Simultaneous detection of the nonlinear restoring and excitation of a forced nonlinear oscillation: an integral approach

We address in this article, how to calculate the restoring characteristic and the excitation of a nonlinear forced oscillating system. Under the assumption that the forced nonlinear oscillator has a periodic solution with period, we constructed a system of linear equations by introducing time-dependent multipliers. The periodicity assumption helps simplify the system of linear equations. The stability and uniqueness are also presented for the inverse problem. Numerical testing is conducted to show the effectiveness of our presented methodology.Peer ReviewedPostprint (author's final draft

Production of L(+)-Lactic Acid from Mixed Acid and Alkali Hydrolysate of Brown Seaweed

The species of brown seaweeds, Laminaria japonica is commercially cultivated in Japan. Mannitol and uronic acid were the main component of mono sugar produced from the saccharification of L. japonica which hydrolysed with H2SO4 or NH4OH. The mannitol concentration of L. japonica (5w/v%) hydrolysate using 0.5v/v% H2SO4 or 1v/v% NH4OH were 15.84g/L and 13.87g/L, respectively. Hydrolysates from both acid and alkali hydrolysis were mixed together for neutralization as well as to obtain higher mannitol concentration of 15.18g/L. Among the mono sugar in the hydrolysate, Mannitol was the main substrate for the lactic acid fermentation by Lactobacillus rhamnosus. L(+)-Lactic acid with 97.9% of optical purity was successfully produced at the yield of 14.42g/L (Yp/s = 94.99%)

Potential Use of Gelidium amansii Acid Hydrolysate for Lactic Acid Production by Lactobacillus rhamnosus

Galactose and glucose are the main monosaccharides produced from the saccharification of Gelidium amansii. They were hydrolysed with 3 % (by volume) H2SO4 at 140 °C for 5 min and obtained at concentrations of 19.60 and 10.21 g/L, respectively. G. amansii hydrolysate (5 %, by mass per volume) was used as a substrate for L(+)-lactic acid production by Lactobacillus rhamnosus. The maximum lactic acid yield (YP/S) was 42.03 % with optical purity of 84.54 %. Lactic acid produced from G. amansii hydrolysate can be applicable, among others, for the production of lactic acid esters, like ethyl or methyl lactate, and disinfectant in seaweed cultivation

To the Edge of M87 and Beyond: Spectroscopy of Intracluster Globular Clusters and Ultra Compact Dwarfs in the Virgo Cluster

We present the results from a wide-field spectroscopic survey of globular clusters (GCs) in the Virgo Cluster. We obtain spectra for 201 GCs and 55 ultracompact dwarfs (UCDs) using the Hectospec on the Multiple Mirror Telescope, and derive their radial velocities. We identify 46 genuine intracluster GCs (IGCs), not associated with any Virgo galaxies, using the 3D GMM test on the spatial and radial velocity distribution.They are located at the projected distance 200 kpc $\lesssim$ R $\lesssim$ 500 kpc from the center of M87. The radial velocity distribution of these IGCs shows two peaks, one at $v_{\rm r}$ = 1023 km s$^{-1}$ associated with the Virgo main body, and another at $v_{\rm r}$ = 36 km s$^{-1}$ associated with the infalling structure. The velocity dispersion of the IGCs in the Virgo main body is $\sigma_{\rm{GC}} \sim$ 314 km s$^{-1}$, which is smoothly connected to the velocity dispersion profile of M87 GCs, but much lower than that of dwarf galaxies in the same survey field, $\sigma_{\rm{dwarf}} \sim$ 608 km s$^{-1}$. The UCDs are more centrally concentrated on massive galaxies, M87, M86, and M84. The radial velocity dispersion of the UCD system is much smaller than that of dwarf galaxies. Our results confirm the large-scale distribution of Virgo IGCs indicated by previous photometric surveys. The color distribution of the confirmed IGCs shows a bimodality similar to that of M87 GCs. This indicates that most IGCs are stripped off from dwarf galaxies and some from massive galaxies in the Virgo.Comment: 19 pages, 20 figures, 8 tables, accepted for publication in Ap

The Association of Maximum Body Weight on the Development of Type 2 Diabetes and Microvascular Complications: MAXWEL Study

Background: Obesity precedes the development of type 2 diabetes (T2D). However, the relationship between the magnitude and rate of weight gain to T2D development and complications, especially in non-White populations, has received less attention. Methods and Findings: We determined the association of rate and magnitude of weight gain to age at T2D diagnosis (AgeT2D), HbA1c at T2D diagnosis (HbA1cT2D), microalbuminuria, and diabetic retinopathy after adjusting for sex, BMI at age 20 years, lifestyles, family history of T2D and/or blood pressure and lipids in 2164 Korean subjects aged ≥30 years and newly diagnosed with diabetes. Body weight at age 20 years (Wt20y) was obtained by recall or from participants’ medical, school, or military records. Participants recalled their maximum weight (Wtmax) prior to T2D diagnosis and age at maximum weight (Agemax_wt). The rate of weight gain (Ratemax_wt) was calculated from magnitude of weight gain (ΔWt = Wtmax–Wt20y) divided by ΔTime (Agemax_wt –20 years). The mean Agemax_wt and AgeT2D were 41.5±10.9 years and 50.1±10.5 years, respectively. The Wt20y and Wtmax were 59.9±10.5 kg and 72.9±11.4 kg, respectively. The Ratemax_wt was 0.56±0.50 kg/year. After adjusting for risk factors, greater ΔWt and higher Ratemax_wt were significantly associated with earlier AgeT2D, higher HbA1cT2D after additional adjusting for AgeT2D, and microalbuminuria after further adjusting for HbA1cT2D and lipid profiles. Greater ΔWt and higher Ratemax_wt were also significantly associated with diabetic retinopathy. Conclusions: This finding supports public health recommendations to reduce the risk of T2D and its complications by preventing weight gain from early adulthood

Emerging Link between Alzheimer’s Disease and Homeostatic Synaptic Plasticity

Alzheimer’s disease (AD) is an irreversible brain disorder characterized by progressive cognitive decline and neurodegeneration of brain regions that are crucial for learning and memory. Although intracellular neurofibrillary tangles and extracellular senile plaques, composed of insoluble amyloid-β (Aβ) peptides, have been the hallmarks of postmortem AD brains, memory impairment in early AD correlates better with pathological accumulation of soluble Aβ oligomers and persistent weakening of excitatory synaptic strength, which is demonstrated by inhibition of long-term potentiation, enhancement of long-term depression, and loss of synapses. However, current, approved interventions aiming to reduce Aβ levels have failed to retard disease progression; this has led to a pressing need to identify and target alternative pathogenic mechanisms of AD. Recently, it has been suggested that the disruption of Hebbian synaptic plasticity in AD is due to aberrant metaplasticity, which is a form of homeostatic plasticity that tunes the magnitude and direction of future synaptic plasticity based on previous neuronal or synaptic activity. This review examines emerging evidence for aberrant metaplasticity in AD. Putative mechanisms underlying aberrant metaplasticity in AD will also be discussed. We hope this review inspires future studies to test the extent to which these mechanisms contribute to the etiology of AD and offer therapeutic targets

Novel roles of striatal enriched protein phosphatase (STEP) in neuronal intrinsic properties and homeostatic synaptic plasticity

STriatal Enrich Protein Phosphatase (STEP) is a brain specific protein tyrosine phosphatase, which is only expressed in the central nervous system (CNS). STEP has two major isoforms, including STEP46 and STEP61 and membrane-bound STEP61 is implicated in multiple neurologic disorders. For example, the level of STEP61 is elevated in animal disease models and postmortem samples of Alzheimer’s disease and Schizophrenia, whereas its activity is reduced in brain ischemia and Huntington’s diseases. STEP61 regulates Hebbian forms of synaptic plasticity, which has been considered as a mechanism by which the information is encoded and stored at the synapse. STEP61 is involved in the internalization of the N-methyl-D-aspartate receptors (NMDARs) and the α-amino-hydroxy-5-methyl-4-isoxazolepropinoic acid receptors (AMPARs) via dephosphorylating Tyr1472 of GluN2B subunit in NMDAR and 3 Tyr (Tyr869, Tyr873, and Tyr876) of GluA2 subunit in AMPAR. Despite extensive studies on the role of STEP61 in activity-dependent synaptic plasticity, including long-term synaptic potentiation and depression, it was unknown whether STEP contributes to homeostatic synaptic plasticity, a compensatory mechanism by which neurons adjust their synaptic strength within a normal range in response to chronic activity challenge. In addition, whether STEP regulates somatic intrinsic properties of hippocampal pyramidal neurons has to be addressed. This dissertation is focused on finding novel roles of STEP in homeostatic adjustment of synaptic strength and neuronal intrinsic properties in the hippocampus. The first chapter of this work describes background information about keywords related to research topics written in this dissertation. In the second chapter, I describe the results on the involvement of STEP in homeostatic synaptic plasticity using in vitro primary hippocampal cultured neurons. In the third and fourth chapter, I describe the alteration of STEP expression and activity and the elevation of amyloid-β following an electroconvulsive seizure (ECS) and Kainic-acid (KA) induced status epilepticus (SE) accompanied by network hyper-excitability. The fifth chapter provides a novel evidence into STEP regulates neuronal intrinsic properties in the hippocampal neurons. In the part of appendix, I describe subcellular fractionation technique using hippocampi from rats which underwent ECS, and molecular and electrophysiological verification of chemical long-term potentiation (cLTP). Taken together, the findings in this dissertation suggest that STEP plays crucial roles in mediating homeostatic responses at the excitatory synapses and regulating intrinsic neuronal properties of hippocampal pyramidal neurons