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Introduction: Galectin-1 (Gal-1) and galectin-3 (Gal-3) are expressed by many immune cells and receive considerable attention in the context of immunity. We aimed to compare between seminal plasma and serum levels of Gal-1 and Gal-3 in azoospermic patients and fertile men. Materials and methods: This cross-sectional study was conducted at the andrology outpatient clinic from January (2022) to September (2022). A total of 90 participants were enrolled and divided into two equal groups: azoospermic and normal group. Semen analysis was done for all participants. Hormonal profile including FSH, LH, serum prolactin, total testosterone and estradiol was performed as well as assessment of serum and seminal levels of Gal-1 and Gal-3 by ELISA commercial kits. Finally, scrotal Duplex was done in standing and supine position. Results: Serum and seminal levels of Gal-1 and Gal-3 were statistically significant higher in azoospermic patients compared with normal individuals (p < 0.001 for all). In addition, in healthy individuals there were statistically significant positive correlations between serum levels of Gal-1 and age, FSH, LH levels (r = 0.296, p = 0.005; r = 0.333, p = < 0.001; r = 0.312, p = 0.003, respectively) and serum levels of Gal-2 and FSH and LH (r = 0.436, p < 0.001; r = 0.350, p < 0.001, respectively), whereas serum Gal-3 showed a borderline positive correlation with age (r = 0.2, p = 0.059). Additionally, statistically significant positive correlations between seminal levels of Gal-1 and Gal-3 and free testosterone in healthy individuals were reported (r = 0.205, p = 0.053; r = 0.219, p = 0.038, respectively). On the other hand, there were negative correlations between serum and seminal levels of Gal-1 and Gal-3, total and progressive sperm motility, sperm count and abnormal sperm forms in healthy individuals (r = -0.382, p < 0.001; r = -0.405, p < 0.001; r = -0.376, p < 0.001; r = -0.364, p < 0.001) (r = -0.394, p < 0.001; r = -0.467, p < 0.001; r = -0.413, p < 0.001; r = -0.433, p < 0.001); (r = -0.372, p < 0.001; r = -0.377, p < 0.001; r = -0.317, p = 0.002; r = -0.311, p = 0.003)(r = -0.445, p < 0.001; r = -0.498, p < 0.001; r = -0.453, p < 0.001; r = -0.463, p < 0.001, respectively). Furthermore, statistically significant positive correlations between serum levels of Gal-1 and Gal-3 and age in azoospermic patients were reported (r = 0.511, p < 0.001; r = 0.390, p = 0.008, respectively). On the other hand, there were negative correlations between seminal Gal-1 and estradiol (E2) and seminal Gal-3 and FSH and LH in azoospermic patients (r= -0.318, p = 0.033; r = -0.322, p = 0.031; r = -0.477, p < 0.001, respectively). Also, negative correlations between serum Gal-3 and total and free testosterone in azoospermic patients were detected (r = -0.396, p = 0.007; r = -0.375, p = 0.011, respectively). Conclusions: Elevated serum and seminal levels of Gal-1 and Gal-3 have detrimental effects on spermatogenesis. Furthermore, the current study demonstrated potential regulatory effects of reproductive hormones on Gal-1 and Gal-3. Thus, future studies are needed to confirm such findings. [ABSTRACT FROM AUTHOR]

Introduction: Galectin-1 (Gal-1) and galectin-3 (Gal-3) are expressed by many immune cells and receive considerable attention in the context of immunity. We aimed to compare between seminal plasma and serum levels of Gal-1 and Gal-3 in azoospermic patients and fertile men. Materials and methods: This cross-sectional study was conducted at the andrology outpatient clinic from January (2022) to September (2022). A total of 90 participants were enrolled and divided into two equal groups: azoospermic and normal group. Semen analysis was done for all participants. Hormonal profile including FSH, LH, serum prolactin, total testosterone and estradiol was performed as well as assessment of serum and seminal levels of Gal-1 and Gal-3 by ELISA commercial kits. Finally, scrotal Duplex was done in standing and supine position. Results: Serum and seminal levels of Gal-1 and Gal-3 were statistically significant higher in azoospermic patients compared with normal individuals (p < 0.001 for all). In addition, in healthy individuals there were statistically significant positive correlations between serum levels of Gal-1 and age, FSH, LH levels (r = 0.296, p = 0.005; r = 0.333, p = < 0.001; r = 0.312, p = 0.003, respectively) and serum levels of Gal-2 and FSH and LH (r = 0.436, p < 0.001; r = 0.350, p < 0.001, respectively), whereas serum Gal-3 showed a borderline positive correlation with age (r = 0.2, p = 0.059). Additionally, statistically significant positive correlations between seminal levels of Gal-1 and Gal-3 and free testosterone in healthy individuals were reported (r = 0.205, p = 0.053; r = 0.219, p = 0.038, respectively). On the other hand, there were negative correlations between serum and seminal levels of Gal-1 and Gal-3, total and progressive sperm motility, sperm count and abnormal sperm forms in healthy individuals (r = -0.382, p < 0.001; r = -0.405, p < 0.001; r = -0.376, p < 0.001; r = -0.364, p < 0.001) (r = -0.394, p < 0.001; r = -0.467, p < 0.001; r = -0.413, p < 0.001; r = -0.433, p < 0.001); (r = -0.372, p < 0.001; r = -0.377, p < 0.001; r = -0.317, p = 0.002; r = -0.311, p = 0.003)(r = -0.445, p < 0.001; r = -0.498, p < 0.001; r = -0.453, p < 0.001; r = -0.463, p < 0.001, respectively). Furthermore, statistically significant positive correlations between serum levels of Gal-1 and Gal-3 and age in azoospermic patients were reported (r = 0.511, p < 0.001; r = 0.390, p = 0.008, respectively). On the other hand, there were negative correlations between seminal Gal-1 and estradiol (E2) and seminal Gal-3 and FSH and LH in azoospermic patients (r= -0.318, p = 0.033; r = -0.322, p = 0.031; r = -0.477, p < 0.001, respectively). Also, negative correlations between serum Gal-3 and total and free testosterone in azoospermic patients were detected (r = -0.396, p = 0.007; r = -0.375, p = 0.011, respectively). Conclusions: Elevated serum and seminal levels of Gal-1 and Gal-3 have detrimental effects on spermatogenesis. Furthermore, the current study demonstrated potential regulatory effects of reproductive hormones on Gal-1 and Gal-3. Thus, future studies are needed to confirm such findings.

Objective: To correlate late spermatid score and sperm count in men with normal semen analysis and oligozoospermia undergoing intracytoplasmic sperm injection (ICSI) to set the average threshold of spermatids/tubule of testicular tissue needed for normal sperm count/ml of semen. Material and methods: This study was conducted on 24 normozoospermic subjects and 18 oligozoospermic patients who underwent wide bore needle biopsy because of failed sperm collection at the day of ICSI. Clinical data were reviewed and testicular biopsy slides were examined for Johnson score and adjusted late spermatid score. Results: The optimum cut off value for adjusted late spermatid score in predicting a sperm count >20 million/ml was 20.75 late spermatid per tubule with 100% specificity. Model equations were produced to predict the sperm count using adjusted late spermatid score and vice versa. Conclusion: This work supports the hypothesis that late spermatid score is a simple and reliable method for quantitation of spermatogenesis and it correlates well with the sperm count. The value of late spermatids needed for normal sperm count in this report is different from some other reports. The better standardization of work in this study may help resetting a new late spermatid threshold for normal sperm count.

Objective: To correlate late spermatid score and sperm count in men with normal semen analysis and oligozoospermia undergoing intracytoplasmic sperm injection (ICSI) to set the average threshold of spermatids/tubule of testicular tissue needed for normal sperm count/ml of semen. Material and methods: This study was conducted on 24 normozoospermic subjects and 18 oligozoospermic patients who underwent wide bore needle biopsy because of failed sperm collection at the day of ICSI. Clinical data were reviewed and testicular biopsy slides were examined for Johnson score and adjusted late spermatid score. Results: The optimum cut off value for adjusted late spermatid score in predicting a sperm count >20 million/ml was 20.75 late spermatid per tubule with 100% specificity. Model equations were produced to predict the sperm count using adjusted late spermatid score and vice versa. Conclusion: This work supports the hypothesis that late spermatid score is a simple and reliable method for quantitation of spermatogenesis and it correlates well with the sperm count. The value of late spermatids needed for normal sperm count in this report is different from some other reports. The better standardization of work in this study may help resetting a new late spermatid threshold for normal sperm count. [ABSTRACT FROM AUTHOR]

In mouse testis, claudin-11 is responsible for the formation of specific parallel TJ strands of the blood–testis barrier (BTB). Concerning the human BTB, there is no information about the transmembrane TJ proteins. We recently demonstrated the loss of functional integrity of the BTB in testicular intraepithelial neoplasia (TIN), associated with a dislocation of the peripheral TJ proteins ZO-1 and ZO-2. Here, we determined the expression and distribution of claudin-11 at the human BTB in seminiferous tubules with normal spermatogenesis (NSP) and TIN. Immunostaining of claudin-11 revealed intense signals at the basal BTB region in seminiferous epithelium with NSP. Within TIN tubules, claudin-11 immunostaining became diffuse and cytoplasmic. Double immunogold labeling demonstrated a co-localization of claudin-11 and ZO-1 at the inter-Sertoli cell junctions. Real-time RT-PCR of laser microdissected tubules showed an up-regulation of claudin-11 mRNA in TIN. Additionally, increased claudin-11 protein was observed by Western blot. We conclude that claudin-11 constitutes a TJ protein at the human BTB. In TIN tubules, claudin-11 is up-regulated and dislocated from the BTB. Therefore, the disruption of the BTB is related to a dysfunction of claudin-11 and not to a failure of its expression. [ABSTRACT FROM AUTHOR]

To evaluate whether defective cyclic adenosine monophosphate responsive element modulator (CREM) expression is the causative factor of spermatid maturation arrest (SMA).Comparative evaluation of the testicular histology in patients with SMA or normal spermatogenesis.University clinic of andrology.Azoospermic patients undergoing testicular biopsy.None.Expression of CREMτ in quantitative immunohistochemistry analysis of testicular biopsy samples.Regular CREM expression was observed in the tubules with round, but not elongated, spermatids of patients with SMA (n = 9). Quantitative analysis showed that round spermatids of patients with SMA had a staining intensity similar to that observed in controls (n = 7).Lack of spermatid elongation was not due to defective CREM expression. Therefore, CREM did not play a pathogenetic role in the onset of SMA in humans. [Copyright &y& Elsevier]