Oil and gas company Jadestone Energy has signed a rig contract for infill drilling on the Stag oilfield located offshore Australia.Jadestone informed on Monday that Ensco Australia had agreed to provide the Ensco 107 jack-up drilling rig to Jadestone, after completion of its current operation in Dampier, Western Australia.Jadestone intends to drill the Stag-49H well from the Stag wellhead platform, as a horizontal oil producer, targeting unswept pay in the Stag reservoir southwest of the platform. The well will target approximately 1.2 mmbbl of incremental oil reserves from the field.The company is planning to spud the Stag-49H well in early March 2019 and drilling operations are expected to take approximately 34 days.Paul Blakeley, President and CEO commented “I am pleased to have signed the rig contract with Ensco to drill Stag-49H, the first infill well at the Stag field since 2013, and an important milestone for the company too.”The Stag oilfield was acquired by Jadestone through its wholly-owned subsidiary Jadestone Australia on November 11, 2016.The field was developed using a fixed leg, 12 slot manned central processing facility platform with a liquids production capacity of 50,000 bbl/d, of which 30,000 bbl/d is for oil. This is connected, by an eight inch underwater export pipeline, to a pipeline end manifold and floating storage and offloading vessel (FSO), via a catenary anchor leg mooring buoy. Shuttle tankers transfer the oil from the FSO to shore.It is worth reminding that the Ensco 107 drilling rig was used last year to drill the Dorado-1 well, which turned out to be one of largest oil discoveries ever on the Australian North West Shelf.
Ubong’s strike against ABS FC of Ilorin was adjudged the best goal of the match-day by online voters in a Nigeria Professional Football League (NPFL) poll and was presented the award on Wednesday by the Akwa Ibom and Cross River State FIRS Coordinator, Agu Bennet at the Godswill Akpabio International Stadium, Uyo.Elated by the recognition, Ubong said he had never won such an award in his career and was delighted that he was beginning to hit the limelight.He said he will share the prize money of N150,000 with the Children Development Centre on IBB Boulevard in Uyo which his club and players have been channeling their charity gestures as part of their community relations.“It is a great thing for me to win this award. I have never received an award like this in my playing career and I am happy that I am the one who has brought it to my club. It is great for me, my family, my teammates, the club and our fans and I am dedicating it to all of them because we are a family.“I will share the proceeds with the Children Development Centre near our camp here in Uyo. That is the only charity I know and that is where we as a club and team mates have been visiting to give support from time to time.“I love children and each time we go there, I remember when I was a child and my younger ones too. I feel very happy that I can personally bring something to them and I thank God for the opportunity. Many of us may have come from homes where our parents have the means to cater for us but when you consider the children at the centre, you are reminded that there are so many children among us who need support from members of the society to go through life. “Ubong who has five goals so far on record this season believes he has just opened a floodgate for more recognition for Akwa United.“I hope to keep scoring this season and I believe my team mates too will score such beautiful goals that will be so celebrated. I believe that Christian’s (Pyagbara) goal today will also win the Wonder Goal Award because it was something you can’t believe. I stood in awe of the effort, the gut and the delivery of that goal and I believe it will count as the best.”Akwa United played Wikki Tourists in a rescheduled Match-day 23 NPFL game at their Nest of Champions ground in Uyo. United defeated the Bauchi team 2-0.Share this:FacebookRedditTwitterPrintPinterestEmailWhatsAppSkypeLinkedInTumblrPocketTelegram Fred EdorehAkwa United winger, Ubong Friday and Match-day 21 VAT Wonder Goal Award winner has spoken of his love for children while revealing that he would be sharing the proceeds of his award with the Children Development Centre in Uyo.
Source:https://ucsdnews.ucsd.edu/pressrelease/caspase_2_enzyme_inhibition_shows_promise_for_ameliorating_fatty_liver_disease Reviewed by James Ives, M.Psych. (Editor)Sep 14 2018Researchers at University of California San Diego School of Medicine have discovered using mice and human clinical specimens, that caspase-2, a protein-cleaving enzyme, is a critical driver of non-alcoholic steatohepatitis (NASH), a chronic and aggressive liver condition. By identifying caspase-2’s critical role, they believe an inhibitor of this enzyme could provide an effective way to stop the pathogenic progression that leads to NASH — and possibly even reverse early symptoms.The findings are published in the September 13 online issue of Cell.”Our results show that caspase-2 is a critical mediator of NASH pathogenesis, not only in mice but probably in humans as well,” said Michael Karin, PhD, Distinguished Professor of Pharmacology at UC San Diego School of Medicine. “While explaining how NASH is initiated, our findings also offer a simple and effective way to treat or prevent this devastating disease.”NASH is the most aggressive form of non-alcoholic fatty liver disease (NAFLD), which includes a spectrum of chronic liver diseases and has become a leading cause of liver transplants. The cause of both NAFLD and NASH remains a mystery, but researchers believe one factor that accelerates the progression of benign NAFLD to aggressive NASH is elevated endoplasmic reticulum (ER) stress, induced by protein misfolding within the liver. This results in excessive buildup of cholesterol and triglycerides in liver tissue.Applying this premise in mice, researchers first identified molecules involved in NASH pathogenesis by combining liver-specific ER stress and a high-fat diet to elicit NASH like disease, duplicating the cardinal features of human NASH, including fat accumulation in liver cells, liver damage, inflammation and scarring. Using this model, researchers found that the onset of NASH correlated with increased expression of caspase-2.In the next phase, Karin and team examined human liver specimens collected from patients with benign NAFLD or aggressive NASH to confirm caspase-2 expression was also elevated in humans. By knocking out the caspase-2 gene in mice subjected to liver ER stress and high-fat diet or treating the mice with a specific caspase-2 inhibitor, they found that caspase-2 was responsible for all aspects of NASH, including lipid droplet accumulation, liver damage, inflammation and scarring.Related StoriesLiver fat biomarker levels linked with metabolic health benefits of exercise, study findsResearchers pinpoint treatment target for rare liver cancer in adolescents, young adultsScientists develop new way to detect and switch off ticking time bomb of liver disease”We now know that by preventing caspase-2 expression or inhibiting its activity that biomarkers of NASH are mitigated,” said Juyoun Kim, PhD, senior fellow in the Karin laboratory and lead author. “This is exciting because now, we not only understand the role of caspase-2 in the disease, but also have a new avenue to find a potential drug treatment.”Through this study, Karin and team also discovered that caspase-2 has a critical role in activating SREBP1 and 2 — the master regulators of lipogenesis, a process that takes place in the liver where nutrients like carbohydrates are turned into fatty acids, triglycerides and cholesterol. Caspase-2 was found to control SREBP1 and 2 activation by cleaving another protein called site-1 protease.”In NASH-free individuals, the activities of SREBP1 and SREBP2 are kept under control, which is essential for preventing excessive lipid accumulation in the liver,” said Karin. “However, in NASH patients, something goes awry and the liver continues to turn out excess amounts of triglycerides and cholesterol. This correlates with elevated SREBP1 and SREBP2 activities and increased caspase-2 expression.”Moving forward, Karin and team would like to embark on development of more effective drug-like caspase-2 inhibitors that could be used for NASH prevention, and ultimately provide a treatment option.”This study was a great step forward in being able to understand the causes, and explore possible new treatments for patients with NASH and NAFLD,” said co-author Rohit Loomba, MD, director of the UC San Diego NAFLD Research Center and director of hepatology at UC San Diego School of Medicine. “It is our hope to eventually translate and validate these study results using a much larger cohort of human subjects.””This study was a great step forward in being able to understand the causes, and explore possible new treatments for patients with NASH and NAFLD,” said co-author Rohit Loomba, MD, director of the UC San Diego NAFLD Research Center and director of hepatology at UC San Diego School of Medicine. “It is our hope to eventually translate and validate these study results using a much larger cohort of human subjects.”