Varkey, A M; Dr.Sebastian, V D(Cochin University of Science and Technology, March 2, 1984)
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Abstract:
The joint stock company is an institution wielding immense socio economic _power over the ultimate progress and well -being of the nation. It is subjected to corresponding definable responsibilities towards all who depend on than. the shareholders.the employees the suppliers of raw materials. the consumers of its product: and society at Large. The company law is changing and must change with time and take note of the dynamics of trade and industry. Obviously it cannot be static and permanent while the basic economic and social philosophies and the technique of production and investment in the industrial sector change.‘ It provides a legal framework for the corporate form of business in which the organization capital and labour are brought. together in a particular form of relationship. The activities carried on within this corporate form is subjected to a gradual but steadily increasing control by the Government. A study of this oontrol is undertaken to better understand the present law and to suggest the path for further change
Description:
Department of Law, Cochin University of Science and Technology
Finla, Chathu; Dr. Paulose, C S(Cochin University of Science and Technology, February , 2007)
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Abstract:
In the present work, the role of oxygen, epinephrine and glucose
supplementation in regulating neurotransmitter contents, adrenergic and glutamate
receptor binding parameters in the cerebral cortex of experimental groups of neonatal
rats were investigated. The study of neurotransmitters and their receptors in the
cerebral cortex and the EEG pattern in the brain regions of neonatal rats were taken as
index for brain damage due to hypoxia, oxygen and epinephrine. Real-Time PCR work was done to confirm the binding parameters. Second messenger, cyclic
Adenosine Monophosphate (cAMP) was assayed to find the functional correlation of
the receptors. Behavioural studies were carried out to confirm the biochemical and
molecular studies. The efficient and timely supplementation of glucose plays a crucial
role in correcting the molecular changes due to hypoxia, oxygen and epinephrine. The
addictive neuronal damage effect due to oxygen and epinephrine treatment is another
important observation. The corrective measures from the molecular study brought to
practice will lead to maintain healthy intellectual capacity during the later
developmental stages, which has immense clinical significance in neonatal care.
Description:
Department of Biotechnology, Cochin
University of Science and Technology
Naijil, George; Dr.Paulose, C S(Cochin University of Science and Technology, May 14, 2014)
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Abstract:
In the present study, the initial phase was directed to confirm the effects of
curcumin and vitamin D3 in preventing or delaying diabetes onset by studying the
blood glucose and insulin levels in the pre-treated and diabetic groups.
Behavioural studies were conducted to evaluate the cognitive and motor function
in experimental rats. The major focus of the study was to understand the cellular
and neuronal mechanisms that ensure the prophylactic capability of curcumin and
vitamin D3. To elucidate the mechanisms involved in conferring the antidiabetogenesis
effect, we examined the DNA and protein profiles using
radioactive incorporation studies for DNA synthesis, DNA methylation and
protein synthesis. Furthermore the gene expression studies of Akt-1, Pax, Pdx-1,
Neuro D1, insulin like growth factor-1 and NF-κB were done to monitor pancreatic beta cell proliferation and differentiation. The antioxidant and antiapoptotic
actions of curcumin and vitamin D3 were examined by studying the
expression of antioxidant enzymes - SOD and GPx, and apoptotic mediators like
Bax, caspase 3, caspase 8 and TNF-α. In order to understand the signalling
pathways involved in curcumin and vitamin D3 action, the second messengers,
cAMP, cGMP and IP3 were studied along with the expression of vitamin D
receptor in the pancreas. The neuronal regulation of pancreatic beta cell
maintenance, proliferation and insulin release was studied by assessing the
adrenergic and muscarinic receptor functional regulation in the pancreas, brain
stem, hippocampus and hypothalamus. The receptor number and binding affinity
of total muscarinic, muscarinic M1, muscarinic M3, total adrenergic, α adrenergic
and β adrenergic receptor subtypes were studied in pancreas, brain stem and
hippocampus of experimental rats. The mRNA expression of muscarinic and
adrenergic receptor subtypes were determined using Real Time PCR.
Immunohistochemistry studies using confocal microscope were carried out to
confirm receptor density and gene expression results. Cell signalling alterations in
the pancreas and brain regions associated with diabetogenesis and antidiabetogenesis
were assessed by examining the gene expression profiles of
vitamin D receptor, CREB, phospholipase C, insulin receptor and GLUT. This
study will establish the anti-diabetogenesis activity of curcumin and vitamin D3
pre-treatment and will attempt to understand the cellular, molecular and neuronal
control mechanism in the onset of diabetes.Administration of MLD-STZ to curcumin and
vitamin D3 pre-treated rats
induced only an incidental prediabetic condition. Curcumin and vitamin D3 pretreated
groups injected with MLD-STZ exhibited improved circulating insulin
levels and behavioural responses when compared to MLD-STZ induced diabetic
group. Activation of beta cell compensatory response induces an increase in
pancreatic insulin output and beta cell mass expansion in the pre-treated group.
Cell signalling proteins that regulate pancreatic beta cell survival, insulin release,
proliferation and differentiation showed a significant increase in curcumin and
vitamin D3 pre-treated rats. Marked decline in α2 adrenergic receptor function in
pancreas helps to relent sympathetic inhibition of insulin release. Neuronal
stimulation of hyperglycemia induced beta cell compensatory response is
mediated by escalated signalling through β adrenergic, muscarinic M1 and M3
receptors. Pre-treatment mediated functional regulation of adrenergic and
cholinergic receptors, key cell signalling proteins and second messengers
improves pancreatic glucose sensing, insulin gene expression, insulin secretion,
cell survival and beta cell mass expansion in pancreas. Curcumin and vitamin D3
pre-treatment induced modulation of adrenergic and cholinergic signalling in brain
stem, hippocampus and hypothalamus promotes insulin secretion, beta cell
compensatory response, insulin sensitivity and energy balance to resist
diabetogenesis. Pre-treatment improved second messenger levels and the gene
expression of intracellular signalling molecules in brain stem, hippocampus and
hypothalamus, to retain a functional neuronal response to hyperglycemia.
Curcumin and vitamin D3 protect pancreas and brain regions from oxidative stress
by their indigenous antioxidant properties and by their ability to stimulate cellular
free radical defence system. The present study demonstrates the role of adrenergic
and muscarinic receptor subtypes functional regulation in curcumin and vitamin
D3 mediated anti-diabetogenesis. This will have immense clinical significance in
developing effective strategies to delay or prevent the onset of diabetes.
Sudha, B; Dr. Paulose, C S(Cochin University of Science And Technology, March , 1997)
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Abstract:
The adult mammalian liver is predominantly in a quiescent state with respect to cell
division. This quiescent state changes dramatically, however, if the liver is injured by
toxic, infectious or mechanic agents (Ponder, 1996). Partial hepatectomy (PH) which
consists of surgical removal of two-thirds of the liver, has been used to stimulate
hepatocyte proliferation (Higgins & Anderson 1931). This experimental model of liver
regeneration has been the target of many studies to probe the mechanisms responsible for
liver cell growth control (Michalopoulos, 1990; Taub, 1996). After PH most of the
remaining cells in the renmant liver respond with co-ordinated waves of DNA synthesis
and divide in a process called compensatory hyperplasia. Hence, liver regeneration is a
model of relatively synchronous cell cycle progression in vivo. In contrast to hepatomas,
cell division is terminated under some intrinsic control when the original cellular mass has
been regained. This has made liver regeneration a useful model to dissect the biochemical
and molecular mechanisms of cell division regulation. The liver is thus, one of the few
adult organs that demonstrates a physiological growth rewonse (Fausto & Mead, 1989;
Fausto & Webber, 1994). The regulation of liver cell proliferation involves circulating or
intrahepatic factors that are involved in either the priming of hepatocytes to enter the cell
cycle (Go to G1) or progression through the cell cycle. In order to understand the basis of
liver regeneration it is mandatory to define the mechanisms which (a) trigger division, (b)
allow the liver to concurrently grow and maintain dilferentiated fimction and (c) terminate
cell proliferation once the liver has reached the appropriate mass. Studies on these aspects
of liver regeneration will provide basic insight of cell growth and dilferentiation, liver
diseases like viral hepatitis, toxic damage and liver transplant where regeneration of the
liver is essential. In the present study, Go/G1/S transition of hepatocytes re-entering the
cell cycle after PH was studied with special emphasis on the involvement of
neurotransmitters, their receptors and second messenger function in the control of cell
division during liver regeneration
Description:
Department of Biotechnology, Cochin University of Science and Technology
Ani Das, V; Paulose,C S(Department of Biotechnology, Faculty of Science, August , 2000)
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Abstract:
In the present study, the changes in the brain EPI (Epinephrine), adrenergic receptors and the receptor gene expression were investigated during pancreatic regeneration and insulin secretion. The changes in the pancreatic islet EPI and adrenergic receptors were also studied in the pancreatectomised rats. The regulatory function of EPI in association with Epidermal growth factor (EGF) and glucose were investigated in rat islet cultures. In vitro studies were carried out using antagonists for adrenergic receptor subtypes to see their involvement in the islet DNA synthesis. The mechanism by which the peripheral EPI regulate insulin secretion was also investigated by studying the nuclear binding proteins in the pancreatic islets during pancreatic regeneration and diabetes. The study reveals that EPI can regulate the pancreatic islet cell proliferation by controlling the insulin synthesis and secretion. The brain adrenergic receptor gene expression and functional correlation regulate the pancreatic adrenergic receptors. The functional balance of α and β-adrenergic receptors controls the insulin secretion and pancreatic β-cell proliferation, which will have immense clinical significance in the treatment of Diabetes mellitus.
Asha,Abraham; Dr. Paulose, C S(Cochin University of Science And Technology, March 30, 1998)
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Abstract:
I) To study the changes in the content of brain rrrorroamirres in streptozotocirr-irrduced
tliabetes as a lirnction of age and to lirrd the role oliadrenal lrornroncs in diabetic state.
2) To assess the adrenergic receptor function in the brain stem ofstreptozotocin-induced
diabetic rats ofdillerent ages.
3) To study the changes in the basal levels of second messenger cAMP in the brain stenr
ofstreptozotocin-induced diabetic rats as a function of age.
4) To study the changes occurring in the content ofmorroamines and their metabolites in
whole pancreas and isolated pancreatic islets of streptozotocin-diabetic rats as a function
ofage and the effect of adrenal hormones.
5) To study the adrenergic receptors and basal levels of cAMP in isolated pancreatic islets
in young and old streptozotoein-diabetic rats.
6) The in virro study of CAMP content in pancreatic islets of young and old rats and its
ellect on glucose induced insulin secretion.
7) 'lhe in vitro study on the involvement of dopamine and corticosteroids in glucose
induced insulin secretion in pancreatic islets as a function of age.
Description:
Department of
Biotechnology, Cochin University of Science and Technology