Graphene, popularly known as the wonder material,But there's a drawback of this material too.
It
has a zero band gap which makes it impossible for pure Graphene to turn
OFF when used as a switch. Hence, it is important that the material is
doped with some impurities. This is where the researchers have really
worked. They have oxidised Graphene to make it impure, but they have
done it without damaging the lattice structure of the material.
Scientists
could resort to only one process called Hummer’s method for making
changes in Graphene’s structural characteristics. This process was
developed in 1940s. But, because of the usage of harsh acids, it tends
to make the Graphene structure unusable. But this latest technique
overcomes such issues. Mark C Hersam, professor of materials science and
engineering at the McCormick School explains the process. Hersam said
that they had exposed hot Tungsten filament to Oxygen at about 1500
degree celsius in an ultra-high vacuum chamber. Molecular oxygen is
transformed into atomic oxygen when both the elements come in contact.
The researchers have introduced nascent Oxygen into Graphene which
oxidises it to make it homogeneous. The researchers discovered that the
electronic properties of Graphene are a result of the amount of Oxygen
introduced.
It is worth mentioning here that like
Silicon and plastic, Graphene has a chance to function efficiently in
the modern day electronics industry.
GRAPHENE NANO RIBBONS.
A
new synthetic strategy toward novel linear two-dimensional graphene
nanoribbons up to 12 nm has been established. The nanoribbons are
characterized by MS, UV/vis, and scanning tunneling microscopy (STM).
Various microscopic studies of these novel structures showed a high
tendency to self-assemble.
Graphene nanoribbons (also
called nano-graphene ribbons), often abbreviated GNRs.Their electronic
states largely depend on the edge structures Zigzag edges provide the
edge localized state with non-bonding molecular orbitals near the Fermi
energy.Graphene nanoribbons with controlled edge orientation have been
fabricated by Scanning Tunneling Microscope (STM) lithography. Opening
of energy gaps up to 0.5 eV in a 2.5 nm wide armchair ribbon was
reported. Zigzag nanoribbons are also semiconducting and present spin
polarized edges. Their gap opens thanks to an unusual antiferromagnetic
coupling between the magnetic moments at opposite edge carbon atoms.
This gap size is inversely proportional to the ribbon width and its
behavior can be traced back to the spatial distribution properties of
edge-state wave functions, and the mostly local character of the
exchange interaction that originates the spin polarization.
Their
2D structure, high electrical and thermal conductivity, and low noise
also make GNRs a possible alternative to copper for integrated circuit
interconnects.
a) Genetic Recombinant technique:PRDM9
During
mammalian meiosis, double-strand breaks are deliberately made
throughout the genome and then repaired, leading to the exchange of
genetic material between copies of chromosomes. How the locations of
breaks are specified was largely unknown until a fortuitous confluence
of statistical genetics and molecular biology uncovered the role of
PRDM9, a DNA binding protein. Many properties of this protein remain
mysterious, however, including how it binds to DNA, how it contributes
to male infertility—both in humans, and in hybrid mice—and why, in spite
of its fundamental function in meiosis, its binding domain varies
extensively among humans and across mammals. We present a brief summary
of what has recently been learned about PRDM9 in different fields,
focusing on the puzzles yet to be resolved.
b) GUT BACTERIA may override genetic protections against diabetes:
Obesity
and type 2 diabetes have risen tremendously over the last 20 years, and
the causes of these epidemics are complex. In both diseases, insulin
resistance manifests early due to a combination of genetic and
environmental factors, with gut bacteria and the immune system playing
key roles. For example, weight gain and insulin resistance are linked to
a group of gut bacteria called Firmicutes, which provide a source of
extra calories by breaking down polysaccharides that are otherwise
indigestible in mammals.
Insulin sensitivity is also
affected by immune system proteins called Toll-like receptors (TLRs)
that recognize microbial compounds. When raised in germ-free
environments, mice that lack TLR2 are protected against obesity-induced
insulin resistance. Intriguingly, the immune system helps regulate gut
bacteria, and previous work suggests that TLRs may affect insulin
sensitivity by altering the composition of enteric microbes.
present
compelling evidence that gut bacteria can nullify the genetic
protection against insulin resistance in TLR2-deficient mice.
To
investigate the relationship between gut bacteria and insulin
sensitivity, the researchers raised TLR2-deficient mice under conditions
that were not germ-free. In contrast to previous findings, these mice
became insulin resistant within 8 weeks, and were fatter at 12 weeks.
Genetic analysis of their gut bacteria revealed that the abundance of
Firmicutes was three times higher than that of wild-type mice, and the
researchers suggest that this explains why these TLR2-deficient mice
were not protected against insulin resistance. Because the composition
of enteric microbes varies with the environment and diet, mice with the
same genetic background can have different gut bacteria, and presumably
this was the case for the TLR2-deficient mice in previous studies.
How
could gut bacteria counteract the innate insulin sensitivity of
TLR2-deficient mice? Insulin resistance can be caused by bacterial cell
membrane compounds called lipopolysaccharides, and several lines of
evidence suggest that this is a likely mechanism for the development of
insulin resistance in the TLR2-deficient mice studied. Notably, they had
higher serum levels of lipopolysaccharides, and absorbed more of them
after oral administration. This suggests that these mice had more
permeable guts, which is supported by the finding that their intestines
had less of a tight junction protein.
The link between
gut microbe composition and insulin resistance was further strengthened
by a number of findings. In particular, treating TLR2-deficient mice
with antibiotics brought their Firmicutes down to normal levels, reduced
their fat, decreased their serum lipopolysaccharides, and increased
their insulin sensitivity. This suggests that changing the composition
of gut microbes reversed their insulin resistance. Moreover, when gut
microbes were transplanted from TLR2-deficient mice into wild-type mice
with only the genus Bacillus in their guts, the latter got fatter, had
higher lipopolysaccharide levels, and were less sensitive to insulin.
This suggests that the Firmicutes-rich gut bacteria from these
TLR2-deficient mice were enough to cause insulin resistance.
Because
obesity and insulin resistance may be promoted by fatty foods in
people, the researchers compared the effects of high-fat diets on
TLR2-deficient and wild-type mice. The TLR2-deficient mice got much
fatter and glucose tolerance tests revealed that they also developed
diabetes, indicating that the high-fat diet exacerbated their insulin
resistance.
By showing that changes in gut bacteria can
cause insulin resistance in mice that are genetically protected against
this condition, this work suggests that the composition of enteric
microbes may cause obesity and diabetes in animals that are predisposed
to be lean. This work also sheds light on the interplay of genetic and
environmental factors that cause metabolic syndrome in people, which is
characterized by obesity and insulin resistance, and increases the risks
of stroke and coronary artery disease along with type 2 diabetes.
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KENISINS-
are group of motor proteins. They move materials faster across nerve
cell end with a velocity of 3 micro meters per second thereby causing
the transmission of nerve impulses in lightening speed.
DYNEIN- cell division is aided with this protein motor.
These natural molecular motors have immense application in bionano
technology, pharmology and medicine. It can be a
promising approach to drug system that can utilize motor transport with
in human cells and mobile components for nanoscale manufacturing in
adding life to nanotechnology.
