A Review on Recent Deep Learning-Based Semantic Segmentation for Urban Greenness Measurement.

Accurate urban green space (UGS) measurement has become crucial for landscape analysis. This paper reviews the recent technological breakthroughs in deep learning (DL)-based semantic segmentation, emphasizing efficient landscape analysis, and integrating greenness measurements. It explores quantitative greenness measures applied through semantic segmentation, categorized into the plan view- and the perspective view-based methods, like the Land Class Classification (LCC) with green objects and the Green View Index (GVI) based on street photographs. This review navigates from traditional to modern DL-based semantic segmentation models, illuminating the evolution of the urban greenness measures and segmentation tasks for advanced landscape analysis. It also presents the typical performance metrics and explores public datasets for constructing these measures. The results show that accurate (semantic) segmentation is inevitable not only for fine-grained greenness measures but also for the qualitative evaluation of landscape analyses for planning amidst the incomplete explainability of the DL model. Also, the unsupervised domain adaptation (UDA) in aerial images is addressed to overcome the scale changes and lack of labeled data for fine-grained greenness measures. This review contributes to helping researchers understand the recent breakthroughs in DL-based segmentation technology for challenging topics in UGS research.

High-Performance Self-Powered Quantum Dot Infrared Photodetector with Azide Ion Solution Treated Electron Transport Layer.

The demand for self-powered photodetectors (PDs) capable of NIR detection without external power is growing with the advancement of NIR technologies such as LIDAR and object recognition. Lead sulfide quantum dot-based photodetectors (PbS QPDs) excel in NIR detection; however, their self-powered operation is hindered by carrier traps induced by surface defects and unfavorable band alignment in the zinc oxide nanoparticle (ZnO NP) electron-transport layer (ETL). In this study, an effective azide-ion (N3 - ) treatment is introduced on a ZnO NP ETL to reduce the number of traps and improve the band alignment in a PbS QPD. The ZnO NP ETL treated with azide ions exhibited notable improvements in carrier lifetime and mobility as well as an enhanced internal electric field within the thin-film heterojunction of the ZnO NPs and PbS QDs. The azide-ion-treated PbS QPD demonstrated a increase in short-circuit current density upon NIR illumination, marking a responsivity of 0.45 A W-1 , specific detectivity of 4 × 1011 Jones at 950 nm, response time of 8.2 µs, and linear dynamic range of 112 dB.

The Monitoring and Management of an Operating Environment to Enhance the Safety of a Container-Type Energy Storage System.

The implementation of an energy storage system (ESS) as a container-type package is common due to its ease of installation, management, and safety. The control of the operating environment of an ESS mainly considers the temperature rise due to the heat generated through the battery operation. However, the relative humidity of the container often increases by over 75% in many cases because of the operation of the air conditioner which pursues temperature-first control. Humidity is a major factor which can cause safety issues such as fires owing to insulation breakdown caused by condensation. However, the importance of humidity control in ESS is underestimated compared to temperature control. In this study, temperature and humidity monitoring and management issues were addressed for a container-type ESS by building sensor-based monitoring and control systems. Furthermore, a rule-based air conditioner control algorithm was proposed for temperature and humidity management. A case study was conducted to compare the conventional and proposed control algorithms and verify the feasibility of the proposed algorithm. The results showed that the proposed algorithm reduced the average humidity by 11.4% compared to the value achieved with the existing temperature control method while also maintaining the temperature.

Depression-like behaviors induced by defective PTPRT activity through dysregulated synaptic functions and neurogenesis.

PTPRT has been known to regulate synaptic formation and dendritic arborization of hippocampal neurons. PTPRT-/- null and PTPRT-D401A mutant mice displayed enhanced depression-like behaviors compared with wild-type mice. Transient knockdown of PTPRT in the dentate gyrus enhanced the depression-like behaviors of wild-type mice, whereas rescued expression of PTPRT ameliorated the behaviors of PTPRT-null mice. Chronic stress exposure reduced expression of PTPRT in the hippocampus of mice. In PTPRT-deficient mice the expression of GluR2 (also known as GRIA2) was attenuated as a consequence of dysregulated tyrosine phosphorylation, and the long-term potentiation at perforant-dentate gyrus synapses was augmented. The inhibitory synaptic transmission of the dentate gyrus and hippocampal GABA concentration were reduced in PTPRT-deficient mice. In addition, the hippocampal expression of GABA transporter GAT3 (also known as SLC6A11) was decreased, and its tyrosine phosphorylation was increased in PTPRT-deficient mice. PTPRT-deficient mice displayed reduced numbers and neurite length of newborn granule cells in the dentate gyrus and had attenuated neurogenic ability of embryonic hippocampal neural stem cells. In conclusion, our findings show that the physiological roles of PTPRT in hippocampal neurogenesis, as well as synaptic functions, are involved in the pathogenesis of depressive disorder.

Effects of histone acetyltransferase inhibitors on L-DOPA-induced dyskinesia in a murine model of Parkinson's disease.

Histone acetylation is a key regulatory factor for gene expression in cells. Modulation of histone acetylation by targeting of histone acetyltransferases (HATs) effectively alters many gene expression profiles and synaptic plasticity in the brain. However, the role of HATs on L-DOPA-induced dyskinesia of Parkinson's disease (PD) has not been reported. Our aim was to determine whether HAT inhibitors such as anacardic acid, garcinol, and curcumin from natural plants reduce severity of L-DOPA-induced dyskinesia using a unilaterally 6-hydroxydopamine (6-OHDA)-lesioned PD mouse model. Anacardic acid 2 mg/kg, garcinol 5 mg/kg, or curcumin 100 mg/kg co-treatment with L-DOPA significantly reduced the axial, limb, and orofacial (ALO) score indicating less dyskinesia with administration of HAT inhibitors in 6-OHDA-lesioned mice. Additionally, L-DOPA's efficacy was not altered by the compounds in the early stage of treatment. The expression levels of c-Fos, Fra-2, and Arc were effectively decreased by administration of HAT inhibitors in the ipsilateral striatum. Our findings indicate that HAT inhibitor co-treatment with L-DOPA may have therapeutic potential for management of L-DOPA-induced dyskinesia in patients with PD.

Gadd45ß ameliorates L-DOPA-induced dyskinesia in a Parkinson's disease mouse model.

The dopamine precursor 3,4-dihydroxyphenyl-l-alanine (L-DOPA) is currently the most efficacious pharmacotherapy for Parkinson's disease (PD). However, long-term L-DOPA treatment leads to the development of abnormal involuntary movements (AIMs) in patients and animal models of PD. Recently, involvement of growth arrest and DNA damage-inducible 45ß (Gadd45ß) was reported in neurological and neurobehavioral dysfunctions. However, little is known about the role of Gadd45ß in the dopaminergic nigrostriatal pathway or L-DOPA-induced dyskinesia (LID). To address this issue, we prepared an animal model of PD using unilateral 6-hydroxydopamine (6-OHDA) lesions in the substantia nigra of Gadd45ß(+/+) and Gadd45ß(-/-) mice. Dyskinetic symptoms were triggered by repetitive administration of L-DOPA in these 6-OHDA-lesioned mice. Whereas dopamine denervation in the dorsal striatum decreased Gadd45ß mRNA, chronic L-DOPA treatment significantly increased Gadd45ß mRNA expression in the 6-OHDA-lesioned striatum of wild-type mice. Using unilaterally 6-OHDA-lesioned Gadd45ß(+/+) and Gadd45ß(-/-) mice, we found that mice lacking Gadd45ß exhibited long-lasting increases in AIMs following repeated administration of L-DOPA. By contrast, adeno-associated virus-mediated expression of Gadd45ß in the striatum reduced AIMs in Gadd45ß knockout mice. The deficiency of Gadd45ß in LID increased expression of ΔFosB and c-Fos in the lesioned striatum 90 min after the last administration of L-DOPA following 11days of daily L-DOPA treatments. These data suggest that the increased expression of Gadd45ß induced by repeated administration of L-DOPA may be beneficial in patients with PD.

Inhibition of adenylyl cyclase type 5 prevents L-DOPA-induced dyskinesia in an animal model of Parkinson's disease.

The dopamine precursor L-3,4-dihydroxyphenylalanine (L-DOPA) is widely used as a therapeutic choice for the treatment of patients with Parkinson's disease. However, the long-term use of L-DOPA leads to the development of debilitating involuntary movements, called L-DOPA-induced dyskinesia (LID). The cAMP/protein kinase A (PKA) signaling in the striatum is known to play a role in LID. However, from among the nine known adenylyl cyclases (ACs) present in the striatum, the AC that mediates LID remains unknown. To address this issue, we prepared an animal model with unilateral 6-hydroxydopamine lesions in the substantia nigra in wild-type and AC5-knock-out (KO) mice, and examined behavioral responses to short-term or long-term treatment with L-DOPA. Compared with the behavioral responses of wild-type mice, LID was profoundly reduced in AC5-KO mice. The behavioral protection of long-term treatment with L-DOPA in AC5-KO mice was preceded by a decrease in the phosphorylation levels of PKA substrates ERK (extracellular signal-regulated kinase) 1/2, MSK1 (mitogen- and stress-activated protein kinase 1), and histone H3, levels of which were all increased in the lesioned striatum of wild-type mice. Consistently, FosB/ΔFosB expression, which was induced by long-term L-DOPA treatment in the lesioned striatum, was also decreased in AC5-KO mice. Moreover, suppression of AC5 in the dorsal striatum with lentivirus-shRNA-AC5 was sufficient to attenuate LID, suggesting that the AC5-regulated signaling cascade in the striatum mediates LID. These results identify the AC5/cAMP system in the dorsal striatum as a therapeutic target for the treatment of LID in patients with Parkinson's disease.

Angiotensin-converting enzyme inhibition prevents l-dopa-induced dyskinesia in a 6-ohda-induced mouse model of Parkinson's disease.

Parkinson's disease (PD) is characterised by severe movement defects and the degeneration of dopaminergic neurones in the midbrain. The symptoms of PD can be managed with dopamine replacement therapy using L-3, 4-dihydroxyphenylalanine (L-dopa), which is the gold standard therapy for PD. However, long-term treatment with L-dopa can lead to motor complications. The central renin-angiotensin system (RAS) is associated with the development of neurodegenerative diseases in the brain. However, the role of the RAS in dopamine replacement therapy for PD remains unclear. Here, we tested the co-treatment of the angiotensin-converting enzyme inhibitor (ACEI) with L-dopa altered L-dopa-induced dyskinesia (LID) in a 6-hydroxydopamine (6-OHDA)-lesioned mouse model of PD. Perindopril, captopril, and enalapril were used as ACEIs. The co-treatment of ACEI with L-dopa significantly decreased LID development in 6-OHDA-lesioned mice. In addition, the astrocyte and microglial transcripts involving Ccl2, C3, Cd44, and Iigp1 were reduced by co-treatment with ACEI and L-dopa in the 6-OHDA-lesioned striatum. In conclusion, co-treatment with ACEIs and L-dopa, such as perindopril, captopril, and enalapril, may mitigate the severity of L-DOPA-induced dyskinesia in a mouse model of PD.

Agathobaculum butyriciproducens improves ageing-associated cognitive impairment in mice.

AIMS: The gut microbiota is increasingly recognised as a pivotal regulator of immune system homeostasis and brain health. Recent research has implicated the gut microbiota in age-related cognitive impairment and dementia. Agathobaculum butyriciproducens SR79 T (SR79), which was identified in the human gut, has been reported to be beneficial in addressing cognitive deficits and pathophysiologies in a mouse model of Alzheimer's disease. However, it remains unknown whether SR79 affects age-dependent cognitive impairment. MAIN METHOD: To explore the effects of SR79 on cognitive function during ageing, we administered SR79 to aged mice. Ageing-associated behavioural alterations were examined using the open field test (OFT), tail suspension test (TST), novel object recognition test (NORT), Y-maze alternation test (Y-maze), and Morris water maze test (MWM). We investigated the mechanisms of action in the gut and brain using molecular and histological analyses. KEY FINDINGS: Administration of SR79 improved age-related cognitive impairment without altering general locomotor activity or depressive behaviour in aged mice. Furthermore, SR79 increased mature dendritic spines in the pyramidal cells of layer III and phosphorylation of CaMKIIα in the cortex of aged mice. Age-related activation of astrocytes in the cortex of layers III-V of the aged brain was reduced following SR79 administration. Additionally, SR79 markedly increased IL-10 production and Foxp3 and Muc2 mRNA expression in the colons of aged mice. SIGNIFICANCE: These findings suggest that treatment with SR79 may be a beneficial microbial-based approach for enhancing cognitive function during ageing.

Ca(V)3.1 is a tremor rhythm pacemaker in the inferior olive.

The rhythmic motor pathway activation by pacemaker neurons or circuits in the brain has been proposed as the mechanism for the timing of motor coordination, and the abnormal potentiation of this mechanism may lead to a pathological tremor. Here, we show that the potentiation of Ca(V)3.1 T-type Ca(2+) channels in the inferior olive contributes to the onset of the tremor in a pharmacological model of essential tremor. After administration of harmaline, 4- to 10-Hz synchronous neuronal activities arose from the IO and then propagated to cerebellar motor circuits in wild-type mice, but those rhythmic activities were absent in mice lacking Ca(V)3.1 gene. Intracellular recordings in brain-stem slices revealed that the Ca(V)3.1-deficient inferior olive neurons lacked the subthreshold oscillation of membrane potentials and failed to trigger 4- to 10-Hz rhythmic burst discharges in the presence of harmaline. In addition, the selective knockdown of Ca(V)3.1 gene in the inferior olive by shRNA efficiently suppressed the harmaline-induced tremor in wild-type mice. A mathematical model constructed based on data obtained from patch-clamping experiments indicated that harmaline could efficiently potentiate Ca(V)3.1 channels by changing voltage-dependent responsiveness in the hyperpolarizing direction. Thus, Ca(V)3.1 is a molecular pacemaker substrate for intrinsic neuronal oscillations of inferior olive neurons, and the potentiation of this mechanism can be considered as a pathological cause of essential tremor.

Causing trouble and being transmissible: COVID-19 survivors' experiences of stigma and discrimination in South Korea.

Background: The stigma associated with coronavirus disease (COVID-19) is relatively neglected in policies for handling the disease. Stigmatization occurs only within specific social contexts in local societies. Objective: This study aims to examine COVID-19 survivors' experiences of social stigma and discrimination in South Korea in the first 2 years of the pandemic. Methods: Semi-structured interviews were conducted. Results: Of 52 participants, 45 reported that they had to cope with stigma and discrimination in their intimate social relationships, workplaces, and children's schools, ranging from subtle actions to job loss. Sexual minorities who were involved in mass disease transmission in the early part of the pandemic experienced a higher level of stigmatization. The stigmatization dealt with in this study was related to two themes: survivors' sense of causing trouble and possibility of transmission. Conclusion: By intertwining this stigma with the experiences of public health measures through the voices of survivors, this study reveals the local context of East Asia in terms of culture-specific aspects of COVID-19-related stigma.

Prevalent toxin types of Clostridium botulinum in South Korean cattle farms.

Clostridium botulinum produces neurotoxic substrates that can cause fatal flaccid paralysis called botulism. These neurotoxins are classified into types A-G. Several botulism cases were recorded in 2012-2013 in the Gyeonggi province, South Korea. We assessed the distribution of C. botulinum types B, C, and D in several South Korean farms. A total of 184 samples collected in 2012-2013, including feces (n = 72), hay and silage (n = 50), soil (n = 26), water trough (n = 21), and stomach contents (n = 15), were subjected to multiplex polymerase chain reaction (PCR) to screen for types B, C, and D. Twenty-four samples tested PCR-positive as follows: type B (n = 11), type C/D (n = 4), and type D (n = 18). Eight of the 11 type B samples were detected in hay and silage. Sixteen of the 18 type D samples were detected in fecal and stomach content samples. PCR-positivity was observed in fecal (n = 9, 12.5%), hay and silage (n = 10, 20.0%), water trough (n = 2, 9.5%), and stomach content (n = 12, 80.0%) samples. Fourteen (42.4%) C. botulinum-positive samples were isolated from the PCR-positive samples (type B [n = 8], type C/D [n = 1], and type D [n = 5]). Our findings demonstrate that C. botulinum types B, C/D, and D were prevalent in South Korean cattle farms between 2012 and 2013.

Impact of vision and hearing impairments on risk of cardiovascular outcomes and mortality in patients with type 2 diabetes: A nationwide cohort study.

AIMS/INTRODUCTION: The purpose of this study was to investigate the impact of vision and hearing impairments on the risk of adverse cardiovascular outcomes and mortality in patients with type 2 diabetes using a nationwide longitudinal cohort. MATERIALS AND METHODS: We enrolled 771,128 patients with type 2 diabetes who underwent the National Health Screening Program in 2009. We carried out Cox proportional hazards regression analyses to calculate the hazard ratios (HR) of myocardial infarction (MI), stroke, and mortality in those with or without vision and hearing impairments. Subgroup analyses of patients stratified by age, sex and diabetic retinopathy were carried out. RESULTS: Diabetes patients with either vision or hearing impairment showed higher risk of MI, stroke or death compared with those without. Among the combinations of impairments, patients with both vision and hearing impairments had the highest risk for MI (adjusted HR [aHR] 1.362, 95% confidence interval [CI] 1.252-1.481) and mortality (aHR 1.591, 95% CI 1.532-1.651). Those with only vision impairment showed higher risk of MI (aHR 1.324, 95% CI 1.275-1.375 and aHR 1.117, 95% CI 1.066-1.170, respectively), stroke (aHR 1.318, 95% CI 1.276-1.362 and aHR 1.134 95% CI 1.089-1.180, respectively) and mortality (aHR 1.417, 95% CI 1.390-1.446 and aHR 1.163, 95% CI 1.135-1.191, respectively) compared with those with only hearing impairment. CONCLUSIONS: Vision and hearing impairments are independently important risk factors for adverse cardiovascular events and mortality in patients with type 2 diabetes. Vision and hearing impairments synergistically increased the risk of MI and all-cause deaths, but not stroke. In addition, in patients aged <65 years, the HR of vision impairment was higher than those with vision and hearing impairments.

Humulus japonicus attenuates LPS-and scopolamine-induced cognitive impairment in mice.

BACKGROUND: Neuroinflammation plays an important role in cognitive decline and memory impairment in neurodegenerative disorders. Previously, we demonstrated that Humulus japonicus (HJ) has anti-inflammatory effects in rodent models of Alzheimer's disease and Parkinson's disease. The present study aimed to examine the protective potential of HJ extracts against lipopolysaccharide (LPS)-induced cognitive impairment and scopolamine-induced amnesia in mouse models. Cognitive improvement of mice was investigated by novel object recognition test. For analyzing effects on neuroinflammation, immunohistochemistry and quantitative real-time polymerase chain reaction (qRT-PCR) assays were performed. RESULTS: We found that the oral administration of HJ significantly improved cognitive dysfunction induced by LPS in a novel object recognition test. The LPS-induced activation of microglia was notably decreased by HJ treatment in the cortex and hippocampus. HJ administration with LPS also significantly increased the mRNA expression of interleukin (IL)-10 and decreased the mRNA expression of IL-12 in the parietal cortex of mice. The increased expression of LPS-induced complement C1q B chain (C1bq) and triggering receptor expressed on myeloid cells 2 (Trem2) genes was significantly suppressed by HJ treatment. In addition, HJ administration significantly improved novel object recognition in a scopolamine-induced amnesia mouse model. CONCLUSIONS: These findings revealed that HJ has a beneficial effect on cognitive impairment and neuroinflammation induced by systemic inflammation and on amnesia induced by scopolamine in mice.

Agathobaculum butyriciproducens Shows Neuroprotective Effects in a 6-OHDA-Induced Mouse Model of Parkinson's Disease.

Parkinson's disease (PD) is the second-most prevalent neurodegenerative disease and is characterized by dopaminergic neuronal death in the midbrain. Recently, the association between alterations in PD pathology and the gut microbiota has been explored. Microbiota-targeted interventions have been suggested as a novel therapeutic approach for PD. Agathobaculum butyriciproducens SR79T (SR79) is an anaerobic bacterium. Previously, we showed that SR79 treatment induced cognitive improvement and reduced Alzheimer's disease pathologies in a mouse model. In this study, we hypothesized that SR79 treatment may have beneficial effects on PD pathology. To investigate the therapeutic effects of SR79 on PD, 6-hydroxydopamine (6-OHDA)-induced mouse models were used. D-Amphetamine sulfate (d-AMPH)-induced behavioral rotations and dopaminergic cell death were analyzed in unilateral 6-OHDA-lesioned mice. Treatment with SR79 significantly decreased ipsilateral rotations induced by d-AMPH. Moreover, SR79 treatment markedly activated the AKT/GSK3ß signaling pathway in the striatum. In addition, SR79 treatment affected the Nrf2/ARE signaling pathway and its downstream target genes in the striatum of 6-OHDA-lesioned mice. Our findings suggest a protective role of SR79 in 6-OHDA-induced toxicity by regulating the AKT/Nrf2/ARE signaling pathway and astrocyte activation. Thus, SR79 may be a potential microbe-based intervention and therapeutic strategy for PD.

Evaluation of substituted triazol-1-yl-pyrimidines as inhibitors of Bacillus anthracis acetohydroxyacid synthase.

Acetohydroxyacid synthase (AHAS), a potential target for antimicrobial agents, catalyzes the first common step in the biosynthesis of the branched-chain amino acids. The genes of both catalytic and regulatory subunits of AHAS from Bacillus anthracis (Bantx), a causative agent of anthrax, were cloned, overexpressed in Escherichia coli, and purified to homogeneity. To develop novel anti-anthracis drugs that inhibit AHAS, a chemical library was screened, and four chemicals, AVS2087, AVS2093, AVS2387, and AVS2236, were identified as potent inhibitors of catalytic subunit with IC(50) values of 1.0 +/- 0.02, 1.0 +/- 0.04, 2.1 +/- 0.12, and 2.0 +/- 0.08 microM, respectively. Further, these four chemicals also showed strong inhibition against reconstituted AHAS with IC(50) values of 0.05 +/- 0.002, 0.153 +/- 0.004, 1.30 +/- 0.10, and 1.29 +/- 0.40 microM, respectively. The basic scaffold of the AVS group consists of 1-pyrimidine-2-yl-1H-[1,2,4]triazole-3-sulfonamide. The potent inhibitor, AVS2093 showed the lowest binding energy, -8.52 kcal/mol and formed a single hydrogen bond with a distance of 1.973 A. As the need for novel antibiotic classes to combat bacterial drug resistance increases, the screening of new compounds that act against Bantx-AHAS shows that AHAS is a good target for new anti-anthracis drugs.

Yeast-hybrid based high-throughput assay for identification of anthrax lethal factor inhibitors.

Inhibitors of anthrax lethal factor (LF) are currently being sought as effective therapeutics for the treatment of anthrax. Here we report a novel screening approach for inhibitors of LF, a yeast-hybrid-based assay system in which the expression of reporter genes from a Gal4 promoter is repressed by LF proteolytic activity. Yeast cells were co-transformed with LF and a chimeric transcription factor that contains an LF substrate sequence inserted between the DNA-binding and activation domains of Gal4. In the resulting yeast cells, LF cleaves the substrate, thus inactivating the chimeric Gal4 and resulting in lack of expression of reporter genes. Compounds that inhibit LF cleavage of its substrate are identified by changes in reporter gene activity. Relative to in vitro screens for inhibitors of LF proteolytic activity, this screen has the advantage of excluding compounds that are toxic or non-permeable to eukaryotic cells. Additionally, the screen has the advantage of being fast, easy and cheap because exogenous LF and substrate are not needed. An initial chemical library screen with this system has identified four candidate inhibitors which were confirmed to inhibit LF protease activity in an in vitro assay. Furthermore, FBS-00831, one of the compounds identified, protects Raw 264.7 macrophages from anthrax lethal toxin and the possible binding site on LF was also evaluated by molecular docking.

Lack of CaV3.1 channels causes severe motor coordination defects and an age-dependent cerebellar atrophy in a genetic model of essential tremor.

T-type Ca(2+) channels have been implicated in tremorogenesis and motor coordination. The α1 subunit of the Ca(V)3.1 T-type Ca(2+) channel is highly expressed in motor pathways in the brain, but knockout of the Ca(V)3.1 gene (α(1G)(-/-)) per se causes no motor defects in mice. Thus, the role of Ca(V)3.1 channels in motor control remains obscure in vivo. Here, we investigated the effect of the Ca(V)3.1 knockout in the null genetic background of α1 GABA(A) receptor (α1(-/-)) by generating the double mutants (α1(-/-)/α(1G)(-/-)). α1(-/-)/α(1G)(-/-) mice showed severer motor abnormalities than α1(-/-) mice as measured by potentiated tremor activities at 20Hz and impaired motor learning. Propranolol, an anti-ET drug that is known to reduce the pathologic tremor in α1(-/-) mice, was not effective for suppressing the potentiated tremor in α1(-/-)/α(1G)(-/-) mice. In addition, α1(-/-)/α(1G)(-/-) mice showed an age-dependent loss of cerebellar Purkinje neurons. These results suggest that α1(-/-)/α(1G)(-/-) mice are a novel mouse model for a distinct subtype of ET in human and that Ca(V)3.1 T-type Ca(2+) channels play a role in motor coordination under pathological conditions.

Sensitive fluorescence assay of anthrax protective antigen with two new DNA aptamers and their binding properties.

A homogeneous assay of the protective antigen in anthrax toxin is reported using two new PA-specific aptamers for selective and sensitive detection, based on reduction in the fluorescence emission according to the formation of the aptamer-PA ternary complex. PA at 1 nM was readily detected using OliGreen as a fluorophore in HEPES buffer. We also demonstrated that the PA detection could be performed in blood serum. The binding interaction between the aptamer and PA was strong enough to dehybridize double-stranded DNA paired completely with 12 bases at room temperature. Moreover, this fluorescence study revealed that the binding sites of the two aptamers were located differently on the PA protein. We believe our approach may lay the groundwork for the real-time detection of PA.