MUMBAI, India (AP) ? India has joined China in saying it will not cut back on oil imports from Iran, despite stiff new U.S. and European sanctions designed to pressure Tehran over its nuclear program.
"It is not possible for India to take any decision to reduce the import from Iran drastically because, after all, the countries which can provide the requirement of the emerging economy, Iran is an important country amongst them," India's finance minister Pranab Mukherjee told reporters Sunday in Chicago.
India and China together accounted for 34 percent of Iran's oil exports from January to September of 2011 ? slightly more than Europe, according to International Energy Agency data.
The move is likely to be seen as a political victory in Iran, but it's unclear how Chinese and Indian companies will actually be able to pay for Iranian oil without running afoul of the sanctions, analysts said.
"It's a blow," said David Hartwell, senior Middle East analyst at IHS Jane's, adding that Iran may have discounted prices to keep the Chinese and Indians on their side. "If you have two major countries like India and China saying they will not abide by the sanctions, that's going to keep a vital line open for the Iranians to continue to sidestep the sanctions and get foreign capital."
He said India and China could just be trying to buy time to diversify their oil supplies and may steer away from Iran, especially if Saudi Arabia ? India's largest source of oil imports ? were to ramp up production and offer an attractively priced alternative.
The European Union last week imposed an oil embargo against Iran and froze the assets of its central bank. In December, the U.S. said it would bar financial institutions from the U.S. market if they do business with Iran's central bank.
India and China are ravenous energy consumers and rely heavily on imported oil. Iranian oil accounts for 9 percent of India's oil consumption and 6 percent of China's, according to the latest data from the IEA.
Iran exports 2.5 million barrels of oil per day, about 3 percent of world supplies. About 500,000 barrels go to Europe and most of the rest goes to China, India, Japan and South Korea.
China has called for negotiations over Iran's nuclear program. South Korea has been non-committal about the sanctions, and Japan is seeking an exemption, saying its Iranian oil imports have steadily declined and probably will continue to do so.
Kyodo News agency reported that senior Japanese and U.S. officials on Thursday will hold their second meeting on the sanctions this month.
"I believe it may not be easy to come to a conclusion on this matter in the upcoming discussions," Foreign Minister Koichiro Gemba said.
Western sanctions could make it harder for India to pay for the oil it gets from Iran. Past sanctions have already delayed payments by Indian oil importers, who have had to scramble to find banks willing to handle transactions with Iran.
India's central bank governor D. Subbarao said last week that the current payment mechanism was "working fine," though India was also "exploring other options," which he declined to discuss.
Indian companies now reportedly route payments through Turkey's Turkiye Halk Bankasi AS, after EU pressure forced German-based Europaisch-Iranische Handelsbank AG to stop handling the payments last year.
IHS Jane's energy analyst said Turkey is unlikely to shut down that route immediately, noting that Turkish oil refiner Tupras also uses this payment mechanism.
"But this route remains susceptible to external pressure," she added by email. "India is now discussing rupee based payments and direct trade ? however that has a number of drawbacks for Iran given the trade imbalance and restrictions on use. China isn't publicly discussing options but I imagine other currency payments are also on the cards there."
The U.S. and its allies believe Iran is using oil revenues to develop nuclear weapons, but Tehran insists its nuclear program is purely for peaceful purposes.
Associated Press
Red Exterior, Red Interior - Factory 271 Horsepower 289
Many of us, especially the current or former graduate students among us, are addicted to our breakfast caffeinated beverage of choice. Mine is tea, but if I had to guess, I?d wager that the most popular option is coffee. We chug it down in the morning to get ready for our day, we sip it thoughtfully at work, and we seek it out in the wee hours when we should be sleeping but instead we?re at the lab or at our desks, telling ourselves that we?ll run just one more gel or write just one more page. The ritual of coffee (or tea!) is deeply ingrained in our daily lives for many of us, but aside from keeping us alert, what else does it do for us? A recent study suggests that certain polyphenolic compounds in tea and coffee may offer protective effects against type 2 diabetes mellitus (T2 diabetes) by interfering with the formation of amyloid fibrils in the pancreas. Wow, that sounds great, doesn?t it? Another excuse to drink more of the stuff! But what the heck does it mean? In order to understand how this might work, we first need to understand some concepts. Specifically, what is an amyloid fibril, and what does it have to do with T2 diabetes?
Amyloids are deposits of proteins that have been folded in a specifically incorrect way (proteins must be folded properly in order to function properly). These misfolded proteins form aggregates (i.e., they clump together) that build up in tissues and cells, similar to the way that calcium deposits might build up in your pipes, for instance. You can see what this looks like in the photo to the left, which shows amyloid deposits (brown) of Abeta protein in the cerebral cortex. Amyloids tend to be associated with diseases such as Parkinson?s and Alzheimer?s disease in addition to T2 diabetes. The exact way that these protein deposits contribute to these diseases is unclear, but it is thought that their presence causes the tissues around them to be deformed, thus interfering with their ability to do their job. They may also cause cell death by interfering with the mitochondria, which are the organelles that supply cells with energy. In the case of T2 diabetes, the presence of amyloid fibrils in the pancreas is thought to kill the beta-cells that produce insulin. The amyloid fibrils in this case are made of a protein called human islet amyloid polypeptide (hIAPP, or amylin), which normally functions as an endocrine (i.e., hormone) that is released along with insulin from the beta-cells. Therefore, one way we can think about treating T2 diabetes is to stop hIAPP amyloid fibrils from forming in the first place.
To the left are transmission electron microscopy images of hIAPP incubated with the compounds listed above (click to enlarge). I have edited the figure slightly to include labels. In part A, which had hIAPP alone, and parts C and D, which had hIAPP incubated with caffeine, you can see the fibrous amyloid protein bundles, which look a little bit like hairs or threads. Caffeine clearly was ineffective at stopping amyloid formation. In part B, EGCG appeared to stop amyloids from forming, as there were no fibrils detected, which is consistent with the existing research leading up to this study. In addition, both CA and CGA also inhibited amyloid fibrils from forming, with greater concentrations causing more complete inhibition. Small aggregates of hIAPP were detected, but they did not form mature bundles. So the coffee polyphenols do seem to stop amyloid fibrils from forming, similar to the tea polyphenol.
Does this inhibition result in less cell death? In fact, that does seem to be the case! The graph to the right shows the percentage of cells that survived when exposed to hIAPP alone or in combination with the study compounds relative to an untreated group of cells (the untreated group = 100% viability; click to enlarge). hIAPP alone caused the survival rate of beta-cells to drop by almost two-thirds, presumably because of the cytotoxic (i.e., cell-killing) effects of amyloid fibrils. In contrast, all four of the study compounds increased the survival rate to various degrees. EGCG (in a 1:1 ratio with hIAPP) and CA (in a 1:5 ratio with?hIAPP) seemed to be the most effective at protecting the beta-cells at 75 and 96%, respectively. Perhaps the most interesting thing is that although caffeine did not stop the amyloid fibrils from forming, it still offered some protection against cell death! It could be that caffeine somehow alters the structure of the amyloid fibrils in a way that makes them less deadly to the beta-cells, even though it doesn?t stop them from forming entirely. It is also possible that caffeine interferes with the receipt of some of the chemical messengers involved in the cell death process.
