Comparison of luteal phase and follicular phase in-vitro maturation in women with oocyte maturation abnormalities.

RESEARCH QUESTION: Are there differences in immature oocyte retrieval following luteal phase in-vitro maturation (IVM) compared with follicular phase IVM in women with oocyte maturation abnormalities (OMAs). DESIGN: From January 2019 to May 2023, a retrospective cohort study at a private IVF centre included 36 women with 53 IVM cycles in Group 1 (follicular phase) and 24 women with 32 IVM cycles in Group 2 (luteal phase). Additionally, nine women had both follicular and luteal phase IVM cycles for intracycle variability analysis. RESULTS: There were no differences in oocyte maturation stages between the groups at collection. Group 1 and Group 2 exhibited comparable median metaphase II oocyte rates per patient at 48 h after collection [40.0%, interquartile range (IQR) 0.0-66.7% versus 22.5%, IQR 0.0-52.9%] (P = 0.53). The median fertilization rate in Group 1 (66.7%, IQR 50.0-66.7%) was found to be comparable with that in Group 2 (66.7%, IQR 50.0-66.7%). There were no significant differences in the yielded embryo grades and pregnancy rates between the groups. Comparing follicular and luteal phase IVM within the same menstrual cycle in nine patients, no differences were observed in metaphase II oocyte maturation rates (P > 0.05). CONCLUSIONS: This study found no significant differences in oocyte maturation, fertilization rate, embryo quality or pregnancy outcomes between luteal phase and follicular phase IVM in women with OMAs. These findings suggest that luteal phase IVM can be used similarly to follicular phase IVM, offering a potential avenue to enhance embryo yield for women with OMAs.

Oocyte in-vitro maturation primed with letrozole-HCG versus FSH-HCG in women with oocyte maturation abnormalities: a retrospective study.

RESEARCH QUESTION: Are there differences between in-vitro maturation (IVM) primed with letrozole-human chorionic gonadotrophin (HCG) and IVM primed with FSH-HCG in women with oocyte maturation abnormalities (OMAs), defined as at least two failed IVF cycles where immature oocytes were retrieved? DESIGN: This retrospective study was conducted at a private fertility clinic from January 2009 to April 2023. The final analysis included 75 women in Group 1 (IVM primed with FSH-HCG) and 52 women in Group 2 (IVM primed with letrozole-HCG). RESULTS: A significantly higher median number of oocytes was obtained in Group 1 compared with Group 2 {9 [interquartile range (IQR) 1-5] versus 5 (IQR 1-18); P < 0.001}. However, no differences in oocyte maturation stage at collection were found between the groups (P > 0.05). At the end of IVM, Group 1 had 73/666 mature oocytes and Group 2 had 106/322 mature oocytes, and the median metaphase II oocyte rate per patient was higher in Group 2 [33.3% (IQR 66.7-100.0%) versus 0.0% (IQR 0.0-22.2%); P < 0.001]. Moreover, Group 2 demonstrated a higher median fertilization rate [66.7% (IQR 50.0-100.0%) versus 50.0% (IQR 0.0-66.7%); P = 0.027]. Group 2 had a higher proportion of Grade 2 embryos (58.5% versus 6.3%), and Group 1 had a higher proportion of Grade 3 embryos (93.8% vs 24.4%; P < 0.001). Notably, all pregnancies obtained in the study were in Group 2 (5 versus 0; P = 0.042). CONCLUSIONS: IVM primed with letrozole-HCG in women with prior failed IVF cycles due to OMAs may result in mature oocytes, clinical pregnancies and live births. The effectiveness of letrozole priming for the subtypes of OMAs needs further investigation, with studies including greater numbers of cases.

Investigation of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels in vitro inflammation model at molecular level.

In our study, we aimed to create an inflammation model in endothelial and macrophage cell lines and to examine the changes in the expression of hyperpolarization activated cyclic nucleotide gated (HCN) channels at the molecular level. HUVEC and RAW cell lines were used in our study. 1 µg/mL LPS was applied to the cells. Cell media were taken 6 h later. TNF-α, IL-1, IL-2, IL-4, IL-10 concentrations were measured by ELISA method. Cell media were cross-applied to cells for 24 h after LPS. HCN1/HCN2 protein levels were determined by Western-Blot method. HCN-1/HCN-2 gene expressions were determined by qRT-PCR method. In the inflammation model, a significant increase in TNF-α, IL-1, and IL-2 levels was observed in RAW cell media compared to the control. While no significant difference was observed in IL-4 level, a significant decrease was observed in IL-10 level. While a significant increase in TNF-α level was observed in HUVEC cell medium, no difference was observed in other cytokines. In our inflammation model, an 8.44-fold increase in HCN1 gene expression was observed in HUVEC cells compared to the control group. No significant change was observed in HCN2 gene expression. 6.71-fold increase in HCN1 gene expression was observed in RAW cells compared to the control. The change in HCN2 expression was not statistically significant. In the Western-Blot analysis, a statistically significant increase in HCN1 level was observed in the LPS group in HUVEC cells compared to the control; no significant increase in HCN2 level was observed. While a statistically significant increase in HCN1 level was observed in the LPS group in RAW cells compared to the control; no significant increase in HCN2 level was observed. In immunofluorescence examination, it was observed that the level of HCN1 and HCN2 proteins in the cell membrane of HUVEC and RAW cells increased in the LPS group compared to the control group. While HCN1 gene/protein levels were increased in RAW and HUVEC cells in the inflammation model, no significant change was observed in HCN2 gene/protein levels. Our data suggest that the HCN1 subtype is dominant in endothelium and macrophages and may play a critical role in inflammation.

Is there any association between low level of serum nesfatin-1 and fibromyalgia syndrome?

OBJECTIVES: This study aims to investigate the relationship between serum level of nesfatin-1 and fibromyalgia syndrome (FMS) clinical parameters such as pain severity, disease activity, fatigue, emotional state, and sleep quality. PATIENTS AND METHODS: Forty-six female patients with FMS (median age 40 years; range, 18 to 53 years) and 46 healthy female controls (median age 36 years; range, 19 to 52 years) were included in the study. Severity of pain, disease activity, fatigue, sleep quality, and emotional status were evaluated by visual analog scale, Fibromyalgia Impact Questionnaire, Multidimensional Assessment of Fatigue (MAF), Pittsburgh Sleep Quality Index (PSQI), Beck Depression Inventory (BDI), and Beck Anxiety Inventory (BAI), respectively. Serum nesfatin-1 concentrations (pg/mL) were measured by enzyme-linked immunosorbent assay method. RESULTS: There was no significant difference with respect to demographic characteristics between the FMS patients and healthy controls. When clinical parameters were compared, MAF, BDI, BAI, and PSQI scores were significantly higher in FMS patients than controls (p<0.05). Serum nesfatin-1 concentration was significantly lower in patients with FMS (p<0.05). When compared to the FMS patients without anxiety, serum nesfatin-1 concentration was significantly increased in FMS patients with anxiety (p<0.05). Serum nesfatin-1 concentration was positively correlated with BAI scores in patients with FMS (p<0.05). CONCLUSION: Low nesfatin-1 serum levels may contribute to pathological changes in FMS. In addition, nesfatin-1 may also be involved in the mediation of anxiety-related responses in FMS.

Effects of smoking on the gingival crevicular fluid levels of interleukin-17A, interleukin-17E, and oxidative stress following periodontal treatment process.

OBJECTIVE AND BACKGROUND: How smoking affects periodontal inflammation and healing still needs to be revealed with all its mechanisms. In this study, the gingival crevicular fluid (GCF) levels of: (a) interleukin-17A (IL-17A) and interleukin-17E(IL-17E) with their ratios and (b) oxidative stress by means of total oxidative stress (TOS), total anti-oxidant capacity (TAOC), and their ratios as the oxidative stress index (OSI) were evaluated and compared for smoking and non-smoking periodontitis patients after a periodontitis management process including both the non-surgical and surgical treatments. MATERIALS AND METHODS: Fifteen smoker and 15 non-smoker generalized periodontitis patients as 2 distinct groups participated in the study. Conventional clinical and radiographical examinations were utilized for the periodontitis diagnosis. The clinical data and GCF samples were collected at baseline, 4 week after non-surgical periodontal treatment (NSPT), and 4 weeks after surgical periodontal treatment (SPT). IL-17A, IL-17E, TOS, and TAOC were determined by ELISA and Rel Assay. RESULTS: Clinical parameters in both smokers and non-smokers improved following periodontal treatment (P < .001) and their clinical data were similar for all the examination times (baseline, NSPT, and SPT) (P > .05). Following the treatment phases, the IL-17A concentration decreased and the IL-17E concentration increased in both the smokers and non-smokers (P < .01). The total amount of IL-17A decreased while the total amount of IL-17E increased in smokers throughout NSPT and SPT (P < .01). Such an alteration was seen only at SPT compared to NSPT and baseline in non-smokers (P < .01). The concentration and total amount of IL-17A were higher at baseline, and the concentration and total amount of IL-17E were lower at all examination time points in non-smokers as compared to smokers (P < .01). The 17A/E ratio decreased in both groups following the treatment phases and was higher in smokers at all the examination times (P < .01). TOS were higher and TAOC were lower in smokers versus non-smokers at all the time points, but the differences were significant only for TOS levels (P < .01). Throughout the treatment phases, the concentration and total amount of TOS decreased in smokers(P < .01) and only the total amount of TOS decreased in non-smokers (P < .01). The concentration and total amounts of TAOC increased throughout the treatments in both smokers and non-smokers without significant changes (P > .05). The baseline OSI was higher in smokers, and it decreased only in smokers following the treatment phases (P < .01). CONCLUSIONS: Smoking and periodontal inflammation were found to alter IL-17A, IL-17E, and oxidant/anti-oxidant statuses in periodontitis patients. The intra-group assessments in smokers demonstrated more apparent alterations in the oxidant/anti-oxidant statuses and IL-17A and IL-17E levels after periodontitis management.