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The development of salinity affects 7% of the world’s land surface, acting as a major constraint to crop productivity. This study attempted to use the co-evolving endophytes of peanut to alleviate salinity stress and enhance the yield of peanut. Diverse and different tissue colonizing endophytes were isolated from peanut and screened in vitro by seed germination bioassay imposing gradients of salinity, with two cultivars TG37A (susceptible) and GG2 (moderately resistant), in potted conditions using saline irrigation water. Finally, nine endophytes capable of producing IAA and ACC-deaminase, promoting root growth and yield in potted conditions were selected for further evaluation in field conditions. They were evaluated with saline water (1.5–2.0 dS/m) in saline soil with susceptible cultivar TG37A. Simultaneously, three endophytes (Bacillus firmus J22N; Bacillus tequilensis SEN15N; and Bacillus sp. REN51N) were evaluated with two cultivars, GG2 and TG37A, during rainy and post-rainy seasons with elevated salinity. The application of endophytes like Bacillus firmus J22N and Bacillus sp. REN51N enhanced the pod and haulm yield of peanuts by 14–19% across cultivars, salinity, and seasons. In addition, there was significant modulation in parameters like relative water content; production of enzymes like superoxide dismutase (SOD), glutathione reductase (GR), catalase (CAT), ascorbate peroxidase (APX), lipid peroxidase (POD), and H2O2 content in leaf; and uptake of potassium. The activities of the enzymes involved in scavenging reactive oxygen species (ROS) increased with salinity, and further increased with endophytes like Bacillus firmus J22N, Bacillus tequilensis SEN15N, and Bacillus sp. REN51N. There was an enhanced accumulation of proline, reduced level of phenol and H2O2, and enhanced uptake of potassium with the inoculation of endophytes. This improved scavenging capacity of plants by endophytic modulation of ROS scavengers, uptake of K, production of ACC deaminase and IAA, root and biomass growth, modulation in relative water content, and enhanced accumulation of osmoprotectant might be the reasons of alleviation of salinity stress. Endophytes could have alleviated salinity stress in peanuts, indicating the mechanisms and potential of peanuts at the field level. These endophytes could be applied to bring agricultural sustainability to salinity-affected areas in the future. Furthermore, few genera viz. Kocuria, Brevundimonas, Agrococcus, Dietzia, and Kytococcus were observed in peanut tissue for the first time.

Oxidative stress plays a fundamental role in abdominal aortic aneurysm (AAA) formation. Activated polymorphonuclear leukocytes (or neutrophils) are associated with AAA and express myeloperoxidase (MPO), which promotes inflammation, matrix degradation, and other pathological features of AAA, including enhanced oxidative stress through generation of reactive oxygen species. Both plasma and aortic MPO levels are elevated in patients with AAA, but the role of MPO in AAA pathogenesis has, heretofore, never been investigated. Here, we show that MPO gene deletion attenuates AAA formation in two animal models: ANG II infusion in apolipoprotein E-deficient mice and elastase perfusion in C57BL/6 mice. Oral administration of taurine [1% or 4% (wt/vol) in drinking water], an amino acid known to react rapidly with MPO-generated oxidants like hypochlorous acid, also prevented AAA formation in the ANG II and elastase models as well as the CaCl2 application model of AAA formation while reducing aortic peroxidase activity and aortic protein-bound dityrosine levels, an oxidative cross link formed by MPO. Both MPO gene deletion and taurine supplementation blunted aortic macrophage accumulation, elastin fragmentation, and matrix metalloproteinase activation, key features of AAA pathogenesis. Moreover, MPO gene deletion and taurine administration significantly attenuated the induction of serum amyloid A, which promotes ANG II-induced AAAs. These data implicate MPO in AAA pathogenesis and suggest that studies exploring whether taurine can serve as a potential therapeutic for the prevention or treatment of AAA in patients merit consideration. NEW & NOTEWORTHY Neutrophils are abundant in abdominal aortic aneurysm (AAA), and myeloperoxidase (MPO), prominently expressed in neutrophils, is associated with AAA in humans. This study demonstrates that MPO gene deletion or supplementation with the natural product taurine, which can scavenge MPO-generated oxidants, can prevent AAA formation, suggesting an attractive potential therapeutic strategy for AAA.

Plant growth-promoting rhizobacteria (PGPR) thrive in the rhizosphere of plants and play a beneficial role in plant growth, and development along with biocontrol activities. The present study was undertaken with the aim of developing rhizobacterial inoculants for groundnut for enhancement of growth and yield and suppression of major soil-borne fungal diseases caused by Sclerotium rolfsii (stem rot) and Aspergillus niger (collar rot). Out of a total of 154 rhizobacterial isolates obtained from groundnut rhizosphere, 78 isolates were selected on the basis of in vitro antifungal activities against three major soil-borne fungal pathogens of groundnut, i.e. Aspergillus niger, Aspergillus flavus and Sclerotium rolfsii. The selected isolates were further screened for the production of 2,4-Diacetylphloroglucinol (2,4-DAPG) by the gene specific PCR amplification of phlD gene. A total of 11 rhizobacterial isolates were found to have DAPG-producing genes and selected for further studies. Gene specific primers were also used for characterization of the isolates for plant growth-promoting and biocontrol traits. The qualitative and quantitative estimation of the various attributes of the isolates were also carried out. Majority of the isolates showed production of IAA, siderophores and fluorescent pigments. The DAPG-producing rhizobacterial isolates have great potential as bio-inoculants for groundnut crop for suppressing soil-borne fungal pathogens and to enhance growth and yield.

Haloarchaea are predominant in the salt crystallizers of the Rann of Kutch when the concentration of salts approaches saturation levels. The obligate and extreme halophilic archaeon 3A1-DGR, isolated from a salt crystallizer pond of the Little Rann of Kutch, India, needs minimum of 10 % NaCl in the growth medium. To understand the mechanism(s) of osmotolerance and adaptation at extreme osmolarity, and to mine relevant gene(s), the genome of this haloarchaeon, 3A1-DGR, was sequenced. We report here, the 2.88 Mb draft genome sequence of the haloarchaeon 3A1-DGR, with G+C content of 68 % and the possible involvement of 43 genes in stress tolerance. Further studies of the genome of this haloarchaeon would be required to identify gene(s) that might be responsible for imparting extreme osmotolerance.

Acute ST elevation myocardial infarction results from atherosclerotic plaque rupture with subsequent thrombus formation, leading to complete or near complete occlusion of an epicardial coronary artery. Minimization of the mechanical obstruction from this thrombus remains the main goal of therapy in ST elevation myocardial infarction. Primary percutaneous coronary intervention for an ST elevation myocardial infarction appears to be the preferred mode of revascularization over thrombolytic therapy if the door-to-balloon time target of 90 min is achievable. The idea of reducing the thrombus burden with the use of devices as an adjunct to percutaneous coronary intervention is an attractive one. Several thrombectomy devices have been studied in randomized clinical trials, but no definitive conclusions have emerged, owing to conflicting results and variable clinical end points. This article intends to shed further light on the potential role of thrombectomy in the treatment of acute myocardial infarction.

Background— Angiotensin II (Ang II) contributes to vascular pathology in part by stimulating NADPH oxidase activity, leading to increased formation of superoxide (O 2 − ). We reported that O 2 − levels, NADPH oxidase activity, and expression of the p47 phox subunit of NADPH oxidase are increased in human abdominal aortic aneurysms (AAAs). Here, we tested the hypothesis that deletion of p47 phox will attenuate oxidative stress and AAA formation in Ang II–infused apoE −/− mice. Methods and Results— Male apoE −/− and apoE −/− p47 phox −/− mice received saline or Ang II (1000 ng · kg −1 · min −1 ) infusion for 28 days, after which abdominal aortic weight and maximal diameter were determined. Aortic tissues and blood were examined for parameters of aneurysmal disease and oxidative stress. Ang II infusion induced AAAs in 90% of apoE −/− versus 16% of apo −/− p47 phox −/− mice ( P −/− p47 phox −/− mice compared with apoE −/− mice ( P −/− p47 phox −/− mice compared with apoE −/− mice. Deletion of p47 phox attenuated the pressor response to Ang II; however, coinfusion of phenylephrine with Ang II, which restored the Ang II pressor response, did not alter the protective effects of p47 phox deletion on AAA formation. Conclusions— Deletion of p47 phox attenuates Ang II–induced AAA formation in apoE −/− mice, suggesting that NADPH oxidase plays a critical role in AAA formation in this model.

We report the 3.98-Mbp first draft genome sequence of Sediminibacillus halophilus strain NSP9.3, a moderate halophile isolated from a seasonal salt marsh of the Great Rann of Kutch, India. Exploring the genome of this organism will facilitate the understanding of the mechanism(s) of osmotolerance and survival in differential osmolarity.

The 4.37-Mbp draft genome of a moderately halophilic Bacillus megaterium strain, MSP20.1, isolated from a saltern of the Little Rann of Kutch, India, is reported here. To understand the mechanism(s) of moderate halophilism and to isolate the gene(s) involved in osmotolerance and adaptation, the genome of MSP20.1 was sequenced.

Here, we report the 4.0-Mbp draft genome of an obligate halophile, Bacillus sp. strain NSP22.2, isolated from a seasonal salt marsh of the Great Rann of Kutch, India. To understand the mechanism(s) of obligate halophilism and to isolate the relevant gene(s), the genome of Bacillus sp. NSP22.2 was sequenced.

We report the 3.93-Mbp first draft genome sequence of a species of the genus Thalassobacillus , Thalassobacillus devorans strain MSP14, a moderate but obligate halophile, isolated from a salt crystallizer of the Little Rann of Kutch, India. Exploring the genome of this organism will facilitate understanding the mechanism(s) of its obligate halophilism.

We report the 4.52-Mbp draft genome sequence of Bacillus sp. strain NSP9.1, a moderately halophilic bacterium isolated from the salt marsh of the Great Rann of Kutch, India. Analysis of the genome of this organism will lead to a better understanding of the genes and metabolic pathways involved in imparting osmotolerance.

Here we report the draft whole-genome sequence (3.72 Mbp) of Bacillus sp. strain SB49, an extremely halophilic bacterium isolated from a salt crystallizer pond of the Little Rann of Kutch in India. Unraveling the genome of this organism will facilitate understanding and isolation of the genes involved in imparting extreme osmotolerance.

Here, we report the 4.46-Mbp draft genome sequence of Bacillus sp. strain SB47, an extreme halophile isolated from a salt pan of the Little Rann of Kutch, India. Exploring the genome of this organism will facilitate the understanding and isolation of the gene(s) involved in its extreme osmotolerance.

The 5.52-Mbp draft genome sequence of Bacillus sp. strain NSP2.1, a nonhalophilic bacterium isolated from the salt marsh of the Great Rann of Kutch, India, is reported here. An analysis of the genome of this organism will facilitate the understanding of its survival in the salt marsh.

We report the 7.42-Mbp draft whole genome sequence of Salinibacillus aidingensis strain MSP4, an obligate halophilic bacterium, isolated from a salt crystallizer of the Rann of Kutch in India. Analysis of the genome of this organism will lead to a better understanding of the genes and metabolic pathways involved in imparting osmotolerance.

Background Recruitment of macrophage precursors to the adventitia plays a key role in the pathogenesis of abdominal aortic aneurysms ( AAA s), but molecular mechanisms remain undefined. The innate immune signaling molecule CD 14 was reported to be upregulated in adventitial macrophages in a murine model of AAA and in monocytes cocultured with aortic adventitial fibroblasts (AoAf) in vitro , concurrent with increased interleukin‐6 (IL‐6) expression. We hypothesized that CD 14 plays a crucial role in adventitial macrophage precursor recruitment early during AAA formation. Methods and Results CD 14 −/− mice were resistant to AAA formation induced by 2 different AAA induction models: aortic elastase infusion and systemic angiotensin II (Ang II ) infusion. CD 14 gene deletion led to reduced aortic macrophage infiltration and diminished elastin degradation. Adventitial monocyte binding to Ang II ‐infused aorta in vitro was dependent on CD 14, and incubation of human acute monocytic leukemia cell line‐1 (THP‐1) monocytes with IL ‐6 or conditioned medium from perivascular adipose tissue ( PVAT ) upregulated CD 14 expression. Conditioned medium from AoAf and PVAT induced CD 14‐dependent monocyte chemotaxis, which was potentiated by IL ‐6. CD 14 expression in aorta and plasma CD 14 levels were increased in AAA patients compared with controls. Conclusions These findings link CD 14 innate immune signaling via a novel IL ‐6 amplification loop to adventitial macrophage precursor recruitment in the pathogenesis of AAA .

Background— Abdominal aortic aneurysms (AAAs) in humans are associated with locally increased oxidative stress and activity of NADPH oxidase. We investigated the hypothesis that vitamin E, an antioxidant with documented efficacy in mice, can attenuate AAA formation during angiotensin II (Ang II) infusion in apolipoprotein E–deficient mice. Methods and Results— Six-month-old male apolipoprotein E–deficient mice were infused with Ang II at 1000 ng/kg per minute for 4 weeks via osmotic minipumps while consuming either a regular diet or a diet enriched with vitamin E (2 IU/g of diet). After 4 weeks, abdominal aortic weight and maximal diameter were determined, and aortic tissues were sectioned and examined using biochemical and histological techniques. Vitamin E attenuated formation of AAA, decreasing maximal aortic diameter by 24% and abdominal aortic weight by 34% ( P P P Conclusions— Vitamin E ameliorates AAAs and reduces the combined end point of fatal+nonfatal aortic rupture in this animal model. These findings are consistent with the concept that oxidative stress plays a pivotal role in Ang II–driven AAA formation in hyperlipidemic mice.

A patient with extensive coronary cameral fistulae (CCF) involving the left ventricle (LV) found incidentally during an emergency coronary angiogram is presented. A 68-year-old woman with a history of hypertension was brought to the emergency room with accelerated anginal symptoms. She was diagnosed with inferior ST segment elevation myocardial infarction, and underwent a coronary angiogram and successful percutaneous intervention to the right coronary artery (RCA). Other than the mid-RCA occlusion, the coronary angiogram was significant for diffuse CCF involving the circumflex-obtuse marginal system and diagonal branches emptying into the LV (Figure 1), delineating the endocardial border very well (Figure 2). After the RCA intervention, the patient remained asymptomatic and was discharged home in stable condition at her excellent baseline functional status. Figure 1) Coronary angiograms demonstrating extensive coronary cameral fistulae (arrowheads) involving the diagonal branches (A) and circumflexobtuse marginal system (B) Figure 2) Coronary angiogram demonstrating extensive coronary cameral fistulae emptying into the left ventricle, delineating the endocardial border (arrowheads) A coronary artery fistula is an abnormal communication between an epicardial coronary artery and a cardiac chamber (CCF) or a major vessel (venae cavae, pulmonary artery or veins, or coronary sinus). CCF are seen in 0.1% of patients undergoing coronary angiograms. Over 90% of the CCF drain into the venous circulation, and most fistulae are single communications. Although most CCF are asymptomatic, sudden or gradual progression of symptoms has also been reported (1). Surgical repair or transcatheter ablations of the fistulae are recommended for symptomatic patients and for asymptomatic patients who are at risk for future complications such as coronary steals, aneurysms and larger shunts. Our case is very rare because of the asymptomatic clinical course and the presence of multiple LV communications.

Zinc is a structural constituent of many proteins, including Cu/Zn superoxide dismutase (SOD), an endogenous antioxidant enzyme. Hypozincemia has been found in patients hospitalized with congestive heart failure, where neurohormonal activation, including the renin-angiotensin-aldosterone system (RAAS), is expected and oxidative stress is present. This study was undertaken to elucidate potential pathophysiological mechanisms involved in Zn dyshomeostasis in aldosteronism. In rats receiving aldosterone/salt treatment (ALDOST) alone for 1 and 4 wk or in combination with spironolactone (Spiro), an ALDO receptor antagonist, we monitored 24-h urinary and fecal Zn excretion and tissue Zn levels in heart, liver, and skeletal muscle, together with tissue metallothionein (MT)-I, a Zn2+-binding protein, and Cu/Zn-SOD activities in plasma and tissues. When compared with unoperated, untreated, age-/sex-matched controls, urinary and, in particular, fecal Zn losses were markedly increased ( P < 0.05) at days 7 and 28 of ALDOST, leading to hypozincemia and a fall ( P < 0.05) in plasma Cu/Zn-SOD activity. Microscopic scars and perivascular fibrosis of intramural coronary arteries first appeared in the right and left ventricles at week 4 of ALDOST and were accompanied by increased ( P < 0.05) tissue Zn, MT-I, and Cu/Zn-SOD activity, which were not found in uninjured liver or skeletal muscle. Spiro cotreatment prevented cardiac injury and Zn redistribution to the heart. Thus increased urinary and fecal Zn losses, together with their preferential translocation to sites of cardiac injury, where MT-I overexpression and increased Cu/Zn-SOD activity appeared, contribute to Zn dyshomeostasis in rats with aldosteronism, which were each prevented by Spiro. These findings may shed light on Zn dyshomeostasis found in patients with decompensated heart failure.

Purpose Fibrosis contributes to an adverse structural remodeling of the failing heart. In morphologic terms, it presents as a perivascular/interstitial fibrosis of intramural coronary arteries and as microscopic scarring, a marker of necrotic cardiomyocyte death. Because these lesions are found in both the right and the left heart, a circulating substance has been incriminated (vis-e-vis a hemodynamic factor). In rats with aldosteronism, such as structural remodeling with fibrosis is found throughout the heart and other organs, together with markers of oxidative stress and redox-sensitive transcription. We hypothesized that it is possible to attenuate the appearance of cardiac fibrosis in rats with aldosteronism by cotreatment with either an aldosterone receptor antagonist, spironolactone (Spiro), or a dietary Zn supplement (Zn+), an antioxidant. Methods and Results Eight-week-old male, uninephrectomized Sprague-Dawley rats received aldosterone via subcutaneous pump (0.75 μg/h) and 1% NaCl in their drinking water (ALDOST) for 4 weeks alone or together with either Spiro (150 mg/kg/d by gavage) or Zn+ (1478.84 mg of Zn/kg chow). At 4 weeks, hearts were harvested for immunohistochemical detection of gp91phox, a subunit of NADPH oxidase and source of superoxide, and histochemical assessment of fibrillar collagen using picrosirius red. In coronal sections taken from the minor axis of the heart, morphometric determination of collagen volume fraction (CVF) was assessed. In contrast to untreated, unoperated controls, there was increased tissue labeling for gp91phox and an increase in cardiac CVF (1.3 ± 0.2 vs 4.5 ± 0.6%; p Conclusion In association with aldosteronism, increased fibrillar collagen deposition as well as increased activity of gp91phox was found in cardiac tissue. These effects were prevented by Spiro cotreatment or diminished by dietary Zn+ supplementation to further implicate oxidative stress in the appearance of cardiac fibrosis in aldosteronism. Fibrosis is a surrogate marker of a previously altered redox state.

Purpose A chronic activation of the circulating renin-angiotensin-aldosterone system, which contributes to a salt-avid state and appearance of congestive heart failure (CHF), is accompanied by a systemic illness. Featured is the presence of reactive oxygen and nitrogen species in such diverse tissues as skin, skeletal muscle, heart, peripheral blood mononuclear cells (PBMC), and blood plasma. This altered redox state appears when endogenous antioxidant defenses are overwhelmed or when they are deficient. Zinc is a micronutrient integral to Cu/Zn superoxide dismutase (Cu/Zn SOD) activity; it protects against superoxide-mediated cytotoxicity. Urinary Zn excretion is increased in chronic hyperparathyroidism (HPT). We hypothesized that hypozincemia would accompany the secondary HPT seen with chronic aldosterone/salt treatment (ALDOST) and thereby would compromise Cu/Zn SOD activity. Methods In plasma, we monitored Zn, parathyroid hormone (PTH), and a1-antiproteinase (AP) activity, an inverse correlate of oxidative stress. In PBMC we measured total SOD activity and that of its isoforms, Cu/Zn-SOD and Mn-SOD. Uninephrectomized rats received ALDOST (0.75 μg/h and 1% NaCl/0.4% KCl in drinking water) and were compared to untreated age-/gender-matched controls. Results In ALDOST vs controls, we found that Zn was reduced (95.2 6 3.5 vs 110 6 1.5 μg/dL, p Conclusions Hypozincemia accompanies the secondary HPT found in rats with aldosteronism, where it may contribute to the systemic appearance of oxidative stress, including reduced plasma a1-AP activity and PBMC Cu/Zn SOD activity. Our findings suggest that monitoring of serum Zn and its supplementation could be beneficial in patients with CHF.

Purpose Congestive heart failure (CHF) has its origins rooted in an activation of the circulating renin-angiotensin-aldosterone system. In patients with protracted CHF of 4 wks or more, where chronic aldosteronism is contributory to their salt-avid state, we found ionized hypocalcemia and hypomagnesemia together with elevations in serum parathyroid hormone (PTH). In a rat model of chronic aldosteronism (ALDOST), extracellular concentrations of these divalent cations are reduced in response to an early and persistent increase in both urinary and fecal excretion. The resultant secondary hyperparathyroidism (SHPT) and continual PTH-mediated resorption of bone is invoked to restore homeostasis of these cations. Bone Ca and Mg are each reduced by 10% at 4 wks and more than 40% at 6 wks of ALDOST with a corresponding fall in bone strength to flexor stress. The time course to the restoration of fallen plasma Ca and Mg that accompanies SHPT in rats with ALDOST remains uncertain. Methods Toward this end, we monitored plasma total Ca and Mg and PTH in uninephrectomized rats with 1, 4, and 6 weeks ALDOST generated by aldosterone infusion (0.75 μg/h, by implanted minipump; and 1% NaCl/0.4% KCl in drinking water), without or with prior parathyroidectomy (PTx). Results In rats with ALDOST and intact parathyroids, plasma PTH was increased (p Conclusions In rats with chronic aldosteronism, accompanied by hypocalcemia and hypomagnesemia, sustained SHPT is required to restore Ca and Mg homeostasis. These findings suggest that supplemental Ca, Mg, and vitamin D may be required to minimize SHPT and preserve Ca and Mg balance in patients with protracted CHF.