New types of bialgebras arising from the Hopf equation

New types of bialgebras arising from the Hopf equation (pentagonal equation) are introduced and studied. They will play from the Hopf equation the same role as the co-quasitriangular do from the quantum Yang Baxter equation.Comment: Latex2e, Comm Algebra, in pres

The Hopf modules category and the Hopf equation

We study the Hopf equation which is equivalent to the pentagonal equation, from operator algebras. A FRT type theorem is given and new types of quantum groups are constructed. The key role is played now by the classical Hopf modules category. As an application, a five dimensional noncommutative noncocommutative bialgebra is given.Comment: 30 pages, Letax2e, Comm. Algebra in pres

The death of recency: Relationship between end-state comfort and serial position effects in serial recall: Logan and Fischman (2011) revisited

Two experiments examined the dynamic interaction between cognitive resources in short-term memory and bimanual object manipulation by extending recent research by Logan and Fischman (2011). In Experiment 1, 16 participants completed a bimanual end-state comfort task and a memory task requiring serial recall of 12 words or pictures. The end-state comfort task involved moving two glasses between two shelves. Participants viewed the items, performed the end-state comfort task, and then serially recalled the items. Recall was evaluated by the presence or absence of primacy and recency effects. The end-state comfort effect (ESCE) was assessed by the percentage of initial hand positions that allowed the hands to end comfortably. The main findings indicated that the ESCE was disrupted; the primacy effect remained intact; and the recency effect disappeared regardless of the type of memory item recalled. In Experiment 2, 16 participants viewed six items, performed an end-state comfort task, viewed another six items, and then serially recalled all 12 items. Results were essentially the same as in Experiment 1. Findings suggest that executing a bimanual end-state comfort task, regardless of when it is completed during a memory task, diminishes the recency effect irrespective of the type of memory item.Keywords: Motor processes, Learning and memor

Role of Protein Farnesylation in Burn-Induced Metabolic Derangements and Insulin Resistance in Mouse Skeletal Muscle

Objective: Metabolic derangements, including insulin resistance and hyperlactatemia, are a major complication of major trauma (e.g., burn injury) and affect the prognosis of burn patients. Protein farnesylation, a posttranslational lipid modification of cysteine residues, has been emerging as a potential component of inflammatory response in sepsis. However, farnesylation has not yet been studied in major trauma. To study a role of farnesylation in burn-induced metabolic aberration, we examined the effects of farnesyltransferase (FTase) inhibitor, FTI-277, on burn-induced insulin resistance and metabolic alterations in mouse skeletal muscle. Methods: A full thickness burn (30% total body surface area) was produced under anesthesia in male C57BL/6 mice at 8 weeks of age. After the mice were treated with FTI-277 (5 mg/kg/day, IP) or vehicle for 3 days, muscle insulin signaling, metabolic alterations and inflammatory gene expression were evaluated. Results: Burn increased FTase expression and farnesylated proteins in mouse muscle compared with sham-burn at 3 days after burn. Simultaneously, insulin-stimulated phosphorylation of insulin receptor (IR), insulin receptor substrate (IRS)-1, Akt and GSK-3β was decreased. Protein expression of PTP-1B (a negative regulator of IR-IRS-1 signaling), PTEN (a negative regulator of Akt-mediated signaling), protein degradation and lactate release by muscle, and plasma lactate levels were increased by burn. Burn-induced impaired insulin signaling and metabolic dysfunction were associated with increased inflammatory gene expression. These burn-induced alterations were reversed or ameliorated by FTI-277. Conclusions: Our data demonstrate that burn increased FTase expression and protein farnesylation along with insulin resistance, metabolic alterations and inflammatory response in mouse skeletal muscle, all of which were prevented by FTI-277 treatment. These results indicate that increased protein farnesylation plays a pivotal role in burn-induced metabolic dysfunction and inflammatory response. Our study identifies FTase as a novel potential molecular target to reverse or ameliorate metabolic derangements in burn patients

Modular Design of a Passive, Low-Cost Prosthetic Knee Mechanism to Enable Able-Bodied Kinematics for Users With Transfemoral Amputation

There is a significant need for low-cost, high-performance prosthetic knee technology for transfemoral amputees in India. Replicating able-bodied gait in amputees is biomechanically necessary to reduce the metabolic cost, and it is equally important to mitigate the socio-economic discrimination faced by amputees in developing countries due to their conspicuous gait deviations. This paper improves upon a previous study of a fully passive knee mechanism, addressing the issues identified in its user testing in India. This paper presents the design, analysis and bench-level testing of the three major functional modules of the new prosthetic knee architecture: (i) a four-bar latch mechanism for achieving stability during stance phase of walking, (ii) an early stance flexion module designed by implementing a fully adjustable mechanism, and (iii) a hydraulic rotary damping system for achieving smooth and reliable swing-phase control

Recruitment, augmentation and apoptosis of rat osteoclasts in 1,25-(OH)2D3 response to short-term treatment with 1,25-dihydroxyvitamin D3in vivo

Background Although much is known about the regulation of osteoclast (OC) formation and activity, little is known about OC senescence. In particular, the fate of of OC seen after 1,25-(OH)2D3 administration in vivo is unclear. There is evidence that the normal fate of OC is to undergo apoptosis (programmed cell death). We have investigated the effect of short-term application of high dose 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) on OC apoptosis in an experimental rat model. Methods OC recruitment, augmentation and apoptosis was visualised and quantitated by staining histochemically for tartrate resistant acid phosphatase (TRAP), double staining for TRAP/ED1 or TRAP/DAPI, in situ DNA fragmentation end labelling and histomorphometric analysis. Results Short-term treatment with high-dose 1,25-(OH)2D3 increased the recruitment of OC precursors in the bone marrow resulting in a short-lived increase in OC numbers. This was rapidly followed by an increase in the number of apoptotic OC and their subsequent removal. The response of OC to 1,25-(OH)2D3 treatment was dose and site dependent; higher doses producing stronger, more rapid responses and the response in the tibiae being consistently stronger and more rapid than in the vertebrae. Conclusions This study demonstrates that (1) after recruitment, OC are removed from the resorption site by apoptosis (2) the combined use of TRAP and ED1 can be used to identify OC and their precursors in vivo (3) double staining for TRAP and DAPI or in situ DNA fragmentation end labelling can be used to identify apoptotic OC in vivo

The carboxyl terminus of myosin binding protein C (MyBP-C, C-protein) specifies incorporation into the A-band of striated muscle

Myosin binding protein-C (MyBP-C), also known as C-protein, is a major constituent of the thick filaments of vertebrate striated muscles. The protein, approximately 130 kDa, consists of a series of 10 globular motifs (numbered I to X) each of approximately 90-100 amino acids, bearing resemblance to the C2-set of immunoglobins (Ig C2) and to the fibronectin type III (FnIII) motifs. Using pure preparations of myosin and MyBP-C, it has been demonstrated that the major myosin binding domain of MyBP-C resides within the C-terminal Ig C2 motif (motif X). However, in the context of the in vivo thick filament, it is uncertain if the latter domain is sufficient to target MyBP-C correctly to the A-band or if other regions of the molecule are required for this process. To answer this question, cultures of skeletal muscle myoblasts were transfected with expression plasmids encoding seven truncation mutants of MyBP-C, and their targeting to the A-band investigated by immunofluorescence microscopy. To distinguish the recombinant proteins from endogenous MyBP-C, a myc epitope was inserted at each amino terminus. Recombinant MyBP-C exhibited an identical distribution in the sarcomere to that of native MyBP-C; i.e. it was found exclusively in the C-zone of the A-band. A mutant encoding the C-terminal 372 amino acids, but lacking motifs I-VI (termed delta 1-6), also targeted correctly to the A-band. This fragment, which is composed of two Ig C2 and two FnIII motifs, was the minimal protein fragment required for correct A-band incorporation. Larger amino-terminal deletions or deletion of motif X, the myosin binding domain, abolished all localization to the A-band. One construct (delta 10) lacking only motif X strongly inhibited myofibril assembly. We conclude that the myosin binding domain of MyBP-C, although essential, is not sufficient for correct incorporation into the A-band and that motifs VII to IX are required for this process. The data suggest a topological model in which MyBP-C is associated with the thick filament through its C terminus.NRC publication: N