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1.
The effect of neurotensin on submaximally-stimulated hepatobiliary and pancreatic secretion was studied in 6 healthy subjects. An intravenous infusion of neurotensin 1.4 ± 0.3 pmol/kg/min, designed to reproduce plasma neurotensin immunoreactivity levels within the physiological range, produced a significant increase in pancreatic bicarbonate output. Plasma concentrations of pancreatic polypeptide rose by 83 ± 16 pmol/l and were associated with a small reduction in trypsin, but no significant change in bilirubin outputs. 相似文献
2.
Melatonin reduces glial reactivity in the hippocampus, cortex, and cerebellum of streptozotocin-induced diabetic rats 总被引:5,自引:0,他引:5
Baydas G Reiter RJ Yasar A Tuzcu M Akdemir I Nedzvetskii VS 《Free radical biology & medicine》2003,35(7):797-804
Hyperglycemia plays a critical role in the development and progression of diabetic neuropathy. One of the mechanisms by which hyperglycemia causes neural degeneration is via the increased oxidative stress that accompanies diabetes. Metabolic and oxidative insults often cause rapid changes in glial cells. Key indicators of this response are increased synthesis of glial fibrillary acidic protein (GFAP) and S100B, both astrocytic markers. In the present study, we examined glial reactivity in hippocampus, cortex, and cerebellum of streptozotocin (STZ)-induced diabetic rats by determining the expression of GFAP and S-100B and we evaluated the effect of melatonin on the glial response. Western blot measurement of contents in brain regions after 6 weeks of STZ-induced diabetes indicated significant increases in these constituents compared with those in nondiabetic controls. Administration of melatonin prevented the upregulation of GFAP in all brain regions of diabetic rats. Using GFAP immunohistochemistry, we observed an increase in GFAP immunostaining in the hippocampus of STZ-diabetic rats relative to levels in the control brains. Treatment with melatonin resulted in an obvious reduction of GFAP-immunoreactive astrocytes in hippocampus. Like GFAP, S100B levels also were increased in all three brain areas of diabetic rats, an effect also reduced by melatonin treatment. Finally, the levels of lipid peroxidation products were elevated as a consequence of diabetes, with this change also being prevented by melatonin. These results suggest that diabetes causes increased glial reactivity possibly due to elevated oxidative stress, and administration of melatonin represents an achievable adjunct therapy for preventing gliosis. 相似文献
3.
We examined, using a Western blot technique, the contents and compositions of a specific neuronal protein, NCAM, and of an
astrocyte marker, GFAP, in the hippocampus and cortex of rats with streptozotocin (STZ)-induced diabetes and compared these
indices with those in control (intact) animals and STZ-diabetic rats treated with melatonin. Behavioral cognitive indices
manifested in the passive avoidance test (PAT) and Morris water maze (MWM) learning performance were also estimated in the
above groups of animals. As was found, STZ-diabetic rats demonstrated clear cognitive deficits according to the values of
the retention latency in the PAT and time of reaching the escape platform in the MWM performance. In these animals, the GFAP
content was elevated, and the amount of degraded products of this protein increased, as compared with the control. Simultaneously,
considerable down-regulation of the NCAM expression and modifications of NCAM isoform composition were found in diabetic animals.
In addition, significantly increased levels of lipid peroxidation (according to the amounts of malondialdehyde + 4-hydroxyalkenals)
were measured in the cortex and hippocampus of rats with stable diabetic hyperglycemia. All the above-mentioned shifts were
significantly smoothed or even nearly completely compensated in the case of treatment of STZ-diabetic rats with melatonin
(10 mg/kg per day). The role of diabetes-related changes in the amount and composition of specific neural and glial proteins
in the development of cognitive deficits, the involvement of oxidative stress in the mechanisms of the respective shifts,
and possible mechanisms of the neuroprotective effect of melatonin with respect to diabetes-related pathological biochemical
and behavioral shifts are discussed.
Neirofiziologiya/Neurophysiology, Vol. 40, No. 2, pp. 105–111, March–April, 2008. 相似文献
4.
We studied the effects of irradiation with X-rays (the total dose of 0.0129 C/kg was attained over 7, 14, or 21 days), increased entry of Al3+ into the organism (0.2% AlCl3 in drinking water), and the combined influence of these factors for 21 days on the contents of the soluble and filamentous forms of glial fibrillary acidic protein (GFAP) in the tissues of the hippocampus, cerebellum, and neocortex of albino rats. After irradiation for 7 days, a clear trend toward drops in the GFAP contents in the structures under study was observed, while irradiation in the same dose, but for 14 or 21 days, resulted in increases in the contents of both GFAP forms (within a range of 13-29%, as compared with the control). Entry of aluminum chloride with water also resulted in an increase in the GFAP contents in all studied structures; changes in the filamentous form were more intensive. The combined influence of irradiation and Al3+ resulted in more intensive shifts in the GFAP levels; the content of its filamentous form increased in all structures by about 50%, while shifts of the soluble form were somewhat smaller. 相似文献
5.
A Puri R Sethi B Singh SK Dwivedi VS Narain RK Saran VK Puri 《Indian pacing and electrophysiology journal》2009,9(3):186-189
A 25-year-old previously asymptomatic pregnant woman at 36 weeks'' gestation was noticed to have repetitive monomorphic ventricular tachycardia. A dilated left ventricle with moderately reduced systolic function was found on echocardiographic examination. This is a very rare presentation of peripartum cardiomyopathy (PPCMP) presenting with repetitive monomorphic ventricular tachycardia. 相似文献
6.
Neurological and structural changes are paralleled by cognitive deficits in diabetes mellitus. The present study was designed to evaluate the expression of neural cell adhesion molecules (NCAM) in the hippocampus, cortex and cerebellum and to examine cognitive functions in diabetic rats. Diabetes was induced in male albino rats via intraperitoneal streptozotocin injection. Learning and memory behaviors were investigated using a passive avoidance test and a spatial version of the Morris water maze test. NCAM expression was detected in the hippocampus, cortex and cerebellum by an immunoblotting method. The diabetic rats developed significant impairment in learning and memory behaviours as indicated by deficits in passive avoidance and water maze tests as compared to control rats. Expression of NCAM 180 and 120 kDa were found to be higher in hippocampus and cortex of diabetic rat brains compared to those of control, whereas expression of NCAM 140 kDa decreased in these brain regions. Our findings suggest that streptozotocin-induced diabetes impairs cognitive functions and causes an imbalance in expression of NCAM in those brain regions involved in learning and memory. Altered expression of NCAM in hippocampus may be an important cause of learning and memory deficits that occur in diabetes mellitus. 相似文献
7.
A recently silenced, duplicate PgiC locus in Clarkia 总被引:1,自引:0,他引:1
Previous electrophoretic analysis showed that 17 diploid species of the
wildflower Clarkia (Onagraceae) have two cytosolic isozymes of
phosphoglucose isomerase (PGIC; EC 5.3.1.9), whereas 15 other diploid
species have a single PGIC. Molecular studies revealed that the two
isozymes in the former species are encoded by duplicate genes, PgiC1 and
PgiC2, whereas the single isozyme in the latter is always encoded by PgiC1.
Phylogenetic analysis of the nucleotide sequences implied that PgiC2 was
silenced four times independently in the genus. Here we describe a psi
PgiC2 from C. mildrediae, a species in which only PgiC1 is expressed. The
discovery of the psi PgiC2 is significant because it confirms a formal
prediction of the phylogenetic analysis. The psi PgiC2 includes 5,039
nucleotides corresponding to 18 of the 23 exons of PgiC, as well as the
intervening introns and 3' nontranslated region. The absence of an increase
of nucleotide substitutions in its "exons" suggests that the gene was
silenced recently. The present study appears to be the first to establish
that a specific duplicate gene locus regularly expressed in a group of
related plant species has been silenced in one of them. The multiple
independent silencings of PgiC2 suggest that it remained functional but
inessential in ancestral lineages. We discuss the possibility that PgiC2
may have been preserved in these lineages by selection against mutants
causing defective PGIC1- PGIC2 heterodimers.
相似文献
8.
9.
Aulus EAD Barbosa Érika VS Albuquerque Maria CM Silva Djair SL Souza Osmundo B Oliveira-Neto Arnubio Valencia Thales L Rocha Maria F Grossi-de-Sa 《BMC biotechnology》2010,10(1):44
Background
Coffee is an important crop and is crucial to the economy of many developing countries, generating around US70 billion per year. There are 115 species in the < i > Coffea < /i > genus, but only two, < i > C. arabica < /i > and < i > C. canephora < /i > , are commercially cultivated. Coffee plants are attacked by many pathogens and insect-pests, which affect not only the production of coffee but also its grain quality, reducing the commercial value of the product. The main insect-pest, the coffee berry borer ( < i > Hypotheneumus hampei < /i > ), is responsible for worldwide annual losses of around US70 billion per year. There are 115 species in the Coffea genus, but only two, C. arabica and C. canephora, are commercially cultivated. Coffee plants are attacked by many pathogens and insect-pests, which affect not only the production of coffee but also its grain quality, reducing the commercial value of the product. The main insect-pest, the coffee berry borer (Hypotheneumus hampei), is responsible for worldwide annual losses of around US500 million. The coffee berry borer exclusively damages the coffee berries, and it is mainly controlled by organochlorine insecticides that are both toxic and carcinogenic. Unfortunately, natural resistance in the genus Coffea to H. hampei has not been documented. To overcome these problems, biotechnological strategies can be used to introduce an α-amylase inhibitor gene (α-AI1), which confers resistance against the coffee berry borer insect-pest, into C. arabica plants. 相似文献10.