Postradical prostatectomy erectile dysfunction (pRP-ED) is a major health issue. There has been a shortage of an effective treatment method until now. In this study, a total of 48 adult male Sprague-Dawley (SD) rats were randomly equally divided into four groups, including group 1-sham surgery with cavernous nerve exposure plus vehicle, group 2-bilateral cavernous nerve injury (BCNI) plus vehicle, group 3-BCNI plus adipose-derived mesenchymal stem cells (ADSCs)-derived exosomes (ADSC-Exo), and group 4-BCNI plus bone marrow-derived mesenchymal stem cell (BMSCs)-derived exosomes (BMSC-Exo). Twenty-one days following surgery, erectile function was measured before tissue harvest. Histologic and Western blot analyses were then performed. Exosomes were capable of internalization into human umbilical vein endothelial cells (HUVEC) in vitro and could be detected in the corpus cavernosum in vivo. The nNOS expression in the penile dorsal nerves (DN) and major pelvic ganglion (MPG), protein level of neurofilament in the DN, endothelial markers vWF, alpha smooth muscle actin (α-SMA), the ratio of smooth muscle to collagen content were obviously lower in BCNI group compared with the sham group, while ADSC-Exo and BMSC-Exo groups resulted in significant restoration of the above histopathological changes. Moreover, BCNI treated with ADSC-Exo or BMSC-Exo had significantly higher mean intracavernous pressure/mean arterial pressure ratio compared with BCNI group. The results demonstrated that both ADSC-Exo and BMSC-Exo treatment could significantly alleviate pathological changes and improve the erectile function in BCNI-related rats. Exosomes derived from ADSCs and BMSCs may be a potential agent for pRP-ED treatment.
Progression to androgen independent (AI) is the main cause of death in prostate cancer, and the mechanism is still unclear. By reviewing the expression profiles of 26 prostate cancer samples in a holistic view, we found a group of genes differentially expressed in AI compared with androgen-dependent groups (P-value<0.01, t-test). Focusing on apoptosis, proliferation, hormone and angiogenesis, we found a group of genes such as thioredoxin domain containing 5 , tumor necrosis factor receptor superfamily, member 10a , ribosomal protein S19 and Janus kinase 2 upregulated in AI prostate cancer, could play important roles in the transition from AD to AI and could be biomarkers of prognosis.
SummaryThe mechanism of disease progression in Hashimoto's thyroiditis (HT) is still unclear. Thyroglobulin antibody (TgAb) is a diagnostic hallmark of HT. The aim of our study was to evaluate the avidity of TgAb in sera from HT patients with different thyroid functional status. Sera from 50 patients with newly diagnosed HT were collected and divided into three groups according to thyroid function: patients with hypothyroidism (H, n = 18), subclinical hypothyroidism (sH, n = 18) and euthyroidism (Eu, n = 14). Titres and avidity of TgAb were determined by enzyme-linked immunosorbent assays (ELISAs). Avidity constant (aK) was determined as the reciprocal value of the thyroglobulin molar concentration in the liquid phase resulting in 50% inhibition of TgAb binding to thyroglobulin in solid-phase ELISAs. The titres and aK of TgAb were performed using log-transformation, and expressed as lgT and lgaK, respectively. Mean lgT of TgAb in sera was 4·19 Ϯ 0·60 in H, 3·77 Ϯ 0·63 in sH, and 3·29 Ϯ 0·64 in Eu, respectively. The median avidity of TgAb was 2·30 ¥ 10 9 in H, 8·80 ¥ 10 8 in sH, 2·00 ¥ 10 7 in Eu, respectively. lgT and lgaK of TgAb were at significantly lower levels in Eu than in sH and H (P < 0·05). Correlation was found between lgT and lgaK (r = 0·594, P < 0·05). lgaK was also related to TSH (r=0·308, P < 0·05). Our study indicated that patients with high-avidity TgAb might be at high risk of developing subclinical, even to overt, hypothyroidism.
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