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Biomedical subjects

W Rohde

Publications and source records attributed to W Rohde.

At least 127 records · Page 7Linked to original sources
PubMed1986

[New aspects of the pathogenesis of acromegaly-somatoliberinomas].

According to modern knowledge, acromegaly can develop in at least three ways. A pituitary adenoma with growth hormone overproduction is the most frequent. Much rarer is ectopic growth hormone secretion by extra-hypophyseal tumors. A further possibility is the production of growth hormone releasing factor (GRF) by hypothalamic or ectopic tumors. This involves the secretion of a substance which selectively stimulates the GH producing cells of the pituitary. Special features of the clinical and morphological picture of this condition are described, based on the authors own observations. Two patients developed acromegaly: one had a retroperitoneal paraganglioma and the other a bronchial carcinoid. Ectopic GRF secretion could be confirmed radioimmunologically and immunohistologically in both cases. As a result of the on-going, tumor related GRF stimulation the patients developed nodular or diffuse GH-cell hyperplasia in the adenohypophysis. Since ectopic GH secretion does not cause hyperplasia of the adenohypophyseal cells, morphologic examination of the hypophysis can contribute to the differential diagnosis in such cases.

Acromegaly↗
PubMed1986

[Experimental studies of the significance and mechanism of desensitization to the gonadotropin-inhibiting effect of estrogen. 2. Detection and mechanisms of preovulatory desensitization in the ovarian cycle].

It has recently been demonstrated in women and several mammalian species that the basal LH secretion increases prior to the ovulation-inducing LH surge in spite of a simultaneous rise of the estrogen level in the blood. The temporary relative inefficiency of estrogen in its negative feedback action may be necessary to make adequate gonadotrophic support of final preovulatory follicle maturation possible. To study the mechanisms underlying this phenomenon, the gonadotrophic response to a single injection of estradiol benzoate (EB) was evaluated in acutely ovariectomized adult rats during the different stages of a 4-day ovarian cycle. The results showed that the sensitivity to the gonadotrophin-inhibiting effect of EB is high during late estrus and early metestrus. Between metestrus and diestrus it suddenly declines, and EB did not inhibit the hypophysial gonadotrophin secretion from diestrus through the morning of the subsequent estrus. The cyclic variation of the sensitivity to the negative estrogen feedback is probably not based upon an endogenous rhythm that is independent of the ovarian hormone secretion, because similar variability of the gonadotrophic response to estrogen was not found in rats that had been castrated three days before the injection of EB. A further experiment demonstrated that bilateral implants of EB placed in the medial preoptic area (MPOA) of ovariectomized rats significantly reduced the gonadotrophin-inhibiting effect of s. c. injected estradiol, whereas similar implants located in the mediobasal hypothalamus were completely ineffective in this regard. Since bilateral lesioning of the MPOA in long-term ovariectomized females also lowered the sensitivity to estrogen, the conclusion may be drawn that preovulatory desensitization to the negative estrogen feedback is probably induced in cyclic female rats by an inhibitory effect on medial preoptic neurones of the increase of circulating estrogen recorded in metestrus. In accordance with this assumption, imitation of the periovulatory diminution of estrogen action on the MPOA of intact rats by the removal of medial preoptic EB implants in castrated females during the afternoon of proestrus, resulted in high sensitivity to estrogen during estrus and metestrus. The possible clinical significance of the hitherto not described preovulatory desensitization is briefly discussed.

Animals↗
PubMed1986

[Clinical use of Gonadorelin as a diagnostic agent in one- and two-step tests].

Synthetic LH/RH Gonadorelin, produced by VEB Berlin-Chemie, was given to 11 women with a normal menstrual cycle during the middle of the follicle phase. It was proved as a very effective drug, which provoked a typical gonadotropin release. Also 10 patients with a secondary amenorrhea responded already to the first intravenous injection of 80 micrograms Gonadorelin with a peak level of gonadotropins, in particular with LH levels, after 30 to 60 minutes (delta 1 = 1 st peak level--0' level). The relative ascent of gonadotropins (delta 2 = 2nd peak level--120' level) after the second step i.v. administration of 80 micrograms Gonadorelin at a 120 minutes interval was not significantly higher than delta 1. The reaction of pituitary on LH/RH does not immediately depend on the basal level of gonadotropin values. It reflects the severity of the hypothalamic-pituitary functional disturbance. The "Gonadorelin-test" ist a good complement to the progesterone- and clomiphene-test.

Adult↗
PubMed1985

Immunoreactive substance P and LH-RH content in median eminence and pituitary gland during proestrus, oestrus, lactation and after anterior hypothalamic deafferentation.

Substance P (SP) and luteinizing hormone releasing hormone (LH-RH) content were measured by radioimmunoassay in median eminence of female rats, SP only in rats pituitary after decapitation on the day of oestrus (E), on the first and second day of dioestrus (D1 and D2), on the day of proestrus (P) and in "constant oestrus" (AD) caused by anterior hypothalamic deafferentation and in lactation (L). During four days of oestrus cycle the highest SP and LH-RH content of median eminence was found in dioestrus. Both during cyclic oestrus and "constant oestrus", SP and LH-RH were significantly lower than on the second day of dioestrus. These results may suggest the reciprocal functional relation of both hypothalamic peptides in the mechanism of the control of gonadotropin release. The highest LH-RH concentration of the median eminence was found in the animals on the 11th to 15th day of lactation, while the SP content in the median eminence of these animals is not significantly different from those of the remaining groups except the value for dioestrus (D2) rats. The SP content in pituitary of lactating rats was significantly higher than those of rats during cyclic or "constant oestrus".

Animals↗
PubMed1985

Postovulatory sensitization to the negative oestrogen feedback in female rats is probably induced by the preceding decline of the oestrogen concentration in the medial preoptic area.

To examine the question if an endogenous oestrogen-independent rhythm is involved in the cyclic variation of sensitivity to the negative feedback of oestrogen recorded in a former study, adult female rats were ovariectomized on subsequent days of a 4-day ovarian cycle, injected with 3 micrograms oestradiol benzoate (OB)/100 g b.w. or oil three days after castration, and autopsied on the following day. Estimation of the serum LH concentration revealed a similar LH-inhibiting effect of OB in all experimental groups. Female rats were then implanted with OB or cholesterol in the medial preoptic area (MPOA) in metoestrus. In part of the rats, the implants were removed on the presumptive day of pro-oestrus to imitate the periovulatory decline of the circulating oestrogen level acting on the MPOA. Evaluation of the sensitivity to the negative oestrogen feedback during oestrus and metoestrus demonstrated that s.c. injected OB was highly effective in suppressing the LH secretion after removal of the OB implants in pro-oestrus, but not in rats with the implants left in place till autopsy. In a final experiment, the pro-oestrous progesterone surge was inactivated by the injection of specific antibodies. An influence of this treatment on the LH-inhibiting effect of OB examined during oestrus and metoestrus could not be found. Taken together the results suggest that the high sensitivity to the negative oestrogen feedback recorded during the postovulatory period in cyclic female rats is mainly induced by the periovulatory fall of the circulating oestrogen level leading to reduction of the medial preoptic oestrogen concentration.

Animals↗
PubMed1985

Successful treatment of prostatic cancer with the orally active depot estrogen ethinylestradiol sulfonate (Turisteron).

Ethinylestradiol sulfonate (Turisteron) is an orally highly active depot-estrogen with relatively low side effects. In men with prostatic cancer, weekly administration of 2 mg Turisteron resulted in a striking decrease of the biologically active free testosterone level to less than 2% of the basal level; i.e., even significantly lower than after orchidectomy. Turisteron was able to normalize the 5 year survival rate in men with advanced non-metastatic cancer (T3NxM0) and to increase the survival rate significantly in men with metastatic cancer (T3-4, Nx, M1). Hence, due to our experience, Turisteron treatment is a very effective, non-expensive and well tolerated therapy for prostatic cancer.

Aged↗
PubMed1985

[Unusual abdominal apudomas. I. Cushing syndrome in association with Zollinger-Ellison syndrome in an endocrine pancreas tumor].

Ectopic production of ACTH is observed in 6% of patients with Cushing syndrome. Ten percent of these cases are related to endocrine pancreatic tumors. In a few cases a multiplicity of hormones are produced. The combination with a Zollinger-Ellison syndrome is very infrequent. In the present case, a female patient aged 54, there was an interval between the onset of Zollinger-Ellison and Cushing syndrome. The combination of bilaterally enlarged adrenals in the absence of an adrenal adenoma and the presence of Crooke-cells in the adenohypophysis in a patient with Cushing syndrome are of diagnostic significance. This trias should always alert the physician to the possibility of extrahypophyseal ACTH production.

Adrenocorticotropic Hormone↗
PubMed1985

[Immunohistological determination of beta-endorphin in chromophobe, clinically hormone-nonproducing hypophyseal adenomas].

Pituitary adenomas are usually classified according to the nature of their proper hormonal production. Silent adenomas of the pituitary are tumors without clinical and biochemical evidence of overproduction of any known adenohypophyseal hormones. The proportion of such seemingly nonfunctioning tumors is 20 to 30%. Silent corticotropic adenomas are able to synthesize some normal or abnormal sequences of proopiomelanocortin precursor without any signs of hypercorticism. These tumors were divided into basophilic adenomas with strong periodic acid-Schiff (PAS) positivity and chromophobic adenomas with moderate or no PAS positivity. All of our cases were chromophobic adenomas. Two of the cases were positive for beta-endorphin by immunofluorescence. ACTH immunoreactivity was not present in the cells. Electron microscopic study of the adenoma cells showed small secretory granules with a halo. The diameter of these granules varied from 50 to 250 nm. Automated morphometric and densitometric investigations of silent corticotropic adenomas and adenomas from patients with Cushing's disease gave different karyometric results. The most important practical problem arising from the present investigation was the high frequency of recurrence of silent corticotropic tumors.

Adenoma, Chromophobe↗
PubMed1984

Sequence of the neuraminidase gene of an avian influenza A virus (A/parrot/ulster/73, H7N1).

The complete sequence of the neuraminidase (NA) gene of the influenza A strain A/parrot/ Ulster /73 ( H7N1 ) has been determined after reverse transcribing and cloning it into the pBR322 plasmid, followed by subcloning into M13 vectors and sequencing with dideoxynucleotide chain terminators. The gene consists of 1458 nucleotides and codes for a protein of 469 amino acids. The neuraminidase has seven potential glycosylation sites. According to the molecular weight as determined by electrophoretic migration in polyacrylamide gel all of these sites might carry a carbohydrate side chain. When the parrot Ulster NA was compared with two other N1 neuraminidases, those of the human PR8 and WSN strains, deletions in the stalk region of 15 amino acids for PR8 NA and of 16 amino acids for WSN NA were apparent. No further rearrangements were found within N1 neuraminidases. Although the parrot Ulster strain was isolated 40 years after the two human strains, the base sequence homology of their NA genes is still 83 or 82%, respectively.

Allantoin↗
PubMed1984

Serum levels of FSH, LH and estradiol-17 beta in female rats around the time of puberty onset.

Groups of female rats were autopsied at daily intervals from 27 days of age through the first vaginal cycle and the serum FSH and LH and plasma estradiol-17 beta (E2) concentrations were estimated. Fluctuating hormone concentrations were recorded between days 27 and 31. Both gonadotropins and E2 dropped to a very low level on days 32 and 33 and showed then a progressive increase that commenced on day 34 and terminated for LH and E2 on day 39, i.e. in proestrus, whereas FSH declined from day 37 to day 39. The circulating gonadotropin level was lower during the first postpubertal diestrus than during most of the prepubertal phase. The findings suggest that a high sensitivity to the gonadotropin -inhibiting effect of estrogen prevented completion of an ovarian cycle up to day 33. After that, desensitization to the negative estrogen feedback as indicated by the simultaneous rise of E2 and gonadotropins makes final maturation of ovarian follicles and the first ovulation possible. In part of the rats aged 27-38 days cell nuclear volumes of medial preoptic neurons were evaluated, because recent results suggest that estrogen induces the desensitization process by an inhibitory action on the medial preoptic area. In accordance with this assumption, an inverse relationship between nuclear size and the E2 level in the blood could be revealed.

Animals↗
PubMed1984

Evidence that desensitization to the negative estrogen feedback is a prepubertal and not a postpubertal event in female rats.

Female rats were ovariectomized at 31 days of age, on the day of proestrus, or on the day of the first vaginal estrus if corpora lutea were seen in the ovaries. Immediately after castration, estradiol-17 beta (E2) or oil was administered via s.c. silastics capsules, or a 1:240 mixture of estradiol benzoate (EB) and cholesterol or cholesterol alone was unilaterally implanted into the hypothalamic ventromedial-arcuate region. Forty-eight hours after surgery the rats were decapitated and the serum concentrations of LH and FSH estimated. In rats implanted s.c. with E2 in anestrus, proestrus or estrus, estrogen treatment reduced the circulating LH level to 9.4; 60.4 and 33.6% and that of FSH to 49.5; 120.3 and 63%, respectively, of the concentration recorded in the corresponding controls implanted with oil. Following the intrahypothalamic implantation of EB, the serum concentration of LH was lowered to 20.8; 67.4 and 68.1% and that of FSH to 48.8; 87.0 and 62.0% as compared to the cholesterol-implanted controls. The findings clearly suggest that a major part of the change in sensitivity to the negative feedback of estrogen occurs prior to the first preovulatory surge of gonadotrophins.

Anestrus↗
PubMed1984

Evidence that inhibition of medial preoptic dopaminergic activity may be involved in the prepubertal desensitization to the negative oestrogen feedback in female rats.

Immature female rats were bilaterally lesioned in the medial preoptic area (MPOA) or hypothalamic ventromedial-arcuate region (VMAR) at 21 days of age and daily injected with the dopamine (DA) agonist bromocriptine (CB-154) through day 26. Estimation of the serum LH and FSH concentrations following ovariectomy and two injections of 0.05 micrograms oestradiol benzoate (OB)/100 g b.w. revealed that the desensitization to the negative feedback effect of OB induced by lesioning of the MPOA was almost completely prevented by CB-154. A similar effect of the drug was not found in rats lesioned in the VMAR. The DA antagonist alpha-methyldopa (alpha-MD) was then bilaterally implanted in the MPOA or VMAR of 28-day-old females. Evaluation of the gonadotrophin-inhibiting effect of OB on days 30-31 showed that medial preoptic, but not hypothalamic implants of alpha-MD reduced the sensitivity to the inhibitory action of OB. It is proposed that diminution of the dopaminergic activity in the MPOA may play a role in the prepubertal desensitization to the negative oestrogen feedback in female rats.

Animals↗
PubMed1984

Serum prolactin levels before and after galactography in patients with pathological nipple discharge.

Serum prolactin levels were determined in 25 women who underwent galactography on account of pathological nipple discharge. The test samples were obtained immediately before galactography as well as 5, 10, 15 and 30 minutes after. There was no significant change in serum prolactin levels following galactography. In 2 cases out of 25, the basal level of prolactin was well above normal while in 1 case it was below normal. Those three were cases of galactorrhea. The clinical aspect of pathological nipple discharge did not correlate with serum prolactin levels, and galactorrhea would appear to be compatible with serum prolactin levels below normal.

Adult↗
PubMed1984

Medial preoptic area, estrogen, and the peripubertal desensitization to the negative estrogen feedback in female rats.

Bilateral lesions placed in the medial preoptic area (MPOA) markedly diminished the luteinizing hormone-(LH-) and follicle-stimulating hormone- (FSH-) inhibiting effects of s.c. injected or intrahypothalamically implanted estradiol benzoate (EB) in ovariectomized immature rats. Desensitization to the negative estrogen feedback was also recorded in immature rats implanted into the MPOA with a mixture of 1 part EB and 240 or 360 parts cholesterol. Estrogen implants located in the hypothalamic ventromedial-arcuate region were ineffective in this regard. Whereas precocious puberty resulted from the implantation of EB into the MPOA, a delay of puberty onset was induced by medial preoptic implants of the antiestrogen clomiphene citrate which also enhanced the LH-suppressing effect of s.c. administered EB in prepubertal females. It is proposed that an increase of the estrogen concentration in the MPOA inactivates medial preoptic neurons that exert a restraining influence on tonic LH (and FSH) secretion by sensitizing the mediobasal hypothalamus to the negative feedback action of estrogen. This mechanism may be involved in the control of the onset of puberty in female rats.

Animals↗
PubMed1984

Varying sensitivity to the negative oestrogen feedback during the ovarian cycle of female rats: evidence for the involvement of oestrogen and the medial preoptic area.

The gonadotrophic response to a single injection of oestradiol benzoate (OB) was studied in acutely ovariectomized adult rats during the different stages of a 4-day ovarian cycle. The results showed a sudden decline of the sensitivity to the gonadotrophin-inhibiting effect of OB between metoestrus and dioestrus. This desensitization to the negative oestrogen feedback was probably caused by an oestrogen action on the medial preoptic area (MPOA). In rats ovariectomized and implanted with OB in the MPOA in metoestrus, an s.c. injection of OB on the presumptive day of pro-oestrus did not lower the circulating LH and FSH levels, whereas a clear suppression of gonadotrophin secretion was seen in females implanted with cholesterol in the MPOA or implanted with OB in the hypothalamic ventromedial-arcuate region. Similar findings were obtained in rats which had been ovariectomized 3-4 weeks before implantation. A final experiment demonstrated that bilateral lesioning of the MPOA also reduced the sensitivity to the negative feedback action of oestrogen in long-term ovariectomized rats. In all experiments performed, diminution of the oestrogen-induced inhibition of LH secretion was more marked than that of suppression of FSH secretion. It is proposed that desensitization to the negative oestrogen feedback, probably resulting from an inhibitory oestrogen action on medial preoptic neurones, is a prerequisite for adequate gonadotrophic support of preovulatory follicle maturation in the presence of a continuously rising oestrogen concentration in the blood.

Animals↗
PubMed1984

[Significance and mechanism of desensitization to the gonadotropin-inhibiting effect of estrogen. 1. Studies on prepubertal desensitization].

In immature female rats, both a distinctive diminution of the gonadotrophin-inhibiting effect of s. c. or intrahypothalamically implanted estradiol and a simultaneous rise of the estrogen and gonadotrophin levels in the blood were revealed during the last days preceding the onset of puberty. Based on these findings, studies on the neurohormonal mechanism underlying this prepubertal desensitization to the negative estrogen feedback were performed. Bilateral lesioning of the medial preoptic area (MPOA) which induced precocious puberty also diminished significantly the gonadotrophin-inhibiting effect of s. c. or intrahypothalamically administered estrogen. Similar responses were recorded following the implantation of very low quantities of estrogen into the MPOA, whereas medial preoptic implants of the antiestrogen clomiphene citrate impaired the spontaneous prepubertal desensitization and delayed the onset of puberty. It is concluded from the results that the prepubertal increase of the estrogen concentration in the blood itself induces the desensitization to estrogen by an inhibitory effect on medial preoptic neurons. Preliminary clinical and experimental findings suggest that a comparable mechanism may be operative in humans, too.

Animals↗