[Clinical efficacy of Manlyman Spray on premature ejaculation].

OBJECTIVE: To observe the clinical effect of Manlyman Spray in the treatment of premature ejaculation (PE). METHODS: From January 2021 to March 2022, a total of 123 patients with PE were enrolled in clinical observation. Manlyman Spray was sprayed on the surface of the glans penis, corona of the glans and frenulum of the penis qd for 4 weeks. Before and after medication and at 4 weeks after drug withdrawal, the intravaginal ejaculation latency time (IELT), Premature Ejaculation Diagnostic Tool (PEDT) scores and Chinese Index of Sexual Function for Premature Ejaculation (ClPE) scores of the patients were obtained and compared. RESULTS: Compared with the baseline, the IELT of the patients was significantly prolonged after 4 weeks of medication (ï¼»1.51 ± 0.42ï¼½ vs ï¼»3.79 ± 1.69ï¼½ min, P < 0.05) and at 4 weeks after drug withdrawal (ï¼»1.51 ± 0.42ï¼½ vs ï¼»3.55 ± 1.62ï¼½ min, P < 0.05), the PEDT scores were remarkably improved after 4 weeks of medication (14.0 ± 1.9 vs 7.7 ± 2.1, P < 0.05) and at 4 weeks after drug withdrawal (14.0 ± 1.9 vs 7.8 ± 2.0, P < 0.05), and so were the CIPE scores (9.0 ± 1.6 vs 20.0 ± 1.7, P < 0.05, and 9.0 ± 1.6 vs 17.3 ± 1.6, P < 0.05). CONCLUSION: Manlyman Spray has a definite effect in the treatment of PE.

[Cytogenetic and molecular analysis of a case of Prader-Willi syndrome].

OBJECTIVE: To investigate the significance of cytogenetic and molecular genetic diagnosis of a special type of secondary sexual dysplasia and the applicability of various methods for its detection. METHODS: Using karyotype analysis, array comparative genomic hybridization (aCGH), multiplex ligation-dependent probe amplification (MLPA) and methylation-specific PCR (MS-PCR), we diagnosed and differentially diagnosed a case of secondary sexual dysplasia. RESULTS: Abnormalities were not found in the karyotype analysis or the SRY and AZF gene detection, nor chromosomal duplication and deletion in the initial SurePrint G3 Human CGH Array Kit8×60K.SurePrint G3 unrestricteda CGH ISCA v2,88×60K, however, identified a 68.9 kb deletion of chromosome 15 (hg19:25190737-25259677). MLPA revealed the deletion of exon 3 of the SNRPN gene. MS-PCR showed a significant decrease in the paternal fragment signals, but no difference in the maternal fragment signals between the sample from the patient and that from the control. CONCLUSIONS: The patient was confirmed with Prader-Willi syndrome by various methods of detection.