Nigeria striker Odion Ighalo hopes that his loan deal at Manchester United is extended until the Premier League season is completed following the coronavirus lockdown.

Odion Ighalo is keen to extend his stay at Manchester United beyond the summer.

Odion Ighalo scored twice as Manchester United beat Derby to reach the FA Cup quarter-finals and leave their all-time top scorer Wayne Rooney on the losing side.

Odion Ighalo hopes his loan deal at Manchester United is extended until the Premier League season is completed.

Pathogenic bacteria of the genera Mycobacterium and Corynebacterium cause severe human diseases such as tuberculosis (Mycobacterium tuberculosis) and diphtheria (Corynebacterium diphtheriae). The cells of these species are surrounded by protective cell walls rich in long-chain mycolic acids. These fatty acids are conjugated to the disaccharide trehalose on the cytoplasmic side of the bacterial cell membrane. They are then transported across the membrane to the periplasm where they act as donors for other reactions. We have previously shown that transient acetylation of the glycolipid trehalose monohydroxycorynomycolate (hTMCM) enables its efficient transport to the periplasm in Corynebacterium glutamicum and that acetylation is mediated by the membrane protein TmaT. Here, we show that a putative methyltransferase, encoded at the same genetic locus as TmaT, is also required for optimal hTMCM transport. Deletion of the C. glutamicum gene NCgl2764 (Rv0224c in M. tuberculosis) abolished acetyltrehalose monocorynomycolate (AcTMCM) synthesis, leading to accumulation of hTMCM in the inner membrane and delaying its conversion to trehalose dihydroxycorynomycolate (h2TDCM). Complementation with NCgl2764 normalized turnover of hTMCM to h2TDCM. In contrast, complementation with NCgl2764 derivatives mutated at residues essential for methyltransferase activity failed to rectify the defect, suggesting that NCgl2764/Rv0224c encodes a methyltransferase, designated here as MtrP. Comprehensive analyses of the individual mtrP and tmaT mutants and of a double mutant revealed strikingly similar changes across several lipid classes compared with WT bacteria. These findings indicate that both MtrP and TmaT have nonredundant roles in regulating AcTMCM synthesis, revealing additional complexity in the regulation of trehalose mycolate transport in the Corynebacterineae.

Pathogenic bacteria of the genera Mycobacterium and Corynebacterium cause severe human diseases such as tuberculosis (Mycobacterium tuberculosis) and diphtheria (Corynebacterium diphtheriae). The cells of these species are surrounded by protective cell walls rich in long-chain mycolic acids. These fatty acids are conjugated to the disaccharide trehalose on the cytoplasmic side of the bacterial cell membrane. They are then transported across the membrane to the periplasm where they act as donors for other reactions. We have previously shown that transient acetylation of the glycolipid trehalose monohydroxycorynomycolate (hTMCM) enables its efficient transport to the periplasm in Corynebacterium glutamicum and that acetylation is mediated by the membrane protein TmaT. Here, we show that a putative methyltransferase, encoded at the same genetic locus as TmaT, is also required for optimal hTMCM transport. Deletion of the C. glutamicum gene NCgl2764 (Rv0224c in M. tuberculosis) abolished acetyltrehalose monocorynomycolate (AcTMCM) synthesis, leading to accumulation of hTMCM in the inner membrane and delaying its conversion to trehalose dihydroxycorynomycolate (h2TDCM). Complementation with NCgl2764 normalized turnover of hTMCM to h2TDCM. In contrast, complementation with NCgl2764 derivatives mutated at residues essential for methyltransferase activity failed to rectify the defect, suggesting that NCgl2764/Rv0224c encodes a methyltransferase, designated here as MtrP. Comprehensive analyses of the individual mtrP and tmaT mutants and of a double mutant revealed strikingly similar changes across several lipid classes compared with WT bacteria. These findings indicate that both MtrP and TmaT have nonredundant roles in regulating AcTMCM synthesis, revealing additional complexity in the regulation of trehalose mycolate transport in the Corynebacterineae.

Pathogenic bacteria of the genera Mycobacterium and Corynebacterium cause severe human diseases such as tuberculosis (Mycobacterium tuberculosis) and diphtheria (Corynebacterium diphtheriae). The cells of these species are surrounded by protective cell walls rich in long-chain mycolic acids. These fatty acids are conjugated to the disaccharide trehalose on the cytoplasmic side of the bacterial cell membrane. They are then transported across the membrane to the periplasm where they act as donors for other reactions. We have previously shown that transient acetylation of the glycolipid trehalose monohydroxycorynomycolate (hTMCM) enables its efficient transport to the periplasm in Corynebacterium glutamicum and that acetylation is mediated by the membrane protein TmaT. Here, we show that a putative methyltransferase, encoded at the same genetic locus as TmaT, is also required for optimal hTMCM transport. Deletion of the C. glutamicum gene NCgl2764 (Rv0224c in M. tuberculosis) abolished acetyltrehalose monocorynomycolate (AcTMCM) synthesis, leading to accumulation of hTMCM in the inner membrane and delaying its conversion to trehalose dihydroxycorynomycolate (h2TDCM). Complementation with NCgl2764 normalized turnover of hTMCM to h2TDCM. In contrast, complementation with NCgl2764 derivatives mutated at residues essential for methyltransferase activity failed to rectify the defect, suggesting that NCgl2764/Rv0224c encodes a methyltransferase, designated here as MtrP. Comprehensive analyses of the individual mtrP and tmaT mutants and of a double mutant revealed strikingly similar changes across several lipid classes compared with WT bacteria. These findings indicate that both MtrP and TmaT have nonredundant roles in regulating AcTMCM synthesis, revealing additional complexity in the regulation of trehalose mycolate transport in the Corynebacterineae.

Hepatic encephalopathy constitutes a spectrum of neuropsychiatric abnormalities, beginning with subtle psychomotor changes and progressing to confusion with asterixis, somnolence, and then coma, arising in patients with impaired liver function. In this podcast, Tim Cross, a consultant hepatologist from the Royal Liverpool University Hospital,...

Gregor Thut
Sep 13, 2006; 26:9494-9502
BehavioralSystemsCognitive

Few epidemiological studies, which included varied exposure assessment, have investigated the relation between drinking-water–disinfection byproducts such as trihalomethanes and hypospadias, and their results have been inconclusive.

Little evidence was found for an association between trihalomethanes and hypospadias, but a novel association between water consumption and hypospadias was found. Factors that influence maternal water consumption, or other contaminants in tap or bottled water, might explain this finding. (Read the full article)

Nonconvulsive status epilepticus (NCSE) is the diagnosis for encephalopathy caused by continuous epileptic activity on EEG. It is a well-known cause of morbidity and mortality in critically ill adults and neonates. NCSE is increasingly reported in critically ill children.

We show that NCSE is common in all inpatient settings, not only in the critically ill. Key risk factors that should dramatically increase suspicion of NCSE in clinical practice include a history of convulsive seizure and acute imaging abnormalities. (Read the full article)

Severe neonatal hyperbilirubinemia can lead to acute bilirubin encephalopathy and, subsequently, chronic bilirubin encephalopathy (CBE). This condition is preventable through routine identification and proper treatment; therefore, it is rare for permanent neurologic complications to occur.

This article describes the incidence of CBE in Canada, which is higher than previously reported in the literature. Furthermore, it describes the underlying causes of CBE and the spectrum of neurologic disease. (Read the full article)

Infants with hypoxic-ischemic encephalopathy suffer a high rate (>40%) of death or moderate to severe disability, even after therapeutic hypothermia. High-dose erythropoietin (Epo) reduces brain injury and improves neurologic function in animal models of neonatal hypoxic-ischemic brain injury.

Multiple doses of Epo (up to 2500 U/kg intravenously) given in conjunction with hypothermia are well tolerated in newborns with HIE. Epo doses of 1000 U/kg intravenously in cooled infants produce plasma concentrations that are neuroprotective in animal studies. (Read the full article)

Most term and late preterm infants with neonatal encephalopathy have not had recognized asphyxial birth events. Several nonasphyxial risk factors for neonatal encephalopathy have been identified in previous studies.

In a large sample, we confirm the association of several nonasphyxial factors with neonatal encephalopathy, including markers of intrauterine exposure to infection or inflammation, intrauterine fetal growth restriction, and birth defects. We identify steps that would improve studies of neonatal encephalopathy. (Read the full article)

Etiology and timing of onset of neonatal hypoxic-ischemic encephalopathy continue to be controversial. Previous studies suggest antepartum events are the main contributing factors, but have used a broad definition of encephalopathy and included infants with genetic, congenital, and developmental abnormalities.

Our study suggests that when strict criteria defining hypoxic-ischemic encephalopathy are applied with supporting neuroimaging evidence of an acute hypoxic-ischemic insult, intrapartum events are the final and necessary pathway leading to this condition. (Read the full article)

Hypothermia treatment of neonatal encephalopathy reduces death and disability from 66% to 50%; additional neuroprotective therapies are needed. We previously found in animal models that adding 50% xenon to the breathing gas during cooling doubled neuroprotection.

This clinical feasibility study used 50% xenon for 3 to 18 hours in 14 cooled infants with cardiovascular, respiratory, and amplitude-integrated EEG monitoring. This depressed seizures, with no blood pressure reduction. Xenon is ready for randomized clinical trials in newborns. (Read the full article)

Computed tomography is commonly used for neuroimaging in newborn infants with neonatal encephalopathy despite concerns over potential harm from radiation exposure. Alternative neuroimaging options include MRI and cranial ultrasound.

Using a very large, international, multicenter database, we demonstrate utilization rates and compare diagnostic findings of computed tomography, MRI, and cranial ultrasound in the evaluation of neonatal encephalopathy. (Read the full article)

Jaundiced newborns without additional risk factors rarely develop kernicterus if the total serum bilirubin is <25 mg/dL. Measuring the bilirubin/albumin ratio might improve risk assessment, but the relationships of both indicators to advancing stages of neurotoxicity are poorly documented.

Both total serum bilirubin and bilirubin/albumin ratio are strong predictors of advancing stages of acute and post-treatment auditory and neurologic impairment. However, bilirubin/albumin ratio, adjusted to the same sensitivity, does not improve prediction over total serum bilirubin alone. (Read the full article)

Surviving infants with neonatal encephalopathy treated with hypothermia have lower rates of moderate to severe cerebral palsy and cognitive impairment at 18 to 24 months. Limited data exist on the association between cognitive functioning and neuromotor, behavioral, and school outcomes.

Although the incidence of death or IQ <55 is reduced after therapeutic hypothermia, survivors of neonatal encephalopathy with and without cerebral palsy are at elevated risk for subnormal IQ and the need for specialized educational services at 6 to 7 years. (Read the full article)

Continuous conventional EEG video is currently gold standard for identifying neonatal seizures and a substantial proportion of neonatal seizures are electrographic. Currently there is no direct evidence that EEG monitoring, seizure identification, or treatment impacts long-term outcomes.

In neonates with hypoxic ischemic encephalopathy, EEG monitoring and treatment of electrographic seizures results in significant reduction in seizure burden. Increasing seizure burden is associated with more severe brain injury and significantly lower performance scores on Bayley Scales of Infant Development III. (Read the full article)

The off-label use of third generation cephalosporin (3GC) during in ovo vaccination or vaccination of newly hatched chicks, was a common practice worldwide. CMY-2-producing Escherichia coli have been disseminated among broiler production. The objectives of this study were to determine the epidemiological linkage of bla_CMY-2-positive plasmids among broilers both within and outside Japan because grandparent stock and parent stock were imported in Japan. We examined the whole genome sequences of 132 3GC-resistant E. coli isolates collected from healthy broilers during 2002-2014. The predominant 3GC-resistance gene was bla_CMY-2, which was detected in the plasmids of 87 (65.9%) isolates. The main plasmid replicon types were IncI1-I (n=21; 24.1%), IncI (n=12; 13.8%), IncB/O/K/Z (n=28; 32.2%), and IncC (n=22; 25.3%). Those plasmids were subjected to gene clustering and network analyses and plasmid multi-locus sequence typing (pMLST). The chromosomal DNA of isolates was subjected to MLST and single nucleotide variant (SNV)-based phylogenetic analysis.

MLST and SNV-based phylogenetic analysis revealed high diversity of E. coli isolates. ST429 harboring bla_CMY-2-positive IncB/O/K/Z was closely related to isolates from broiler in Germany harboring bla_CMY-2-positive IncB/O/K/Z. pST55-IncI and pST12-IncI1-I and pST3-IncC were prevalent in western Japan. pST12-IncI1-I and pST3-IncC were closely related to those detected in E. coli isolates from chicken in American continent, whereas 26 IncB/O/K/Z were related to those in Europe. These data will be useful to reveal the whole picture of transmission of CMY-2-producing bacteria in and out of Japan.

When it comes to electric vehicles, there’s no denying the multitude of benefits for manufacturers, consumers, and the environment – from reduced emissions to lower fuel costs, increased efficiency, and lower noise pollution. These benefits continue to...

Title: Haldol (haloperidol) vs. Abilify (aripiprazole)
Category: Medications
Created: 7/30/2019 12:00:00 AM
Last Editorial Review: 4/10/2020 12:00:00 AM

ABSTRACT

The archaeal cytoplasmic membrane provides an anchor for many surface proteins. Recently, a novel membrane anchoring mechanism involving a peptidase, archaeosortase A (ArtA), and C-terminal lipid attachment of surface proteins was identified in the model archaeon Haloferax volcanii. ArtA is required for optimal cell growth and morphogenesis, and the S-layer glycoprotein (SLG), the sole component of the H. volcanii cell wall, is one of the targets for this anchoring mechanism. However, how exactly ArtA function and regulation control cell growth and morphogenesis is still elusive. Here, we report that archaeal homologs to the bacterial phosphatidylserine synthase (PssA) and phosphatidylserine decarboxylase (PssD) are involved in ArtA-dependent protein maturation. Haloferax volcanii strains lacking either HvPssA or HvPssD exhibited motility, growth, and morphological phenotypes similar to those of an artA mutant. Moreover, we showed a loss of covalent lipid attachment to SLG in the hvpssA mutant and that proteolytic cleavage of the ArtA substrate HVO_0405 was blocked in the hvpssA and hvpssD mutant strains. Strikingly, ArtA, HvPssA, and HvPssD green fluorescent protein (GFP) fusions colocalized to the midcell position of H. volcanii cells, strongly supporting that they are involved in the same pathway. Finally, we have shown that the SLG is also recruited to the midcell before being secreted and lipid anchored at the cell outer surface. Collectively, our data suggest that haloarchaea use the midcell as the main surface processing hot spot for cell elongation, division, and shape determination.

IMPORTANCE The subcellular organization of biochemical processes in space and time is still one of the most mysterious topics in archaeal cell biology. Despite the fact that haloarchaea largely rely on covalent lipid anchoring to coat the cell envelope, little is known about how cells coordinate de novo synthesis and about the insertion of this proteinaceous layer throughout the cell cycle. Here, we report the identification of two novel contributors to ArtA-dependent lipid-mediated protein anchoring to the cell surface, HvPssA and HvPssD. ArtA, HvPssA, and HvPssD, as well as SLG, showed midcell localization during growth and cytokinesis, indicating that haloarchaeal cells confine phospholipid processing in order to promote midcell elongation. Our findings have important implications for the biogenesis of the cell surface.

Objective

De novo missense mutations in the RHOBTB2 gene have been described as causative for developmental and epileptic encephalopathy.

ABSTRACT

Members of family Coronaviridae cause a variety of diseases in birds and mammals. Porcine hemagglutinating encephalomyelitis virus (PHEV), a lesser-researched coronavirus, can infect naive pigs of any age, but clinical disease is observed in pigs ≤4 weeks of age. No commercial PHEV vaccines are available, and neonatal protection from PHEV-associated disease is presumably dependent on lactogenic immunity. Although subclinical PHEV infections are thought to be common, PHEV ecology in commercial swine herds is unknown. To begin to address this gap in knowledge, a serum IgG antibody enzyme-linked immunosorbent assay (ELISA) based on the S1 protein was developed and evaluated on known-status samples and then used to estimate PHEV seroprevalence in U.S. sow herds. Assessment of the diagnostic performance of the PHEV S1 ELISA using serum samples (n = 924) collected from 7-week-old pigs (n = 84; 12 pigs per group) inoculated with PHEV, porcine epidemic diarrhea virus, transmissible gastroenteritis virus, porcine respiratory coronavirus, or porcine deltacoronavirus showed that a sample-to-positive cutoff value of ≥0.6 was both sensitive and specific, i.e., all PHEV-inoculated pigs were seropositive from days postinoculation 10 to 42, and no cross-reactivity was observed in samples from other groups. The PHEV S1 ELISA was then used to estimate PHEV seroprevalence in U.S. sow herds (19 states) using 2,756 serum samples from breeding females (>28 weeks old) on commercial farms (n = 104) with no history of PHEV-associated disease. The overall seroprevalence was 53.35% (confidence interval [CI], ±1.86%) and herd seroprevalence was 96.15% (CI, ±3.70%).

IMPORTANCE There is a paucity of information concerning the ecology of porcine hemagglutinating encephalomyelitis virus (PHEV) in commercial swine herds. This study provided evidence that PHEV infection is endemic and highly prevalent in U.S. swine herds. These results raised questions for future studies regarding the impact of endemic PHEV on swine health and the mechanisms by which this virus circulates in endemically infected populations. Regardless, the availability of the validated PHEV S1 enzyme-linked immunosorbent assay (ELISA) provides the means for swine producers to detect and monitor PHEV infections, confirm prior exposure to the virus, and to evaluate the immune status of breeding herds.

A fosfomycin-resistant and carbapenemase (OXA-48)-producing Klebsiella pneumoniae isolate was recovered, and whole-genome sequencing revealed ISEcp1-bla_CTX-M-14b tandemly inserted upstream of the chromosomally encoded lysR-fosA locus. Quantitative evaluation of the expression of lysR and fosA genes showed that this insertion brought a strong hybrid promoter leading to overexpression of the fosA gene, resulting in fosfomycin resistance. This work showed the concomitant acquisition of resistance to broad-spectrum cephalosporins and fosfomycin due to a single genetic event.

Publisher Microsoft and developer 343 Industries announced Halo 2: Anniversary will launch for the Windows PC version of Halo: The Master Chief Collection via Steam and Microsoft Store on Tuesday, May 12.

Here is an overview of the game:

Halo 2: Anniversary comes to PC as the next installment in Halo: The Master Chief Collection. Now optimized for PC, experience the impeccably remastered edition of the original Halo 2 game. Following the destruction of Halo, humankind experiences a short-lived victory. Eager for revenge, the Covenant launches a surprise attack on Earth, but they find themselves ill-prepared to defeat the UNSC’s home fleet and are forced to flee into slipspace. When the Master Chief pursues his overzealous enemies, they discover yet another Halo ring, uncovering long-buried secrets, including an unlikely ally, that will dramatically alter the course of the Human-Covenant Conflict forever.

Key Features:

• PC Settings/Optimizations: Halo 2: Anniversary is now optimized for PC and looking better than ever at up to 4k UHD and at 60+ FPS.* Other PC native settings include customizable mouse and keyboard support, ultrawide support, FOV customization, and more.
• Campaign: Experience the next chapter in the Halo saga and fight your way through 15 unforgettable missions. Play as both Spartan-117, the Master Chief, and for the first time, the Covenant Elite, known as the Arbiter, and experience the Human-Covenant Conflict in a whole new way.
• Anniversary Edition/Update: Toggle between the remastered graphics in the Anniversary edition and the graphics from the original Halo 2 campaign. In the Anniversary edition, view Blur Studio’s spectacularly remastered cutscenes from the original Halo 2 game.
• Multiplayer: Continue your Halo adventure with 7 remastered multiplayer maps from Halo 2: Anniversary and 25 multiplayer maps from the original Halo 2, featuring a completely updated progression system.

A life-long and avid gamer, William D'Angelo was first introduced to VGChartz in 2007. After years of supporting the site, he was brought on in 2010 as a junior analyst, working his way up to lead analyst in 2012. He has expanded his involvement in the gaming community by producing content on his own YouTube channel and Twitch channel dedicated to gaming Let's Plays and tutorials. You can contact the author at wdangelo@vgchartz.com or on Twitter @TrunksWD.

Full Article - https://www.vgchartz.com/article/443396/halo-2-anniversary-for-halo-the-master-chief-collection-for-pc-launches-may-12/

Manchester United are yet to offer Odion Ighalo a permanent deal with Ole Gunnar Solskjaer undecided over his plans to sign a striker this summer.

Manchester United have been warned that Odion Ighalo could be set to land a 'big money move' to one of their major European rivals if they do not sign him permanently this summer.

Manchester United striker Odion Ighalo has heaped praise on fellow January arrival Bruno Fernandes and warned the rest of the Premier League: "We've not seen the best of him yet!"

Odion Ighalo says Manchester United will be "a different team" when Paul Pogba is back fit and firing.

Odion Ighalo believes Victor Osimhen has huge potential, with the Manchester United striker praising his compatriot as the "future of Nigerian football."

Loan sensation Odion Ighalo has revealed he felt the benefits of working under Ole Gunnar Solskjaer instantly upon arriving at Manchester United.