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Biomedical subjects

A Minenko

Publications and source records attributed to A Minenko.

17 recordsLinked to original sources
PubMed1993

Host risk factors for the development of reactive arthritis: a family study.

OBJECTIVE: To determine if the same arthritogenic microorganisms can trigger reactive arthritis (ReA) in both HLA-B27 positive and HLA-B27 negative individuals. To determine risk factors (other than HLA-B27) for the development of ReA. METHODS: Following a common food source outbreak of Salmonella enteritidis, 2 family groups of individuals with dysentery and new onset ReA signs and symptoms were identified. HLA typing was performed for all family members exposed to the dysenteric organism. RESULTS: ReA occurred in HLA-B27 positive members of Family A. No member of Family B possessed HLA-B27 or CREG phenotype, but 3 members developed ReA. The HLA identical sibling of the proband in Family B developed dysentery but did not develop ReA. CONCLUSION: In this epidemic, interaction of the microorganism with an HLA-B27 positive host predictably produced ReA but B27 was not necessary to produce it in other dysenteric patients. Host factors including amount of ingested microorganisms, age and sex but excluding HLA type may account for the differential development of ReA in the siblings in Family B.

Arthritis, Infectious↗
PubMed1988

Decreased SP-stimulated diesteratic hydrolysis of inositol phospholipids in adrenal medulla slices from spontaneously hypertensive rats.

The effects of substance P on inositol phospholipids of adrenal medulla slices from spontaneously hypertensive and normotensive Wistar-Kyoto rats were investigated. Substance P reduces [32P] incorporation into inositol phospholipids of both rat strains. This effect was most expressed in hypertensive rats, which showed a higher basal 32P incorporation into phosphatidylinositol phosphates compared to normotensive control rats (probably due to the higher turnover of monoester-phosphate groups). Substance P causes a less potent diesteratic hydrolysis of [3H]inositol prelabelled phospholipids in spontaneously hypertensive rats compared with Wistar-Kyoto rats. A possible consequence of the reduced diesteratic hydrolysis by endogenous substance P and related substances of inositol phospholipids in adrenal medulla from spontaneously hypertensive rats is discussed.

Adrenal Medulla↗
PubMed1988

Effects of substance P (SP) and the N-terminal SP-analogue SP (1-4) on inositol phospholipids in rat adrenal medulla slices.

We previously demonstrated that SP (1.10(-6) M) stimulates the hydrolysis of inositol phospholipids from adrenal medulla slices of Wistar rats (Biomed. Biochim. Acta 46, 461-467 (1987]. In this study we compared the effects of SP and the N-terminal SP-analogue SP(1-4) on inositol phospholipids and their water-soluble metabolites. The effect of SP (1-4) on 32P incorporation into inositol PL is substantially smaller than that of SP. However, the results obtained with [3H]inositol-prelabelled slices show that both peptides cause a diesteratic hydrolysis of inositol phospholipids. For both peptides a significant decrease in [3H]phosphatidylinositol-4,5-bisphosphate as well as an accumulation of [3H]inositol-bisphosphates were observed. There is a significant difference between the effects of SP and SP (1-4): SP stimulates the accumulation of glycerophosphorylinositols, whereas SP (1-4) inhibits its production. These effects of both peptides are discussed in the light of their effects on the catecholamine system.

Adrenal Medulla↗
PubMed1987

Substance P action on inositol phospholipids in rat adrenal medulla slices.

The effect of SP (1.10(-6) M) on the 32P incorporation into inositol phospholipids from rat adrenal medulla slices has been examined. After 20 s, a decreased 32P incorporation into all inositol phospholipids was found (most expressed for phosphatidyl-inositol-4,5-bisphosphate) without changes in phosphatidylcholine/phospatidylserine fraction. During 5 min exposure to SP the 32P incorporation into phosphatidylinositol-4,5-bisphosphate returned up to the control level, whereas that into phosphatidylcholine/phosphatidylserine fraction strongly decreased. A within-one-sample comparison of the radioactivity of each phospholipid against that in the phosphatidylcholine/phosphatidylserine fraction reveals a "phosphatidylinositol effect". A possible regulation mechanism of catecholamine secretion by SP in relation to changes in inositol phospholipids is discussed.

Adrenal Medulla↗
PubMed1987

Nicotinic stimulation of polyphosphoinositide turnover in rat adrenal medulla slices.

When rat adrenal medulla slices, treated with atropine (1 X 10(-6) mol X l-1], were stimulated with acetylcholine (1 X 10(-5) mol X l-1), an enhanced 32P incorporation into phosphatidylinositol-bis-phosphate (PIP2) and phosphatidylphosphate (PIP) was observed. On the ather hand, stimulation of myo-[3H] inositol prelabelled slices led to a decline in radioactivity of PIP2, indicating an increased turnover of this phospholipid. A possible affection of monoesterphosphate groups of PIP2 or of both PIP2 and PIP during cholinergic nicotinic stimulation is assumed.

Acetylcholine↗
PubMed1983

[Effect of nicotine on polyphosphoinositides of erythrocytes from spontaneously hypertensive rats].

We have investigated the in vitro action of nicotine (1 . 10(-6)M) on the content of and 32P incorporation into di- and triphosphoinositides of erythrocyte membranes from spontaneously hypertensive rats (SHR) and WKY control rats (both 10 weeks of age). The triphosphoinositide content was found increased after incubation with nicotine for 0.5 min and decreased after incubation for 20 min in both strains. The diphosphoinositide content was decreased after 5 min and much more after 20 min. The specific activity for the phosphate groups of phosphoinositides increased during incubation with nicotine for 0.5 min in rats of both strains. Recovery of preincubation activity values ("normalization") was faster in SHR than in WKY rats. Explanations are given concerning the rate of 32P incorporation into polyphosphoinositides and recovery of cholinergic excitability of erythrocyte membranes.

Animals↗
PubMed1983

[Effect of naloxone on polyphosphoinositide in erythrocytes of spontaneously hypertensive rats].

We investigated the in vitro action of naloxone (1 X 10(-6) M) on the content and 32P incorporation into di-and triphosphoinositides of erythrocytes from spontaneously hypertensive rats (SHR) and WKY controls (both 10 weeks of age). We found that the content of diphosphoinositides was decreased and the specific activity of their phosphate groups was increased after incubation with naloxone for 1 min in both rat strains. The effect was faster in SHR than in WKY rats.

Animals↗
PubMed1982

[Effect of morphine on polyphosphoinositides of erythrocytes of spontaneously hypertensive rats].

Morphine (1 X 10(-5) mol/l) did not affect the incorporation of 32P into the phosphoinositides of erythrocytes from spontaneously hypertensive and normotensive Wistar Kyoto rats, whereas the content of triphosphoinositides was decreased. In spontaneously hypertensive rats the content of total phospholipids was decreased in the same ratio. Thus, the effect of morphine (at this concentration) on the membrane phospholipids of spontaneously hypertensive rats seems to be unspecific.

Animals↗
PubMed1975

[On the composition of fatty acids in Chlorella pyrenoidosa under the influence of dimethyl- and diethylaminoazobenzene (author's transl)].

The composition of bulk fatty acids in Chlorella pyrenoidosa under the influence of the carcinogenic dimethylaminoazobenzene and the non carcinogenic diethylaminoazobenzene was examined. In the presence of dimethylaminoazobenzene cultivated algae showed parallel to morphological changes distinct deviations in the composition of their fatty acids compared with the control. This especially concerns the unsaturated C18-fatty acids as the C16:0-, C16:2- and C16:3-acids respectively. By treatment of algae with diethylaminoazobenzene no morphological variations were observed and only little changes in composition of their fatty acids was demonstrated.

Azo Compounds↗