Attorneys Must Manifest Express Authority in Order to Create a Binding Settlement Agreement on Behalf of Their Client: \u3cem\u3eReutzel v. Douglas\u3c/em\u3e

The Pennsylvania Supreme Court held that an attorney may enter into a binding settlement agreement on behalf of his client only if the attorney is acting with express authority. Reutzel v. Douglas, 870 A.2d 787 (Pa. 2005)

Measurement and Creation of Map Documentation of the Mokrsko Západ Area of the Josef Mine

Táto diplomová práca sa zaoberá mapovaním a vytvorením banskej mapovej dokumentácie štôlne Josef v oblasti Mokrsko Západ. Na začiatku bolo nutné urobiť zameranie oblasti pomocou laserového skeneru – Leica ScanStation P40. Výstupom z merania bolo mračno bodov, ktoré sa spracovalo v softvéri Leica Cyclone. Výsledné mapové diela štôlne boli vytvorené v softvéri MicroStation s nadstavbou DULMAP.This diploma thesis deals with the mapping and creation of mining map documentation of the Josef mine in the Mokrsko Západ area. Initially, it was necessary to measure the area using a laser scanner – Leica ScanStation P40. The output of the measurement was a point cloud, which was processed in Leica Cyclone software. The resulting map works of the mine were created in MicroStation software with the DULMAP extension

3D documentation of the St.Henry church in Jindrisska street, Prague

Táto bakalárska práca sa zaoberá vytvorením 3D modelu historickej pamiatky. Na začiatku bolo nutné urobiť meranie pomocou laserového skeneru ? Surphaser 25HSX. Následne sa zamerané mračno bodov spracovalo v softvéri Geomagic Studio, kde sa upravovalo až do finálnej podoby.This bachelor´s project deals with creating 3D model of historical sight. At the beginning, it was necessary to make measurement using laser scanner ? Surphaser 25HSX. Then, the measured point cloud was processed in the Geomagic Studio software, where it was modified to the final form

Simultaneous blockade of histamine H3H_{3} receptors and inhibition of acetylcholine esterase alleviate autistic-like behaviors in BTBR T+ tf/J mouse model of autism

Autism spectrum disorder (ASD) is a heterogenous neurodevelopmental disorder defined by persistent deficits in social interaction and the presence of patterns of repetitive and restricted behaviors. The central neurotransmitters histamine (HA) and acetylcholine (ACh) play pleiotropic roles in physiological brain functions that include the maintenance of wakefulness, depression, schizophrenia, epilepsy, anxiety and narcolepsy, all of which are found to be comorbid with ASD. Therefore, the palliative effects of subchronic systemic treatment using the multiple-active test compound E100 with high H3R antagonist affinity and AChE inhibitory effect on ASD-like behaviors in male BTBR T+tf/J (BTBR) mice as an idiopathic ASD model were assessed. E100 (5, 10 and 15 mg/kg, i.p.) dose-dependently palliated social deficits of BTBR mice and significantly alleviated the repetitive/compulsive behaviors of tested animals. Moreover, E100 modulated disturbed anxiety levels, but failed to modulate hyperactivity parameters, whereas the reference AChE inhibitor donepezil (DOZ, one milligram per kilogram) significantly obliterated the increased hyperactivity measures of tested mice. Furthermore, E100 mitigated the increased levels of AChE activity in BTBR mice with observed effects comparable to that of DOZ and significantly reduced the number of activated microglial cells compared to the saline-treated BTBR mice. In addition, the E100-provided effects on ASD-like parameters, AChE activity, and activated microglial cells were entirely reversed by co-administration of the H3R agonist (R)-α-methylhistamine (RAM). These initial overall results observed in an idiopathic ASD mice model show that E100 (5 mg/kg) alleviated the assessed behavioral deficits and demonstrate that simultaneous targeting of brain histaminergic and cholinergic neurotransmissions is crucial for palliation of ASD-like features, albeit further in vivo assessments on its effects on brain levels of ACh as well as HA are still needed.Autism spectrum disorder (ASD) is a heterogenous neurodevelopmental disorder defined by persistent deficits in social interaction and the presence of patterns of repetitive and restricted behaviors. The central neurotransmitters histamine (HA) and acetylcholine (ACh) play pleiotropic roles in physiological brain functions that include the maintenance of wakefulness, depression, schizophrenia, epilepsy, anxiety and narcolepsy, all of which are found to be comorbid with ASD. Therefore, the palliative effects of subchronic systemic treatment using the multiple-active test compound E100 with high H3R antagonist affinity and AChE inhibitory effect on ASD-like behaviors in male BTBR T+tf/J (BTBR) mice as an idiopathic ASD model were assessed. E100 (5, 10 and 15 mg/kg, i.p.) dose-dependently palliated social deficits of BTBR mice and significantly alleviated the repetitive/compulsive behaviors of tested animals. Moreover, E100 modulated disturbed anxiety levels, but failed to modulate hyperactivity parameters, whereas the reference AChE inhibitor donepezil (DOZ, one milligram per kilogram) significantly obliterated the increased hyperactivity measures of tested mice. Furthermore, E100 mitigated the increased levels of AChE activity in BTBR mice with observed effects comparable to that of DOZ and significantly reduced the number of activated microglial cells compared to the saline-treated BTBR mice. In addition, the E100-provided effects on ASD-like parameters, AChE activity, and activated microglial cells were entirely reversed by co-administration of the H3R agonist (R)-α-methylhistamine (RAM). These initial overall results observed in an idiopathic ASD mice model show that E100 (5 mg/kg) alleviated the assessed behavioral deficits and demonstrate that simultaneous targeting of brain histaminergic and cholinergic neurotransmissions is crucial for palliation of ASD-like features, albeit further in vivo assessments on its effects on brain levels of ACh as well as HA are still needed

Apigenin Alleviates Autistic-like Stereotyped Repetitive Behaviors and Mitigates Brain Oxidative Stress in Mice

Studying the involvement of nicotinic acetylcholine receptors (nAChRs), specifically α7-nAChRs, in neuropsychiatric brain disorders such as autism spectrum disorder (ASD) has gained a growing interest. The flavonoid apigenin (APG) has been confirmed in its pharmacological action as a positive allosteric modulator of α7-nAChRs. However, there is no research describing the pharmacological potential of APG in ASD. The aim of this study was to evaluate the effects of the subchronic systemic treatment of APG (10–30 mg/kg) on ASD-like repetitive and compulsive-like behaviors and oxidative stress status in the hippocampus and cerebellum in BTBR mice, utilizing the reference drug aripiprazole (ARP, 1 mg/kg, i.p.). BTBR mice pretreated with APG (20 mg/kg) or ARP (1 mg/g, i.p.) displayed significant improvements in the marble-burying test (MBT), cotton-shredding test (CST), and self-grooming test (SGT) (all p \u3c 0.05). However, a lower dose of APG (10 mg/kg, i.p.) failed to modulate behaviors in the MBT or SGT, but significantly attenuated the increased shredding behaviors in the CST of tested mice. Moreover, APG (10–30 mg/kg, i.p.) and ARP (1 mg/kg) moderated the disturbed levels of oxidative stress by mitigating the levels of catalase (CAT) and superoxide dismutase (SOD) in the hippocampus and cerebellum of treated BTBR mice. In patch clamp studies in hippocampal slices, the potency of choline (a selective agonist of α7-nAChRs) in activating fast inward currents was significantly potentiated following incubation with APG. Moreover, APG markedly potentiated the choline-induced enhancement of spontaneous inhibitory postsynaptic currents. The observed results propose the potential therapeutic use of APG in the management of ASD. However, further preclinical investigations in additional models and different rodent species are still needed to confirm the potential relevance of the therapeutic use of APG in ASD

The Effects of Snake Venom (<em>Bitis arietans</em>) on Embryonic Development

Venomous snake bites in pregnant women can lead to poor survival rates in both the foetus and mother; early bites can precipitate teratogenesis, miscarriages, preterm delivery, foetal death and antepartum haemorrhage. The chicken embryo poses as a valuable research model for venom research due to its advantages such as ease of availability, economic feasibility and its non-invasiveness. This study evaluates the embryotoxic effects of Puff adder venom (Bitis arietans) from Namibia, Kenya, South Africa and non-specified region of Africa at varying concentrations. The venoms were applied to chicken embryos on the fourth day of incubation and assessed on a ninth day, focusing on body weight, heart weight, liver weight and mortality rate. Nile blue staining was also performed to observe the occurrence of apoptosis amongst the venoms at the strongest concentrations. The information provided from our results suggested that there was a regional variation in venom toxicity, with the Kenyan venom producing the largest weight changes, whereas the non-specified African venom proved the most lethal across the concentrations. Further studies to assess venom protein concentrations in comparison with regional diet disparities are required

Curcumin potentiates the function of human α \u3csub\u3e7\u3c/sub\u3e -nicotinic acetylcholine receptors expressed in SH-EP1 cells

© 2018 Elsevier Ltd Effects of curcumin, a biologically active ingredient of turmeric, were tested on the Ca 2+ transients induced by the activation of α 7 subunit of the human nicotinic acetylcholine (α 7 nACh) receptor expressed in SH-EP1 cells. Curcumin caused a significant potentiation of choline (1 mM)-induced Ca 2+ transients with an EC 50 value of 133 nM. The potentiating effect of curcumin was not observed in Ca 2+ transients induced by high K + (60 mM) containing solutions or activation of α 4 β 2 nACh receptors and the extent of curcumin potentiation was not altered in the presence of Ca 2+ channel antagonists nifedipine (1 μM), verapamil (1 μM), ω-conotoxin (1 μM), and bepridil (10 μM). Noticeably the effect of curcumin was not observed when curcumin and choline were co-applied without curcumin pre-incubation. The effect of curcumin on choline-induced Ca 2+ transients was not reversed by pre-incubation with inhibitors of protein C, A, and CaM kinases. Metabolites of curcumin such as tetrahydrocurcumin, demethylcurcumin, and didemethylcurcumin also caused potentiation of choline-induced Ca 2+ transients. Notably, specific binding of [ 125 I]-bungarotoxin was not altered in the presence of curcumin. Collectively, our results indicate that curcumin allosterically potentiate the function of the α7-nACh receptor expressed in SH-EP1 cells

Curcumin Potentiates the Function of Human α7-nicotinic Acetylcholine Receptors Expressed in SH-EP1 Cells

Effects of curcumin, a biologically active ingredient of turmeric, were tested on the Ca2+transients induced by the activation of α7 subunit of the human nicotinic acetylcholine (α7nACh) receptor expressed in SH-EP1 cells. Curcumin caused a significant potentiation of choline (1 mM)-induced Ca2+ transients with an EC50 value of 133 nM. The potentiating effect of curcumin was not observed in Ca2+ transients induced by high K+ (60 mM) containing solutions or activation of α4β2 nACh receptors and the extent of curcumin potentiation was not altered in the presence of Ca2+ channel antagonists nifedipine (1 μM), verapamil (1 μM), ω-conotoxin (1 μM), and bepridil (10 μM). Noticeably the effect of curcumin was not observed when curcumin and choline were co-applied without curcumin pre-incubation. The effect of curcumin on choline-induced Ca2+ transients was not reversed by pre-incubation with inhibitors of protein C, A, and CaM kinases. Metabolites of curcumin such as tetrahydrocurcumin, demethylcurcumin, and didemethylcurcumin also caused potentiation of choline-induced Ca2+ transients. Notably, specific binding of [125I]-bungarotoxin was not altered in the presence of curcumin. Collectively, our results indicate that curcumin allosterically potentiate the function of the α7-nACh receptor expressed in SH-EP1 cells