Identification of 16SrII-V Phytoplasma Associated with Mungbean Phyllody Disease in Taiwan.

Mungbean (Vigna radiata (L.) R. Wilczek), an important legume crop in Asia, is primarily cultivated in the central-southern region of western Taiwan. In 2020, mungbean exhibiting typical phytoplasma-induced disease symptoms such as witches' broom, phyllody, virescence, and proliferation was observed in Yunlin County, Taiwan. Moreover, the seed harvested from diseased plants displayed premature germination. Transmission electron microscopy examination of leaf veins prepared from symptomatic mungbean demonstrated that the occlusion of sieve tubes resulted from the accumulation of phytoplasma-like bodies in sieve elements along with filament-like structures in sieve pores. The association of phytoplasma in symptomatic mungbean was confirmed by PCR analyses of the 16S ribosomal RNA (rRNA) and immunodominant membrane protein genes. Further analyses of the 16S rRNA-based phylogenetic tree and the iPhyClassifier-based virtual restriction fragment length polymorphism study demonstrated that the phytoplasma-associated mungbean phyllody disease identified in this study belongs to the 16SrII-V subgroup. BLAST analysis and the phylogenetic analysis indicated that the SAP11-like protein identified in mungbean phyllody disease is identical to peanut witches' broom phytoplasma SAP11, which explains the witches' broom phenotype observed in symptomatic mungbean. The results described in this report confirm that the 16SrII-V phytoplasma, a widely distributed phytoplasma associated with peanut witches' broom disease in Taiwan, has also infected mungbean. This is not only the first instance of mungbean phyllody disease found in Taiwan but also the first instance of mungbean phyllody disease caused by 16SrII-V subgroup phytoplasma.

Nano-colorimetrically determined refractive index variation with ultra-high chromatic resolution.

We develop a front-to-end solution where the shift of chromaticity from scattering of plasmonic nanoparticles is used as the reporter for nano-environmental refractive index variation. By co-projecting possible power combinations of RGB LEDs and digitized color grid density of CCD with various luminance onto the CIE 1931 chromaticity diagram, optimum condition for nanoenvironment sensing can be achieved. The highest resolution for local refractive index change is 0.0021 per distinguishable color, which is higher than that of a typical handheld spectrometer by 4.8 times. This result shows great potential in simplifying nano-environment sensing instruments and is particularly useful for multi-point dynamical process.

Neuronal levels and sequence of tau modulate the power of brain rhythms.

Neural network dysfunction may contribute to functional decline and disease progression in neurodegenerative disorders. Diverse lines of evidence suggest that neuronal accumulation of tau promotes network dysfunction and cognitive decline. The A152T-variant of human tau (hTau-A152T) increases the risk of Alzheimer's disease (AD) and several other tauopathies. When overexpressed in neurons of transgenic mice, it causes age-dependent neuronal loss and cognitive decline, as well as non-convulsive epileptic activity, which is also seen in patients with AD. Using intracranial EEG recordings with electrodes implanted over the parietal cortex, we demonstrate that hTau-A152T increases the power of brain oscillations in the 0.5-6 Hz range more than wildtype human tau in transgenic lines with comparable levels of human tau protein in brain, and that genetic ablation of endogenous tau in Mapt-/- mice decreases the power of these oscillations as compared to wildtype controls. Suppression of hTau-A152T production in doxycycline-regulatable transgenic mice reversed their abnormal network activity. Treatment of hTau-A152T mice with the antiepileptic drug levetiracetam also rapidly and persistently reversed their brain dysrhythmia and network hypersynchrony. These findings suggest that both the level and the sequence of tau modulate the power of specific brain oscillations. The potential of EEG spectral changes as a biomarker deserves to be explored in clinical trials of tau-lowering therapeutics. Our results also suggest that levetiracetam treatment is able to counteract tau-dependent neural network dysfunction. Tau reduction and levetiracetam treatment may be of benefit in AD and other conditions associated with brain dysrhythmias and network hypersynchrony.

Autistic-like behaviour in Scn1a+/- mice and rescue by enhanced GABA-mediated neurotransmission.

Haploinsufficiency of the SCN1A gene encoding voltage-gated sodium channel Na(V)1.1 causes Dravet's syndrome, a childhood neuropsychiatric disorder including recurrent intractable seizures, cognitive deficit and autism-spectrum behaviours. The neural mechanisms responsible for cognitive deficit and autism-spectrum behaviours in Dravet's syndrome are poorly understood. Here we report that mice with Scn1a haploinsufficiency exhibit hyperactivity, stereotyped behaviours, social interaction deficits and impaired context-dependent spatial memory. Olfactory sensitivity is retained, but novel food odours and social odours are aversive to Scn1a(+/-) mice. GABAergic neurotransmission is specifically impaired by this mutation, and selective deletion of Na(V)1.1 channels in forebrain interneurons is sufficient to cause these behavioural and cognitive impairments. Remarkably, treatment with low-dose clonazepam, a positive allosteric modulator of GABA(A) receptors, completely rescued the abnormal social behaviours and deficits in fear memory in the mouse model of Dravet's syndrome, demonstrating that they are caused by impaired GABAergic neurotransmission and not by neuronal damage from recurrent seizures. These results demonstrate a critical role for Na(V)1.1 channels in neuropsychiatric functions and provide a potential therapeutic strategy for cognitive deficit and autism-spectrum behaviours in Dravet's syndrome.

Impaired excitability of somatostatin- and parvalbumin-expressing cortical interneurons in a mouse model of Dravet syndrome.

Haploinsufficiency of the voltage-gated sodium channel NaV1.1 causes Dravet syndrome, an intractable developmental epilepsy syndrome with seizure onset in the first year of life. Specific heterozygous deletion of NaV1.1 in forebrain GABAergic-inhibitory neurons is sufficient to cause all the manifestations of Dravet syndrome in mice, but the physiological roles of specific subtypes of GABAergic interneurons in the cerebral cortex in this disease are unknown. Voltage-clamp studies of dissociated interneurons from cerebral cortex did not detect a significant effect of the Dravet syndrome mutation on sodium currents in cell bodies. However, current-clamp recordings of intact interneurons in layer V of neocortical slices from mice with haploinsufficiency in the gene encoding the NaV1.1 sodium channel, Scn1a, revealed substantial reduction of excitability in fast-spiking, parvalbumin-expressing interneurons and somatostatin-expressing interneurons. The threshold and rheobase for action potential generation were increased, the frequency of action potentials within trains was decreased, and action-potential firing within trains failed more frequently. Furthermore, the deficit in excitability of somatostatin-expressing interneurons caused significant reduction in frequency-dependent disynaptic inhibition between neighboring layer V pyramidal neurons mediated by somatostatin-expressing Martinotti cells, which would lead to substantial disinhibition of the output of cortical circuits. In contrast to these deficits in interneurons, pyramidal cells showed no differences in excitability. These results reveal that the two major subtypes of interneurons in layer V of the neocortex, parvalbumin-expressing and somatostatin-expressing, both have impaired excitability, resulting in disinhibition of the cortical network. These major functional deficits are likely to contribute synergistically to the pathophysiology of Dravet syndrome.

Dissecting the phenotypes of Dravet syndrome by gene deletion.

Neurological and psychiatric syndromes often have multiple disease traits, yet it is unknown how such multi-faceted deficits arise from single mutations. Haploinsufficiency of the voltage-gated sodium channel Nav1.1 causes Dravet syndrome, an intractable childhood-onset epilepsy with hyperactivity, cognitive deficit, autistic-like behaviours, and premature death. Deletion of Nav1.1 channels selectively impairs excitability of GABAergic interneurons. We studied mice having selective deletion of Nav1.1 in parvalbumin- or somatostatin-expressing interneurons. In brain slices, these deletions cause increased threshold for action potential generation, impaired action potential firing in trains, and reduced amplification of postsynaptic potentials in those interneurons. Selective deletion of Nav1.1 in parvalbumin- or somatostatin-expressing interneurons increases susceptibility to thermally-induced seizures, which are strikingly prolonged when Nav1.1 is deleted in both interneuron types. Mice with global haploinsufficiency of Nav1.1 display autistic-like behaviours, hyperactivity and cognitive impairment. Haploinsufficiency of Nav1.1 in parvalbumin-expressing interneurons causes autistic-like behaviours, but not hyperactivity, whereas haploinsufficiency in somatostatin-expressing interneurons causes hyperactivity without autistic-like behaviours. Heterozygous deletion in both interneuron types is required to impair long-term spatial memory in context-dependent fear conditioning, without affecting short-term spatial learning or memory. Thus, the multi-faceted phenotypes of Dravet syndrome can be genetically dissected, revealing synergy in causing epilepsy, premature death and deficits in long-term spatial memory, but interneuron-specific effects on hyperactivity and autistic-like behaviours. These results show that multiple disease traits can arise from similar functional deficits in specific interneuron types.

Fuzzy logic feedback control for fed-batch enzymatic hydrolysis of lignocellulosic biomass.

A fuzzy logic feedback control system was developed for process monitoring and feeding control in fed-batch enzymatic hydrolysis of a lignocellulosic biomass, dilute acid-pretreated corn stover. Digested glucose from hydrolysis reaction was assigned as input while doser feeding time and speed of pretreated biomass were responses from fuzzy logic control system. Membership functions for these three variables and rule-base were created based on batch hydrolysis data. The system response was first tested in LabVIEW environment then the performance was evaluated through real-time hydrolysis reaction. The feeding operations were determined timely by fuzzy logic control system and efficient responses were shown to plateau phases during hydrolysis. Feeding of proper amount of cellulose and maintaining solids content was well balanced. Fuzzy logic proved to be a robust and effective online feeding control tool for fed-batch enzymatic hydrolysis.

Label-free multi-color superlocalization of plasmonic emission within metallic nano-interstice using femtosecond chirp-manipulated four wave mixing.

We demonstrate an as yet unused method to sieve, localize, and steer plasmonic hot spot within metallic nano-interstices close to percolation threshold. Multicolor superlocalization of plasmon mode within 60 nm was constantly achieved by chirp-manipulated superresolved four wave mixing (FWM) images. Since the percolated film is strongly plasmonic active and structurally multiscale invariant, the present method provides orders of magnitude enhanced light localization within single metallic nano-interstice, and can be universally applied to any region of the random film. The result, verified by the maximum likelihood estimation (MLE) and deconvolution stochastic optical reconstruction microscopy (deconSTORM) algorithm, may contribute to label-free multiplex superlocalized spectroscopy of single molecule and sub-cellular activity monitoring combining hot spot steering capability.

Optimal control strategy for fed-batch enzymatic hydrolysis of lignocellulosic biomass based on epidemic modeling.

A mathematical optimal control strategy for feeding operation was developed for fed-batch enzymatic hydrolysis of dilute acid pretreated lignocellulosic biomass based on a modified epidemic model. Cellulose conversion was maximized and glucose concentration achieved highest possible value over a fixed hydrolysis time. Boundaries of feeding rate and lignin content were set for feasible controls. Using the optimal control feeding strategy, glucose concentration and accumulated cellulose conversion reached up to 77.31 g/L and 72.08% in 100 h, which are 108.76% and 37.50% higher than in batch hydrolysis with same amount of enzyme consumption. Solids content in feeding source has a significant interference on system mass transfer. Optimal control is a useful tool for guiding operations in fed-batch and continuous processes as it enables process optimization through clear objective functions and feasible controls.

Methylmercury photodegradation in surface water of the Florida Everglades: importance of dissolved organic matter-methylmercury complexation.

Photodegradation is the major pathway of methylmercury (MeHg) degradation in many surface waters. However, the mechanism of MeHg photodegradation is still not completely understood. Dissolved organic matter (DOM) is expected to play a critical role in MeHg photodegradation. By using several techniques, including N2/O2 purging and the addition of stable isotope (Me(201)Hg), scavengers, competing ligands, and a singlet oxygen ((1)O2) generator, the role played by MeHg-DOM complexation in MeHg photodegradation of Everglades surface water was investigated. DOM appeared to be involved in MeHg photodegradation via the formation MeHg-DOM complexes based on three findings: (1) MeHg was quickly photodegraded in solutions containing DOM extracts; (2) degradation of MeHg did not occur in deionized water; and (3) addition of competing complexation reagents (dithiothreitol-DTT) dramatically prohibited the photodegradation of MeHg in Everglades water. Further experiments indicated that free radicals/reactive oxygen species, including hydroxyl radical (·OH), (1)O2, triplet excited state of DOM ((3)DOM*), and hydrated electron (e(-)aq), played a minor role in MeHg photodegradation in Everglades water, based on the results of scavenger addition, (1)O2 generator addition and N2/O2 purging. A pathway, involving direct photodegradation of MeHg-DOM complexes via intramolecular electron transfer, is proposed as the dominant mechanism for MeHg photodegradation in Everglades water.