US busts online drugs ring Farmer’s Market

first_img Tweet 14 Views   no discussions HealthInternationalLifestylePrint US busts online drugs ring Farmer’s Market by: – April 17, 2012 Sharing is caring! Sharecenter_img Share Share The secret ring supplied drugs to clients in 35 countries around the world, the US saidThe US authorities say they have busted a secret internet drugs market, where people around the world could buy LSD, ecstasy and other illegal substances.The ring – The Farmer’s Market – is said to have operated through a computer network which allows users to communicate anonymously.At least eight people have been held in the US, the Netherlands and Colombia.They have been charged with drug trafficking and money laundering and will face trial in the US.‘Clear message’The arrests were the culmination of the two-year Operation Adam Bomb, officials from the US Drug Enforcement Administration (DEA) announced late on Monday.The sophisticated ring had tried to hide its activities “through the use of advanced anonymising online technology,” said Briane Grey, the DEA’s acting special agent in charge.He added that the arrests “should send a clear message to organisations that are using technology to conduct criminal activity that the DEA and our law enforcement partners will track them down and bring them to justice”.The US authorities have identified Marc Willems, 42, as the “lead defendant”, who is believed to have created and run the network. He has been arrested at his home in the Netherlands.It is alleged that more than $1m (£630,000) worth of drugs sales were processed through the sophisticated ring which used the TOR computer network between 2007-09.The Farmer’s Market reportedly provided order forms, customer service and accepted payments through PayPal, Western Union and other means.It had customers in every US state as well as in 34 countries around the world.BBC Newslast_img read more

Absolute Stunner! Gabriel five-for sucker-punches Pakistan for 81

first_imgBRIDGETOWN, Barbados (CMC) – A rampant West Indies flattened Pakistan for a record-equalling low at Kensington Oval, as they romped to an emphatic 106-run victory in the second Test here yesterday, to level the three-match series and set up a decider in Dominica next week.Set 188 for victory on the final day of the pivotal contest, Pakistan folded meekly for a paltry 81, about 38 minutes before the scheduled tea interval, to slump to their fourth loss in seven games at the historic venue and maintain their unenviable record of having never won a Test at the ground.The total equalled the previous lowest posted by India 20 years ago here and was also Pakistan’s second lowest-ever against West Indies, surpassing their record low of 77 in Lahore, 31 years ago.For West Indies, the victory came just 11 days after they lost the opening Test in Jamaica by seven wickets and marked only their third Test win in 17 outings over the last two years.“It was obviously a very good game for us. It was a collective team effort,” captain Jason Holder said afterwards.Yasir Shah has his off-stump uprooted by Shannon Gabrielas West Indies players celebrate the wicket. (WICB)“I always thought once we could give them in excess of 170, I felt we would be in with a very good chance on a day-five pitch, the way it has deteriorated here.”West Indies were fired by speedster Shannon Gabriel who turned in a man-of-the-match effort with five for 11 from 11 overs, to claim his second five-wicket haul in Tests and end with match figures of nine for 92.Holder claimed three for 23 while 20-year-old pacer Alzarri Joseph supported with two for 42.Resuming the morning on 264 for nine, West Indies added only four runs before the innings ended, when Devendra Bishoo holed out to Azhar Ali at mid-off for 20, off the fifth ball of the day from leg-spinner Yasir Shah who ended with seven for 94.Gabriel then produced a lethal three-wicket burst to wipe out Pakistan’s top order and reduce the innings to rubble at 35 for five at lunch.He prised out Azhar in the seventh over of the innings for 10, pulling a short ball to Shimron Hetmyer at short mid-wicket with as many runs on the board and four balls later in the next over, Babar Azam completed a pair in the match when he touched a leg-side catch to wicketkeeper Shane Dowrich off Joseph.West Indies struck a major blow when they got the prized wicket of veteran Younis Khan for five, lbw to Holder at 27 for three but it was in the fifth over before the break that Gabriel turned the game on its head.With the second delivery, he removed skipper Misbah-ul-Haq without scoring to a catch at gully by Shai Hope after that batsman edged one into his pads, and was given out via DRS after the initial appeal went unheeded.Two balls later, new batsman Asad Shafiq also fell without scoring, nicking Gabriel to first slip where Kieran Powell held a juggling catch.Needing a virtual miracle after lunch to survive, Pakistan found themselves in deeper trouble when they lost two further wickets in the first 16 balls on resumption.Alzarri Joseph sentback Babar AzaOpener Ahmed Shehzad, unbeaten on 14 at the interval after being dropped on six by Powell at slip, off Joseph in the 10th over, failed to add when he was lbw on the back foot in the second over after the break to one from Joseph which kept low.Shadab Khan then followed in the next over for one, caught at the wicket off Holder, leaving Pakistan flailing on 36 for seven and in danger of their lowest Test score of 49.Wicketkeeper Sarfraz Ahmed, who top-scored with 23, briefly raised hopes of a Pakistan comeback, staging the best partnership of the innings by adding 42 for the eighth wicket with tail-ender Mohammad Amir who made 20.Sarfraz, unbeaten on five at lunch, spent just 50 balls and just over 1-1/2 hours at the crease and struck two fours while Mohammad Amir was his usual self, stroking four boundaries in a 34-ball knock.However, once Amir’s enterprise got the better of him and he slashed Gabriel to Vishaul Singh at backward point on the stroke of the first hour, the innings quickly declined as the last two wickets tumbled for just three runs in the space of 18 balls.Yasir was bowled neck and crop by Gabriel without scoring and Sarfraz was last to fall, holing out to Chase at long-on off Holder.The decisive third Test begins next Wednesday at Windsor Park.last_img read more

Cancer cells coopt painsensing neural channel to increase tolerance against oxidative stress

first_imgMay 25 2018Anyone who’s taken a bite of a sandwich with too much spicy mustard or a piece of sushi with too much wasabi can attest to the tear-inducing sensation these condiments can cause. These loud warnings to the nervous system of exposure to potentially harmful chemicals are triggered by TRPA1, a calcium channel protein sometimes referred to as the “wasabi receptor.”Found primarily in sensory neurons, TRPA1 is a sensor for environmental irritants and has been widely studied for its roles in detecting sensations such as pain and cold, and in airway inflammation conditions such as asthma.Certain cancers express unusually high levels of TRPA1, particularly lung and breast cancers, but why they do so has thus far remained unclear.Now, in a new study published online in Cancer Cell on May 24, Harvard Medical School researchers show that tumor cells use TRPA1 as a unique defense mechanism against reactive oxygen species (ROS), toxic byproducts of cell metabolism.”This was quite an unexpected finding. Tumor cells appear to have co-opted this neural protein channel, which is associated with multiple types of cancer, to protect themselves against oxidative stress,” said senior study author Joan Brugge, the Louise Foote Pfeiffer Professor of Cell Biology at HMS.The team’s analyses revealed that TRPA1 allows cancer cells to tolerate elevated ROS by inhibiting programmed self-destruction, which severely damaged or stressed cells normally undergo. They found that TRPA1 expression is regulated by a cellular pathway that also produces antioxidant compounds that neutralize ROS. Antioxidants and TRPA1 appear to complement each other to increase tumor survival, according to the authors.Experiments that blocked TRPA1 activity in mice curbed tumor growth and made cancer cells more vulnerable to chemotherapy. Drugs that target TRPA1 are being developed, with some entering clinical trials, for a variety of conditions, including asthma and pain, Brugge pointed out.”Our results suggest that TRPA1 could be a promising target for new treatments against cancer as well,” said Brugge, who is co-director of the Harvard Ludwig Cancer Center.Damage PreventionVirtually every cell uses oxygen to power the metabolic processes necessary for life, but metabolism also generates ROS, oxygen-based chemicals that are highly reactive and potentially harmful to cellular structures.ROS must be carefully managed to prevent cell damage or death. This is especially important for cancer cells, which accumulate large amounts of ROS as they multiply and metastasize beyond control.Previous work by Nobuaki Takahashi, HMS instructor in cell biology in the Brugge laboratory, and colleagues showed that ROS can activate TRPA1 in neurons.To investigate this connection in cancer, Brugge, Takahashi and colleagues grew human breast and lung cancer cells under laboratory conditions into 3-D spheroids that mimic a tumor’s natural structure.They found that ROS levels were substantially higher inside the spheroids compared to the surface, but this disparity had little effect on cell survival.When TRPA1 was blocked, however, cancer cells in the interior of the spheroids began to die and were cleared within a few days.Antioxidant ComplementThe team’s analyses revealed that an influx of calcium ions through TRPA1 triggers a cascade of cellular signals that suppress programmed cell death. They found that TRPA1 expression is induced by NRF2, a transcription factor that controls the production of antioxidants.Related StoriesStudy reveals link between inflammatory diet and colorectal cancer riskNew research links “broken heart syndrome” to cancerUsing machine learning algorithm to accurately diagnose breast cancerWhen exposed to high levels of ROS, cancer cells appear to rely on NRF2 to activate antioxidant production and to prevent programmed cell death through TRPA1, the authors said.”The cellular program that increases production of antioxidants also simultaneously activates this unique TRPA1-dependent defense mechanism, which allows cancer cells to tolerate enhanced levels of ROS,” said Takahashi, who is lead author on the study. “These two very different pathways work together to help tumors survive and adapt to oxidative stress.”In mice with transplanted human breast cancer tumors, the researchers showed that blocking TRPA1 with drugs slowed tumor growth. Inhibition of TRPA1 also increased the sensitivity of cancer cells to chemotherapy agents that kill tumors by encouraging programmed cell death. When given together, TRPA1 blockers and chemotherapy significantly reduced tumor size.Because of its central role in pain sensation and asthma, numerous research efforts and clinical trials are underway to develop small molecules that can safely and effectively inhibit TRPA1 activity. Taken together, the results show that TRPA1 could be an enticing target for therapies against cancer, the researchers said.”In lung cancer, for example, radiation is an important primary therapy that kills cancer cells by flooding them with ROS,” Brugge said. “But cancer cells expressing TRPA1 may be able to tolerate radiotherapy better.””Inhibiting TRPA1 activity and decreasing this buffering ability might make TRPA1-positive tumors more vulnerable to radiation,” she added. “We think this could be a possible first-use scenario, if indeed good TRPA1 inhibitors are developed.”Buyer BewareThe study findings also add to a growing body of evidence that defense against oxidative stress is important to cancer progression.Previous research by Brugge’s lab was among the first to show that antioxidants help cancer cells survive high ROS conditions, particularly when cells travel away from the original tumor site, as is the case with metastases.Subsequent studies in cell and animal models have supported this observation. In humans, large-scale clinical trials of antioxidant dietary supplements have not found evidence that supplements are beneficial for cancer, and in some cases have suggested that their use may worsen outcomes.Further research is needed to better understand the effects of dietary antioxidants in cancer patients, the authors said, and the National Cancer Institute recommends that such supplements be used with caution.Brugge and colleagues are now further investigating the biological underpinnings of TRPA1 activity in cancer and its role in defending against ROS.”There is an abundance of evidence that the mechanisms cancer cells use to defend against oxidative stress could be exploited to enhance the sensitivity of tumors to existing therapies,” Takahashi said. “In the case of TRPA1, inhibiting its activity blocks pain, which is almost always a good thing, and our study highlights its potential clinical utility for cancer treatment.” Source:https://hms.harvard.edu/news/no-pain-all-gainlast_img read more