years he would have celebrated his birthday on the 100th year of college football, #1 playing #2 in the "Game of the Century" with Arkansas versus Texas, and the longest living member of the original 14.
One of Lee Roy's grandchildren wrote this football-related comment for the family history:
"When I was about 8 years old, I went with my parents, Granny, and Grandad to Fayetteville for a University of Arkansas Homecoming. Grandad was the last survivor of the first football team U of A had in 1894. He was honored at half-time and given a white letter sweater with a large red "A" on the front. He said in 1894 Arkansas played Texas and they nearly killed them. Grandad got a broken nose, ribs, and a toe. He said those Texas boys were really mean (laughingly)."
Sadly, Campbell is not listed on the roster of the 1896 football team picture. However, the University has indicated that the 1896 team picture is the earliest one that they have for the football program.There are no pictures for the 1894 or 1895 teams.
"...the last living member of the 1894 team."
As best as I can determine, Campbell may have graduated in the 1895 class, which by the way, is missing from Senior Walk. However, he is listed on the 1894 team roster, but not on the 1895 team which leads me to believe that he may have graduated in the spring of 1895. Because of this, I was not able to get a picture of him since the earliest Cardinal yearbook that the University has is the 1897 issue. Although he only played for one year, Campbell was a very significant part of the team that became the foundation of what is now the present day football program. Thanks, Paul for leading me down this path!
Join us next month, as we once again recall tales of the games, players, and coaches from the past.
Send us your name and e-mail address to receive a reminder of "hawg-tales" each month plus a FREE copy of the 1960's 45-rpm records in mp3 format to play on your computer, tablet, or smart phone. They make a great gift for any Razorback football history buff. Don't forget to let us know where you are from. WPS!
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Check if human
Glenn Short authors this blog. He is shown here with his daughter, although he didn't notice the orange and white outfit on her at the time. It would soon be burned.
1947 Cotton Bowl
1951 Ark. Vs Texas
1963 Texas Tech
1965 Texas Vs. Ark.
1971 Liberty Bowl
1982 Ark. Vs.SMU
1988 Ark. Vs UH
1998 Ark. Vs Tennessee
2001 Ark. Vs. Ole Miss
2003 Independence Bowl
7 Overtimes
Bill Montgomery
Billy Moore
Bobby Burnett
Brandon Burlsworth
Buddy Bob Benson
Callin' The Razorbacks
Damn Texas Refs
Dennis Winston
Dickey Morton
First Bowl Game
First Conference Champs
Francis A. Schmidt
Hogs First Bowl Game
Hogs Vs. #1
Hugo Bezdek
Jack Mitchell
James Street
Jim Lindsey
Joe Ferguson
John Clinton Futrall
Ken Hatfield
Lee Roy Campbell
"Lighthorse" Harry Jones
Light Hoss Harry
Powder River Pass Play
Preston Carpenter
Quarterbackin Man
Quinn Grovey
Razorback Red
Short Squashed Texan
Steve Little
The Big Red
The Ice Bowl
"Tommy" Thomsen
http://www.hawg-tales.com


All About Counseling's directory of Tampa therapy services is your trusted resource to find a top therapy center provider to find ways to deal with every day issues or more complicated psychological concerns in a clinical setting, deal with problems head on in a clinical environment or get related help.
Each month thousands use our guide to find local professional psychotherapists in Tampa, Florida by simply browsing our therapy center listings, many of which contain ratings and reviews. Helping yourself to improve your self-esteem, mental clarity, emotional wellbeing can be just a click or call away!
Reviews of Tampa professional psychotherapists include ratings, and provider details to assist you in finding the best local therapy center to improve your self-esteem, mental clarity, emotional wellbeing or address related issues. Additionally, searching our directories will allow you to find Tampa counseling psychologists and Tampa therapy providers review and rating information. Locating a Tampa therapy center, psychology expert, or licensed psychiatrist to find ways to deal with every day issues or more complicated psychological concerns in a clinical setting is simple!


text:
Q: Chrome extension - Messaging with multiple ports In my extension, different content scripts connect to background.js to communicate with each other. The problem I'm having, is that when I receive a message on one port, I am not able to forward this information to the other port. The error I'm getting is:
Error: Attempting to use a disconnected port object

My code in background.js
chrome.runtime.onConnect.addListener(function(port) {
  if(port.name === "menuport") {
    port.onMessage.addListener(function(msg) {
      console.log('BGJS from menuport')
      console.log(msg)
      var page_port = chrome.runtime.connect({name: "pageport"});
      page_port.postMessage(msg);
    });
  } else if (port.name === "pageport") {
    port.onMessage.addListener(function(msg) {
      console.log('BGJS from pageport')
      console.log(msg)
    });
  }
});

The pageport is activated in content.js:
var page_port = chrome.runtime.connect({name: "pageport"});
page_port.postMessage({source: "page", status: "ready"});
page_port.onMessage.addListener(function(msg) {
    console.log(msg)
});

The menuport works with a similar script. The activation of both ports works, I can see in the console. However I can't post a message to a port from background.js.

A: On background.js, when you receive the onConnect callback, you need to store that port as a variable, so you can reuse it later. I see that you discard the port variable under the port.name=="pageport", which causes it to be garbage collected (and disconnected). Store it as window.page_port.
I think you are trying to "connect" from both sides, which does not make sense.
One side connects, the other waits for the onConnect event.