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1 ne epithelium, and female UtEpialphaERKO are infertile.
2 orn and grow normally but are reproductively infertile.
3 t for members of the CatSper gene family are infertile.
4 anulosa cell tumors that renders the animals infertile.
5 but all PTM-ARKO males were azoospermic and infertile.
6 n-Crtc1(-/-) mice are hyperphagic, obese and infertile.
7 ant mice were phenotypically normal but were infertile.
8 of mice expressing the hypomorphic allele is infertile.
9 ps per month, Bmp2d/d females are completely infertile.
10 sequently, the Ant4-deficient male mice were infertile.
11 ient in both AtATM and AtNBS1 are completely infertile.
12 wever, both males and females are completely infertile.
13 have normal fertility, Tpst2(-/-) males are infertile.
14 The female C/EBPbeta-null mice are infertile.
15 tic fringe null female mice were found to be infertile.
16 ts in meiotic chromosome segregation and are infertile.
17 action of adult "escapers" that are weak and infertile.
18 protein results in mice that are healthy but infertile.
19 in, and all of these high-titer monkeys were infertile.
20 eriod were hyperphagic, obese, diabetic, and infertile.
21 s observed only when cases were concurrently infertile.
22 le and grossly normal, Zar1(-/-) females are infertile.
23 tility, yet CatSper2-/- males are completely infertile.
24 and immune deficient, and mutant males were infertile.
25 le and female Ercc1-deficient mice were both infertile.
26 Cpe(fat/fat) mice are obese, diabetic, and infertile.
27 6-deficient males surviving to maturity were infertile.
28 e and found that homozygous mutant males are infertile.
29 ficient mice, and some of the male mice were infertile.
30 show progressive motility and male mice were infertile.
31 esults in Man2a2 null males that are largely infertile.
32 gic, cold intolerant, insulin resistant, and infertile.
33 ice lacking VDAC3 are healthy, but males are infertile.
34 HDLs, ovulate dysfunctional oocytes, and are infertile.
35 y the NHE3 knockout and alpha ERKO mice were infertile.
36 ritestin (ADAM 3) and found mutant males are infertile.
37 ry, have low levels of progesterone, and are infertile.
38 nd approximately 60% of Tnp1-null males were infertile.
39 ause mice lacking PR fail to ovulate and are infertile.
40 exception that males, but not females, were infertile.
41 id of Cdk4 are viable, but small in size and infertile.
42 ormal reproductive tract development but are infertile.
43 ctasia and Atm-deficient mice are completely infertile.
44 tm/tm)) do not form a zona pellucida and are infertile.
45 ngle disrupted zona gene lack a zona and are infertile.
46 tdh knock-out mice are viable, but males are infertile.
47 ble to conceive after a year and are labeled infertile.
48 ts receptor fail to complete puberty and are infertile.
49 ons that inactivate kisspeptin signaling are infertile.
50 Mice deficient in this Fue homologue are infertile.
51 t (Lep(ob/ob)) mice are obese, diabetic, and infertile.
53 ring asexual development in both fertile and infertile adults, and was also enriched in a population
57 the transgene in the gonads and the mice are infertile, allowing examination of the function of BRCA2
58 ations in both GSL1 and GSL5 rendered pollen infertile, although such a chromosome could be transmitt
61 Smad5 Smad8 conditional knockout mice become infertile and develop metastatic granulosa cell tumors.
63 cking the transcription factor C/EBPbeta are infertile and display markedly reduced estrogen (E)-indu
64 at male mice with a null mutation in Hrb are infertile and display round-headed spermatozoa that lack
66 ce deficient in the tyrosine kinase cSrc are infertile and exhibit improper cauda epididymis developm
70 d obesity (DIO) wild-type (DIO-WT) mice were infertile and experienced increased circulating testoste
74 hin populations of single spermatocytes from infertile and fertile men who reported for assisted repr
78 termined that Akita homozygous male mice are infertile and have reduced testis size and abnormal morp
81 nitis biovar of Chlamydia trachomatis became infertile and sustained high rates of hydrosalpinx forma
83 ing the sperm tail-specific CATSPERdelta are infertile and their spermatozoa lack both Ca(2+) current
85 of full-length ERalpha, renders the animals infertile, and inhibits the induction of female sexual b
86 ce homozygous null for alpha2(alpha2-/-) are infertile, and spermatogenesis is disrupted at mid- or l
92 s of the N-end rule proteolytic pathway, are infertile associated with meiotic arrest at prophase I.
94 Female mice lacking TAFII105 are viable but infertile because of a defect in folliculogenesis correl
96 this protein are viable, but female mice are infertile because of complete failure of mature follicle
98 bly, adult FOXA2-deleted mice are completely infertile because of defects in blastocyst implantation
99 Similar to Pgr null mice, Pgr null rats were infertile because of deficits in sexual behavior, ovulat
100 Male mice deficient in Spem1 were completely infertile because of deformed sperm characterized by a b
101 meric and heterozygous males were completely infertile because of disrupted spermiogenesis characteri
102 eletion ofMsxgenes (Msx1(d/d)/Msx2(d/d)) are infertile because of implantation failure associated wit
106 These pseudohermaphrodites are frequently infertile because sperm passage is blocked by the presen
107 normal number of oocytes but were completely infertile, because ovulated oocytes were arrested at the
111 Vglut2-ires-Cre;Esr1(lox/lox) mice were also infertile but displayed a wider range of deficits, inclu
117 who were previously thought to be hopelessly infertile, but who are now able to conceive their own bi
118 e initially fertile, Taf4b-null males become infertile by 3 mo of age and eventually exhibit seminife
119 gressive dominants render their subordinates infertile by inducing chronic physiological "stress." Ho
120 diment infilling, croplands will be rendered infertile by salt, and water scarcity will pit growing d
122 ording ionic currents from spermatozoa of an infertile CatSper-deficient patient, we demonstrate that
123 e induces fertilizing capacity in sperm from infertile CatSper1 (Ca(2+) channel), Adcy10 (soluble ade
124 M2 (fertilin beta) or ADAM3 (cyritestin) are infertile; cauda epididymal sperm (mature sperm) from th
125 arf8 double-null mutant flowers arrested as infertile closed buds with short petals, short stamen fi
128 nfertility who did not have tubal occlusion (infertile controls) and 584 primigravid women (pregnant
129 lving the women with tubal occlusion and the infertile controls, the odds ratio for tubal occlusion a
130 cimens from each of the male partners in 765 infertile couples and 696 fertile couples at nine sites.
134 ouse and human embryos, embryos from fertile/infertile couples, and following growth factor supplemen
135 utinely used to evaluate the male partner in infertile couples, sperm measurements that discriminate
137 so observed between embryos from fertile and infertile couples, which were largely equalized in respo
144 om the retroposition from its parental gene, Infertile crescent (Ifc), and integrated into heterochro
148 ntation of spermatogonial stem cells from an infertile donor to a permissive testicular environment c
154 dditionally, the homozygous male mutants are infertile due to azoospermia, a condition that was not a
155 cKO males sired up to two litters but became infertile due to collapse of spermatogenesis and loss of
157 le, the homozygous males unexpectedly proved infertile due to defective spermatogenesis, which was ev
162 r, these mice are growth retarded, males are infertile due to meiotic failure, and the mammary gland
163 Prolactin receptor knockout females are infertile due to multiple reproductive defects, but epit
166 sequences lead to the production of flaccid, infertile eggs with a soluble, rather than insoluble, vi
168 risingly, in spite of the fact that they are infertile, ERKO mice showed normal motivation to mount f
169 rred in mountainous regions due to abandoned infertile farmland, secondary succession, and government
171 d from these conditions were all found to be infertile fish that possessed minimally-developed gonads
172 mmersion is an effective strategy to produce infertile fish without introducing transgenic modificati
175 te, randomized trial, 666 women who had been infertile for more than 1 year and were scheduled to und
177 stological evaluation of the testes from the infertile group showed variable degrees of Leydig cell h
178 The median of the lower allele size in the infertile group was only 2.5 kb compared with 3.4 kb in
179 nomics program at The Jackson Laboratory are infertile, have low epididymal sperm concentrations, and
180 uction of diploid males that are inviable or infertile, imposing a high cost on matings between close
182 eduction in testicular Usp14 levels and were infertile, indicating that Usp14 is required for develop
183 unmodified centrioles, engaged or not, were "infertile," indicating that engagement specifically bloc
184 entially clinically important for asthmatic, infertile individuals and society because treatment of t
185 leles whose interaction produces inviable or infertile interspecific hybrids but does not reduce fitn
186 Consistent with this notion, 12 PEGs in the infertile interspecific hybrids matched MEGs in fertile
187 ting (W), to determine if stem cells from an infertile male were capable of generating spermatogenesi
189 ion, the diagnosis should be suspected in an infertile male with oligospermia or azoospermia with low
192 te future mapping of deletion breakpoints in infertile males and elucidation of mechanisms behind fre
193 Because of these severe abnormalities, these infertile males presented with diaphragmatic hernias, he
195 Instead, brca2(Q658X) homozygotes develop as infertile males with meiotic arrest in spermatocytes.
199 valence of Y-chromosome microdeletions among infertile men and to correlate the clinical presentation
201 were collected from 35 healthy donors and 35 infertile men at the Andrology laboratory from August 20
202 smission to the offspring of these otherwise infertile men conceived using an assisted reproductive t
203 berrations in testicular tissue samples from infertile men confirmed to have impaired spermatogenesis
204 ns relevant to immune infertility, sera from infertile men containing antisperm antibodies (ASA) were
208 <0.05) and mRNA (P<0.05) in spermatozoa from infertile men were significantly lower than those from f
212 chemical and biophysical changes in HSF from infertile men with spinal cord injury compared to age-ma
213 xtensive overlap between the fertile and the infertile men within both the subfertile and the fertile
216 te that TAS1R3 and GNAT3 activators may help infertile men, particularly those that are affected by s
217 protamine-2 have been identified in sperm of infertile men, suggesting that our results may have clin
228 tic mutant Mei1 was isolated in a screen for infertile mice descended from chemically mutagenized emb
229 r pituitary of fertile mice lacking Ink4c or infertile mice doubly deficient for Ink4c and Ink4d prod
233 que of spermatogonial transplantation in two infertile mouse strains, Steel (Sl) and dominant white s
234 changes in the reproductive cycle in obese, infertile ob/ob mice with no circulating leptin and infe
235 le ob/ob mice with no circulating leptin and infertile, obese, agouti (Ay/a) mice with high circulati
236 d9(-/-) and Izumo1(-/-) mice are healthy but infertile or severely subfertile due to defective sperm-
237 Atm-deficient mice are viable but completely infertile, our studies suggest that the Rad51 assembly d
239 yos, whereas UBR2(-/-) males were viable but infertile, owing to the postnatal degeneration of the te
240 e-transcription PCR on spermatozoal RNA from infertile patients with wide-ranging sperm concentration
241 les (22-54 years; 44 fertile controls and 27 infertile patients), along with total levels and localis
244 onderance of patients with varicocele in the infertile population leads to the search for causality a
245 ogesterone receptor knockout (PRKO) mice are infertile primarily due to ovulatory failure and lack th
247 the transduced stem cells into the testes of infertile recipient mice, approximately 4.5% of progeny
248 of spermatogenesis upon transplantation into infertile recipient testes, were present almost exclusiv
251 eceptor -- we show that Ep2(-/-) females are infertile secondary to failure of the released ovum to b
255 attributed to either explosive radiation on infertile soils under fire-prone, summer-dry climates or
257 ockout parasites with a male-deficient, self-infertile strain of P. berghei, which restored fertility
261 ls from infertile Sl/Sld mutant male mice to infertile W/Wv or Wv/W54 mutant male mice restored ferti
262 Although Prl receptor (PrlR)-null mice are infertile, we were able to maintain pregnancies in a few
267 ransgenic males that either kills or renders infertile wild-type female recipients and an antidote ex
270 h2-/- mice are microphallic, hypogonadal and infertile with alterations in circulating gonadotropins,
272 with a high level of mutant germ cells were infertile with low sperm counts and a high frequency of
275 are small, hypermetabolic, hyperactive, and infertile, with markedly reduced leptin levels and fat s
276 mice in which Csnk2a2 has been disrupted are infertile, with oligospermia and globozoospermia ('round
279 PAG1 antibodies derived from the serum of an infertile woman were reported to cause sperm agglutinati
280 from the peripheral blood lymphocytes of an infertile woman who exhibited high sperm-immobilizing an
282 d obesity in different PCOS phenotypes among infertile women (n = 213), of whom 159 had PCOS and 54 w
285 er was similar to the US national mean among infertile women of a similar age undergoing in vitro fer
286 ce serum antibody titers were recorded among infertile women seen at St. Michael's Hospital in Bristo
287 in 27 hospitals in the Netherlands in which infertile women who were undergoing hysterosalpingograph
288 d the pregnancy rate in overweight and obese infertile women who were undergoing in vitro fertilizati
290 re female germ cells for future treatment of infertile women with a diminishing ovarian reserve and f
291 ts could provide a new treatment regimen for infertile women with low responses to the traditional go
293 rior to metformin in achieving live birth in infertile women with the polycystic ovary syndrome, alth
295 orylation of STAT3 in eutopic endometrium of infertile women with this disorder leading to over-expre
296 on 3347 consecutive treatment cycles in 1494 infertile women, 441 of which resulted in pregnancy.
298 ncidence of high-order multiple pregnancy in infertile women, though only to a limited extent and at
300 k of formation of the outer segment, whereas infertile wpk males developed spermatids with very short
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