Lignocellulosic‐based bioenergy and water quality parameters: a review

High rates of crop residue removal as biofuel feedstocks could increase losses of nonpoint source pollutants, negatively affecting water quality. An alternative to residue removal can be growing dedicated bioenergy crops such as warm season grasses (WSGs) and short‐rotation woody crops (SRWCs). Yet, our understanding of the implications of growing dedicated bioenergy crops on water quality is limited. Thus, we (i) synthesized and compared the impacts of crop residue removal, WSGs, and SRWCs on water quality parameters (i.e., sediment and nutrient runoff, and nutrient leaching) and (ii) identified research gaps for growing dedicated energy crops. Literature indicates that residue removal at rates >50% (residue retention up to 4.71 Mg ha^?1) can increase runoff by 5–15 mm, sediment loss by 0.2–7 Mg ha^?1, NO₃–N by 0.58–1 kg ha^?1, and sediment‐associated C by 0.3–57 kg ha^?1 per rainstorm event compared to no residue removal. Crop residue removal may also increase nutrient leaching. Studies on the impacts of growing WSGs as dedicated bioenergy crops at field scale on water quality parameters are few. However, WSGs when used as conservation buffers reduce losses of sediment by 66–97%, nutrients by 21–94%, and contaminants by 9–98%. This suggests that if WSGs were grown as dedicated bioenergy crops at larger scales, they could reduce losses of nonpoint source pollutants. Literature indicates that SRWCs can consistently reduce NO₃–N leaching. More modeled than field data are available, warranting further field research on (i) field data collection from WSGs and SRWCs from marginal lands, (ii) growing monoculture or polyculture of WSGs, and (iii) large‐scale production of energy crops. Overall, dedicated bioenergy crops, particularly WSGs, can reduce losses of nonpoint source pollutants compared to residue removal and be an important strategy to improve water quality if grown at larger scales.     

Responses exhibited by various microbial groups relevant to uranium exposure

There is a strong interest in knowing how various microbial systems respond to the presence of uranium (U), largely in the context of bioremediation. There is no known biological role for uranium so far. Uranium is naturally present in rocks and minerals. The insoluble nature of the U(IV) minerals keeps uranium firmly bound in the earth’s crust minimizing its bioavailability. However, anthropogenic nuclear reaction processes over the last few decades have resulted in introduction of uranium into the environment in soluble and toxic forms. Microbes adsorb, accumulate, reduce, oxidize, possibly respire, mineralize and precipitate uranium. This review focuses on the microbial responses to uranium exposure which allows the alteration of the forms and concentrations of uranium within the cell and in the local environment. Detailed information on the three major bioprocesses namely, biosorption, bioprecipitation and bioreduction exhibited by the microbes belonging to various groups and subgroups of bacteria, fungi and algae is provided in this review elucidating their intrinsic and engineered abilities for uranium removal. The survey also highlights the instances of the field trials undertaken for in situ uranium bioremediation. Advances in genomics and proteomics approaches providing the information on the regulatory and physiologically important determinants in the microbes in response to uranium challenge have been catalogued here. Recent developments in metagenomics and metaproteomics indicating the ecologically relevant traits required for the adaptation and survival of environmental microbes residing in uranium contaminated sites are also included. A comprehensive understanding of the microbial responses to uranium can facilitate the development of in situ U bioremediation strategies.     

An unusual case of complete atrioventricular block causing Takotsubo syndrome

Complete atrioventricular (AV) block in association with Takotsubo syndrome (TS) has been well recognized, but the cause and effect relationship has not been elucidated. We describe a 78-year-old female who presented with complete AV block but one week later developed new-onset, diffuse T-wave inversions, QT prolongation, and acceleration of junctional escape rate. Left ventriculogram revealed features typical of TS. One year after permanent pacemaker implantation, complete AV block persisted despite the reversal of wall motion defects implying that conduction abnormality was the trigger of TS rather than its consequence.     

Defining Optimal Head-Tilt Position of Resuscitation in Neonates and Young Infants Using Magnetic Resonance Imaging Data

Head-tilt maneuver assists with achieving airway patency during resuscitation. However, the relationship between angle of head-tilt and airway patency has not been defined. Our objective was to define an optimal head-tilt position for airway patency in neonates (age: 0–28 days) and young infants (age: 29 days–4 months). We performed a retrospective study of head and neck magnetic resonance imaging (MRI) of neonates and infants to define the angle of head-tilt for airway patency. We excluded those with an artificial airway or an airway malformation. We defined head-tilt angle a priori as the angle between occipito-ophisthion line and ophisthion-C7 spinous process line on the sagittal MR images. We evaluated medical records for Hypoxic Ischemic Encephalopathy (HIE) and exposure to sedation during MRI. We analyzed MRI of head and neck regions of 63 children (53 neonates and 10 young infants). Of these 63 children, 17 had evidence of airway obstruction and 46 had a patent airway on MRI. Also, 16/63 had underlying HIE and 47/63 newborn infants had exposure to sedative medications during MRI. In spontaneously breathing and neurologically depressed newborn infants, the head-tilt angle (median ± SD) associated with patent airway (125.3° ± 11.9°) was significantly different from that of blocked airway (108.2° ± 17.1°) (Mann Whitney U-test, p = 0.0045). The logistic regression analysis showed that the proportion of patent airways progressively increased with an increasing head-tilt angle, with > 95% probability of a patent airway at head-tilt angle 144–150°.     

Schistosome immunomodulators

Schistosomes are long lived, intravascular parasitic platyhelminths that infect >200 million people globally. The molecular mechanisms used by these blood flukes to dampen host immune responses are described in this review. Adult worms express a collection of host-interactive tegumental ectoenzymes that can cleave host signaling molecules such as the “alarmin” ATP (cleaved by SmATPDase1), the platelet activator ADP (SmATPDase1, SmNPP5), and can convert AMP into the anti-inflammatory mediator adenosine (SmAP). SmAP can additionally cleave the lipid immunomodulator sphingosine-1-phosphate and the proinflammatory anionic polymer, polyP. In addition, the worms release a barrage of proteins (e.g., SmCB1, SjHSP70, cyclophilin A) that can impinge on immune cell function. Parasite eggs also release their own immunoregulatory proteins (e.g., IPSE/α1, omega1, SmCKBP) as do invasive cercariae (e.g., Sm16, Sj16). Some schistosome glycans (e.g., LNFPIII, LNnT) and lipids (e.g., Lyso-PS, LPC), produced by several life stages, likewise affect immune cell responses. The parasites not only produce eicosanoids (e.g., PGE2, PGD2—that can be anti-inflammatory) but can also induce host cells to release these metabolites. Finally, the worms release extracellular vesicles (EVs) containing microRNAs, and these too have been shown to skew host cell metabolism. Thus, schistosomes employ an array of biomolecules—protein, lipid, glycan, nucleic acid, and more, to bend host biochemistry to their liking. Many of the listed molecules have been individually shown capable of inducing aspects of the polarized Th2 response seen following infection (with the generation of regulatory T cells (Tregs), regulatory B cells (Bregs) and anti-inflammatory, alternatively activated (M2) macrophages). Precisely how host cells integrate the impact of these myriad parasite products following natural infection is not known. Several of the schistosome immunomodulators described here are in development as novel therapeutics against autoimmune, inflammatory, and other, nonparasitic, diseases.     

Portal systemic shunting of insulin does not lead to insulin resistance in patients with extrahepatic portal vein obstruction.

There is no clear relation between portal systemic shunting, reduced hepatic insulin extraction leading to an increased systemic delivery of insulin, and, resultant peripheral hyperinsulinemia and insulin resistance. Extrahepatic portal vein obstruction is a natural human model of portal systemic shunting with essentially normal liver function. To investigate the role of portal systemic shunting of insulin in creating systemic hyperinsulinemia and insulin resistance, we studied nine subjects with portal systemic shunting and nine controls matched for age (+/- 2 years), body weight (+/- 2 kg) and height (+/- 5 cm). We carried out an oral glucose tolerance test and hyperinsulinemic euglycemic clamp study at insulin infusion rate of 40 mU/m2/ min. Comparable (p = 0.61) basal insulin concentrations in the two groups (Mean (SE): 21.0 (3.98) vs. 24.1 (4.28) mU/L) demonstrated a lack of hyperinsulinemia in the presence of portal systemic shunting. The lower (p = 0.03) insulin area under curve on oral glucose tolerance test in presence of portal systemic shunting (7.40 (0.95) vs. 10.83 (1.15) U/L-min) indicated that lower extraction of insulin by the liver leads to a lower requirements in the periphery. The coefficient of variation for plasma glucose between 60 and 120 min of the clamps was 4.44 (0.55)%. Comparable (p = 0.82) M-values (6.21 (0.67) vs. 6.38 (0.45) mg/kg/min) in the two groups proved a lack of significant insulin resistance in the presence of portal systemic shunting. We conclude that isolated portal systemic shunting leads to neither hyperinsulinemia nor insulin resistance.