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Biomedical subjects

H Vorherr

Publications and source records attributed to H Vorherr.

At least 37 records · Page 2Linked to original sources
PubMed1981

Pathobiology of breast cancer: hypothesis of biological predetermination and long-term survival.

Th pathobiology of breast cancer is complex: clinically "early" breast cancer may be tumor biologically "late" progressing rapidly toward death. Accordingly, it has been suggested that two different breast cancer populations (slow tumor growth and long survival-fast tumor growth and short survival) exist, which cannot be identified by pathohistological criteria. However, these "populations" are most likely either patients with localized disease and occult metastases (long survival) or with diagnosable regional and occult or overt systemic spread (short survival). Since even small tumors (0.1 to 0.3 cm in diameter) can spread systemically, in most patients breast cancer upon clinical diagnosis may be considered an inevitably lethal disease. Present treatment modalities can only improve the quality of life and delay death, even though the overall long-term survival rates of breast cancer are better or at least equal to those of other cancers. However, with other cancers (Table 2) it is decided within the first 5 years which patients are cured because the survival rates for 5, 10, 15, and 20 years are similar. In contrast, survival rates of patients with breast cancer steadily decline and there is no point in time when patients can feel really safe; this is indicative of a peculiar tumor pathobiology of this disease, the nature of which remains to be investigated. Progress in the fight against breast cancer is only possible by application of sensitive physical, reliable immunological, and specific biochemical methods for early diagnosis and development of efficient therapeutic modalities for inhibition of growth or complete eradication of metastasized cancer cells.

Adult↗
PubMed1980

Vaginal absorption of povidone-iodine.

In 12 nonpregnant women, total iodine, protein-bound iodine, inorganic iodine, and thyroxine values were measured in serum before and 15, 30, 45 or 60 minutes after a two-minute vaginal disinfection with povidone-iodine (Betadine). Only 15 minutes after application, serum iodine levels were raised and remained significantly elevated 30, 45 and 60 minutes after disinfection. Serum concentrations of total iodine and inorganic iodine were increased up to fivefold to 15-fold, respectively; during the relative short period of observation, thyroxine levels were not altered. An overload of iodine can suppress thyroid hormonogenesis, and the fetal and neonatal thyroid glands are especially sensitive. In pregnant women, vaginitis should not be treated with povidone-iodine because of the possible development of iodine-induced goiter and hypothyroidism in the fetus and newborn. The risk is especially high when povidone-iodine is used repeatedly.

Absorption↗
PubMed1980

Antimicrobial effect of chlorhexidine on bacteria of groin, perineum and vagina.

The antimicrobial effects of two chlorhexidine preparations, Hibiclens and Hibitane Tincture, were evaluated in 154 obstetric patients. Both agents produced bacterial kills of over 99% on skin bacteria of groin and perineum ten and 30 minutes after their application. Five minutes after vaginal cleansing with Hibiclens more than 99% of bacteria originally present were destroyed. Even though both preparations proved to be potent bactericidal agents, Hibitane Tincture cannot be recommended as a perigenital antiseptic since it causes vulvar irritation due to its high isopropanol content. With Hibiclens application to groin and perineal skin no side effects were observed. In one of 51 patients treated vaginally with Hibiclens a rather strong burning sensation occurred, without any aftereffect. Hibiclens seems to be a promising antiseptic for obstetric and gynecologic patients.

Antisepsis↗
PubMed1979

Renal and vascular activity of prolactin preparations. Contamination of prolactin preparations with ADH and implications on renal and vascular prolactin research.

Prolactin, as a "broad spectrum hormone", has been described to exert also vascular and renal actions in laboratory animals and in humans. However, prolactin preparations of various species are contaminated with neurohypophysial hormones (ADH, oxytocin) which possess vascular and renal activities. Antisera against ADH, oxytocin and prolactin are rather specific inactivators of the biologic activity of the respective hormone; the oxytocinasevasopressinase system of pregnancy plasma destroys ADH and oxytocin. Incubation-identification procedures with antisera against ADH, oxytocin and prolactin and with pregnancy plasma revealed that changes in blood pressure, urine flow and urinary osmolarity cannot be ascribed to prolactin per se but to the ADH impurity of prolactin preparations. Furthermore, recent metabolic studies in normally hydrated, overhydrate and dehydrated animals and humans have shown that prolactin does not affect renal water and electrolyte excretion. Thus, earlier reports on vascular and renal activity of prolactin in laboratory animals and humans should be viewed with great caution. Elimination of neurohypophysial hormone impurities of prolactin preparations by incubation with either ADH and oxytocin antisera or with pregnancy plasma provides techniques for better assessment of the real biologic effects of the prolactin molecule.

Animals↗
PubMed1979

Effect of prostaglandins (F2 alpha, E1, and E2) on blood pressure and oxytocin-induced intramammary pressure responses in rats.

In lactating rats, vasoactive prostaglandin (PG) doses of F2 alpha (4 and 8 microgram/kg), E1, and E2 (2 and 4 microgram/kg each) reduced the intramammary pressure response to standard iv doses of 300 microU oxytocin by 50--80%. Adrenergic blockers, phenoxybenzamine and/or propranolol (1 mg/kg each sc) did not influence the blood pressure response to PGF2 alpha, PGE1, or PGE2. The oxytocin-antagonistic action of a single iv PGF2 alpha dose (4 microgram/kg) could not be altered by adrenergic blockers. In contrast, the oxytocin-antagonistic effects of PGE1 and PGE2 (2 microgram/kg each) were completely eliminated after alpha-receptor blockade, while the activity of oxytocin was augmented. Under beta-receptor or alpha- and beta-receptor blockade, the oxytocin-antagonistic effects of PGE1 and PGE2 were almost abolished. alpha-Receptor blockade reduced the oxytocin-antagonistic action of infused PGF2 alpha (8 microgram/kg.min for 15 min) by 38%. beta- or alpha- and beta-receptor blockade had no effect. The oxytocin-antagonistic actions of PGE1 and PGE2 (4 microgram/kg.min for 15 min each) were greatly reduced under alpha-receptor blockade. beta-Receptor blockade had no influence on the oxytocin-antagonistic activities of PGE1 or PGE2; under alpha- and beta-receptor blockade, the inhibitory actions of PGE1 and PGE2 were reduced by 60--70%. Mechanisms of PG-induced inhibition of the oxytocin response may involve mammary vasoconstriction and/or alterations in myoepithelial activity of cAMP and cGMP.

Animals↗
PubMed1979

Effect of prostaglandins on milk ejection.

Prostaglandins (PGs) of type F2 alpha, E1, and E2 have been reported both, to inhibit or to facilitate posterior pituitary oxytocin release in lactating animals and women, and to suppress or to stimulate the mammary myoepithelium. Prostaglandin-induced milk ejection in women and cows has been attributed to central oxytocin release, but no oxytocin blood levels were determined. Moreover, for lactating cows, sows, rabbits, guinea pigs, and rats a direct PG effect on the mammary myoepithelium resulting in milk ejection has been suggested. On the other hand, PGs were found to antagonize the milk-ejection response to oxytocin in rabbits and rats. The mechanisms involved in PG synergism or antagonism of oxytocin-induced milk ejection are not understood. Studies in lactating rats showed that blood pressure active PG doses of F2 alpha, E1, and E2 largely inhibited the intramammary pressure response to oxytocin. Whereas the oxytocin-antagonistic action of PGF2 alpha was not affected by adrenergic blockers (phenoxybenzamine, propranolol), the anti-oxytocin effects of PGE1 and E2 were eliminated after alpha-receptor blockade while the activity of oxytocin increased. Under beta-receptor or alpha- plus beta-receptor blockade, the oxytocin-inhibitory effects of PGE1 and E2 were almost abolished. Mechanisms of PG-induced inhibition of the oxytocin response may involve mammary vascular changes and/or alterations in myoepithelial activity of cyclic adenosine-3,5-monophosphate (c-AMP), cyclic guanosine-3,5-monophosphate (c-GMP), and phosphodiesterase (PDE). It seems unlikely that PGs bring about significant posterior pituitary oxytocin release in rats.

Animals↗
PubMed1979

Pregnancy and lactation in relation to breast cancer risk.

In the past, numerous efforts have been made to define risk and protective factors of breast cancer. Among these, pregnancy and lactation have been extensively discussed in connection with breast cancer. Unfortunately, many of the reports on the protective effects of pregnancy and lactation are equivocal; caution needs to be exercised when interpreting the results of a single publication. Development of breast cancer is often preceded by the occurrence of preneoplastic mammary lesions, which may be the result of long-term exposure to estrogens and prolactin. Since endogenous estrogen levels regulate pituitary prolactin secretion to some extent, it has been postulated that a hormonal imbalance exists in early mammary carcinogenesis. Exogenous estrogens directly increase pituitary prolactin secretion. During gestation, greatly increased levels of endogenous sex steroids efficiently stimulate pituitary prolactin secretion; during lactation, the stimulus of suckling is responsible for hyperprolactinemia. However, most studies did not reveal a cause-effect relationship between prolactin levels and enhanced risk of breast cancer. At present, the role of pregnancy and lactation in the development and prognosis of breast cancer is not determined.

Adolescent↗
PubMed1978

Thyroid disease in relation to breast cancer.

A controversy exists in regard to thyroid function and breast cancer. Hypothyroidism has been suggested as being either protective from breast cancer or predisposing to the disease. It has been hypothesized that a deficiency in circulating thyroid hormones may hypersensitize the mammary glandular epithelium toward prolactin and estrogens, thus aiding the development of breast neoplasia. On the other hand, thyroid hormone replacement therapy has been connected with an increased risk of breast cancer, but this has been contested. At this time the American Thyroid Association recommends that, if indicated, hypothyroid patients should take their thyroid hormone medication. Hyperthyroidism has been associated with a decreased risk of breast cancer. Also, in hyperthyroid patients with inoperable breast cancer, the malignant growth is thought to be slowed. However, this, too has been disputed. Moreover, hyperthyroidism has been connected with the development of breast cancer in premenopausal women. At present no role of thyroid hormone in the pathobiology of breast cancer can be defined. It seems that the "thyroid-breast cancer controversy" can only be resolved by a prospective study preferably on postmenopausal women correlating thyroid (T3, T4, PBI), pituitary (TSH, TRH, Prolactin), and adrenocortical (androgens) function tests with the clinical examination of thyroid, breast, and genital apparatus and determination of the estrogen status (vaginal smear, plasma estrogens) as well.

Adult↗
PubMed1978

Breast cancer: potentially predisposing and protecting factors. Role of pregnancy, lactation, and endocrine status.

Risk factors of breast cancer have been correlated with the availability of estradiol and estrone. Mechanisms protecting from breast cancer are thought to be due to the mitotic rest of mammary epithelium (low deoxyribonucleic acid synthesis), as encountered during pregnancy and lactation, and to the actions of estriol and progesterone in opposing the "carcinogenic" estradiol and estrone.

Adult↗
PubMed1978

Contamination of prolactin preparations by antidiuretic hormone and oxytocin.

Since impurities consisting of neurohypophysical hormones in prolactin powder may be responsible for the vascular and renal effects attributed to prolactin, rat (NIH-RP-1), ovine (NIH-P-S-10, S-12), and bovine (NIH-P-B4) prolactin preparations were examined for their content of ADH and oxytocin by rat antidiuresis, milk-ejection, and blood pressure assays. Activities were identified as due to ADH or oxytocin by incubation of prolactin solutions with antisera against ADH, oxytocin, and prolactin, or with pregnancy plasma. The ADH content of rat, ovine (P-S-10, P-S-12) and bovine prolactin was found to be 104.5 +/- 7.1 (means +/- SE), 2.5 +/- 0.2, 1.6 +/- 0.1, and 1.6 +/- 0.5 mU/mg powder, respectively; the corresponding values for oxytocin content were 155.3 +/- 3.5, 1.2 +/- 0.1, 0.5 +/- 0.1, and 1.2 +/- 0.01 mU/mg powder, respectively. Because antidiuretic, milk-ejection, and blood pressure activities of the various prolactins were eliminated after incubation with antisera against ADH and oxytocin, or with pregnancy plasma, but not with prolactin antisera, it is concluded that the reported vascular and renal prolactin effects are attributable to ADH contamination of the prolactin preparation rather than to the prolactin molecule itself. These findings have implications for renal and vascular prolactin research.

Animals↗
PubMed1977

Rat mammary deoxyribonucleic acid synthesis during the estrous cycle, pregnancy, and lactation in relation to mammary tumorigenesis: its implication for human breast cancer.

Rat mammary DNA synthesis is greatly reduced during late pregnancy and lactation; this corresponds to the decreased incidence of induced mammary tumors by chemical carcinogens during these periods. The protective effects of pregnancy and lactation against mammary tumorigenesis of rats and human subjects may be explained by the prolonged phases of mitotic rest encountered during pregnancy and lactation.

Animals↗
PubMed1975

Placental insufficiency in relation to postterm pregnancy and fetal postmaturity. Evaluation of fetoplacental function; management of the postterm gravida.

As pregnancy extends post term, incidence of placental insufficiency, fetal postmaturity (dysmaturity), and fetal perinatal death increases rapidly as a consequence of reduced respiratory and nutritive placental function. Despite a compensatory fetoplacental respiratory reserve capacity, fetal distress is observed in about one third of postterm pregnancies. On a biochemical level, placental pathophysiology in postterm-postmaturity pregnancies is not well understood. Postmaturity is correlated with increased incidence of placental lesions, fetal hypoxia-asphyxia, intrauterine growth retardation, increased perinatal death, and neonatal morbidity. Early diagnosis of fetal postmaturity is difficult because currently applied test methods allow recognition only when placental insufficiency is far progressed. Therefore, in postterm gravidas with a favorable cervix, induction of labor should be considered; in older primigravidas, in whom fetal losses may be sevenfold increased, or in multiparas with a history of obstetric complications, pregnancy may require termination by cesarean section. Pregnancy may be allowed to continue under close supervision in cases of uncertainty of duration of gestation, in gravidas carrying small babies, in young primigravidas, and in multigravidas in whom placentofetal function tests are normal. As long as fetal scalp blood sampling during labor does not show fetal acidosis, despite abnormal fetal heart rate pattern and meconium release, vaginal delivery may be attempted when deemed possible within a few hours. In parturients attention must be paid to the extent of uterine activity and type of medication; lateral positioning of the gravida and maternal oxygen breathing, facilitating fetal oxygen supply, are important features. Because during bearing-down efforts placentofetal respiratory reserves of postterm gravidas may become further compromised, immediate delivery by forceps or vacuum extraction may be considered. After delivery the umbilical cord should not be clamped immediately in order to allow increased fetal blood supply and to counteract fetal hypovolemia. Dysmature newborn infants require special care by the neonatologist.

Adrenocorticotropic Hormone↗