ライフサイエンスコーパス: gonadal

1 on of leukemic stem cells (LSCs) can utilize gonadal adipose tissue (GAT) as a niche to support their

2 ty were reduced, respectively, 75 and 70% in gonadal adipose tissue (GAT), 90 and 80% in subcutaneous

3 n of genes involved in metabolic pathways in gonadal adipose tissue of WT and APNko, but this effect

4 hat chemotherapy-resistant CD36+ LSCs co-opt gonadal adipose tissue to support their metabolism and s

5 intrauterine growth restriction (IUGR) with gonadal, adrenal, and bone marrow failure, predispositio

6 hormone is disrupted most often, followed by gonadal, adrenal, and thyroid hormones, leading to abnor

7 lism, and action) and at all relevant sites (gonadal, adrenal, intratumoral) simultaneously at the ti

8 mechanism that is influenced by circulating gonadal and adrenal hormones.

9 Cases of gonadal and extragonadal primary were included in the na

10 etal macrophages are associated with nascent gonadal and mesonephric vasculature during the initial p

11 are signaled through complex interconnecting gonadal and neurological control mechanisms that general

12 profound influence of TSD on male pituitary-gonadal and pituitary-thyroid axis hormones characterize

13 her TSD affects the course of male pituitary-gonadal and pituitary-thyroid axis related hormones duri

14 mouse models that allow distinction between gonadal and sex chromosome effects.

15 oatrophy with approximately 90% reduction in gonadal and subcutaneous white adipose tissue and brown

16 Gonadal androgen suppression (castration via orchiectomy

17 Novel inhibitors of extra-gonadal androgen synthesis and androgen receptor functio

18 Suppression of gonadal androgens by medical or surgical castration rema

19 ators of the pituitary-thyroid and pituitary-gonadal axes.

20 s associated with the hypothalamic-pituitary-gonadal axis (HPG axis) in fish had become a conventiona

21 tores function of the hypothalamic-pituitary-gonadal axis and, thus, normalizes hormone levels of lut

22 The hypothalamic-pituitary-gonadal axis controls puberty and reproduction and is ti

23 e following: (a) the hypothalamic-pitutitary-gonadal axis in female FHMs, where aromatase inhibition

24 role in regulating the hypothalamo-pituitary-gonadal axis in vivo through the activation of nNOS in n

25 ole in regulating the hypothalamic-pituitary-gonadal axis in vivo.

26 Control of the hypothalamic-pituitary-gonadal axis is dependent on correct migration of gonado

27 ormal function of the hypothalamic-pituitary-gonadal axis is dependent on gonadotropin-releasing horm

28 lic information to the hypothalamo-pituitary-gonadal axis is mediated by leptin receptors on AgRP neu

29 nce of the male on the hypothalamo-pituitary-gonadal axis of the inseminated female.

30 es to orchestrate the hypothalamus-pituitary-gonadal axis physiology.

31 ent of the estrogenic hypothalamic-pituitary-gonadal axis regulation in females showed that leptin ac

32 rly activation of the hypothalamic-pituitary-gonadal axis results in central precocious puberty.

33 educed activity of the hypothalamo-pituitary-gonadal axis such as delayed puberty, hypothalamic ameno

34 r of the adult female hypothalamus-pituitary-gonadal axis, is paradoxically produced by neurons in th

35 modifications to the hypothalamic-pituitary-gonadal axis.

36 adal function via the hypothalamic-pituitary-gonadal axis.

37 rine system along the hypothalamus-pituitary-gonadal axis; however, most studies address either devel

38 -1, NR5A1) is a key regulator of adrenal and gonadal biology.

39 imally expressed by the endothelial cells of gonadal blood vessels.

40 d higher responses than women, likely due to gonadal cancer-testis-antigen expression.

41 diagnosis, and treatment of infertility and gonadal cancers, and in efforts to augment human and ani

42 c division is involved in the acquisition of gonadal cell fates.

43 d transcriptional regulation in an embryonic gonadal cell line demonstrated partial activation of dow

44 hway to suppress endogenous mobile elements, gonadal cell TE landscapes can still dramatically change

45 This pivotal decision in a single gonadal cell type ultimately controls sexual differentia

46 nscription collapses in germline and somatic gonadal cells and TEs are activated, resulting in germli

47 , a portion of excessive early-stage somatic gonadal cells are found to originate from early-stage ge

48 We have previously shown that somatic gonadal cells are required for male GSC specification an

49 We find excessive early-stage somatic gonadal cells in E(z) mutant testes, which originate fro

50 In Drosophila, Nup107 knockdown in somatic gonadal cells resulted in female sterility, whereas male

51 KN-1 localizes to the plasma membrane of all gonadal cells, with apical and lateral bias.

52 ansposable elements (TEs) from mobilizing in gonadal cells.

53 e ablated the corresponding genes in somatic gonadal cells.

54 Drosophila Piwi is the founding member of a gonadal clade of Argonaute proteins that serve as silenc

55 ines and discovered dynamic TE landscapes in gonadal cultures that were defined by a subset of active

56 This effect is partially dependent on gonadal DAF-16/FOXO activity.

57 e cancer survivors, but endocrine effects of gonadal damage are likewise central to long-term health

58 transgenic overexpression of Map3k4 rescues gonadal defects in Gadd45gamma-deficient embryos.

59 Subordinates experience gonadal development if separated from the queen.

60 Gonadal development in C. elegans is well studied, but r

61 zooplankton to the diet, somatic growth and gonadal development of whitefish.

62 sexual differentiation, especially later in gonadal development, remains poorly elucidated.

63 us to study sex-specific gene expression and gonadal development.

64 MRT1 is an essential sex-linked regulator of gonadal differentiation in avians, and that it likely ac

65 t, expression of thermoresponsive genes, and gonadal differentiation in fathead minnows, Pimephales p

66 In mice, Dmrt1 is required for male gonadal differentiation in somatic cells and germ cells

67 proof for an essential role of NF-kappaB in gonadal differentiation of zebrafish and represents an i

68 of WwTW effluent exposure on reproduction or gonadal disruption in roach down the female germ line an

69 es a DAF-1/TGFbetaR signaling cascade in the gonadal distal tip cell (DTC), the germline stem cell ni

70 opituitarism, obesity, diabetes mellitus, or gonadal dysfunction between survivors and siblings.

71 n (mTOR) inhibition has been associated with gonadal dysfunction.

72 Patients with 46,XY gonadal dysgenesis (GD) exhibit genital anomalies, which

73 XX female gonadal dysgenesis (XX-GD) is a rare, genetically hetero

74 ic problems including nephropathy, blastoma, gonadal dysgenesis and genital discordance.

75 Mutations in SRY cause XY gonadal dysgenesis and somatic sex reversal.

76 nd generated XY(DMY-) mutants to investigate gonadal dysgenesis in medaka.

77 ovel mutant that is useful for investigating gonadal dysgenesis in phenotypic female patients with th

78 Mutations in human SRY cause gonadal dysgenesis leading to XY female development (Swy

79 l mice and provide a molecular basis for the gonadal dysgenesis observed in ataxia telangiectasia, th

80 Mutations in SRY cause 46 XY gonadal dysgenesis with female somatic phenotype (Swyer

81 Mutations in SRY cause gonadal dysgenesis with female somatic phenotype.

82 ed dogs with XY chromosomal sex but complete gonadal dysgenesis, which is classified as 78, XY disord

83 ns of mitochondrial translation in mammalian gonadal dysgenesis.

84 ive comorbidities and hypothalamic-pituitary-gonadal dysregulation.

85 n of the gonads and/or are determined by non-gonadal effects of the sexual inequality in the number a

86 rammed death of the linker cell, which leads gonadal elongation, proceeds independently of caspases a

87 gene fkh-6, but mutagenesis of a short male gonadal enhancer element in egl-5 suggested that this re

88 on AIB1 transgenic (AIB1-tg) mice to prevent gonadal estrogen production and by crossing AIB1-tg mice

89 females was not solely reflective of absent gonadal estrogen, as chronically ovariectomized Kiss1r K

90 ssion but did not affect Sox9 mRNA levels in gonadal explants.

91 d outperformed gonadal expression levels and gonadal expression correlations in predicting germ cell-

92 Our method outperformed gonadal expression levels and gonadal expression correla

93 nt relationship to Sex-lethal is revealed by gonadal expression of RBP9, providing a maternal fail-sa

94 al dwarfism, extreme insulin resistance, and gonadal failure and identified compound heterozygous fra

95 Transfusional iron overload and gonadal failure are addressed, followed by options for f

96 ressed in this chapter, including fertility, gonadal failure, erectile dysfunction, and menstrual iss

97 erol was the same in Bhmt(+/+) and Bhmt(-/-) gonadal fat depots (GWAT), but it was 62% lower in Bhmt(

98 Gonadal fat develops postnatally, whereas subcutaneous f

99 Robustly enhanced lipolysis was found in gonadal fat of Adipoq(-/-) dams.

100 that EGL-5 plays an instructive role in male gonadal fate determination.

101 a Wnt/beta-catenin pathway to regulate male gonadal fates and can physically interact with the Wnt p

102 Our studies also implicate microRNAs in gonadal feedback control of gonadotropin synthesis and s

103 exual maturity had altered susceptibility to gonadal feminization and an impaired capacity to reprodu

104 There was no difference in the severity of gonadal feminization in roach derived from either WwTW e

105 g hormone (FSH) is an essential regulator of gonadal function and fertility.

106 terize the effect of sirolimus (SRL) on male gonadal function in an experimental model.

107 Preservation of gonadal function is an important priority for the long-t

108 placode to the forebrain where they control gonadal function via the hypothalamic-pituitary-gonadal

109 such as treatment-induced menopause, altered gonadal function, and significant surgical disfigurement

110 anscription factor with an essential role in gonadal function.

111 regulator of gonadotropins, which stimulate gonadal function.

112 PRL levels, decrease tumor size, and restore gonadal function.

113 drugs can adversely affect hypothalamic and gonadal functioning.

114 Therefore, we analyzed gonadal functions in survivors of HL.

115 nd histologically similar to the more common gonadal GCTs.

116 hermaphrodites is sufficient to induce male gonadal gene expression, indicating that EGL-5 plays an

117 roliferation, survival and expression of the gonadal germline program as marked by MVH.

118 efish activity levels as well as somatic and gonadal growth all peaked during the summer, coinciding

119 e sets indicative of teleost brain-pituitary-gonadal-hepatic (BPGH) axis function indicated that WWTP

120 or arrested egg deposition with no observed gonadal histopathology.

121 dence from animal studies indicates that the gonadal hormone 17beta-estradiol (E(2)) impacts the stru

122 in photic responsiveness are independent of gonadal hormone effects during development.

123 nation of underlying genetic differences and gonadal hormone exposure.

124 ted status, suggesting that dysregulation of gonadal hormone function may be a characteristic trait o

125 changes during puberty that may be driven by gonadal hormone secretion during this developmental peri

126 ence indicates that prenatal exposure to the gonadal hormone, testosterone, influences the developmen

127 ie a two-way interaction between circulating gonadal hormones and behavioral responses to socially sa

128 dimorphism have emphasized the importance of gonadal hormones and cell-autonomous influences in mamma

129 central nervous system (CNS) factors, genes, gonadal hormones and receptors, genitalia, and social/en

130 Here, we review the mechanisms by which gonadal hormones and sex chromosome complement each cont

131 e organizational and activational effects of gonadal hormones and to genes on the sex chromosomes.

132 Many effects of these gonadal hormones are mediated by nuclear steroid hormone

133 Gonadal hormones contribute to ischemic neuroprotection,

134 y and provide a potential mechanism by which gonadal hormones could regulate the maturation of the as

135 Among evolocumab-treated patients, gonadal hormones did not change from baseline to week 52

136 Here, we report that manipulations of gonadal hormones do significantly alter the maturation o

137 ned for a female phenotype unless exposed to gonadal hormones during a perinatal sensitive period.

138 inatal sensitive period, when organizational gonadal hormones establish the sexually dimorphic brain,

139 specting the breadth and depth of the impact gonadal hormones have on brain functioning and its rich

140 astrocytes persisted even in the absence of gonadal hormones in adulthood, suggesting that androgens

141 discriminable, suggesting opposite roles for gonadal hormones in influencing male and female olfactor

142 tivity are sexually dimorphic or affected by gonadal hormones in the MePD.

143 ffects of stress, where the rapid decline of gonadal hormones in women combined with cellular aging p

144 nt work illustrating how sex differences and gonadal hormones influence sleep and circadian rhythms t

145 of these sex differences, but whether adult gonadal hormones maintain the increased number and compl

146 Gonadal hormones modulate behavioral responses to sexual

147 ural mechanisms underlying the influences of gonadal hormones on human behavior are beginning to be i

148 The influence of gonadal hormones on multiple sclerosis (MS) is not well

149 printed genes is most likely attributable by gonadal hormones rather than by sex chromosome complemen

150 rentiation of the gonads, which then secrete gonadal hormones that act directly on tissues to induce

151 , cortisol, adrenocorticotropic hormone, and gonadal hormones were analyzed at baseline and week 52.

152 An emerging hypothesis is that fluctuating gonadal hormones, especially estrogen, in the menstrual

153 adverse effects were observed in steroid or gonadal hormones, even at very low LDL-C levels.

154 In adulthood, gonadal hormones, including both androgens and estrogens

155 itary males independent of pheromonal input, gonadal hormones, opponents, or social context.

156 s were not the consequence of the actions of gonadal hormones, we induced gonadal sex reversal to alt

157 al to hippocampal function and influenced by gonadal hormones.

158 pe are caused by the differential effects of gonadal hormones.

159 ary-adrenal (HPA) and hypothalamic-pituitary-gonadal (HPG) axes in underlying some of these complex i

160 e, which inhibits the hypothalamic-pituitary-gonadal (HPG) axis and reduces both testosterone and LH

161 s associated with the hypothalamic-pituitary-gonadal (HPG) axis in female fathead minnows, specifical

162 The hypothalamic-pituitary-gonadal (HPG) axis is a key biological system required f

163 The hypothalamic-pituitary-gonadal (HPG) axis is a prime candidate for adaptive pla

164 al pathway within the hypothalamic-pituitary-gonadal (HPG) axis is profoundly influenced by neonatal

165 ral components of the hypothalamic-pituitary-gonadal (HPG) axis.

166 itary development and hypothalamic-pituitary-gonadal (HPG) function in adulthood.

167 h have focused on the hypothalamic-pituitary-gonadal (HPG)-axis and reproduction, but other effects h

168 nt, suggesting that sex hormones act via the gonadal-hypophyseal axis.

169 Gonadal intact Dmp1-ERalpha(-/-) female mice had no sign

170 rce of niche Dpp, but instead is required in gonadal intermingled cells (ICs, the progenitor cells of

171 riptional analysis of hypothalamic-pituitary-gonadal-liver axis revealed negligible effects.

172 ssociated with embryonic testis development, gonadal loss of Fog2 resulted in an early partial block

173 We show that gonadal macrophages are derived from primitive yolk-sac

174 global sex determination gene tra-1 and the gonadal masculinizing gene fkh-6, but mutagenesis of a s

175 rmal tissue remodeling to gain access to the gonadal mesoderm and are unable to migrate through intac

176 both in delivering germ cells to the somatic gonadal mesoderm, and in specifying the niche where thes

177 eract while PGCs are en route to the somatic gonadal mesoderm, and previous studies have shown that C

178 e in an identical manner to vertebrate aorta-gonadal-mesonephros (AGM) HSCs.

179 to detect germ cell-specific expression from gonadal microarray data.

180 The embryonic gonadal microenvironment has recently been shown to dete

181 zyme DAF-36, HSD-1 is dispensable for proper gonadal migration and lifespan extension induced by germ

182 abolished in mutants, indicating a defective gonadal negative feedback control.

183 Somatic gonadal niche cells control the survival, differentiatio

184 fore, defines a secondary role for planarian gonadal niche cells in promoting GSC differentiation.

185 atic chimeras and stem cell competitions for gonadal niches.

186 ion analysis in isolated adipocytes from the gonadal pad of Pparg2-KO mice in 2 different backgrounds

187 onversely, alcohol drinking was predicted by gonadal phenotype independent of sex chromosome compleme

188 with biological effects on metamorphosis and gonadal phenotypes, respectively, that were observed in

189 de-differentiate toward their common adrenal-gonadal precursor cell type.

190 involving the fusion of clusters of somatic gonadal precursor cells (SGPs) and their ensheathment of

191 o form a gonad, germ cells (GCs) and somatic gonadal precursor cells (SGPs) must migrate to the corre

192 primordial germ cells (PGCs) towards somatic gonadal precursor cells (SGPs).

193 Somatic gonadal precursor cells and germ cells fail to prolifera

194 e hub, but development of CySCs from somatic gonadal precursors (SGPs) was not examined.

195 sets differential cell affinity for somatic gonadal precursors to specify stromal intermingled cells

196 ments dihydrotestosterone synthesis from non-gonadal precursors.

197 d PGCs and captured time-lapse movies as the gonadal primordium formed.

198 Dmrt1 is expressed in the genital ridge (the gonadal primordium) in both sexes and then becomes testi

199 , which localizes adjacent to the developing gonadal primordium, is required to prevent the SGPs from

200 genetic events that lead to formation of the gonadal primordium, we generated transgenic strains to l

201 The simple Caenorhabditis elegans gonadal primordium, which contains two somatic gonad pre

202 from WT1(+) somatic progenitor pools in the gonadal primordium.

203 vidual treatment exposure assessment such as gonadal radiation doses.

204 g of beta-catenin and variable expression of gonadal receptors and both CYP11B1 and CYP11B2.

205 The molecular expression of CYP11B2 and gonadal receptors in adenomas were also explored.

206 way, and expressed LHCGR and GNRHR, encoding gonadal receptors, at levels that were more than 100 tim

207 ich up-regulated dio3 expression and induced gonadal regression.

208 product of which plays an important role in gonadal responsiveness to FSH.

209 Expression of Sry in the gonadal ridge activates a Sox9-dependent gene regulatory

210 Germ cell migration to the embryonic gonadal ridge is unimpaired in brca2(Q658X) homozygotes;

211 in a cellular model of the rat embryonic XY gonadal ridge) was reduced by 2-fold relative to wild-ty

212 ertoli cell differentiation in the embryonic gonadal ridge, is initiated by SRY, a Y-encoded architec

213 the differential effects of male and female gonadal secretions (commonly referred to as sex hormones

214 cs" mixture during embryonic days 8 to 14 of gonadal sex determination and the incidence of adult ons

215 distinct between germ cells at the onset of gonadal sex determination at embryonic day 13 (E13) and

216 an F0 gestating female rat during embryonic gonadal sex determination, the F1 and F3 generation prog

217 3) following ancestral exposure during fetal gonadal sex determination.

218 ns following ancestral exposure during fetal gonadal sex determination.

219 ar, the thermosensitive genetic triggers for gonadal sex differentiation are largely unknown.

220 ally dimorphic expression pattern, preceding gonadal sex differentiation, and is capable of respondin

221 the best candidate master regulator of avian gonadal sex differentiation.

222 embryonic expression, preceding the onset of gonadal sex differentiation.

223 ne (ESR2) polymorphism rs2978381, one of two gonadal sex hormone genes, significantly mitigate the ne

224 Female gonadal sex hormones are responsible for this sexual dim

225 ctively, these studies establish that female gonadal sex hormones underlie the sexual dimorphic diffe

226 , and competing regulatory networks maintain gonadal sex long after the fetal choice between male and

227 onism between Dmrt1 and Foxl2 for control of gonadal sex may therefore extend beyond mammals.

228 hat mice lacking Gadd45gamma also exhibit XY gonadal sex reversal caused by disruption to Sry express

229 Gonadal sex reversal did not alter the sexually dimorphi

230 of the kinase MAP3K4 causes mouse embryonic gonadal sex reversal due to reduced expression of the te

231 the actions of gonadal hormones, we induced gonadal sex reversal to alter the hormonal environment o

232 arrying a Cys342Tyr substitution displays XY gonadal sex reversal with variable expressivity.

233 ng both p38alpha and p38beta also exhibit XY gonadal sex reversal.

234 DMRT1 also maintains male gonadal sex: its loss, even in adults, can trigger sexua

235 Somatic gonadal sheath cell interaction is necessary for INX-14

236 secreted VPR-1 MSPd acts at least in part on gonadal sheath cell precursors in L1 to early L2 stage h

237 ling, protein kinase A (PKA), is required in gonadal sheath cells for oocyte meiotic maturation and d

238 neurons into the brain, resulting in reduced gonadal size.

239 at expresses Neo controlled by the zebrafish gonadal soma derived factor (gsdf) promoter.

240 First, gonadal somatic cell-targeting Amhr2-Cre mice were cross

241 Yb is specifically expressed in gonadal somatic cells and regulates piwi in somatic nich

242 for transplantation of PGCs aggregated with gonadal somatic cells and showed that reconstituted ovar

243 ctivation of p38 MAPK signaling in embryonic gonadal somatic cells for testis determination in the mo

244 fficient to promote a male identity in adult gonadal somatic cells suggests that the sexual identity

245 demonstrate the presence of a functional non-gonadal somatic piRNA pathway in the adult fat body that

246 cells outside the gonads, the role of a non-gonadal somatic piRNA pathway is not well characterized.

247 This defense system acts in germline and gonadal somatic tissue to preserve germline development.

248 Declines in the gonadal-somatic index (GSI) and increased mortality were

249 However, this was dependent on the gonadal status of the male housing partner, since those

250 eing paired with a male, irrespective of his gonadal status, increased female weight.

251 that Drosophila p53 is selectively active in gonadal stem cells after exposure to stressors that dest

252 reproductive axis is primarily regulated by gonadal steroid and circadian cues, but the starvation-s

253 n regressed oviducts (P<0.001) demonstrating gonadal steroid control, typical of an oviduct and egg s

254 Severe gonadal steroid deficiency induces bone loss in adult me

255 s, uncovering of X chromosome mutations, and gonadal steroid deficiency may all contribute to altered

256 Part of the sex difference, but not the gonadal steroid dependence, resulted from differential p

257 ostaglandin signal to mate and show that the gonadal steroid DHP modulates mRNA levels of the putativ

258 In mice, we used gonadectomy to eliminate gonadal steroid hormone-dependent expression of AVP in t

259 male mice after castration is independent of gonadal steroid hormones and their receptors; thus, we h

260 Circulating gonadal steroid hormones are thought to modulate a wide

261 Because BDNF and gonadal steroid hormones conjointly influence neuronal g

262 ss, nutrition, and seasonal cues, as well as gonadal steroid hormones.

263 , the investigation into sex differences and gonadal steroid modulation of sleep and biological rhyth

264 serelin acetate, which suppresses endogenous gonadal steroid production, and were randomized to treat

265 g season is driven, at least in part, by the gonadal steroid testosterone.

266 er observed that exogenous RFRP-3 suppresses gonadal steroidogenesis and mating behavior in NMRs give

267 Examination of adrenal and gonadal steroidogenesis showed no defects in Tspo(-/-) m

268 on/development in NMRs, we quantified plasma gonadal steroids and GnRH-1- and kisspeptin-immunoreacti

269 sleep are also reported to be independent of gonadal steroids and may involve sex chromosome compleme

270 Adrenal and gonadal steroids are essential for life and reproduction

271 While gonadal steroids delivered via circulation can affect be

272 ges are influenced by changes in circulating gonadal steroids during development.

273 We found that a primary effect of gonadal steroids in the highly sexually dimorphic preopt

274 Gonadal steroids modulate CNS plasticity, including phre

275 We examined here whether gonadal steroids modulated the excitability of kisspepti

276 Pharmacological inhibition of Dnmts mimicked gonadal steroids, resulting in masculinized neuronal mar

277 ale sexual behavior is highly dependent upon gonadal steroids, sexual behavior in a large proportion

278 RH pulsatile secretion, negative feedback by gonadal steroids, the onset of puberty, and the ovulator

279 lopment and low circulating levels of LH and gonadal steroids.

280 n on POP-1 by recruiting it to male-specific gonadal target genes.

281 in 3-week-old Mrp4(-/-) mice, disruption of gonadal testosterone production up-regulates hepatic Cyp

282 atic bud initiation lags behind the onset of gonadal testosterone synthesis by about three days.

283 androgen deprivation therapy by depletion of gonadal testosterone.

284 ation and corrected the abnormalities in the gonadal, thyroid, growth hormone, and adrenal axes.

285 Cryopreservation and transplantation of gonadal tissue in both males and females remains experim

286 If gonadal tissue is spared-as in somatic genomic mosaicism

287 steroids, steroidogenic enzyme inhibitors or gonadal tissue itself.

288 duces robust wasting of adipose, muscle, and gonadal tissues that are distant from the tumor, phenoty

289 dhesion system that connects the uterine and gonadal tissues through their juxtaposed BMs at the site

290 pregnenolone, is synthesized in adrenal and gonadal tissues to initiate steroid synthesis by catalyz

291 In gonadal tissues, the Piwi-interacting (piRNA) pathway pr

292 oson regulation in both germline and somatic gonadal tissues.

293 omparative evaluation of long-term renal and gonadal toxicity is crucial to decisions regarding futur

294 of HL provides well-grounded information on gonadal toxicity of currently used treatment regimens an

295 both germ cells and somatic cells complicate gonadal transcriptome studies.

296 mal ovarian phenotype but with a "male-like" gonadal transcriptome.

297 Further, most neomales had gonadal transcriptomes similar to that of regular males.

298 I-III ovarian, I-II extragonadal, or stage I gonadal tumors with subsequent recurrence) received thre

299 s, hematologic malignancies, carcinomas, and gonadal tumors.

300 FD) gained 56% less body weight and 74% less gonadal white adipose tissue (WAT) than WT mice.

301 t VEGFA expression was lower in inguinal and gonadal white adipose tissues of ESR1 total body knockou