MATERIALS AND METHODS: Eighty pregnant SD female rats were used in this study for three treatment groups and a control group, each consisting of 20 pregnant female rats. Three doses of 850mg/kg/day (Low-dose), 1700mg/kg/day (Mid-dose) and 3400mg/kg/day (High-dose) were selected for the study, whereas 10mL/kg distilled water was served as the control. Examinations were conducted on pregnant rats and fetuses respects to mortality, body weight, body weights gains, food consumption and clinical observations. The pregnant females were gross necropsied on G20, followed by maternal and fetus examination, to evaluate the teratogenicity, reproductive and developmental performance of L. rhinocerotis mycelium.
RESULTS: Results showed that no L. rhinocerotis mycelium-related animal death and abnormal clinical sign were noted. No statistical differences were noted in maternal mean body weight and maternal mean body weight gains. Some animals in the high-dose group appeared audible respiration due to dosing accident, it resulted in lower food consumption but not relevant to L. rhinocerotis mycelium treatment. In maternal gross necropsy, no L. rhinocerotis mycelium-related gross lesion was noted. In maternal examination, parameters of gravid uterus weight, implantation number, corpora lutea number, litter size, live or dead fetal number, male or female fetus number, resorption number, fetal sex ratio (M/F), pre-implantation loss and post-implantation loss were all within the normal reference ranges and showed no significant difference when compared to the control group. In fetus examination, including external, visceral and skeletal evaluations, there were no significant changes between any of the L. rhinocerotis mycelium treated groups and the control group.
CONCLUSIONS: Based on the study results, the no-observable-adverse-effect level (NOAEL) for pregnant female rats under the conditions of this study was 3400mg/kg/day.
METHODS: This was a retrospective study involving archived data sets of women seen between November 2013 and May 2014. All underwent a clinical interview, POPQ examination, and 4D translabial ultrasound (TLUS). The main outcome measure was organ descent on clinical examination and TLUS. Offline analysis for organ descent was undertaken blinded against all other data.
RESULTS: A total of 224 women were assessed. Mean age was 57 (23-84) years. Median parity was 3 (0-7). Ninety-three percent (n=208) were vaginally parous. Fifty-eight percent (n=129) complained of symptoms of prolapse: 49% (n=110) of a vaginal lump, 27% (n=61) of a dragging sensation. Clinically, mean point B anterior (Ba) was -0.86 (-3 to +7.5) cm, mean cervical station (C) was -4.1 (-9 to +8) cm, mean point B posterior (Bp) was -1.1 (-3 to +5) cm. On imaging, mean bladder, uterine, and rectal descent were -8.3 (-68.0 to 34) mm, +18.6 (-56.4 to 46.3) mm, and -5.3 (-39.8 to 36) mm respectively. On univariate analysis, both symptoms were strongly associated with objective prolapse clinically and on TLUS, with "vaginal lump" consistently the stronger predictor.
CONCLUSIONS: The symptom of a "vaginal lump or bulge" was consistently a stronger predictor of objective POP than "dragging sensation." This finding was insensitive to adjustments for potential confounders. However, a "dragging sensation" is clearly a symptom of prolapse.
Methods: This cross-sectional study included 50 patients with late-onset (≥ 32 weeks gestation) PE. Maternal serum was obtained before delivery, and placentas were obtained immediately after delivery. SEMA3B and CUL1 levels were evaluated by ELISA. Results were statistically analysed by Spearman correlation test, with a P < 0.05 considered statistically significant.
Results: While elevated serum SEMA3B levels significantly correlated with increased placental SEMA3B levels in late-onset PE (R = 0.620, P = 0.000), alteration of serum CUL1 levels did not correlate with alteration of placental CUL1.
Conclusion: Alteration of circulating maternal SEMA3B, but not CUL1, levels can potentially be used to monitor PE progression during pregnancy.
MATERIALS AND METHODS: Intact pregnant rats were administered 1 mg/kg/day testosterone alone or in combination with flutamide, finasteride or anastrozole, subcutaneously on day-1 of pregnancy till day 3. The rats were sacrificed at day 4 of pregnancy, which was considered as the uterine receptivity period for determining the expression and distribution of connexin 26 and connexion 43 by immunohistochemistry and quantitative polymerase chain reaction, respectively.
RESULTS: Treatment with 1 mg/kg/day testosterone increased connexin 26 and decreased connexin 43 mRNA expression and protein distribution in the uterus of early pregnancy rats.
CONCLUSION: Changes in the uterine connexin 26 and connexin 43 expression by testosterone could disrupt embryo implantation, resulting in early pregnancy loss.