Evaluation of quality and readability of online patient information on osteoporosis and osteoporosis drug treatment and recommendations for improvement.

Patient information is important to help patients fully participate in their healthcare. Commonly accessed osteoporosis patient information resources were identified and assessed for readability, quality, accuracy and consistency. Resources contained inconsistencies and scored low when assessed for quality and readability. We recommend optimal language and identify information gaps to address. INTRODUCTION: The purpose of this paper is to identify commonly accessed patient information resources about osteoporosis and osteoporosis drug treatment, appraise the quality and make recommendations for improvement. METHODS: Patient information resources were purposively sampled and text extracted. Data extracts underwent assessment of readability (Flesch Reading Ease and Flesch-Kincaid Grade Level) and quality (modified International Patient Decision Aid Standards (m-IPDAS)). A thematic analysis was conducted, and keywords and phrases were used to describe osteoporosis and its treatment identified. Findings were presented to a stakeholder group who identified inaccuracies and contradictions and discussed optimal language. RESULTS: Nine patient information resources were selected, including webpages, a video and booklets (available online), from government, charity and private healthcare providers. No resource met acceptable readability scores for both measures of osteoporosis information and drug information. Quality scores from the modified IPDAS ranged from 21 to 64% (7-21/33). Thematic analysis was informed by Leventhal's Common-Sense Model of Disease. Thirteen subthemes relating to the identity, causes, timeline, consequences and controllability of osteoporosis were identified. Phrases and words from 9 subthemes were presented to the stakeholder group who identified a predominance of medical technical language, misleading terms about osteoporotic bone and treatment benefits, and contradictions about symptoms. They recommended key descriptors for providers to use to describe osteoporosis and treatment benefits. CONCLUSIONS: This study found that commonly accessed patient information resources about osteoporosis have highly variable quality, scored poorly on readability assessments and contained inconsistencies and inaccuracies. We produced practical recommendations for information providers to support improvements in understanding, relevance, balance and bias, and to address information gaps.

Children Exposed to IPV: Impact of Multiple Father Figures.

PURPOSE: Exposure to intimate partner violence (IPV) has been associated with adverse infant developmental outcomes; however, the influence of the number of father-figures (abusive vs non-abusive) has on young infants' risk for neurodevelopmental delays has not been examined. PROCEDURES: A secondary data analysis was conducted from the Domestic Violence Enhanced Perinatal Home Visits (DOVE) study of abused pregnant women (N = 239) and their infants' neurodevelopment from baseline through 12-months postpartum. RESULTS: Although all women reported decreased violence from baseline to 12 months postpartum, there was a significant main effect between baseline IPV scores and infant risk for developmental delay at 12 months (ß = .19; p < .05) and a significant interaction between baseline IPV scores and multiple partner categories (ß = .89; p < .01). Women in the single abusive partner category demonstrated a negative association between baseline IPV and 12-month infant risk scores (ß = -.56; p < .01). Whereas women in the mixed and multiple abusive partner groups demonstrated a positive association between IPV and infant risk scores (ß = .32; p < .05). CONCLUSION: This study provides evidence that an infant's neurodevelopment is impacted by exposure to violence in the home. Additional research is needed to examine the full impact, not only the effects of single and/or abusive partners on child development, but also the possible effect of multiple non-abusive partners on development.

Identifying and managing osteoporosis before and after COVID-19: rise of the remote consultation?

The COVID-19 pandemic is influencing methods of healthcare delivery. In this short review, we discuss the evidence for remote healthcare delivery in the context of osteoporosis. INTRODUCTION: The COVID-19 pandemic has undoubtedly had, and will continue to have, a significant impact on the lives of people living with, and at risk of, osteoporosis and those caring for them. With osteoporosis outpatient and Fracture Liaison Services on pause, healthcare organisations have already moved to delivering new and follow-up consultations remotely, where staffing permits, by telephone or video. METHODS: In this review, we consider different models of remote care delivery, the evidence for their use, and the possible implications of COVID-19 on osteoporosis services. RESULTS: Telemedicine is a global term used to describe any use of telecommunication systems to deliver healthcare from a distance and encompasses a range of different scenarios from remote clinical data transfer to remote clinician-patient interactions. Across a range of conditions and contexts, there remains unclear evidence on the acceptability of telemedicine and the effect on healthcare costs. Within the context of osteoporosis management, there is some limited evidence to suggest telemedicine approaches are acceptable to patients but unclear evidence on whether telemedicine approaches support informed drug adherence. Gaps in the evidence pertain to the acceptability and benefits of using telemedicine in populations with hearing, cognitive, or visual impairments and in those with limited health literacy. CONCLUSION: There is an urgent need for further health service evaluation and research to address the impact of remote healthcare delivery during COVID-19 outbreak on patient care, and in the longer term, to identify acceptability and cost- and clinical-effectiveness of remote care delivery on outcomes of relevance to people living with osteoporosis.

Quality and effectiveness of osteoporosis treatment decision aids: a systematic review and environmental scan.

Decision aids (DAs) are evidence-based tools that support shared decision-making (SDM) implementation in practice; this study aimed to identify existing osteoporosis DAs and assess their quality and efficacy; and to gain feedback from a patient advisory group on findings and implications for further research. We searched multiple bibliographic databases to identify research studies from 2000 to 2019 and undertook an environmental scan (search conducted February 2019, repeated in March 2020). A pair of reviewers, working independently selected studies for inclusion, extracted data, evaluated each trial's risk of bias, and conducted DA quality assessment using the International Patient Decision Aid Standards (IPDAS). Public contributors (patients and caregivers with experience of osteoporosis and fragility fractures) participated in discussion groups to review a sample of DAs, express preferences for a new DA, and discuss plans for development of a new DA. We identified 6 studies, with high or unclear risk of bias. Across included studies, use of an osteoporosis DA was reported to result in reduced decisional conflict compared with baseline, increased SDM, and increased accuracy of patients' perceived fracture risk compared with controls. Eleven DAs were identified, of which none met the full set of IPDAS criteria for certification for minimization of bias. Public contributors expressed preferences for encounter DAs that are individualized to patients' own needs and risk. Using a systematic review and environmental scan, we identified 11 decision aids to inform patient decisions about osteoporosis treatment and 6 studies evaluating their effectiveness. Use of decision aids increased accuracy of risk perception and shared decision-making but the decision aids themselves fail to comprehensively meet international quality standards and patient needs, underpinning the need for new DA development.

Pseudohermaphrodite rat: end organ insensitivity to testosterone.

The pseudohermaphrodite rat is characterized by lack of androgen-dependent differentiation. Treatment of these rats with testosterone failed to produce the expected changes in preputial and adrenal gland weights and hexobarbital metabolism. This insitivity of the end organ to testosterone could not be explained by defective formation of dihydrotestosterone.

Early androgen action in kidney of normal and androgen-insensitive (tfm/y) mice. Changes in RNA polymerase and chromatin template activities.

Intranuclear accumulation of testosterone was compared with early changes in transcriptional events in kidneys from normal female and androgen-insensitive (tfm/y) mice. Following a subcutaneous injection of [3H] testosterone, total nuclear uptake of the steroid was maximal at 30 min and declined to about 40% of the peak value by 4 h after hormone administration. After a single subcutaneous dose of testosterone, RNA polymerase activity assayed in intact nuclei in the presence of Mg2+ and alpha-amanitin (nucleolar RNA polymerase I), as well as the enzyme activity sensitive to low concentration of the toxin (nucleoplasmic RNA polymerase II), increased within 15 min and attained peak values at 2 and 1 h, respectively. The activity of both polymerases declined almost to the control level by 4 h and then increased again with a second peak at 20 and 12 h for RNA polymerase I and II, respectively. Similarly, the template capacity of mouse kidney chromatin, as measured with mammalian RNA polymerase II, increased by 15 min, reached a peak at 1 h and returned to control level by 4 h following hormone treatment. A second dose of testosterone given at the nadir (4 h) was not capable of stimulating renal chromatin template activity significantly as compared to the effect observed after the initial hormone treatment. Contrary to the testosterone-stimulated changes in transcriptional events observed in normal female mice, androgens elicited no response in androgen-insensitive tfm/y mice, animals lacking cytosol androgen receptors. These results strongly support the contention that hormone-specific receptors are obligatory to steroid-mediated modifications in gene transcription.

Synthetic peptide inhibitors of complement serine proteases--III. Significant increase in inhibitor potency provides further support for the functional equivalence hypothesis.

Synthetic peptides based on functionally equivalent (as defined by similar patterns of chemically equivalent amino acids) serine protease inhibitor (serpin) C-terminal sequences inhibit both classical and alternative pathways of complement activation. Inhibition was also found with hybrid peptides consisting of the cleavage site of one serpin (antithrombin III, alpha-1-antitrypsin, or antichymotrypsin) attached to the short and long functionally equivalent protease binding cores of the other two serpins. A hybrid peptide composed of the sequence at the site of cleavage of C4 by C1s attached to the long binding core of antithrombin III was selective in inhibiting the classical pathway with no effect on the alternative pathway at a concn of 10 microM. Extension of the functional equivalence hypothesis has produced inhibitors of complement activation named generic and generic +, whose sequences differ by 77% or 87%, respectively, from those of all three serpin sequences. A hybrid peptide composed of the antithrombin III cleavage site attached to the generic peptide is an inhibitor of complement activation at 500 nM, the most potent inhibitor found in this study.

A hormone priming regimen and hibernation affect oviposition in the boreal toad (Anaxyrus boreas boreas).

Declines of the southern Rocky Mountain population of boreal toad (Anaxyrus boreas boreas) have led to the establishment of a captive assurance population and reintroduction program, in an attempt to preserve and propagate this geographically isolated population. One of the unique adaptations of this species is its ability to survive in cold environments by undergoing long periods of hibernation. In captivity, hibernation can be avoided altogether, decreasing morbidity caused by compromised immune systems. However, it is not entirely clear how essential hibernation is to reproductive success. In this study, the effects of hibernation versus nonhibernation, and exogenous hormones on oviposition, were examined in boreal toad females in the absence of males. In the summers of 2011 and 2012, 20 females housed at Mississippi State University were treated with a double priming dose of hCG and various ovulatory doses of hCG and LH-releasing hormone analog but denied hibernation. Exogenous hormones, in the absence of hibernation, could not induce oviposition over two breeding seasons (2011-2012). In contrast, during the summer of 2012 and 2013, 17 of 22 females (77%) housed at the Native Aquatic Species Restoration Facility (Alamosa, CO, USA) oviposited after they were treated with two priming doses of hCG (3.7 IU/g each) and a single ovulation dose of hCG (13.5 IU/g) and LH-releasing hormone analog (0.4 µg/g) after hibernation. There was a significant difference in oviposition between females that were hibernated and received hormones (2012, P < 0.05 and 2013, P < 0.01) compared to hibernated control females. In 2013, 12 of 16 remaining Mississippi State University females from the same group used in 2011 and 2012 were hibernated for 1, 3, and 6 months, respectively and then treated with the same hormone regimen administered to females at the Native Aquatic Species Restoration Facility. Together, hibernation and hormone treatments significantly increased oviposition (P < 0.05), with 33% of females ovipositing. These results suggest that (1) hibernation is a key factor influencing oviposition that cannot be exclusively circumvented by exogenous hormones; (2) females do not require the presence of a male to oviposit after hormone treatments; and (3) longer hibernation periods are not beneficial for oviposition. The hormonal induction of oviposition in the absence of males and shorter hibernation periods could have important captive management implications for the boreal toad. Furthermore, the production of viable offspring by IVF where natural mating is limited could become an important tool for genetic management of this boreal toad captive population.

Androgen and progestin stimulation of ornithine decarboxylase activity in the mouse kidney.

This study was designed to characterize mouse kidney ornithine decarboxylase (ODC) activity as an androgenic end point and to use ODC activity to detect an androgenic effect of antiandrogens. Enzyme activity was not affected by freezing the whole kidney or the 15,000 X g supernatant for up to 7 days. ODC activity in female mice had a diurnal variation that peaked at midday. This diurnal variation did not affect the androgenic response of ODC. Enzyme activity was lower in females than in males and, in both sexes, could be induced further to similar levels with testosterone treatment. A single dose of crystalline testosterone induced a marked increase in activity, which peaked sharply, up to 100-fold above baseline, 12-17 h after treatment. Enzyme activity could be maintained with continued treatment for at least 28 days and reached levels up to 1,000-fold above baseline. The response was specific for androgens and required a functional androgen receptor. Other hormones had permissive effects. The early androgen-stimulated response (less than 24 h) was partially diminished by hypophysectomy. Propylthiouracil reduced both early and chronic responses. Genetic factors were also involved. The testosterone-stimulated response of C57BL/6J mice was consistently approximately half that of DBA/2J mice. Using this very specific and sensitive increase in ODC activity as an end point, we did not detect an androgenic response to treatment with the antiandrogens, cyproterone acetate (6-chloro - 17 alpha - acetoxyl - 1,2 alpha - methylene - 4,6- pregnadiene- 3,20-dione) and flutamide (4'-nitro-3'-trifluoromethylisobutyranilide), despite an increase in RNA polymerase activity. The functionality of the polymerase activity induced by antiandrogens thus remains in question. These data suggest that mouse renal ODC activity can be a useful tool for future study of androgen action at the physiological and molecular level.

The prosence of estrogen receptor in kidneys from normal and androgen-insensitive tfm/y mice.

In vitro and in vivo binding of [3H]estradiol to cytosol proteins and nuclei was studied in kidneys from normal and androgen-insensitive tfm/y mice. The use of tfm/y mice permitted study of the estrogen-receptor complex in the absence of androgen receptor. A high affinity, [3H]estradiol-labeled, 8S molecule was demonstrated in low salt sucrose gradients. This macromolecule sedimented more slowly in gradients containing KC1 (0.5 M). Binding of [3H]estradiol was inhibited by 100-fold excess estrone, estradiol, or diethylstillbestrol but was not affected by testosterone, androstenedione, or progesterone. Studies of equilibrium-binding kinetics for estradiol indicated a Kd of 1.4 X 10(-9) M and 4.4 X 10(-14) mol of binding sites/mg cytosol protein. Furthermore, the binder was an acidic, heat-labile protein (pI = 4.8) which could be precipitated from cytosol with 33% ammonium sulfate, and needed sulfhydryl groups for activity. The demonstration of an estradiol-binding protein in vitro was correlated with specific [3H]estradiol uptake by tfm/y kidney nuclei in vivo. We concluded that the mouse kidney contains an estradiol-binding protein, distinct from that for androgens, which has many of the characteristics of a steroid receptor. The presence of an estrogen receptor in both normal and tfm/y mice indicates that a genetic defect in one receptor does not influence the properties of another. We concluded that androgen and estrogen receptors are under independent genetic control.

The effect of progestins on submaxillary gland epidermal growth factor: demonstration of androgenic, synandrogenic and antiandrogenic actions.

The effects of progestins (0.1, 1.0, 6-10 mg/day) alone and in combination with testosterone (0.1 mg/day) on immunoreactive epidermal growth factor (EGF) concentrations in submaxillary glands from normal and androgen-insensitive (tfm/y) mice were studied. Since androgens are known to stimulate increased EGF levels, the responses to progestins were interpreted as androgenic, synandrogenic or antiandrogenic if they simulated, potentiated or inhibited androgen response, respectively. Of the progestins studied, medroxyprogesterone acetate (MPA) caused the greatest androgenic response when given alone; 10 mg produced a greater than 40-fold increase of EGF over control values. Lesser responses were achieved when progesterone or megestrol acetate (Meg Ac) were given alone. Cyproterone acetate (Cyp Ac) had no androgenic activity when administered alone and acted as a potent antiandrogen at all doses used. Progesterone and Meg Ac had weak antiandrogenic activity. The only synandrogenic response elicited was with a high dose (10 mg) of progesterone caproate. Neither MPA nor progesterone alone had any effect on EGF levels in tfm/y mice. These patterns of response differ from those seen in mouse kidney. The data indicate that progestins as a class are capable of androgenic, synandrogenic and antiandrogenic action in the mouse submaxillary gland, but that no single progestin is capable of all three actions. Since tfm/y mice lack a functional androgen receptor, the absence of EGF response in these mice to progestins as well as androgens suggest that the action of progestins may be mediated by the androgen receptor in the submaxillary gland.

Inherited congenital adrenal hyperplasia in the rabbit: absent cholesterol side-chain cleavage cytochrome P450 gene expression.

We investigated adrenal steroidogenic enzymes, their activity and mRNA expression, and in vitro biosynthesis of an enzyme in rabbits with congenital adrenal hyperplasia (CAH; weight: CAH, 19 +/- 5 mg/adrenal; normal, 2.7 +/- 1.0 mg/adrenal). Serum pregnenolone (delta 5-P) levels in CAH newborn rabbits (12-36 h) were normal (mean/range, 438/51-2191 ng/dl), but corticosterone levels were low [0.05 +/- 0.05 microgram/dl; P less than 0.001 vs. normal (0.66 +/- 0.57)]. Serum Na+ levels in CAH newborn rabbits were in the normal range (143 +/- 30 meq/liter), but K+ levels were elevated [7 +/- 1.1 meq/liter; P less than 0.05 vs. normal (5.9 +/- 0.6 meq/liter)]. Minced normal adrenal tissue incubated with [3H] cholesterol (30-100 pmol/flask) and ACTH (100 mU/flask) produced [3H]delta 5-P (newborn, 21 and 45 fmol/100 mg; adult, 3 and 5 fmol/100 mg) and [3H]corticosterone (newborn, 23 fmol/100 mg; adult, 11.3 fmol/100 mg), but CAH adrenals produced no product (less than 1.3 fmol/100 mg). Adrenal mitochondria from normal newborn rabbits produced delta 5-P (4.4-7 nmol/mg protein), but CAH adrenals did not, while CAH adrenal mitochondria demonstrated over 4 times greater 11 beta-hydroxylase activity. A Western blot of adrenal homogenate from normal newborn rabbits revealed a cholesterol side-chain cleavage cytochrome P450 (P450scc)-immunoreactive species (mol wt, 53 x 10(3), but this species was absent in CAH adrenals; CAH adrenals had a normal adrenodoxin and intensified 17 alpha-hydroxylase cytochrome P450 (P450(17)alpha) band compared to normal adrenals. In vitro translation of RNA in a cell-free rabbit reticulocyte lysate system containing [35S] methionine yielded a precursor P450scc protein (mol wt, 58.5 x 10(3)) with normal adrenal RNA, but not with CAH adrenal RNA. P450scc mRNA was detected in all normal adrenals, but was not detected in all CAH adrenals. 21-Hydroxylase cytochrome P450 mRNA expression was detected at a similar level in both normal and CAH adrenals. We conclude that CAH in the rabbit is caused by inherited absent P450scc gene expression. The clinical, pathological, and biochemical manifestations of P450scc deficiency in the rabbit are nearly identical to the human disorder. Increased 11 beta-hydroxylase activity and increased P450(17)alpha on Western blot of CAH adrenals indicate altered gene expression of other steroidogenic enzymes due to CAH. Further molecular analysis of the P450scc gene in this animal CAH model will facilitate understanding of P450scc deficiency CAH.

Thyroid hormone antibodies and Hashimoto's thyroiditis in mongrel dogs.

Abnormally elevated serum T3 concentrations measured by RIA were observed in 19 clinically euthyroid or hypothyroid mongrel dogs. The serum T4 concentrations in these sera were low, normal, or high. Measurement of the intensity of thyroid hormone binding to serum proteins was determined by equilibrium dialysis. A marked decrease in the percent free T3 was observed in these abnormal sera. Polyacrylamide gel electrophoresis, pH 7.4, of normal dog serum enriched with tracer 125I-labeled thyroid hormones demonstrated binding of [125I]T4 to transthyretin, thyroid hormone-binding globulin, and albumin and of [125I]T3 primarily to thyroid hormone-binding globulin. In all abnormal sera, polyacrylamide gel electrophoresis demonstrated strikingly higher binding of T3 to immunoglobulin (Ig). Eleven of 16 abnormal sera had minimal to moderate binding of T4 to Ig. The percent free T4 was lower only in dogs whose sera demonstrated markedly increased binding of T4 to Ig. All abnormal sera tested had positive antithyroglobulin antibodies, consistent with the diagnosis of autoimmune lymphocytic thyroiditis. As in humans, antibodies to thyroid hormones in dogs are more common in the presence of Hashimoto's thyroiditis and should be considered when elevated serum thyroid hormone concentrations are observed in the absence of clinical thyrotoxicosis. When an antibody to only one thyroid hormone is present, a marked discrepancy in the serum concentrations of T3 and T4 will be observed.

Brief overview of selected aspects of testicular hormone action.

This paper is designed to give an overview of the mechanism of androgen action and some of the factors that can affect it. The discussion of androgen action includes androgen transport in the blood, metabolism, receptor binding, nuclear activation and selected aspects of biological response. The importance of recognizing interspecies and interstrain differences in specific aspects of androgen action is mentioned. Some examples of the effects of environmental agents on androgen metabolism, receptor binding and biological response are included.

Two forms of ornithine decarboxylase activity in mouse kidney.

Renal ornithine decarboxylase (ODC) activity was evaluated in normal female, male, testosterone-treated female and androgen-insensitive Tfm/Y mice for its heat sensitivity and in vivo half-life. ODC activity in normal female kidney consisted of 2 forms which differed in their heat sensitivity at 46 degrees C. Androgens, either endogenous in normal males or administered exogenously to females, induced primarily the heat-sensitive form. Results from mixing experiments indicated that the heat-sensitive form represented a change in the property of the ODC activity rather than a change in cytoplasmic factors. The in vivo half-life of ODC activity was increased slightly in males and short-term androgen-treated females over normal females and was markedly increased by prolonged androgen treatment. In vivo, the androgen-induced, heat-sensitive form decayed faster than did the heat-resistant form. We conclude that androgens have specific effects on both the amount as well as the biochemical properties of ODC activity in mouse kidney.

Weak androgen reduces the rate constant of beta-glucuronidase induction.

Administration of androgen to mice induces kidney beta-glucuronidase. Measuring beta-glucuronidase activity, rate of beta-glucuronidase synthesis, beta-glucuronidase mRNA activity and beta-glucuronidase mRNA concentration, the time course of induction was compared using a strong androgen, dihydrotestosterone (DHT), and a weakly androgenic progestin, medroxyprogesterone acetate (MPA). Using MPA resulted in a longer lag, a 3-4-fold slower rate of induction as defined by the forward rate constant, ka, a lower final extent of induction, and a slightly lower turnover constant, kb. Differences in kinetics of induction were consistent for all 4 measured parameters, and mimicked previously described genetic differences in these rate constants. The coordinate induction of beta-glucuronidase protein and beta-glucuronidase mRNA indicates that the response to androgen is regulated at a pre-translational level. That substitution of MPA for DHT decreases ka, rather than increasing kb, suggests that induction of beta-glucuronidase follows an increased rate of mRNA synthesis rather than a decreased rate of mRNA turnover. Finally, the results are consistent with a model in which the kinetic constants for beta-glucuronidase induction are dependent on the concentration of receptor molecules in the active conformational state.

Androgenic, synandrogenic, and antiandrogenic actions of progestins.

In addition to their action on the uterus and vagina, progestins exert diverse metabolic effects on a variety of tissues. These actions include androgenic, synandrogenic, and antiandrogenic effects on androgen-responsive tissues of rats and mice. The androgenic and antiandrogenic effects of progestins have been demonstrated in multiple tissues. These actions appear to be mediated via the androgen receptor. A synandrogenic effect of progestins has also been detected in some tissues. However, there are few data to indicate how this response is mediated. Progestins may also alter androgen action indirectly through changes in steroid synthesis and metabolism. The overall biologic effect of a steroid may thus be determined by the sum of its actions on a variety of tissues.

Thyroid growth immunoglobulins in feline hyperthyroidism.

Feline hyperthyroidism bears a strong clinical and pathologic resemblance to toxic nodular goiter in humans. To evaluate whether the observed thyroid growth might be due to circulating thyroid antibodies, as has been postulated in humans, we studied the effect of purified immunoglobulin (Ig) G preparations on a rat thyroid follicular (FRTL-5) cell line. When compared with control, hyperthyroid cat IgG caused significantly increased [3H]-thymidine (Tdr) incorporation into DNA (p less than 0.02) and stimulated cellular proliferation 15-fold. Stimulation of 3H-Tdr incorporation tended to be biphasic and could be inhibited completely by a potent, specific TSH receptor blocking antibody. Hyperthyroid cat IgG also significantly inhibited 125I-bTSH binding to porcine thyroid membranes, an effect that could be reproduced using electrophoretically pure IgG and normal cat thyroid membranes. Unlike its effect on growth, hyperthyroid cat IgG did not stimulate intracellular cAMP, and there was no correlation between thyroid function in vivo and IgG growth-promoting activity in vitro. These data suggest that elevated titers of thyroid growth IgGs, probably acting through the TSH receptor, are present in feline hyperthyroidism and may play a role in goiter formation. Unlike growth, the thyroid hyperfunction observed is not IgG dependent. Further study of feline hyperthyroidism may contribute important insights into human nodular goiter and into the mediation of thyroid growth in general.

In vivo androgen retention in mouse kidney.

The in vivo retention of 3-H-testosterone, dihydrotestosterone (DHT), 3alpha-androstanediol (3alpha-DIOL), 3beta-DIOL, androstenedione, progesterone and cortisol by renal cytoplasm and nuclei of male and female mice was studied. Testosterone was the major androgen isolated from cytoplasm and nuclei following testosterone or androstenedione administration. By contrast, DHT was the major intracellular androgen after DHT, 3alpha- or 3beta-DIOL injection. The uptake of 3-H-testosterone or 3-H-DHT was abolished by excess unlabeled testosterone, DHT or cyproterone acetate. Androgen concentrations in kidney fractions from female mice were similar to those from males. There was no appreciable concentration of the isolated steroids following 3-H-progesterone administration. 3H-cortisol was concentrated in both cytoplasm and nuclei but was not displaced by non-radioactive androgens. These findings suggest that in contrast to prostate, mouse kidney can concentrate both testosterone and DHT. However, since testosterone is the major androgen in blood and since it is not metabolized in kidney, it is the major effector androgen in this organ. Androstenedione is active via conversion to testosterone while DIOLS are androgenic via metabolism to DHT.