Although not a major determinant of receptivity, underexpression of the vitamin D receptor (VDR) is associated with endometrial dysfunction. This study aimed to determine VDR expression in the endometrium of patients with recurrent implantation failure (RIF) and unexplained infertility (UEI) using polymerase chain reaction (PCR) and immunohistochemistry. A total of 75 patients (25 RIF, 25 UEI, and 25 fertile controls) were enrolled in the study. In the control group, only patients with early luteal phase histology according to Noyes’ criteria were included to match the endometrial sampling timing of the RIF and UEI groups; patients with follicular and mid-luteal phase histology were excluded, and enrollment continued until 25 eligible patients were identified. Serum vitamin D (VD) levels were measured in all participants. Endometrial tissue was collected using a Pipelle cannula at the time of oocyte retrieval. VDR transcript variant 2 (VDR2) and 4 (VDR4) expression was analyzed using PCR. Endometrial tissue was subjected to VDR immunostaining. VDR2 expression in the RIF group (0.37 ± 0.02 vs. 1.01 ± 0.03, p < 0.001) and UEI group (0.28 ± 0.01 vs. 1.01 ± 0.03, p < 0.001) was significantly lower compared to the control group. VDR2 expression was similar in the RIF and UEI groups. VDR4 expression in the RIF group (0.46 ± 0.02) was significantly lower than that in the UEI (1.16 ± 0.07) and control (1.02 ± 0.05) groups (p < 0.001 for each comparison). VDR4 expression in the UEI and control groups was similar. The histo-score values of the RIF (0.49 ± 0.03) and UEI (0.35 ± 0.03) groups were significantly lower than those of the control group (1.24 ± 0.13) (p < 0.001 for both). In the RIF group, VDR2 was positively correlated with VD (r = 0.593, p = 0.002) and endometrial thickness (r = 0.627, p < 0.001). Low serum vitamin D levels in patients with RIF and UEI were found concomitantly with low VDR expression in the endometrium. Further research is needed to determine whether VD supplementation and adjustment of serum VD concentrations modulate VDR expression and its effects on embryo implantation.

To analyze the effects of hyperandrogenemia (HA) in polycystic ovary syndrome (PCOS) on negative and positive regulators of endometrial receptivity. Fifty-four women with PCOS undergoing total embryo freezing were classified into four phenotypes: classical type A, classical type B, ovulatory type C, and normoandrogenic type D. Hyperandrogenemia was present in phenotypes A-C and absent in phenotype D. Twenty-five age-matched infertile women without clinical or biochemical features of PCOS served as controls. Endometrial sampling was performed on day five after oocyte retrieval. Relative PCX mRNA and protein levels, together with HOXA10 and HOXA11 mRNA expression, were evaluated. Immunohistochemical analysis was performed to assess the spatial distribution of PCX, and H-score values were compared between the PCOS and control groups. PCX mRNA expression and protein concentration were significantly higher in the PCOS group compared with controls (all p < 0.001), consistent with the significantly higher H-score values observed in the PCOS group (p < 0.001). In contrast, HOXA10 and HOXA11 mRNA expression levels were significantly reduced in PCOS patients (all p < 0.001). Among PCOS phenotypes, those associated with hyperandrogenemia exhibited significantly lower HOXA10 and HOXA11 expression than the normoandrogenic phenotype (all p < 0.005). PCX mRNA and protein levels were significantly higher in classical and ovulatory hyperandrogenic phenotypes compared with the normoandrogenic group (all p < 0.005). PCX was identified as a negative predictor of HOXA10 and HOXA11 expression, while testosterone negatively predicted HOXA10 and HOXA11. Insulin resistance and testosterone were positive predictors of PCX expression, whereas progesterone levels on the day of oocyte retrieval and on day five after retrieval were negative predictors of PCX expression. Hyperandrogenemia disrupts the physiological mid-luteal downregulation of PCX and the upregulation of HOXA10 and HOXA11, leading to impaired endometrial receptivity and displacement of the implantation window in PCOS.

PROBLEM:Immunomodulatory agents (IVIG, intralipid, corticosteroids, and G-CSF) and platelet-rich plasma (PRP) are increasingly used in infertility despite inconsistent clinical outcomes. A critical but overlooked question is whether these agents exert their effects through systemic immune modulation or require direct access to target cells within the ovary and endometrium. HYPOTHESIS:We propose that insufficient tissue accessibility, rather than intrinsic biological inefficacy, may contribute to inconsistent clinical outcomes. This framework examines the physical constraints governing therapeutic effectiveness if local action were necessary, while acknowledging that benefits may also be mediated systemically. FINDINGS:Anatomical and biophysical barriers differ by administration route. For systemic agents, the vascular endothelium (continuous capillaries) restricts macromolecular extravasation via capacity-limited transcytosis. For local agents, epithelial tight junctions (0.5-2 nm pores), follicular basal lamina (40-100 nm), granulosa cell layers (∼20 nm), and the zona pellucida (5-10 nm) create sequential barriers. Molecular size analysis suggests that large immunomodulators like IVIG (∼150 kDa, 10-15 nm) and intralipid particles (200-500 nm) face substantial limitations in reaching target compartments. PRP growth factors face identical barriers. By contrast, smaller molecules (<1 kDa) and FSH (∼30 kDa, 5 nm) penetrate more readily. Ovarian tissue stiffness (1.5-5 kPa in normal ovaries; 0.9-11.3 kPa in premature ovarian insufficiency) further impedes macromolecular diffusion. The proposed Mathematical Access Index integrates molecular size, barrier pore dimensions, and tissue stiffness to predict accessibility. CONCLUSION:Accessibility of immunomodulators and PRP growth factors to reproductive tissues is more limited than commonly assumed. If these therapies act predominantly through systemic immune modulation (e.g., Fc receptor saturation, Th1/Th2 modulation), direct tissue penetration may not be necessary. For PRP, observed effects likely result from indirect mechanisms (paracrine signaling, angiogenesis). Distinguishing between systemic and local mechanisms is essential. Until pharmacokinetic studies quantify drug concentrations in reproductive tissues, clinical use should remain cautious.

Reproductive aging in the ovary, endometrium, and testis is characterized by progressive decline in regenerative capacity, yet the upstream mechanisms coordinating stem cell dysfunction across these tissues remain incompletely understood. Emerging evidence suggests that alterations in extracellular matrix (ECM) mechanics, particularly age and disease associated increases in tissue stiffness, may contribute to impaired stem cell function through mechanotransductive signaling pathways. In the testis, increased matrix stiffness has been associated with activation of mechanosensitive pathways such as Piezo1, leading to calcium influx, mitochondrial stress, and downstream effects on steroidogenic and stem cell populations. In the ovary, age-related fibrosis and cortical stiffening correlate with disrupted follicular development and altered signaling through Hippo-YAP/TAZ pathways. Similarly, the endometrium exhibits stiffness-dependent functional changes, where excessive ECM remodeling is associated with impaired decidualization and reduced regenerative potential. Across these reproductive tissues, mechanotransduction pathways involving calcium signaling, reactive oxygen species generation, and YAP/TAZ activity appear to integrate biomechanical cues with cellular stress responses, potentially contributing to stem cell exhaustion. However, current evidence remains largely correlative, and direct causal links between tissue stiffness and stem cell failure in human reproductive tissues are still limited. We propose the “Hardened Ground” framework as a unifying working model suggesting that increased ECM stiffness may represent a contributory biomechanical factor influencing stem cell function across the reproductive axis. Importantly, this model does not replace established molecular and hormonal mechanisms of aging but instead integrates mechanical properties of the tissue microenvironment as an additional regulatory layer. Notably, clinical observations such as preserved follicular reserve in polycystic ovary syndrome despite increased ovarian stiffness, and dynamic changes in endometrial stiffness across the menstrual cycle, indicate that mechanotransduction outcomes are context-dependent and influenced by hormonal and inflammatory states. Future studies integrating quantitative elastography with stem cell and molecular markers in human tissues are needed to clarify the causal role of stiffness in reproductive aging. This framework generates testable predictions and highlights potential therapeutic avenues targeting extracellular matrix remodeling and mechanosensitive signaling pathways to preserve reproductive tissue function.

Anti-Müllerian hormone (AMH) is widely used as a clinical biomarker of ovarian reserve and is traditionallyinterpreted as a surrogate measure of remaining oocyte quantity. However, accumulating biological and clinicalevidence challenges this quantitative paradigm. AMH is exclusively produced by granulosa cells of growing folliclesrather than by primordial follicles themselves, suggesting that circulating AMH primarily refl ects somatic follicularactivity instead of dormant oocyte pool size. Here, we propose a conceptual framework redefi ning ovarian aging as aprocess that may be strongly infl uenced by progressive somatic ovarian dysfunction. In this model, granulosa cells, stromal integrity, vascular support, immune regulation, and metabolicenvironment collectively form a somatic support network that determines follicular survival and developmentalcompetence. Disruption of this somatic ecosystem, through aging, surgery, chemotherapy, autoimmunity,environmental toxicants, smoking, or metabolic stress, results in reduced granulosa cell functionality, declining AMHsecretion, impaired follicle maturation, and secondary oocyte loss. Evidence from granulosa cell biology, controlledovarian stimulation, ovarian surgery, autoimmune ovarian disease, chemotherapy exposure, and fertility outcomestudies consistently demonstrates that AMH responds dynamically to changes in somatic ovarian health and doesnot reliably predict natural fecundability or absolute follicle number. Primordial follicle depletion progresses continuously throughout life, yet circulating AMH levels often showabrupt declines in response to somatic ovarian injury such as surgery, chemotherapy, or metabolic stress.Continuous primordial follicle attrition therefore does not translate into continuous AMH decline, supporting the viewthat AMH represents the functional cohort of biologically supported follicles rather than the total ovarian reserve. It isimportant to recognize, however, that ovarian reserve markers including AMH have limited predictive value fornatural fecundability with area under the curve values ranging from 0.60 to 0.65. We introduce the concept of somatic ovarian function as an integrated framework for AMHinterpretation, proposing AMH as a biomarker of ovarian functional capacity. Reframing AMH from a purelyquantitative reserve marker to a functional systems biomarker that refl ects granulosa cell integrity, metabolichealth, and environmental infl uences may help reconcile longstanding clinical paradoxes and open new translationalavenues for fertility preservation, ovarian aging research, and therapeutic intervention.

Research question: Does endometrial thinning affect the physiological transition of the endometrium from a non-receptive to a receptive state? Design: Fifty-eight women who underwent total embryo freezing were divided into three groups according to their endometrial thickness (EMT): group 1, EMT <= 7 mm; group 2, 7 mm < EMT <= 10 mm; and group 3, EMT > 10 mm. Group 1 was considered as having a thin EMT and groups 2 and 3 as a normal EMT. Endometrial sampling was performed at the time of oocyte retrieval. Anti-adhesive podocalyxin (PDX), adhesive homeobox A10 and A11 (HOXA10, HOXA11) and leukaemia inhibitory factor (LIF) mRNA, proinflammatory cytokines, oxidative stress markers and collagen deposition were determined. Results: Compared with groups 2 and 3, the relative expression of HOXA10, HOXA11 and LIF mRNA was down-regulated in group 1 (all P < 0.001), while PDX levels significantly increased (P < 0.001). The nuclear factor-kappa B, long pentraxin 3 (PTX3), tumour necrosis factor-alpha and total oxidant status of the thin endometrium group were significantly higher than those of participants with normal endometrium (all P < 0.001), while total antioxidant status was significantly lower (P < 0.001). The histoscore values for PTX3, PDX and Masson's trichrome were significantly higher in the thin endometrium group (P < 0.001 for each). Each millimetre increase in EMT decreased the risk of down-regulation of adhesive receptivity genes. The adjusted odds ratio for PDX was 1.69, representing a 69% increase in PDX expression. Conclusion: Endometrial thinning causes defective expression of anti-adhesive and adhesive receptivity modulators, restricting the transition of the endometrium from a non-receptive to a receptive state.

Background/Objectives: This study aimed to investigate the effects of thyroxine replacement therapy (TRT) on serum Maresin 1 and nuclear factor kappa beta (NF-kB) levels in patients with Hashimoto’s thyroiditis (HT). Methods: A total of 90 patients were included in this study, 60 with HT and 30 without. Patients in the HT group were divided into two groups according to whether they received TRT. Group 1 included 30 patients who underwent TRT, and Group 2 comprised 30 patients who were newly diagnosed with HT, either euthyroid or hypothyroid. The analysis included serum levels of thyroid-stimulating hormone (TSH), free thyroxine (FT4), free triiodothyronine (FT3), thyroid peroxidase antibody (TPOAb), Maresin 1, and NF-kB. Results: The serum NF-kB level in the TRT group was significantly higher than that in the control and non-TRT groups. In the subgroup analysis of patients who did not receive TRT, the serum NF-kB level in euthyroid patients was significantly lower than that in hypothyroid patients. Maresin 1 levels in the control group were significantly higher than those in patients who did and did not receive TRT. The serum Maresin 1 level in the TRT group was significantly lower than that in the untreated group. Maresin 1 levels were higher in the euthyroid group than in the hypothyroid group. TPOAb levels were positively correlated with NF-kB and negatively correlated with Maresin 1. Conclusions: TRT maintains the euthyroid state in patients with HT, but may not contribute positively to the pro-anti-inflammatory balance in these patients.

(Abstracted from Reprod Biomed Online 2025;51(2):104697, doi:10.1016/j.rbmo.2024.104697) Receptivity modulators control and facilitate cell differentiation and embryo development as well as inflammatory pathways and suppression of paternal alloantigens. Molecular changes driven by the microenvironment of the endometrium drive endometrial thickening that prepares the uterus for implantation.

Background A fine-tuned pro-inflammatory and anti-inflammatory balance in the follicular unit is essential for cumulus expansion and successful ovulation. While the long pentraxin 3 (PTX3) gene is required for the expansion of cumulus cells (CCs), ovulation, resumption of meiosis and fertilization, the vitamin D receptor gene (VDR-X2) is required for intra-follicle redox balance. This study was planned to determine the expression pattern of VDR-X2 and PTX3 mRNA in CCs isolated from germinal vesicle (GV), metaphase I (MI), and metaphase II (MII) oocytes of PCOS patients with ovulatory dysfunction. Methods The relative expression of CC-PTX3 and CC-VDR-X2 mRNA were evaluated using qRT-PCR in a total of 79 CC samples collected from individual cumulus-oocyte complex of 40 infertile patients (20 PCOS and 20 non-PCOS normal responders) who underwent ovarian stimulation with the GnRH antagonist protocol. Results Relative PTX3 mRNA expressions of CCMI-control and CCMII-control showed 3- and 9-fold significant upregulation compared to CCGV-control, respectively. The relative PTX3 mRNA expression of CCMII-control increased approximately three fold compared to CCMI-control. Compared to CCGV-pcos, a 3-fold increase was noted in the relative PTX3 mRNA expression of CCMI-pcos and an approximately 4-fold increase in the PTX3 mRNA expression of CCMII-pcos. Relative PTX3 mRNA expression values of CCMII-pcos and CCMI-pcos were similar. A 6-fold upregulation of relative PTX3 mRNA and a 4-fold upregulation of VDR-X2 mRNA were detected in CCMII-control compared to CCMII-pcos. CC-VDR-X2 expression patterns of the PCOS and control groups overlapped with the CC-PTX3 pattern. Fertilization rates of the PCOS group exhibiting failed transcript expression were similar to normal responders. Conclusion The fact that relative CC-PTX3 and CC-VDR mRNA expression does not increase during the transition from MI to MII stage in PCOS as in normal responders suggests that PTX3 and VDR expression may be defective in cumulus cells of PCOS patients with ovulatory dysfunction.

Objective: To determine whether the urinary excretion of podocyte degradation products varies according to PCOS phenotype and metabolic syndrome (MetS). Methods: The concentrations of podocalyxin (PDX) and nephrin, chronic markers of podocyte damage, and neutrophil gelatinase-associated lipocalin (NGAL), a marker of acute glomerular damage, were analyzed in the morning urine samples of 50 PCOS patients and 50 healthy controls matched by age and BMI. Albuminuria was assessed by calculating the urine albumin–creatinine ratio (uACR). Results: The PDX, nephrin and NGAL concentrations of PCOS participants were significantly higher than those of the control group. While PDX, nephrin and NGAL levels of classic phenotypes were similar, they were higher than ovulatory and non-hyperandrogenic phenotypes. Significant increases in urinary levels of each podocyte protein were detected in PCOS patients with MetS compared to patients without MetS. A positive significant correlation between podocyte proteins and BMI, systolic blood pressure, testosterone, glucose, HOMA-IR and uACR. After adjusting for age and BMI, podocyte proteins were an independent risk factor for microalbuminuria. The incidence of microalbuminuria in PCOS increased 6-fold compared to controls. The frequency of microalbuminuria was higher in classical phenotypes than in ovulatory phenotype. The frequency of microalbuminuria in PCOS patients with MetS was 6.5 times higher than in PCOS patients without MetS. Conclusions: In PCOS accompanied by hyperandrogenemia or metabolic syndrome, leakage of acute and chronic podocyte breakdown products into the urine becomes more pronounced.

OBJECTIVE:The aim of the study was to determine the expression pattern of long pentraxin 3 (PTX3) mRNA in cumulus cells (CCs) isolated from metaphase II oocytes of women with unilateral endometrioma undergoing controlled ovarian stimulation using a gonadotropin-releasing hormone antagonist (GnRHa) protocol. PATIENTS AND METHODS:A total of 60 CC samples, 30 from the affected ovary and 30 from the contralateral ovary, were collected from 12 patients with unilateral endometrioma who underwent flexible GnRHa protocol with recombinant human chorionic gonadotropin (rhCG) trigger. Thirty CC samples collected from the left ovary of 12 women with male factor infertility were used as external controls. Long PTX3 mRNA expression in each group was analyzed by real-time polymerase chain reaction (RT-PCR). Relative gene expression (fold-change) was calculated according to the 2-ΔΔCt equation. Fertilization rates after intracytoplasmic sperm injection (ICSI) were recorded for each group. RESULTS:CC-PTX3 mRNA expression in the unilateral endometrioma group was significantly lower than the mRNA expression of the disease-free ovary (0.90±0.01 vs. 0.25±0.02, p<0.01). CC-PTX3 mRNA expression of MII oocytes of the disease-free ovary was found to be similar to the control group (1.02±0.03 vs. 0.90±0.01, p=0.107). A significant 3.6-fold downregulation was observed in the CC-PTX3 mRNA expression of the endometrioma group compared to the CC-PTX3 mRNA expression in the contralateral ovary. CC-PTX3 mRNA expression in the endometrioma group was downregulated 4.08-fold compared to the CC-PTX3 mRNA expression of the control group (1.02±0.03 vs. 0.25±0.02, p<0.001). The cumulus morphologies of the endometrioma group with low CC-PTX3 expression and the groups with normal CC-PTX3 levels were similar. Fertilization rates of the endometrioma group were similar to the contralateral ovary and control groups. CONCLUSIONS:Unilateral endometrioma reduces CC-PTX3 expression but does not affect disease-free ovaries. The GnRHa protocol improved the fertilization rates, suggesting that failed CC-PTX3 expression is an in vivo pathology.

Objectives To determine the effects of hyperandrogenemia and other phenotypic parameters on endometrial vitamin D receptor (VDR-X2 and VDR-X4) expression in women with polycystic ovary syndrome (PCOS) undergoing ovarian stimulation and total embryo freezing.Methods Forty-four PCOS patients were divided into four phenotypes according to the criteria for hyperandrogenemia (HA), ovulatory dysfunction (OD), and polycystic ovary morphology (PCOM): phenotype A (HA+OD+PCOM), phenotype B (HA+OD), phenotype C (HA+PCOM), and phenotype D (OD+PCOM). Endometrial VDR expression was determined by real-time PCR and immunohistochemistry. Twenty age- and body mass index (BMI)-matched couples with male infertility were included as controls.Results VDR-X2 and VDR-X4 expression levels were significantly lower in the PCOS group than in the control group. A significant downregulation was detected in the relative VDR-X2 and X4 expression in phenotypes A, B, and C compared to the control group. VDR-X2 and X4 expression in phenotype D was significantly higher than in phenotypes A and B. A significant negative correlation was detected among VDR-X2, VDR-X4, serum testosterone (T), androstenedione (A), DHEAS, and insulin resistance (IR). Multivariate analysis revealed that serum T, A, DHEAS, and IR levels were independently associated with both VDR-X2 and VDR X4 relative gene expression after adjusting for age and BMI. The VDR mRNA and immunoreactivity of each phenotype overlapped. The clinical pregnancy rates for each phenotype were similar.Conclusion VDR expression in the endometria of patients with PCOS was defective. Hyperandrogenemia and insulin resistance are the key drivers of defective VDR expression in the endometrium of patients with PCOS.

Amaç: Korona virüs enfeksiyonu olan hastalarda yoğun bakım ünitesi (YBÜ) gereksinimi için prediktif belirteçlerin belirlenmesi amaçlandı. Gereç ve Yöntem: Bu çalışma, Yerköy Devlet Hastanesi'ne koronavirüs tanısı ile yatırılan hastaların verilerinden retrospektif olarak yapılmıştır. Çalışmaya COVID-19 tanılı toplam 170 hasta dahil edildi. Toraks bilgisayarlı tomografi (BT), hematolojik veriler, karaciğer ve böbrek fonksiyon testleri, lipid profilleri, bazal hormon verileri ve bazı vitamin düzeyleri değerlendirildi. Cinsiyet, yaş ve hastanede kalış süreleri belirlendi. Biyokimyasal parametreler ile YBÜ yatış riski arasındaki bağımsız ilişkinin varlığı binary lojistik regresyon analizi ile araştırıldı. Bulgular: Hastaların ortalama yaşı 69,12±13,72 yıl idi. 145 (%85,3) hasta şifa ile hastaneden taburcu edildi, 25 (%14,7) hasta ise yoğun bakım ihtiyacı nedeniyle başka bir hastaneye sevk edildi. Hastanede ortalama kalış süresi 5 (1-64) gündü. 143 (%84,1) hastada toraks BT'de patoloji saptandı. Hastanede kalış süresi, sevk edilen hastalarda taburcu edilen hastalara göre anlamlı olarak daha düşük saptandı (p<0,001). Koroner arter hastalığı (KAH) yüzdesi yoğun bakım gereksinimi olan hastalarda anlamlı olarak yüksekti (p=0,010). Yoğun bakım gereksinimi olan ve olmayan hastalar arasında yaş, cinsiyet ve BT bulguları açısından anlamlı fark bulunmadı. Trombosit sayısı (p=0,004) ve monosit yüzdesi (p=0,018) YBÜ gereksinimi olan hastalarda anlamlı olarak düşük, Laktat Dehidrogenaz (LDH) anlamlı olarak yüksekti (p=0,007). Sonuç: COVID-19 tanısı ile yatırılan hastalarda LDH artışı, trombosit ve monositte azalma ve eşlik eden KAH varlığı yoğun bakım ihtiyacı açısından uyarıcı olabilir.

OBJECTIVE:To investigate the effects of body mass index (BMI) values and 25(OH) vitamin D levels determined by Endocrine Society on serum Anti Mullerian Hormone (AMH) and antral follicle count (AFC) in women with polycystic ovary syndrome (PCOS).PATIENTS AND METHODS:Sixty infertile women with PCOS and 30 age-matched women with unexplained infertility (UEI), were included. Patients in PCOS and control groups were divided into three subgroups according to their BMI values as normal, overweight and obese. Each BMI group was divided into three subgroups according to vitamin D levels. While AMH and vitamin D levels were determined at first admission, AFC was measured on the third day of cycle.RESULTS:BMI, AFC, and AMH levels of women with PCOS were significantly higher than the UEI group. AMH values of women with PCOS with normal BMI were found to be significantly higher than UEI controls with normal BMI. AMH values of overweight and obese PCOS patients and controls were similar. As BMI values of the PCOS group increased, vitamin D levels decreased significantly. Vitamin D levels of the patients in the PCOS group were found to be significantly lower than the control group. When evaluated according to BMI, the vitamin D levels of normal, overweight and obese women with PCOS were significantly lower than the UEI.CONCLUSIONS:Rising BMI in PCOS leads to a significant decrease in vitamin D and AMH. Deficiency, insufficiency or normality of vitamin D do not affect the main markers of ovarian reserve.

BACKGROUND:Homeobox genes A10 (HOXA10) and A11 (HOXA11), members of the abdominal B gene family, are responsible for embryonic survival and implantation. This study was planned to investigate whether endometrial injury alters the expression of both transcripts in women with implantation failure.METHODS:A total of 54 women with implantation failure were divided into two equal groups as experimental (scratching) and sham (no scratching). Participants in the scratching group were exposed to endometrial injury in the mid-luteal phase, and those in the sham group were exposed to endometrial flushing. The scratching group, but not the sham group, underwent prior endometrial sampling. A second endometrial sampling was performed on the scratching group in the mid-luteal phase of the following cycle. The mRNA and protein levels of the HOXA10 and 11 transcripts were determined in endometrial samples collected before and after injury/flushing. Participants in each group underwent IVF/ET in the cycle after the second endometrial sampling.RESULTS:Endometrial injury caused a 60.1-fold (p < 0.01) increase in HOXA10 mRNA and a 9.0-fold increase in HOXA11 mRNA (p < 0.02). Injury resulted in a significant increase in both HOXA10 (p < 0.001) and HOXA11 protein expression (p < 0.003). There was no significant change in HOXA10 and 11 mRNA expressions after flushing. Clinical pregnancy, live birth, and miscarriage rates of the both groups were similar.CONCLUSIONS:Endometrial injury increases homeobox transcript expression at both mRNA and protein levels.

OBJECTIVE:Although host microbiome play a role in both hormonal status and fertility, this issue has not yet been clarified. Since the endometrium is a sterile tissue, it is accepted that microbiota does not grow under normal conditions. The aim of the study was to reveal the characteristics of endometrial microbiota according to serum AMH levels in women with implantation failure. PATIENTS AND METHODS:Forty-five women aged 20-30 years with two or more implantation failures were included in the study. They were divided into 3 groups according to their serum AMH values: Group 1 -AMH <1.3 ng/ml; Group 2 - AMH between 1.3-2.6 ng/ml; Group 3 - AMH >2.6 ng/ml. Twenty-two healthy fertile women who were the same age as the infertile group and applied for cervical smear screening were accepted as the control group. Following the embryo transfer, the tip of the catheter was inserted into the transport medium under sterile conditions. Sowing was carried out by touching the tips of the catheter to the blood agar medium. After the evaluation of the petri dishes at the end of 48 hours of incubation, colonies were stained with Gram stain. Microorganisms in the colonies were identified with the Vitek-2 device according to their gram-staining characteristics and their antibiograms were made. RESULTS:A negative correlation was detected between low AMH values and the microbiome detection rates in endometrial cultures. In patients with low serum AMH levels, the chance of endometrial microbiota growth was higher in the endometrial culture medium. The most common bacteria were found to be MSSA, MRKNS and lactobacillus. Clinical pregnancy rates were found to be significantly higher in the group with high AMH levels. As AMH levels increased, positive flora detection rates decreased, while clinical pregnancy rates increased. CONCLUSIONS:Low serum AMH level increases the rate of positive endometrial microbiome in culture and decreases clinical pregnancy rates.

Background : Analyzing expression patterns of receptivity genes is a minimally invasive diagnostic method to identify the underlying cause of subfertility in women with uterine fibroid with a history of implantation failure or recurrent pregnancy loss. This updated systematic review was designed to determine the molecular and genetic changes in the endometrium of women with fibroid and how myomctomy affect the outcome of spontaneous or assisted conception treatment. We also discussed the extent to which we should consider the effects of fibroids on endometrial receptivity when deciding whether or not to perform myomectomy. Methods : A total of 184 articles reached as a result of PubMed research and meeting the selection criteria, were evaluated. Of these, 28 full text articles on uterine leiomyoma and endometrium, leiomyoma and receptivity, fibroid and implantation, myomectomy and implantation, fibroid and genes, fibroid surgery and receptivity, fibroid and uterine peristalsis, fibroid and immune cell were evaluated. Results : The endometrium of subfertile women with fibroid appears to have a disease specific pattern according to the type of the fibroid. The response of the endometrium to a fibroid may vary depending on whether the fibroid is close or far from it. Leiomyomas that contribute to subfertility must be near to or in contact with the endometrium, as is the case for Types 0, 1 and 2 leiomyomas. The proximity to the endometrial cavity makes the effect of fibroid on the endometrium more pronounced. While Type 3 fibroid causes subfertility similar to submucosal fibroids, the subfertility-producing effects of Type 4 fibroids have not been clearly clarified. However, the fact that the fibroid is far from the cavity should not mean that it has no effect on the endometrium. The mechanical stress created by a Type 4 fibroid that is not connected to the endometrium may be converted into biological signal and disrupt receptivity. Data on whether myomectomy restores impaired receptivity are mostly based on clinical observations, and studies evaluating endometrial receptivity before and after myomectomy are very few. Conclusions : Analysis of receptivity genes in subfertile women with fibroid may assist the clinician in deciding whether or not to perform myomectomy. If it is determined whether fibroids affect receptivity other than their mechanical effects, the indications for myomectomy may expand or narrow.

OBJECTIVES: We aimed to calculate analytical variation and reference change value for biochemistry analytes studied on the Roche Cobas 8000 analyzer that we routinely use in our laboratory.MATERIALS and METHODS: The reference change value for our analytes;calculated with formula 2 1/2 x Z x (CV A 2 + CV I 2 ) 1/2 .( 95% probability, two-way; Z=2.58 taken) Three-month, two-level internal quality control results were used to calculate analytical coefficient of variation (CV A ). Median values from meta-analysis studies in EFLM biological variation database were used for intraindividual (CV I ) and inter-individual (CV G ) coefficients of variation.The formulas CVA < 0.25 x CVI for optimum performance, CVA < 0.50 x CVI for acceptable performance and CVA < 0.75 x CVI for minimum performance were used to determine quality specifications developed for precision.RESULTS: When evaluated accordingly, the reference change values (%) for our analytes are in order; glucose 16, urea 39, creatinine 19, total cholesterol 15, triglyceride 55, HDL-cholesterol 19, LDL-cholesterol 24, AST 27, ALT 29, sodium 5, potassium 13, chlorine 8, calcium 7, magnesium 10, phosphorus 23, iron 57 calculated.Optimum for urea, triglyceride, AST and iron from our analytes; acceptable for total cholesterol, LDL-cholesterol, ALT and phosphorus; it meets the minimum performance quality specifications f or g lucose, HDL c holesterol a nd potassium; creatinine, sodium, chlorine, calcium and magnesium do not seem to provide.CONCLUSIONS: Analytical and biological sources of variation should be considered for reliability of laboratory results.Tests that do not meet quality specifications require root cause analysis followed by corrective and preventive action.

OBJECTIVE: The aim of our study was to investigate the protective effect of taxifolin on ovarian damage and reproductive dysfunction created by cisplatin administration. MATERIALS AND METHODS: A total of 36 albino Wistar female adult rats were equally divided into 3 groups as cisplatin administered only (CIS), taxifolin+cisplatin (T+C) and healthy control group (HG). Taxifolin 50 mg/kg was administered orally by gavage in the T+C (n=12) group. In the HG (n=12) and CIS (n=12) groups, the same volume of distilled water as a solvent was orally administered. One hour after administration of taxifolin or distilled water, animals in the T+C and CIS groups were injected with cisplatin at a dose of 2.5 mg/kg intraperitoneally. This procedure was repeated once a day for 14 days. Six animals from each group were sacrificed on day 15, and their ovaries were removed for histopathological and biochemical analysis. Ovarian tissue malondialdehyde (MDA), total Glutathione (tGSH), Nuclear Factor-Kappa B (NF-kB), Tumor Necrosis Factor-α (TNF-α), Interleukin 1 beta (IL-1β), and Interleukin-6 (IL-6) levels were measured. The remaining animals (n=6 in each group) were kept in the laboratory with mature male rats for two months to breed. RESULTS: CIS administration led to an increase in inflammatory molecules and membrane lipid peroxidation products, and decreased the synthesis of antioxidant molecules. Compared to the CIS group, the ovarian tissue MDA, NF-kB, TNF-α, IL-1β and IL-6 levels were found to be significantly decreased in the T+C group (p<0.001 for all comparisons). On the other hand, the tGSH levels of the T+C group were significantly higher than the CIS group (p<0.001). Milder ovarian necrosis, fibrosis and follicle damage were detected in animals which were given taxifolin. Four out of the six rats (67%) treated with taxifolin gave birth within 27 days. CONCLUSIONS: We demonstrated, for the first time, that taxifolin ameliorates cisplatin-induced ovarian injury by decreasing MDA and proinflammatory cytokines and increasing the antioxidant enzyme. The fact that more than half of the animals receiving taxifolin became pregnant suggests that the cytoprotective effect of taxifolin is strong enough to preserve fertility.