The occurrence of a stable quinone radical accumulating in vivo during natural and induced senescence in a range of plants

Author(s):  
George A. F. Hendry ◽  
N. M. Atherton ◽  
Wendy Seel ◽  
Olivier Leprince

SynopsisA correlation has been firmly established, in a wide range of plants, between environmental stress, the onset of senescence, loss of viability in seeds and the development and accumulation of a stable organic free radical. On the basis of the EPR response obtained at 95 GHz (W-band) and ENDOR spectra, and comparisons with quinone radical anions, we present evidence from contrasted plant species, plant tissues and sub-cellular fractions that this stable radical originates from one or more quinones possibly, though perhaps not exclusively, associated with stressed or age-impaired photosynthetic and respiratory electron transport chains. The radical appears to be ubiquitously associated with sub-lethal stress-induced damage and with senescence and arises during the sub-cellular structural and biochemical processes associated with the final phases of metabolism prior to death. As the free radical persists for some considerable time after death, it may have value in long-term studies of seed viability and in broader areas of plant pathology and stress physiology.

1993 ◽  
Vol 264 (2) ◽  
pp. C457-C463 ◽  
Author(s):  
I. Dorup ◽  
T. Clausen

In young rats fed a Mg(2+)-deficient diet for 3 wk, Mg2+ and K+ contents in soleus and extensor digitorum longus muscles were significantly reduced and closely correlated. In isolated soleus muscles, Mg2+ depletion induced an even more pronounced loss of K+, and Mg2+ and K+ contents were correlated over a wide range (r = 0.95, P < 0.001). Extracellular Mg2+ (0-1.2 mM) caused no change in total or ouabain-suppressible 86Rb influx. After long-term incubation in Ca(2+)-Mg(2+)-free buffer with EDTA and EGTA, cellular Mg2+ and K+ contents were reduced by 35 and 15%, respectively, without any reduction in ATP and total or ouabain-suppressible 86Rb influx. In Mg(2+)-depleted muscles 42K efflux was increased by up to 42%, and repletion with Mg2+ produced a graded decrease. We conclude that Mg2+ and K+ contents are closely correlated in muscles Mg2+ depleted in vivo or in vitro and that neither extracellular nor moderate intracellular Mg2+ depletion affects total or Na(+)-K+ pump-mediated K+ influx. The reduced K+ content may rather be related to increased K+ efflux from the muscles.


1996 ◽  
Vol 183 (6) ◽  
pp. 2523-2531 ◽  
Author(s):  
M López-Hoyos ◽  
R Carrió ◽  
R Merino ◽  
L Buelta ◽  
S Izui ◽  
...  

The bcl-2 protooncogene has been shown to provide a survival signal to self-reactive B cells, but it fails to override their developmental arrest after encounter with antigen. Furthermore, constitutive expression of bcl-2 in B cells does not promote the development of autoimmune disease in most strains of mice, indicating that signals other than those conferred by bcl-2 are required for long-term survival and differentiation of self-reactive B cells in vivo. To further examine the factors that are required for the pathogenesis of autoimmune disease, we have assessed the effect of bcl-2 overexpression on the development of host-versus-graft disease, a self-limited model of systemic autoimmune disease. In this model, injection of spleen cells from (C57BL/6 x BALB/c)F1 hybrid mice into BALB/c newborn parental mice induces immunological tolerance to donor tissues and activation of autoreactive F1 donor B cells through interactions provided by allogeneic host CD4+ T cells. BALB/c newborns injected with spleen cells from (C57BL/6 x BALB/c)F1 mice expressing a bcl-2 transgene in B cells developed high levels of anti-single-stranded DNA and a wide range of pathogenic autoantibodies that were not or barely detectable in mice injected with nontransgenic spleen cells. In mice injected with transgenic B cells, the levels of pathogenic autoantibodies remained high during the course of the study and were associated with long-term persistence of donor B cells, development of a severe autoimmune disease, and accelerated mortality. These results demonstrate that bcl-2 can provide survival signals for the maintenance and differentiation of autoreactive B cells, and suggest that both increased B cell survival and T cell help play critical roles in the development of certain forms of systemic autoimmune disease.


2019 ◽  
Vol 3 (4) ◽  
pp. 944-968 ◽  
Author(s):  
Pablo Rojas ◽  
Jenny A. Plath ◽  
Julia Gestrich ◽  
Bharath Ananthasubramaniam ◽  
Martin E. Garcia ◽  
...  

The circadian clock of the nocturnal Madeira cockroach is located in the accessory medulla, a small nonretinotopic neuropil in the brain’s visual system. The clock comprises about 240 neurons that control rhythms in physiology and behavior such as sleep-wake cycles. The clock neurons contain an abundant number of partly colocalized neuropeptides, among them pigment-dispersing factor (PDF), the insects’ most important circadian coupling signal that controls sleep-wake rhythms. We performed long-term loose-patch clamp recordings under 12:12-hr light-dark cycles in the cockroach clock in vivo. A wide range of timescales, from milliseconds to seconds, were found in spike and field potential patterns. We developed a framework of wavelet transform–based methods to detect these multiscale electrical events. We analyzed frequencies and patterns of events with interesting dynamic features, such as mixed-mode oscillations reminiscent of sharp-wave ripples. Oscillations in the beta/gamma frequency range (20–40 Hz) were observed to rise at dawn, when PDF is released, peaking just before the onset of locomotor activity of the nocturnal cockroach. We expect that in vivo electrophysiological recordings combined with neuropeptide/antagonist applications and behavioral analysis will determine whether specific patterns of electrical activity recorded in the network of the cockroach circadian clock are causally related to neuropeptide-dependent control of behavior.


2019 ◽  
Vol 37 (3) ◽  
pp. 9-10
Author(s):  
Rafael Vindas Bolaños ◽  
Jos Malda ◽  
René Van Weeren ◽  
Janny De Grauw

The paper provides results published or to be published of long-term in vivo equine studies to evaluate techniques of possible regenerative matrices of cartilage and bone, by means of cell-free implants or stimulation of the bone marrow. From the fixation techniques analyzed, it can be concluded that the best alternatives are the pressure technique for subchondral defects and a novel hydrogel with self-adhesive capacity for chondral defects. The equine coxal tuberosity was used for the first time as a model for regeneration studies of bone defects, analyzing scaffolds based on tricalcium phosphate, polymers and nanoparticles, by means of 3-D printing. Osteoconductivity, osteoinductivity, and the importance of microporosity were documented.Given that decellularized materials do not always give significant desired results in the regeneration of cartilage, it is important to conduct long-term studies. The technique of nanofracture and a novel self-adhesive hydrogel in the knee of the equine showed promising preliminary results in the regeneration of cartilage.The knee and the coxal tuberosity of the horse represent models of studying cartilage and bone regeneration in a true translational sense as a source of highly valuable information for clinical studies, for both horses and humans.


2016 ◽  
Vol 397 (12) ◽  
pp. 1287-1292 ◽  
Author(s):  
Petr Kasparek ◽  
Zuzana Ileninova ◽  
Radka Haneckova ◽  
Ivan Kanchev ◽  
Irena Jenickova ◽  
...  

Abstract Netherton syndrome (NS) is caused by mutations in the SPINK5 gene. Several Spink5-deficient mouse models were generated to understand the mechanisms of NS in vivo. However, Spink5-deficiency in mice is associated with postnatal lethality that hampers further analysis. Here we present a viable mouse model for NS generated by mosaic inactivation of the Spink5 gene. We propose that these mice are a valuable experimental tool to study NS, especially for long-term studies evaluating potential therapeutic compounds. Furthermore, we show that mosaic inactivation of a gene using TALENs or CRISPR/Cas9 systems can be used to study lethal phenotypes in adult mice.


FACETS ◽  
2017 ◽  
Vol 2 (1) ◽  
pp. 575-609 ◽  
Author(s):  
Alyssa Zucchet ◽  
Grégory Schmaltz

Electronic cigarettes (ECs) are devices that are used recreationally or as smoking cessation tools, and have become increasingly popular in recent years. We conducted a review of the available literature to determine the health effects caused by the use of these devices. A heating element in the EC aerosolizes a solution of propylene glycol, glycerol, nicotine (optional), and flavouring (optional). These compounds are generally harmless on their own. However, upon heating, they produce various carcinogens and irritants. We found that concentrations of these toxicants vary significantly depending on the type of EC device, the type of EC liquid, and the smoking behaviour of the user. Exposure to these vapours can cause inflammation and oxidative damage to in vitro and in vivo cells. EC aerosol can also potentially affect organ systems and especially cardiovascular and lung function. We concluded that EC use causes acute effects on health but not as severe as those of conventional cigarettes (CCs). These devices could, therefore, be of use for smokers of CCs wishing to quit. However, as EC aerosol introduces new toxicants not found in CCs, long-term studies are needed to investigate possible chronic effects associated with EC use.


Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Mitchell Butler ◽  
Joseph R Geraghty ◽  
Deepshika Sudhakar ◽  
Tyler Lung ◽  
Fernando Testai ◽  
...  

Objective: Studies in subarachnoid hemorrhage (SAH) animal models are limited to early timepoints, after which the brain is extracted to confirm hemorrhage. For long-term studies, blood is resorbed by the time of euthanasia and thus alternative methods of confirming SAH are necessary. Here, we used in vivo MRI to determine the presence, extent, and location of blood in the endovascular perforation rat model of SAH. Methods: Animals were divided into two groups - SAH and sham controls (no perforation). Rats were imaged at 24 hours in a 9.4T MRI scanner. T2-weighted imaging (T2WI) was used to quantify and localize the volume and extension of blood. T2WI was performed with a fast spin echo sequence with TR/TE = 5000/60 ms, FOV = 40x40 mm 2 , 0.75 mm slice thickness, and no interslice gap. SAH was identified as hypointense signal at the skull base, a normally hyperintense region due to cerebrospinal fluid in the basal cisterns. Regions of interest were identified and segmented manually. Pixels were converted to areas, and the total hypointense volume (V hypo ) was computed by summing all areas. V hypo was normalized to total brain volume (TBV) for each animal. Ability to detect blood via MRI was compared to the gold standard of direct visualization of blood after brain extraction using receiver operating characteristic (ROC) curves. The location of blood was plotted along a standardized antero-posterior axis. 3D reconstructions were developed in 3D Slicer to visualize the spatial distribution of hemorrhage. Results: V hypo values were 1.6±1.4 mm 3 sham (n = 8) and 7.5±3.9 mm 3 for SAH (n = 10) [p=0.0003]. This difference persisted when V hypo was normalized to TBV (p=0.0005). There was no difference in the TBV between groups (p=0.1493). V hypo distinguished between SAH and sham animals (p=0.001, area under curve = 0.963). A cutoff of V hypo = 4.63 mm 3 corresponded to 100% specificity and 80% sensitivity for confirming SAH. The spatial distribution of bleeding varied along the antero-posterior axis within the subarachnoid space. Conclusions: We developed an in vivo MRI method for the quantification of SAH blood volume and location in rats. This will be used for future long-term studies to confirm and grade severity of SAH.


2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Alex Burton ◽  
Sang Min Won ◽  
Arian Kolahi Sohrabi ◽  
Tucker Stuart ◽  
Amir Amirhossein ◽  
...  

AbstractImplantable deep brain stimulation (DBS) systems are utilized for clinical treatment of diseases such as Parkinson’s disease and chronic pain. However, long-term efficacy of DBS is limited, and chronic neuroplastic changes and associated therapeutic mechanisms are not well understood. Fundamental and mechanistic investigation, typically accomplished in small animal models, is difficult because of the need for chronic stimulators that currently require either frequent handling of test subjects to charge battery-powered systems or specialized setups to manage tethers that restrict experimental paradigms and compromise insight. To overcome these challenges, we demonstrate a fully implantable, wireless, battery-free platform that allows for chronic DBS in rodents with the capability to control stimulation parameters digitally in real time. The devices are able to provide stimulation over a wide range of frequencies with biphasic pulses and constant voltage control via low-impedance, surface-engineered platinum electrodes. The devices utilize off-the-shelf components and feature the ability to customize electrodes to enable broad utility and rapid dissemination. Efficacy of the system is demonstrated with a readout of stimulation-evoked neural activity in vivo and chronic stimulation of the medial forebrain bundle in freely moving rats to evoke characteristic head motion for over 36 days.


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