The problems here stem from a lack of comprehensiveness, interoperability, and critical mass uptake as the de facto platform for PPPR. The result of this is a mess of different platforms having different types of commentary on different articles, or sometimes the same ones, none of which can be viewed easily in a single, standardised way. That doesn’t seem very efficient.

Présidentielles et bulles de filtres: le référencement politique de Facebook passé au crible

Pivotal roles are played by three enzymes, (phospho-fructokinase (PFK), pyruvate kinase (PK) and phosphofructoki-nase/fructose-2,6-bisphosphatase (PFKFB)) through their inhibi-tion or activation by three reaction intermediates (fructose-1,6-bisphosphate (F16BP), fructose-2,6-bisphosphate (F26BP), andphosphoenolpyruvate (PEP)) in glycolysis. These enzymes havemultiple isoforms (PFKL/M/P, PKM1/M2/L/R and PFKFB1-4)which are subjected to contrasting allosteric regulations [9–11].Each isoform, therefore, affects the glycolytic activity in a distinctmanner.All three isoforms of PFK are activated by F6P and F26BP [12],but only PFKM and PFKL are activated by F16BP [13–15].PFKFB is a bifunctional enzyme whose kinase and bisphosphatasedomains catalyze the formation and hydrolysis reaction of F26BP,respectively [9,16]. Isozymes of PFKFB differ in their kinase andphosphatase activities as well as in their sensitivity to feedbackinhibition by phosphoenolpyruvate (PEP) [17–19]. Thus, eachisozyme of PFKFB has a profoundly distinct capacity inmodulating PFK activity. Pyruvate kinase (PK) in mammaliansystems is encoded by two genes that can produce two isoformseach. Except for the PKM1 isoform, the other three isoformsof PK, PKM2, PKL and PKR, are activated by F16BP to varyingextents [11]. The M2 isoform of PK, in addition to activation byF16BP, is also under the control of a host of allosteric modulatorsincluding serine, succinylaminoimidazolecarboxamide ribose-5-phosphate (SAICAR) and phenylalanine among others [

Author and peer reviewer anonymity haven’t been shown to have an overall benefit, and they may cause harm. Part of the potential for harm is if journals act as though it’s a sufficiently effective mechanism to prevent bias.

Peer reviewers were more likely to substantiate the points they made (9, 14, 16, 17) when they knew they would be named. They were especially likely to provide extra substantiation if they were recommending an article be rejected, and they knew their report would be published if the article was accepted anyway (9, 15).