https://novaprd-lb.newcastle.edu.au/vital/access/manager/Index ${session.getAttribute("locale")} 5 https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:53876 Wed 28 Feb 2024 15:19:00 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:50480 Wed 28 Feb 2024 15:16:01 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:45249 Wed 26 Oct 2022 19:43:42 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:45260 Wed 26 Oct 2022 18:02:18 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:42962 Wed 22 Feb 2023 17:05:53 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:44188 Wed 19 Apr 2023 14:52:52 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:51036 Wed 16 Aug 2023 10:16:23 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17021 Wed 11 Apr 2018 17:14:33 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:15648 Wed 11 Apr 2018 17:00:24 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:27033 Xenopus and is expressed during ovarian development in Drosophila. In mammals Musashi is important for spermatogenesis and male fertility, but its role in the ovary has yet to be characterized. In this study we determined the expression of mammalian Musashi proteins MSI1 and MSI2 during mouse folliculogenesis, and through the use of a MSI2-specific knockout mouse model we identified that MSI2 is essential for normal follicle development. Time-course characterization of MSI1 and MSI2 revealed distinct differences in steady-state mRNA levels and protein expression/localization at important developmental time-points during folliculogenesis. Using a gene-trap mouse model that inactivates Msi2, we observed a significant decrease in ovarian mass, and change in follicle-stage composition due to developmental blocking of antral stage follicles and pre-antral follicle loss through atresia. We also confirmed that hormonally stimulated Msi2-deficient mice produce significantly fewer MII oocytes (60.9% less than controls, p < 0.05). Furthermore, the majority of these oocytes are of poor viability (62.2% non-viable/apoptotic, p < 0.05), which causes a reduction in female fertility evidenced by decreased litter size in Msi2-deficient animals (33.1% reduction to controls, p < 0.05). Our findings indicate that MSI1 and MSI2 display distinct expression profiles during mammalian folliculogenesis and that MSI2 is required for pre-antral follicle development.]]> Wed 11 Apr 2018 16:39:10 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:16815 fl/fl with Zp3-cre+ mice, or in ovarian granulosa cells and uterine stroma by crossing with Amhr2-Cre+ mice. Surprisingly, deletion of STAT3 in oocytes had no effect on fertility indicating that the abundance of STAT3 protein in maturing oocytes and fertilized zygotes is not essential to these developmental stages. In Stat3^fl/fl;Amhr2-cre+ females impaired fertility was observed through significantly fewer litters and smaller litter size. Ovulation rate, oocyte fertilization and development to blastocyst were unaffected in this line; however, poor recombination efficiency in granulosa cells had yielded no net change in STAT3 protein abundance. In contrast, uteri from these mice showed STAT3 protein depletion selectively from the stomal compartment. A significant reduction in number of viable fetuses on gestational day 18, increased fetal resorptions and disrupted placental morphology were evident causes of the reduced fertility. In conclusion, this study defines an important role for STAT3 in uterine stromal cells during embryo implantation and the development of a functional placenta.]]> Wed 11 Apr 2018 15:06:51 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:30985 Wed 11 Apr 2018 14:34:15 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14944 Wed 11 Apr 2018 14:30:16 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:15133 Wed 11 Apr 2018 14:23:25 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:4594 Wed 11 Apr 2018 14:21:05 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:26301 Wed 11 Apr 2018 14:11:17 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:20977 TM), approved by the U.S. Food and Drug Administration for the treatment of adult basal cell carcinoma. In this perspective we outline the current state of Hh pathway inhibitors with a particular focus on potential limitations of upstream Hh pathway inhibition in relation to resistance mutations and crosstalk pathways. Together, these limitations indicate that inhibition of downstream components, specifically the Gli family of transcription factors, may represent a next generation approach to suppress tumours associated with aberrant Hh pathway signalling. © 2014 The Royal Society of Chemistry.]]> Wed 11 Apr 2018 14:10:20 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:27762 in vitro fertilization (IVF) success. Furthermore, reduced expression of HSPA2 from the human sperm proteome leads to an impaired capacity for cumulus matrix dispersal, sperm-egg recognition and fertilization following both IVF and ICSI. In this review, we consider the evidence supporting the role of HSPA2 in sperm function and explore the potential mechanisms by which it is depleted in the spermatozoa of infertile patients. Such information offers novel insights into the molecular mechanisms governing sperm function.]]> Wed 11 Apr 2018 13:54:40 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:15689 Wed 11 Apr 2018 13:43:52 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:26480 Wed 11 Apr 2018 13:21:00 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:2442 Wed 11 Apr 2018 12:48:34 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:15105 Wed 11 Apr 2018 12:24:43 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:30804 Wed 11 Apr 2018 12:10:05 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:27739 Wed 11 Apr 2018 11:56:44 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:30207 350 microRNAs (miRNAs), a developmentally important sRNA class, the majority (~60%) of which are also represented by the miRNA signature of spermatozoa. This includes >50 miRNAs that were found exclusively in epididymal sperm and epididymosomes, but not in the surrounding soma. We also documented substantial changes in the epididymosome miRNA cargo, including significant fold changes in almost half of the miRNAs along the length of the epididymis. Finally, we provide the first direct evidence for the transfer of several prominent miRNA species between mouse epididymosomes and spermatozoa to afford novel insight into a mechanism of intercellular communication by which the sRNA payload of sperm can be selectively modified during their post-testicular maturation.]]> Wed 11 Apr 2018 11:13:04 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:28064 Wed 11 Apr 2018 09:24:57 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:33905 Tnfa, mitogen-activated protein kinase 8 (Mapk8/Jnk1), and growth differentiation factor 9 (Gdf9) (P < 0.05). Mass spectrometry and cell signaling pathway analysis indicated upregulation of cellular pathways associated with acute phase signaling, and cellular survival and assembly. Apoptosis assessed by terminal deoxynucleotidyl transferase dUTP nick end labeling indicated significantly increased positive staining in the ovaries of LPS-treated neonates. These findings suggest that increased proinflammatory signaling within the neonatal ovary may be responsible for the LPS-induced depletion of the primordial follicle pool. These findings also have implications for female reproductive health, as the ovarian reserve is a major determinate of female reproductive longevity.]]> Wed 09 Feb 2022 15:58:52 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:30359 Wed 04 Sep 2019 09:47:44 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:45607 Wed 02 Nov 2022 14:14:14 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:27738 Tue 26 Feb 2019 13:24:45 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:35834 Kifc1 and Kifc5b, in aged oocytes; family members selectively targeted for expression regulation by endo-siRNAs of elevated abundance. The implications of reduced Kifc1 and Kifc5b expression were explored using complementary siRNA-mediated knockdown and pharmacological inhibition strategies, both of which led to increased rates of aneuploidy in otherwise healthy young oocytes. Collectively, our data raise the prospect that altered sRNA abundance, specifically endo-siRNA abundance, could influence the quality of the aged oocyte.]]> Tue 10 Dec 2019 16:34:23 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:34061 Tue 05 Feb 2019 14:14:54 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:43897 Tue 04 Oct 2022 13:59:41 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:34016 Thu 30 May 2019 15:47:52 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:34014 Thu 30 May 2019 15:41:20 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:38608 Chlamydia is the most common sexually transmitted bacterial pathogen worldwide. Male and female infections occur at similar rates and both cause serious pathological sequelae. Despite this, the impact of chlamydial infection on male fertility has long been debated, and the effects of paternal chlamydial infection on offspring development are unknown. Using a male mouse chronic infection model, we show that chlamydial infection persists in the testes, adversely affecting the testicular environment. Infection increased leukocyte infiltration, disrupted the blood:testis barrier and reduced spermiogenic cell numbers and seminiferous tubule volume. Sperm from infected mice had decreased motility, increased abnormal morphology, decreased zona-binding capacity, and increased DNA damage. Serum anti-sperm antibodies were also increased. When both acutely and chronically infected male mice were bred with healthy female mice, 16.7% of pups displayed developmental abnormalities. Female offspring of chronically infected sires had smaller reproductive tracts than offspring of noninfected sires. The male pups of infected sires displayed delayed testicular development, with abnormalities in sperm vitality, motility, and sperm-oocyte binding evident at sexual maturity. These data suggest that chronic testicular Chlamydia infection can contribute to male infertility, which may have an intergenerational impact on sperm quality.]]> Thu 18 Nov 2021 11:59:22 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:43352 Thu 15 Sep 2022 15:32:31 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:43344 Thu 15 Sep 2022 15:19:01 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:19748 Thu 13 Aug 2015 09:19:17 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:32118 Thu 03 May 2018 12:11:55 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:32117 Thu 03 May 2018 12:04:54 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:30490 Thu 03 Feb 2022 12:19:24 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:30367 Thu 03 Feb 2022 12:18:59 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:29938 Thu 03 Feb 2022 12:18:20 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:8095 Sat 24 Mar 2018 08:39:59 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:7505 Sat 24 Mar 2018 08:38:29 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:7044 Sat 24 Mar 2018 08:37:51 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:8504 Sat 24 Mar 2018 08:36:25 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:9651 Sat 24 Mar 2018 08:35:26 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:1294 Sat 24 Mar 2018 08:32:44 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:1079 Sat 24 Mar 2018 08:32:08 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:1851 Sat 24 Mar 2018 08:31:16 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:1595 Sat 24 Mar 2018 08:30:41 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:908 Sat 24 Mar 2018 08:30:00 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:987 Sat 24 Mar 2018 08:29:49 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:3072 Sat 24 Mar 2018 08:29:16 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:1163 Sat 24 Mar 2018 08:28:42 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:1172 Sat 24 Mar 2018 08:28:29 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:2473 Sat 24 Mar 2018 08:27:46 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:13040 Sat 24 Mar 2018 08:16:38 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:11322 Sat 24 Mar 2018 08:12:34 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:11354 Sat 24 Mar 2018 08:08:14 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:21584 Sat 24 Mar 2018 08:00:44 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:21158 FZR1 activity in the male germline led to both a mitotic and a meiotic testicular defect resulting in infertility due to the absence of mature spermatozoa. Spermatogonia in the prepubertal testes of such mice had abnormal proliferation and delayed entry into meiosis. Although early recombination events were initiated, male germ cells failed to progress beyond zygotene and underwent apoptosis. Loss of APC/C^FZR1 activity was associated with raised cyclin B1 levels, suggesting that CDK1 may trigger apoptosis. By contrast, female FZR1Δ mice were subfertile, with premature onset of ovarian failure by 5 months of age. Germ cell loss occurred embryonically in the ovary, around the time of the zygotene-pachytene transition, similar to that observed in males. In addition, the transition of primordial follicles into the growing follicle pool in the neonatal ovary was abnormal, such that the primordial follicles were prematurely depleted. We conclude that APC/C^FZR1 is an essential regulator of spermatogonial proliferation and early meiotic prophase I in both male and female germ cells and is therefore important in establishing the reproductive health of adult male and female mammals.]]> Sat 24 Mar 2018 08:00:18 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:19602 Sat 24 Mar 2018 07:58:23 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17664 Sat 24 Mar 2018 07:57:48 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17663 Sat 24 Mar 2018 07:57:48 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17662 Sat 24 Mar 2018 07:57:47 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:17701 Sat 24 Mar 2018 07:57:31 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:20640 Sat 24 Mar 2018 07:55:44 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:20695 Sat 24 Mar 2018 07:55:41 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:20323 Sat 24 Mar 2018 07:55:12 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:20166 Sat 24 Mar 2018 07:51:44 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:18819 Sat 24 Mar 2018 07:51:08 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:27976 50 = 6.7 nM) led to a significant reduction in dynamin phosphorylation (10.3% vs. 27.3%; P < 0.001), acrosomal exocytosis (9.7% vs. 25.7%; P < 0.01), and in vitro fertilization (53% vs. 100%; P < 0.01). GSK3 was shown to be present in developing germ cells where it colocalized with dynamin in the peri-acrosomal domain. However, additional GSK3 was acquired by maturing mouse spermatozoa within the male reproductive tract, via a novel mechanism involving direct interaction of sperm heads with extracellular structures known as epididymal dense bodies. These data reveal a novel mode for the cellular acquisition of a protein kinase and identify a key role for GSK3 in the regulation of sperm maturation and acrosomal exocytosis.—Reid, A. T., Anderson, A. L., Roman, S. D., McLaughlin, E. A., McCluskey, A., Robinson, P. J., Aitken, R. J., Nixon, B. Glycogen synthase kinase 3 regulates acrosomal exocytosis in mouse spermatozoa via dynamin phosphorylation.]]> Sat 24 Mar 2018 07:38:43 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:26158 Sat 24 Mar 2018 07:35:27 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:26416 Sat 24 Mar 2018 07:27:57 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:27749 Drosophila and also shown to be vital to sperm development and reproductive potential in the mouse. We focus in depth on the role and function of the vertebrate Musashi ortholog Musashi-1 (MSI1). Through detailed expression studies and utilizing our novel transgenic Msi1 testis-specific overexpression model, we have identified 2 unique RNA-binding targets of MSI1 in spermatogonia, Msi2 and Erh, and have demonstrated a role for MSI1 in translational regulation. We have also provided evidence to suggest that nuclear import protein, IPO5, facilitates the nuclear translocation of MSI1 to the transcriptionally silenced XY chromatin domain in meiotic pachytene spermatocytes, resulting in the release of MSI1 RNA-binding targets. This firmly establishes MSI1 as a master regulator of posttranscriptional control during early spermatogenesis and highlights the significance of the subcellular localization of RNA binding proteins in relation to their function.]]> Sat 24 Mar 2018 07:27:45 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:30867 H)-one based Hedgehog signalling pathway (HSP) inhibitors we have developed two new classes of HSP inhibitors based on: L-tryptophan and benzo[1,3]dioxol-5-ylmethyl-[2-(1H-indol-3-yl)-ethyl]-amine. Synthesis of focused compound libraries identified six _L-tryptophan based inhibitors, and two stimulators, of Gli at 10 μM compound concentration. 2,4-Dichloro-13 and indole 16 suppressed mRNA expression of Ptch₁ in Shh LIGHT2 cells, with 13 suppressing and 16 stimulating Gli₂ mRNA expression. Focused library development of the benzo[1,3]dioxol-5-ylmethyl-[2-(1H-indol-3-yl)-ethyl]-amine scaffold afforded two sub-micro molar potent inhibitors of Gli expression with 5-methoxy-1H-indole-2-carboxylic acid benzo[1,3]dioxol-5-ylmethyl-[2-(1H-indol-3-yl)-ethyl]-amide 29 and 5-chloro-1H-indole-2-carboxylic acid benzo[1,3]dioxol-5-ylmethyl-[2-(1H-indol-3-yl)-ethyl]-amide 30 returning IC₅₀ values of 0.5 and 0.24 μM, respectively. Neither 29 nor 30 acted directly on Smo with our data supporting inhibition of the HSP downstream of Smo.]]> Sat 24 Mar 2018 07:26:40 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:26537 95% of sperm. Anapparent molecular rearrangement in the complex occurs, bringing PRKACA and TCP11 into proximity. Taken together, these results suggest a role for the novel complex of SPIF, PRKACA, and TCP11 during spermcapacitation, fertilization, and embryogenesis.]]> Sat 24 Mar 2018 07:23:27 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:3443 Sat 24 Mar 2018 07:20:29 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:25153 Sat 24 Mar 2018 07:17:08 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:25107 Sat 24 Mar 2018 07:17:06 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:24140 Danio rerio and Xenopus laevis, the Tob1 gene is expressed from the one-cell stage through to early gastrula stages, followed in later development by discrete expression in many tissues including the notochord and somites. In both mouse and human, Tob1 is expressed in many adult tissues including the testis and ovary; however, the specific cell types are unknown. We examine Tob1 gene expression in mouse in developing germ cells and in sorted male germ cells (gonocytes, spermatogonia, pachytene spermatocytes and round spermatids) by reverse transcription and droplet digital polymerase chain reaction (RT-ddPCR) and in adult ovary and testis by immunofluorescence with anti-Tob1 protein staining. By RT-ddPCR, Tob1 expression was low in developing male germ cells but was highly expressed in round spermatids. In developing female germ cells undergoing entry into meiosis, it increased 10-fold. Tob1 was also highly expressed in round spermatids and in oocytes in all stages of folliculogenesis. Notably, a marker for P-bodies, Dcp-2, was also highly expressed in round spermatids and all oocyte stages examined. The cytoplasmic presence of Tob1 protein in round spermatids and oocytes and the association of Tob1 protein with Dcp2 in both cell types suggest that Tob1 protein plays a role in post-transcriptional mechanisms.]]> Sat 24 Mar 2018 07:16:33 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:24127 Sat 24 Mar 2018 07:16:32 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:21996 Sat 24 Mar 2018 07:14:33 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:22692 Kpna1, Kpna2, Kpna3, Kpna4, Kpna6, Kpna7, Kpnb1, Ipo5 and Xpo1), all were expressed in the embryonic ovary with up-regulation of protein levels concomitant with meiotic entry for KPNA2, accompanied by the redistribution of the cellular localisation of KPNA2 and XPO1. In contrast, postnatal folliculogenesis revealed significant up-regulation of Kpna1, Kpna2, Kpna4, Kpna6 and Ipo5 and down-regulation of Kpnb1, Kpna7 and Xpo1 at the primordial to primary follicle transition. KPNAs exhibited different localisation patterns in both oocytes and granulosa cells during folliculogenesis, with three KPNAs – KPNA1, KPNA2 and IPO5 – displaying marked enrichment in the nucleus by antral follicle stage. Remarkably, varied subcellular expression profiles were also identified in isolated pre-ovulatory oocytes with KPNAs KPNA2, KPNB1 and IPO5 detected in the cytoplasm and at the nuclear rim and XPO1 in cytoplasmic aggregates. Intriguingly, meiotic spindle staining was also observed for KPNB1 and XPO1 in meiosis II eggs, implying roles for KPNAs outside of nucleo-cytoplasmic transport. Thus, we propose that KPNAs, by targeting specific cargoes, are likely to be key regulators of oocyte development.]]> Sat 24 Mar 2018 07:11:11 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:46833 Mon 29 Jan 2024 18:41:10 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:37797 Mon 26 Apr 2021 12:23:37 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:44774 Mon 24 Oct 2022 09:03:57 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:32849 Mon 23 Sep 2019 13:04:11 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:46268 Mon 14 Nov 2022 15:06:53 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:47962 Mon 13 Feb 2023 15:03:17 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:42487 Chlamydia be found in the testes of infertile men? Summary Answer: Chlamydia can be found in 16.7% of fresh testicular biopsies and 45.3% of fixed testicular biopsies taken from a selection of infertile men. What is known already: Male chlamydial infection has been understudied despite male and female infections occurring at similar rates. This is particularly true of asymptomatic infections, which occur in 50% of cases. Chlamydial infection has also been associated with increased sperm DNA damage and reduced male fertility. Study Design, Size, Duration: We collected diagnostic (fixed, n = 100) and therapeutic (fresh, n = 18) human testicular biopsies during sperm recovery procedures from moderately to severely infertile men in a cross-sectional approach to sampling. Participants/Materials, Setting, Methods: The diagnostic and therapeutic biopsies were tested for Chlamydia-specific DNA and protein, using real-time PCR and immunohistochemical approaches, respectively. Serum samples matched to the fresh biopsies were also assayed for the presence of Chlamydia-specific antibodies using immunoblotting techniques. Main Results and the Role of Chance: Chlamydial major outer membrane protein was detected in fixed biopsies at a rate of 45.3%. This was confirmed by detection of chlamydial DNA and TC0500 protein (replication marker). C. trachomatis DNA was detected in fresh biopsies at a rate of 16.7%, and the sera from each of these three positive patients contained C. trachomatis-specific antibodies. Overall, C. trachomatis-specific antibodies were detected in 72.2% of the serum samples from the patients providing fresh biopsies, although none of the patients were symptomatic nor had they reported a previous sexually transmitted infection diagnosis including Chlamydia. Limitations, Reasons for Caution: No reproductively healthy male testicular biopsies were tested for the presence of Chlamydia DNA or proteins or Chlamydia-specific antibodies due to the unavailability of these samples. Wider Implications for the Findings: Application of Chlamydia-specific PCR and immunohistochemistry in this human male infertility context of testicular biopsies reveals evidence of a high prevalence of previously unrecognised infection, which may potentially have a pathogenic role in spermatogenic failure.]]> Fri 26 Aug 2022 09:47:49 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:36974 Fri 24 Jul 2020 14:55:41 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:53082 Fri 17 Nov 2023 12:07:40 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:38444 Fri 05 Nov 2021 14:28:07 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:36766 Fri 03 Jul 2020 14:13:41 AEST ]]>