Is Narmada water being made to flow in Sabarmati not supplied to city of Ahmedabad? This has furthered the idea of river...
I have been selling glass for commercial buildings talking about light, thermal/solar heat gain etc.etc..but I...
Dear Saxena ji,
Thank you for inquiry.
West facing windows can be a big source of heat, first measure which you...
the high density lipoprotein (hdl) or the 'good' cholesterol protects blood vessels from getting clogged. But how exactly it safeguards the arteries was not clear till today. Researchers now claim to have found the receptors that enable hdl particles capture cholesterol from the blood stream. The conventional theory proposes that the hdl removes the cholesterol-laden cells of atherosclerotic plaques lining blood vessels through blood stream to the liver and other tissues. While it appears attractive, still researchers have not been able to find the receptor system that gives the molecular handle for hdl particles to transport away the bad cholesterol.
A team led by Monty Krieger of the Massachusetts Institute of Technology (mit), Massachusetts, usa, has recently reported the clinical evidence. Krieger's group knocked off the gene coding for the molecule designated sr - b1 in laboratory mice. They found that blood cholesterol levels in such mice increased, while the concentrations in organs that pick up cholesterol from the hdl such as the steroid-producing adrenal gland, dropped (Proceedings of the National Academy Sciences usa , Vol 94, No 23).
The mit group was not originally looking for the hdl receptor. For the last 15 years, the researchers had been trying to unravel the mystery of how the sub-cellular scavenging system works. For example, if there is a tissue damage due to an infection how the remains of damaged cells and modified lipoproteins are vacuumed up by the macro pathogens using the scavenger receptors. The receptors which they identified were named as sr - b1 for scavenging receptor b1. But the researchers soon realised that the receptor system discovered and cloned by them, was not only binding the damaged tissue but was also binding other lipoproteins such as the low density lipoprotein (ldl). The ldl causes heart disease in humans.
Last year, the team confirmed this finding by transferring the gene for sr - b1 into cells that do not take up cholesterol from the hdl. The cells acquired such abilities. The gene is expressed primarily in the right places for the proposed function including the liver and glands that produce steroid hormones such as the ovary and adrenals. The researchers have also found that adenovirus carrying the sr - b1 gene system induces over expression in the liver cells of mice. All the circulating hdl disappears from the animals' blood stream while the concentration of cholesterol in their bile doubles.
The sr - b1 system was also found to pass the test in mice. When the researchers inactivated the sr - b1 gene in mice, they found that plasma cholesterol levels in the knockout animals were more than doubled.
In fact, knocking out the gene had nearly the same effect on total serum cholesterol levels as a known contributor to atherosclerosis: loss of the ldl receptor that causes blood cholesterol levels to soar.
The knockout mice showed a dramatic drop in adrenal cholesterol and indicated that the tissues were being starved of the hdl . It made clear that the receptor is the one which takes up the hdl .
Now, the researchers are examining whether people who accumulate cholesterol in their blood have a defective or not fully functional receptor system. It will also be interesting to know whether those genetically prone to heart disease have a partially functional or non-functional receptor system.