Alkalimonas mucilaginosa sp. nov. and Alkalimonas cellulosilytica sp. nov. isolated from alkaline Lonar lake, India.

Two alkaliphilic, Gram-stain-negative bacterial strains (MEB004T and MEB108T) were isolated from water samples collected from Lonar lake, India. The phylogenetic analysis of their 16S rRNA gene sequences showed the highest similarity to A. delamerensis DSM 18314T (98.4%), followed by A. amylolytica DSM 18337T and A. collagenimarina JCM 14267T (97.9%). The genome sizes of strains MEB004T and MEB108T were determined to be 3,858,702 and 4,029,814 bp, respectively, with genomic DNA G + C contents of 51.4 and 51.9%. Average Nucleotide Identity, DNA-DNA Hybridization and Amino Acid Identity values between strains (MEB004T and MEB108T) and A. amylolytica DSM 18337T were (82.3 and 85.5), (25.0 and 29.2) and (86.7 and 90.2%). Both novel strains produced industrially important enzymes, such as amylase, lipase, cellulase, caseinase, and chitinase at pH 10 evidenced by the genomic presence of carbohydrate-active enzymes encoding genes. Genomic analyses further identified pH tolerance genes, affirming their adaptation to alkaline Lonar Lake. Dominant fatty acids were Summed feature 8 (C18:1 ω7c and/or C18:1 ω6c), C16:0, Summed feature 3, Sum In Feature 2 and C12:0 3OH. The prevalent polar lipids included phosphatidyl ethanolamine, phosphatidyl glycerol, and diphosphatidyl glycerol. The major respiratory quinone was ubiquinone-8. Based on the polyphasic data, we propose the classification of strains MEB004T and MEB108T as novel species within the genus Alkalimonas assigning the names Alkalimonas mucilaginosa sp. nov. and Alkalimonas cellulosilytica sp. nov., respectively. The type strains are MEB004T (= MCC 5208T = JCM 35954T = NCIMB 15460T) and MEB108T (= MCC 5330T = JCM 35955T = NCIMB 15461T).

Sub-exponential Time Parameterized Algorithms for Graph Layout Problems on Digraphs with Bounded Independence Number.

Fradkin and Seymour (J Comb Theory Ser B 110:19-46, 2015) defined the class of digraphs of bounded independence number as a generalization of the class of tournaments. They argued that the class of digraphs of bounded independence number is structured enough to be exploited algorithmically. In this paper, we further strengthen this belief by showing that several cut problems that admit sub-exponential time parameterized algorithms (a trait uncommon to parameterized algorithms) on tournaments, including Directed Feedback Arc Set, Directed Cutwidth and Optimal Linear Arrangement, also admit such algorithms on digraphs of bounded independence number. Towards this, we rely on the generic approach of Fomin and Pilipczuk (in: Proceedings of the Algorithms-ESA 2013-21st Annual European Symposium, Sophia Antipolis, France, September 2-4, 2013, pp. 505-516, 2013), where to get the desired algorithms, it is enough to bound the number of k-cuts in digraphs of bounded independence number by a sub-exponential FPT function (Fomin and Pilipczuk bounded the number of k-cuts in transitive tournaments). Specifically, our main technical contribution is a combinatorial result that proves that the yes-instances of the problems (defined above) have a sub-exponential number of k-cuts. We prove this bound by using a combination of chromatic coding, inductive reasoning and exploiting the structural properties of these digraphs.

Parameterized Complexity of Directed Spanner Problems.

We initiate the parameterized complexity study of minimum t-spanner problems on directed graphs. For a positive integer t, a multiplicative t-spanner of a (directed) graph G is a spanning subgraph H such that the distance between any two vertices in H is at most t times the distance between these vertices in G, that is, H keeps the distances in G up to the distortion (or stretch) factor t. An additive t-spanner is defined as a spanning subgraph that keeps the distances up to the additive distortion parameter t, that is, the distances in H and G differ by at most t. The task of Directed Multiplicative Spanner is, given a directed graph G with m arcs and positive integers t and k, decide whether G has a multiplicative t-spanner with at most m - k arcs. Similarly, Directed Additive Spanner asks whether G has an additive t-spanner with at most m - k arcs. We show that (i) Directed Multiplicative Spanner admits a polynomial kernel of size O ( k 4 t 5 ) and can be solved in randomized ( 4 t ) k · n O ( 1 ) time, (ii) the weighted variant of Directed Multiplicative Spanner can be solved in k 2 k · n O ( 1 ) time on directed acyclic graphs, (iii) Directed Additive Spanner is W [ 1 ] -hard when parameterized by k for every fixed t ≥ 1 even when the input graphs are restricted to be directed acyclic graphs. The latter claim contrasts with the recent result of Kobayashi from STACS 2020 that the problem for undirected graphs is FPT when parameterized by t and k.

Possible role of thromboxane A2 in remote hind limb preconditioning-induced cardioprotection.

Remote hind limb preconditioning (RIPC) is a protective strategy in which short episodes of ischemia and reperfusion in a remote organ (hind limb) protects the target organ (heart) against sustained ischemic reperfusion injury. The present study was designed to investigate the possible role of thromboxane A2 in RIPC-induced cardioprotection in rats. Remote hind limb preconditioning was performed by four episodes of 5 min of inflation and 5 min of deflation of pressure cuff. Occlusion of the hind limb with blood pressure cuff is most feasible, non-invasive, clinically relevant, and safe method for inducing RIPC. Isolated rat hearts were perfused on Langendorff apparatus and were subjected to global ischemia for 30 min followed by 120-min reperfusion. The levels of lactate dehydrogenase (LDH) and creatine kinase (CK) were measured in coronary effluent to assess the degree of myocardial injury. The extent of myocardial infarct size along with the functional parameters including left ventricular developed pressure (LVDP), dp/dtmax, and dp/dtmin were also measured. Ozagrel (thromboxane synthase inhibitor) and seratrodast (thromboxane A2 receptor antagonist) were employed as pharmacological modulators of thromboxane A2. Remote hind limb preconditioning significantly attenuated ischemia/reperfusion-induced myocardial injury and produced cardioprotective effects. However, administration of ozagrel and seratrodast completely abolished the cardioprotective effects of RIPC suggesting the key role of thromboxane A2 in RIPC-induced cardioprotection. It may be concluded that brief episodes of preconditioning ischemia and reperfusion activates the thromboxane synthase enzyme that produces thromboxane A2, which may elicit cardioprotection either involving humoral or neurogenic pathway.

Bradykinin in ischemic conditioning-induced tissue protection: Evidences and possible mechanisms.

Ischemic conditioning is an intrinsic protective mechanism in which repeated short episodes of reversible ischemia protects the tissue and increases its tolerance against a subsequent longer period of ischemia (index ischemia). Bradykinin is a physiologically and pharmacologically active peptide of the kallikrein-kinin system. Besides the involvement of bradykinin in a variety of physiological and pathological responses such as pain, inflammation and in cardiovascular system as a potent vasodilator, it also acts as an endogenous cytoprotective mediator in the ischemic tissue. Pretreatment with various pharmacological modulators of bradykinin has confirmed the involvement of bradykinin in ischemic conditioning-induced protection. The protective actions of bradykinin in three major paradigms of ischemic conditioning i.e. ischemic preconditioning, ischemic postconditioning and remote ischemic preconditioning involves activation and regulation of various endogenous signaling cascades to render the heart resistant to infarction. In ischemic preconditioning, bradykinin exerts cardioprotective effect via activation of PI3K/Akt/eNOS signaling pathway and regulation of redox state via NO release. The role of bradykinin and its B2 receptors in ischemic-postconditioning induced neuroprotection has been described mainly due to its increased redox signaling cascade and activation of mitochondrial anti-apoptotic pathway. Furthermore, its cardioprotective role during remote ischemic preconditioning has been associated with activation of B2 receptors mediated neurogenic pathway and internalization of B2 receptors along with the formation of signalosomes that activates intracellular cytoprotective transduction pathways. The present review focuses on the potential role of bradykinin in mediating different forms of ischemic conditioning (pre/post/remote)-induced cardioprotection and neuroprotection along with the possible mechanisms.