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Biomedical subjects

P Tuohimaa

Publications and source records attributed to P Tuohimaa.

At least 127 records · Page 7Linked to original sources
PubMed1984

Absence of nuclear progesterone receptor in LH releasing hormone in laying hens.

Using a double immunohistochemical technique, LH releasing hormone (LHRH) neurones and 110kDa nuclear progesterone receptor were localized in the hypothalamus of the laying hen. Nuclear progesterone receptor was widely distributed throughout the hypothalamus, occurring in the preoptic, septal, anterior and basal areas. The region where progesterone receptor was revealed in nuclei of neurones overlapped that containing LHRH neurones. However, LHRH cell bodies did not contain progesterone nuclear receptor. It is concluded that the positive feedback action of progesterone on LH release is not mediated by a genomic mechanism within the LHRH neurone.

Animals↗
PubMed1983

Protein kinase activity of purified components of the chicken oviduct progesterone receptor.

Preparations of the 90K and 110K components of the chick oviduct progesterone receptor (PR) purified to near homogeneity were tested for protein kinase activity. The 90K component was shown to incorporate radioactive phosphate from [gamma-32P]-ATP in the presence of Ca2+ but not of Mg2+ ions, while the 110K component was phosphorylated in the presence of Mg2+, but not of Ca2+. The enzymatic activity of the 90K polypeptide appeared selective, since added proteins (histones) did not become phosphorylated. However, all proteins present in the 110K preparations were phosphorylated in the presence of Mg2+. These data suggest that components of the chick oviduct PR display protein kinase activity.

Animals↗
PubMed1983

Avidin is induced in chicken embryo fibroblasts by viral transformation and cell damage.

Synthesis and secretion of avidin was studied in cultured chicken embryo fibroblasts infected with transforming retroviruses (Rous sarcoma virus, its mutants temperature-sensitive for transformation, OK-10 virus) or a nontransforming retrovirus (RAV-1). Avidin was detectable in both transformed and untransformed cultures, and was identical to chicken egg white avidin by several criteria: biotin-binding, heat-induced biotin exchange, subunit size (mol. wt. 15 600), immunoprecipitation of metabolically labeled proteins and immunoblotting. Transformation increased the production of avidin up to 50-fold, but several experiments suggested that the induction was not a direct consequence of virus-induced cell transformation. The production of avidin seemed to relate to cellular damage both in cultures of virus-transformed and of normal fibroblasts. It may represent a response to cellular damage and viral transformation may activate the process.

Alpharetrovirus↗
PubMed1983

Studies of vestibular cortical areas with short-living 15O2 isotopes.

The oxygen-15 inhalation technique has been applied to the quantification of regional cerebral blood flow and metabolism with positron emission tomography. These findings support the notion that vestibular cortex is not only one small area in the temporal or parietal cortex but a wider area in the temporoparietal cortex. During caloric reactions cortical potential changes were found on the contralateral temporoparietal cortex. The recent development of positron emission tomography (PET) is theoretically capable of changing considerably the research of the pathophysiology in central vestibular disturbances. Validity of the 15O2 inhalation model and the feasibility of the PET technique does have - like any physiological measurement - some limitations, but it obviously has a tremendous clinical potential.

Adult↗
PubMed1982

Induction of avidin in chickens infected with the acute leukemia virus OK 10.

The presence of avidin, a progesterone-dependent oviductal glycoprotein, was studied in viral tumors. Newborn chickens were infected with the acute leukemia virus OK 10, and the first tumors occurred within 2-3 weeks. Avidin was assayed using a [14C]biotin-binding method and radioimmunoassay. In the control chickens, avidin concentrations were less than 0.3 microgram/g in the plasma and less than 1.5 microgram/g in various tissues including the immature oviduct. In the OK 10 virus-infected chickens, no significant induction was observed during the acute infection or any time thereafter if no tumors were seen. In chickens that developed tumors, avidin concentrations were significantly increased in tumorous tissue only located in the mesenterium and occasionally in the oviduct. In tumors occurring elsewhere (kidney, ovary, muscle, testis, liver, colon) avidin concentrations were not elevated. Tumor-associated avidin had extraordinary biotin-binding capacity after treatment at +90 degrees C similar to the progesterone-dependent avidin, whereas antibody-binding properties suggested that tumor-associated avidin may have a somewhat altered antigenic structure.

Animals↗
PubMed1982

Characterization of progesterone-independent avidin production of chicken tissues in culture.

1. Primary cell cultures of chick oviduct, intestine, peritoneal membrane and lung, but not those of wing muscle or calcaneal tendon, produced avidin progesterone-independently through a 5-week culture. 2. Actinomycin D and cycloheximide, but not hydroxyurea, inhibited the avidin production. 3. The common feature of the cultures producing avidin was a fibroblast-like cell type. 4. Similarly, oviduct and lung, but not muscle or tendon, also produced avidin in hormone-free short-term organ cultures, where the avidin synthesis began during the first 8 h of culture. 5. Induction of the general protein synthesis does not explain the avidin production, since another egg-white protein, ovalbumin, was not induced by the culture procedure.

Animals↗
PubMed1982

Effects of glucocorticoids and disodium cromoglycate on avidin production in chick tissues.

The effects of anti-inflammatory glucocorticoids and a membrane stabilizer (disodium cromoglycate) on avidin induction were studied. Chicks were primed for 0, 3 or 7 days with diethylstilboestrol (DES; 0.5 mg/day per animal, s.c.). Actinomycin D (0.2 mg/kg, i.p.) stimulated avidin production in the oviduct, intestine, lung and wing muscle of both DES-primed and unprimed chicks. Prednisolone (5 mg/animal, i.m.) given 1 h before actinomycin D reduced the avidin amounts to control levels in the unprimed oviducts and in non-oviductal tissues. The signs of inflammation (ascites, oedema) in chicks receiving actinomycin D also disappeared with prednisolone premedication. Cortisol (50 mg/animal, i.m. or 1, 5 or 50 microgram/ml medium), prednisolone (5 mg/animal, i.m. or 0.5, 5, 10 or 50 microgram/ml medium) and dexamethasone (1 mg/animal, i.m. or 0.05 or 0.5 microgram/ml medium) stimulated avidin production in DES-primed oviducts in vivo and in vitro. Culture in vitro induced avidin production in lung and oviduct but not in wing muscle. This avidin production in culture was not inhibited by cortisol, prednisolone or disodium cromoglycate. It is concluded that actinomycin D induces avidin production through its inflammatory effect and that the induction can be prevented by anti-inflammatory glucocorticoids. It is proposed that the 'spontaneous' avidin production in culture is not the effect of trauma during tissue preparation but rather a new form of avidin induction.

Animals↗
PubMed1981

Progesterone-independent avidin in chick oviduct fibroblast culture.

The production of avidin was studied in chick oviduct cell cultures derived from immature chicks or from chicks with 4, 8, or 14 days of estrogen priming in vivo. Cells were grown for 5--7 weeks, and the monolayers formed were composed of collagen-producing fibroblasts. In some cultures, epithelial cells were also found, but only in the original explants. Two-day avidin production of cultures was measured in the media weekly. Cultures produced avidin spontaneously, the amount being fairly stable during the 7-week culture period. No difference was found in avidin production or cell morphology when estrogen-containing medium was used. Cultures from 4- to 8-day-estrogen-primed chick oviducts produced the same amount of avidin as cultures from immature oviducts, whereas further estrogen pretreatment seemed to reduce avidin production. Progesterone did not enhance avidin production with or without estrogen priming but, due to its inhibition of growth, clearly inhibited avidin when it was continuously in the culture medium. It is concluded that chick oviductal fibroblasts have an inherent capacity for avidin production and that this is independent of progesterone.

Animals↗
PubMed1981

Quantitative assessment of steroid hormone binding sites by thaw-mount autoradiography.

A procedure for the quantitative assessment of nuclear receptors for steroid hormones--and other substances--in individual cells is presented. Thaw-mount autoradiography, a procedure developed earlier in our laboratory, is utilized. The silver grain yield (specific activity) is 16.6 disintegrations per silver as determined fo tritium in guinea pig uterine tissues. An integrated formula is presented and applied for 3H-estradiol, 3H-diethylstilbestrol, and 3H-aldosterone in sampled tissue. A comparison with data derived from the literature that are based on the homogenization of whole uteri and biochemical analysis shows comparable values wtih the autoradiographic data if the latter are pooled. The pooled ata indicated 12-14,00 molecules of 3H-estradiol per uterine nucleus, while subpopulations of target cells vary between 5,000 and 28,000 per nucleus.

Animals↗
PubMed1980

Progesterone-binding properties of the microsomal fraction from chick oviduct.

Progesterone binds to specific high-affinity and limited-capacity binding sites of chick-oviduct microsomes of estrogen-primed chicks. The dissociation constant is 2 x 10(-9) M (range 1.6--3.0) and the number of binding sites 500 femtomoles/mg microsomal protein (range 464--551). Treatment of the estrogen-primed chicks by progesterone had no apparent effect on the progesterone-binding capacity or affinity. Competition studies showed that testosterone, R-5020, Org-2058, D-norgestrel, 5 alpha-dihydrotestosterone and R-2323 were effective competitors of progesterone, in that order, whereas cortisol, estradiol and estrone exhibited only minimal displacement. No displacement of microsome-bound [3H]progesterone was found with fenoterol or prostaglandin F2 alpha. No high-affinity progesterone-binding sites were found in the microsomal fractions of liver, muscle, intestine or brain. On the basis of steroid-binding affinity and steroid-specificity determinations, the microsomal progesterone-binding components seem to be different from the progesterone receptor previously described in chick oviduct cytosol.

Animals↗
PubMed1980

Progesterone-dependent and -independent avidin production in chick oviduct organ culture.

Progesterone-dependent and -independent avidin inductions were found in chick oviduct culture. The effects of oestrogen priming and actinomycin D on these inductions were studied. Priming comprised daily diethylstilboestrol (DES) injections in vivo and one day's incubation in vitro with DES before experimental treatment. After 0 or 1 day of DES pretreatment no measurable amount of avidin was found. Avidin was present in progesterone-untreated incubated tissues after 4 days' DES pretreatment. Incubation with progesterone for 24 h increased avidin levels only after 4 or more days of oestrogen priming. No induction of avidin by actinomycin D similar to that found in vivo was observed in vitro. Actinomycin D inhibited both progesterone-dependent and -independent avidin production, but this effect diminished as oestrogen pretreatment was prolonged. Actinomycin D also significantly reduced total oviductal RNA synthesis. It is concluded that oestrogen priming enhances both progesterone-dependent and -independent avidin production in vitro and that both inductions are partially dependent on new RNA synthesis.

Animals↗
PubMed1979

Myringotomy in the treatment of acute otitis media in children.

The treatment of acute otitis media was studied in 158 children. All children (mean age 4 years) received penicillin orally 80 000--100 000 IU per day for 10 days. Myringotomy was performed on 68 children at the time of the diagnosis. The other 90 children were treated with penicillin and ear drops. The bacteriological findings from the nasopharynx at the time of diagnosis were equivalent in both groups. After 2 weeks, 42% of the children without myringotomy and 71% of the children with myringotomy were cured. The children who were not cured were treated with amoxicillin for 10 days. Four weeks after diagnosis 71% and 90% of the children respectively were cured. The differences between the two groups are significant. The observations indicate that myringotomy clearly accelerates the recovery from acute otitis media.

Acute Disease↗
PubMed1978

Induction of avidin in the chick oviduct by tissue damage and prostaglandins.

In immature, diethylstilboestrol-treated chicks, ligation of the oviduct caused local avidin synthesis in the immediate vicinity of the ligature. PGF-2alpha injected directly into the oviduct also induced avidin synthesis, whereas saline or PGE-2 had no effect. PGE and PGF-2alpha concentrations increased in the oviduct within 24 h of ligation: the PGE increase could be partly inhibited by indomethacin, whereas that of PGF-2alpha was less inhibited. An LD50 dose of indomethacin alone and with ligation had a clear stimulatory effect on avidin synthesis, whereas aspirin alone, or with ligation, was not effective. Ligation alone and with indomethacin appeared to alter the PGF-2alpha/PGE ratio. These results suggest that PGF-2alpha may be involved in the regulation of avidin synthesis in the chick oviduct.

Animals↗