Search Results - (Author, Cooperation:E. Peles)

2014-05-30

Nature Publishing Group (NPG)

0028-0836

1476-4687

Biology

Chemistry and Pharmacology

Medicine

Natural Sciences in General

Physics

Animals ; Antipsychotic Agents/pharmacology ; Behavior, Animal/drug effects/physiology ; Dopamine/*metabolism ; Electrical Synapses/genetics/ultrastructure ; Female ; Genotype ; Humans ; Male ; Membrane Proteins/*genetics/*metabolism ; Mice ; Nerve Tissue Proteins/*genetics/*metabolism ; Polymorphism, Single Nucleotide ; *Signal Transduction ; Synaptic Transmission/*genetics ; gamma-Aminobutyric Acid/*metabolism

1476-4687

Nature Archives 1869 - 2009

Biology

Chemistry and Pharmacology

Medicine

Natural Sciences in General

Physics

[Auszug] The protein tyrosine kinase PYK2, which is highly expressed in the central nervous system, is rapidly phosphorylated on tyrosine residues in response to various stimuli that elevate the intracellular calcium concentration, as well as by protein kinase C activation. Activation of PYK2 ...

Electronic Resource

0960-0760

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Biology

Chemistry and Pharmacology

Electronic Resource

1432-8798

Springer Online Journal Archives 1860-2000

Medicine

Summary The ability of several strains and recombinants of herpes simplex virus 1 (HSV-1) to proliferate in the adrenal glands and to invade the spinal cord was studied. After intraperitoneal infection, pathogenic HSV-1 strains replicated in the adrenal glands, penetrated the spinal cord and migrated to the brain. The nonpathogenic strain HFEM could not replicate in the adrenal glands, but the recombinant virus MLC1 was able to do so after rescue by reinsertion of theHpaI-P sequence into theBamHI fragment of HFEM DNA. However the recombinant MLC1 virus could not penetrate the spinal cord. The effect of HSV-1 infection on the expression of the cellular genes for multidrug resistance (in the adrenal glands) and proenkephalin A (in the spinal cord) was also studied.

Electronic Resource

1619-1560

stress ; sympathetic nervous system ; catecholamines ; parasympathetic nervous system ; heart rate ; spectral analysis

Springer Online Journal Archives 1860-2000

Medicine

Abstract Overstimulation of sympathetic nervous system activity is related to atherosclerotic cardiovascular disease risk, but the role of parasympathetic activity in this association is not clear. This study evaluated sympathetic and parasympathetic function by spectral analysis of heart rate variability and plasma levels of norepinephrine (NE) epinephrine (EPI), dihydroxyphenylglycol (DHPG), dihydroxyphenylalanine (DOPA) and dihydroxyphenylacetic acid (DOPAC). It also examined the interrelationships among these parameters and established atherosclerotic cardiovascular disease risk factors in 53 men (mean age 59.5 years). During supine rest, low-frequency power correlated positively with high-frequency power (r = 0.58, p 〈 0.001), plasma NE correlated with plasma DHPG (r = 0.41, p 〈 0.001) and plasma DOPA with DOPAC (r = 0.47, p 〈 0.001) but neither low- nor high-frequency power was correlated with plasma levels of any catechol. Among risk factors, plasma NE correlated with fasting insulin and mean arterial blood pressure, and urine NE correlated with body mass index. Both low- and high-frequency power correlated positively with insulin levels. Orthostasis decreased high-frequency power and increased low-frequency power and plasma NE levels. During the oral glucose tolerance test, both high- and low-frequency power increased, plasma NE levels were unchanged, and plasma EPI levels decreased [88.5 ± 18 (SEM) versus 52.5 ± 12 pM,p = 0.001]. The results suggest that orthostasis decreases and the oral glucose tolerance test increases parasympathetic outflows, whereas both stimuli increase sympathetic outflows. Among all atherosclerotic cardiovascular disease risk factors, hyperinsulinaemia showed the strongest association with autonomic nervous system activity, especially parasympathetic activity. Estimates of sympathetic responses obtained from power spectral analysis of heart rate variability agree poorly with those from plasma levels of catechols, possibly because of a parasympathetic contribution to low-frequency power and independence of sympathoneural outflows to the arm and heart.

Electronic Resource

1619-1560

insulin resistance ; sympathetic nervous system ; catecholamines ; parasympathetic nervous system ; amputees ; spectral analysis

Springer Online Journal Archives 1860-2000

Medicine

Abstract This study examined plasma insulin response to oral glucose load and autonomic nervous system activity in male lower limb amputees (n = 52) aged 50–65 years, compared to matched controls (n = 53). The groups had similar body mass index, blood pressure and plasma lipid levels. The amputees had higher mean fasting plasma insulin levels (18.4 ± 9.7 (SD) versus 13.7 ± 5.1 m U/l,p = 0.005) and during an oral glucose tolerance test (OGTT) (1 h levels 88.1 ± 45.3 versus 62.1 ± 42.7,p = 0.016) with similar plasma glucose levels, indicating insulin resistance. At baseline with the subjects supine, there were no group differences in low- or high-frequency power of heart rate variability or in plasma levels of norepinephrine (NE) or epinephrine (EPI). In response to orthostasis, the groups had similarly increased plasma NE levels. During the OGTT, amputees had significantly larger increments in low-frequency power than did controls (2.2 ± 1.3 versus 1.6 ± 0.9 (beats/min)2 respectively,p 〈 0.01) and plasma NE levels increased significantly in amputees (1595 ± 849 versus 1941 ± 986 pM,p = 0.0008) but not in controls. At 1 h after glucose administration, plasma EPI levels were decreased significantly from baseline in both groups; at both 1 and 2 h after glucose administration, plasma EPI levels were higher in the amputees than controls. Amputees appear to have a combination of enhanced sympathoneural responsiveness and attenuated suppression of adrenomedullary secretion during glucose challenge. As catecholamines antagonize insulin effects, one possible explanation for insulin resistance in amputees is hyperglycaemia-induced sympathoneural activation and a failure of hyperglycaemia to decrease adrenomedullary secretion.

Electronic Resource