Accumulation rates and sediment deposition in the G?kova Bay in Aegean Sea Turkish Coast.

Sediment accumulation rates were estimated from the vertical distribution of excess 210Pb in sediment cores collected at six stations in the G?kova Bay near the heavily industrialized Turkish Coastal zone of the Aegean Sea. Total 210Pb was determined by measuring 210Po activities. The sediment accumulation rates were calculated to vary from 0.32+/-0.01 cm yr(-1) (0.17 +/- 0.01 g cm(-2) yr(-1)) to 1.92 +/- 0.20 cm yr(-1) (1.13 +/- 0.10 g cm(-2) yr(-1)). The unsupported 210Pb flux was calculated from the accumulated dry matter of the examined slices and their unsupported 210Pb concentrations. The flux of unsupported 210Pb varies between 62 +/- 5 and 105 +/- 8 Bq m(-2) yr(-1). The average depositional flux was found to be considerably higher for cores from the Mediterranean.     

The effects of hydergine on the MAO activity of the aged and adult rat brain

Despite the fact that hydergine has been used in the treatment of dementia for many years, its mechanism of action is still not clear. Current studies imply that the major effect of hydergine may be the modulation of synaptic neurotransmission rather than solely increasing blood flow as was once thought. A prominent feature that accompanies aging is an increase in monoamine oxidase (MAO) levels which results in decreased availability of catecholamines in the synaptic cleft. The aim of this study was to determine the effects of hydergine on the MAO activity in different brain regions (cortex, olfactory bulb, hypothalamus, hippocampus, striatum, cerebellum) of old (30 months) and adult (12 months) male Sprague-Dawley rats. In cortex and olfactory bulb MAO levels were higher in the aged group. In hippocampus and hypothalamus hydergine treatment caused significant decreases in MAO levels. An interaction between age and hydergine treatment was observed in the hypothalamus, hippocampus and cerebellum. The hydergine effect was more pronounced in the aged group in the hypothalamus and cerebellum, and more pronounced in the adult in the hippocampus. Our findings imply that increased brain MAO activity in aging can be modified by hydergine treatment in some brain regions.     

Increased frontal phase-locking of event-related theta oscillations in Alzheimer patients treated with cholinesterase inhibitors.

This is a pilot study describing event-related oscillations in patients with Alzheimer-type dementia (AD). Theta responses of 22 mild probable AD subjects according to NINCDS-ADRDA criteria (11 non-treated, 11 treated by cholinesterase inhibitors), and 20 healthy elderly controls were analyzed by using the conventional visual oddball paradigm. We aimed to compare theta responses of the three groups in a range between 4-7 Hz at the frontal electrodes. At F(3) location, theta responses of healthy subjects were phase locked to stimulation and theta oscillatory responses of non-treated Alzheimer patients showed weaker phase-locking, i.e. average of Z-transformed means of correlation coefficients between single trials was closer to zero. In treated AD patients, phase-locking following target stimulation was two times higher in comparison to the responses of non-treated patients. The results indicate that the phase-locking of theta oscillations at F(3) in the treated patients is as strong as the control subjects. The F(4) theta responses were not statistically significant between the groups. Our findings imply that the theta responses at F(3) location are highly unstable in comparison to F(4) in non-treated mild AD patients and cholinergic agents may modulate event-related theta oscillatory activities in the frontal regions.     

The effect of yield damage on the viscoelastic properties of cortical bone tissue as measured by dynamic mechanical analysis

We have previously shown, using Dynamic Mechanical Analysis (DMA), that the presence of a defect in cortical bone tissue affects the apparent viscoelastic properties of that bone. However, mechanically induced damage is more complex than a machined defect making it difficult to predict its effect on bone viscoelasticity. We performed DMA measurements before and after introduction of yield damage into cortical bone beams from sheep radii. The specimens were placed in a DMA machine and baseline measurements of storage modulus (E1) and loss factor (tandelta) were performed using a 3-point bending configuration for a frequency range of 1-10 Hz. Measurements were done in all four bending directions (cranial, caudal, medial, and lateral) in random order. After subjecting the specimens to monotonic yield damage in a servohydraulic testing machine with the load applied to the cranial surface, oscillatory tests were repeated. To supplement results from the current experiment, additional analyses were performed on data from experiments where bone was either cut or fatigue-loaded between viscoelasticity measurements. Introduction of mechanical damage increased tan delta and frequency sensitivity of E1, consistent with the assertion that increased energy dissipation in damaged bone might contribute to its increased resistance to fatigue and fracture.     

Selenium prevents interferon-gamma induced activation of TRPM2 channel and inhibits inflammation,mitochondrial oxidative stress,and apoptosis in microglia

Microglia as the primary immune cells of brain act protective effects against injuries and infections in the central nervous system. Inflammation via excessive Ca²⁺ influx and oxygen radical species (ROS) generation is a known factor in many neurodegenerative disorders. Importantly, the Ca²⁺ permeable TRPM2 channel is activated by oxidative stress. Thus, TRPM2 could provide the excessive Ca²⁺ influx in the microglia. Although TRPM2 expression level is high in inflammatory cells, the interplay between mouse microglia and TRPM2 channel during inflammation is not fully identified. Thus, it is important to understand the mechanisms and factors involved in order to enhance neuronal regeneration and repair. The data presented here indicate that TRPM2 channels were activated in microglia cells by interferon-gamma (IFNγ). The IFNγ treatment further increased apoptosis (early and late) and cytokine productions (TNF-α, IL-1β, and IL-6) which were due to increased lipid peroxidation and ROS generations as well as increased activations of caspase −3 (Casp-3) and − 9 (Casp-9). However, selenium treatment diminished activations of TRPM2, cytokine, Casp-3, and Casp-9, and levels of lipid peroxidation and mitochondrial ROS production in the microglia that were treated with IFNγ. Moreover, addition of either PARP1 inhibitors (PJ34 or DPQ) or TRPM2 blockers (2-APB or ACA) potentiated the modulator effects of selenium. These results clearly suggest that IFNγ leads to TRPM2 activation in microglia cells; whereas, selenium prevents IFNγ-mediated TRPM2 activation and cytokine generation. Together the interplay between IFNγ released from microglia cells is importance in brain inflammation and may affect oxidative cytotoxicity in the microglia.

Summary of pathways involved in IFNγ-induced TRPM2 activation and microglia death through excessive reactive oxygen species (ROS): Modulator role of selenium (Se). The IFNγ causes the microglia activation. Nudix box domain of TRPM2 is sensitive to ROS. The ROS induces DNA damage and ADPR-ribose (ADPR) production in the nucleus via PARP1 enzyme activation. ADPR and ROS-induced TRPM2 activation stimulates excessive Ca²⁺ influx. ROS are produced in the mitochondria through the increase of free cytosolic Ca²⁺ (via TRPM2 activation) by the IFNγ treatment, although they are diminished by the TRPM2 channel blocker (ACA and 2-APB) and PARP1 inhibitor treatments. The main mechanism in the cell death and inflammatory effects of IFNγ is mediated by stimulation of ROS-mediated caspase (caspase −3 and − 9) activations and cytokine production (TNF-α, IL-1β, and IL-6) via TRPM2 activation, respectively. The apoptotic, inflammatory, and oxidant actions of IFNγ are modulated through TRPM2 inhibition by the Se treatment

     

Prospective study of muscle cramps in Charcot‐Marie‐Tooth disease

Introduction: This study aims to assess the frequency, location, severity, duration, and fluctuation over time of muscle cramps in Charcot‐Marie‐Tooth disease (CMT). Methods: Inherited Neuropathies Consortium Contact Registry participants recorded the occurrence and characteristics of muscle cramps using an 11‐question survey administered 3 times over 8 weeks. Results: A total of 110 adult patients with CMT completed the survey. Weekly cramp frequency was 9.3 (SD 12.3), and 23% had daily muscle cramps. Twenty‐two percent reported a significant impact on quality of life. Over 8 weeks, the daily frequency and severity of muscle cramps did not change significantly. Conclusions: Patients with CMT have muscle cramps that vary little over an 8‐week period, and they may interfere with quality of life. These data may be useful in the planning of clinical trials of agents to treat adults with CMT‐associated muscle cramps. Muscle Nerve 51: 485–488, 2015