ATP-sensitive cation-channel in wheat (triticum durum Desf.): Identification and characterization of a plant mitochondrial channel by patch-clamp

Indirect evidence points to the presence of K + channels in plant mitochondria. In the present study, we report the results of the first patch clamp experiments on plant mitochondria. Single-channel recordings in 150 mM potassium gluconate have allowed the biophysical characterization of a channel with a conductance of 150 pS in the inner mitochondrial membrane of mitoplasts obtained from wheat (Triticum durum Desf.). The channel displayed sharp voltage sensitivity, permeability to potassium and cation selectivity. ATP in the mM concentration range completely abolished the activity. We discuss the possible molecular identity of the channel and its possible role in the defence mechanisms against oxidative stress in plants

Pore-blockade Times for Field-Driven Polymer Translocation

We study pore blockade times for a translocating polymer of length $N$, driven by a field $E$ across the pore in three dimensions. The polymer performs Rouse dynamics, i.e., we consider polymer dynamics in the absence of hydrodynamical interactions. We find that the typical time the pore remains blocked during a translocation event scales as $\sim N^{(1+2\nu)/(1+\nu)}/E$, where $\nu\simeq0.588$ is the Flory exponent for the polymer. In line with our previous work, we show that this scaling behaviour stems from the polymer dynamics at the immediate vicinity of the pore -- in particular, the memory effects in the polymer chain tension imbalance across the pore. This result, along with the numerical results by several other groups, violates the lower bound $\sim N^{1+\nu}/E$ suggested earlier in the literature. We discuss why this lower bound is incorrect and show, based on conservation of energy, that the correct lower bound for the pore-blockade time for field-driven translocation is given by $\eta N^{2\nu}/E$, where $\eta$ is the viscosity of the medium surrounding the polymer.Comment: 14 pages, 6 figures, slightly shorter than the previous version; to appear in J. Phys.: Cond. Ma

Generalized β\beta-conformal change and special Finsler spaces

In this paper, we investigate the change of Finslr metrics $$L(x,y) \to\bar{L}(x,y) = f(e^{\sigma(x)}L(x,y),\beta(x,y)),$$ which we refer to as a generalized $\beta$-conformal change. Under this change, we study some special Finsler spaces, namely, quasi C-reducible, semi C-reducible, C-reducible, $C_2$-like, $S_3$-like and $S_4$-like Finsler spaces. We also obtain the transformation of the T-tensor under this change and study some interesting special cases. We then impose a certain condition on the generalized $\beta$-conformal change, which we call the b-condition, and investigate the geometric consequences of such condition. Finally, we give the conditions under which a generalized $\beta$-conformal change is projective and generalize some known results in the literature.Comment: References added, some modifications are performed, LateX file, 24 page

Inhibition or knock out of Inducible nitric oxide synthase result in resistance to bleomycin-induced lung injury

BACKGROUND: In the present study, by comparing the responses in wild-type mice (WT) and mice lacking (KO) the inducible (or type 2) nitric oxide synthase (iNOS), we investigated the role played by iNOS in the development of on the lung injury caused by bleomycin administration. When compared to bleomycin-treated iNOSWT mice, iNOSKO mice, which had received bleomycin, exhibited a reduced degree of the (i) lost of body weight, (ii) mortality rate, (iii) infiltration of the lung with polymorphonuclear neutrophils (MPO activity), (iv) edema formation, (v) histological evidence of lung injury, (vi) lung collagen deposition and (vii) lung Transforming Growth Factor beta1 (TGF-β1) expression. METHODS: Mice subjected to intratracheal administration of bleomycin developed a significant lung injury. Immunohistochemical analysis for nitrotyrosine revealed a positive staining in lungs from bleomycin-treated iNOSWT mice. RESULTS: The intensity and degree of nitrotyrosine staining was markedly reduced in tissue section from bleomycin-iNOSKO mice. Treatment of iNOSWT mice with of GW274150, a novel, potent and selective inhibitor of iNOS activity (5 mg/kg i.p.) also significantly attenuated all of the above indicators of lung damage and inflammation. CONCLUSION: Taken together, our results clearly demonstrate that iNOS plays an important role in the lung injury induced by bleomycin in the mice

Envenomations by Bothrops and Crotalus Snakes Induce the Release of Mitochondrial Alarmins

Skeletal muscle necrosis is a common manifestation of viperid snakebite envenomations. Venoms from snakes of the genus Bothrops, such as that of B. asper, induce muscle tissue damage at the site of venom injection, provoking severe local pathology which often results in permanent sequelae. In contrast, the venom of the South American rattlesnake Crotalus durissus terrificus, induces a clinical picture of systemic myotoxicity, i.e., rhabdomyolysis, together with neurotoxicity. It is known that molecules released from damaged muscle might act as ‘danger’ signals. These are known as ‘alarmins’, and contribute to the inflammatory reaction by activating the innate immune system. Here we show that the venoms of B. asper and C. d. terrificus release the mitochondrial markers mtDNA (from the matrix) and cytochrome c (Cyt c) from the intermembrane space, from ex vivo mouse tibialis anterior muscles. Cyt c was released to a similar extent by the two venoms whereas B. asper venom induced the release of higher amounts of mtDNA, thus reflecting hitherto some differences in their pathological action on muscle mitochondria. At variance, injection of these venoms in mice resulted in a different time-course of mtDNA release, with B. asper venom inducing an early onset increment in plasma levels and C. d. terrificus venom provoking a delayed release. We suggest that the release of mitochondrial ‘alarmins’ might contribute to the local and systemic inflammatory events characteristic of snakebite envenomations