The relationship among body image, psychological distress, and quality of life in young breast cancer patients: a cross-sectional study.

Purpose: The aim of this study is to explore the interrelationships among body image perception, levels of psychological distress, and the quality of life (QOL) experienced by young breast cancer patients. Methods: This study analyzed data from 339 young female breast cancer patients aged between 18 and 40 years (mean age was 33.47 years) from August 2023 to February 2024. Data on demographic characteristics, psychological distress, body image, medical coping, and QOL of young breast cancer patients were collected. Psychological distress, body image, medical coping, and QOL were measured using the Distress Thermometer (DT), Hospital Anxiety and Depression Scale (HADS), Body Image Scale (BIS), Medical Coping Modes Questionnaire (MCMQ), and Functional Assessment of Cancer Therapy-Breast (FACT-B), respectively. Multiple regression analysis was conducted to examine factors influencing QOL. Results: After adjusting for covariates, significant predictors of QOL in young survivors included psychological distress (ß = -3.125; p = 0.002), anxiety and depression (ß = -4.31; p < 0.001), cognitive dimension of body image (ß = -0.218; p = 0.027), behavioral dimension of body image (ß = 0.579; p = 0.047), and confrontational dimension of medical coping (ß = -0.124; p = 0.01). Conclusion: The findings suggest that higher levels of body image concerns and psychological distress are associated with poorer QOL among young female breast cancer patients. Furthermore, breast cancer patients facing with more positive medical coping strategies predicted a higher QOL.

LncRNA MIAT facilitated BM-MSCs differentiation into endothelial cells and restored erectile dysfunction via targeting miR-200a in a rat model of erectile dysfunction.

BACKGROUND: Bone-marrow derived mesenchymal stem cells (BM-MSCs) implantation effectively restored rats' erectile dysfunction (ED). Long noncoding RNA (LncRNA)-myocardial infarction-associated transcript (MIAT) has been reported to play an important role in regulating endothelial cells (ECs) function via vascular endothelial growth factor (VEGF) that induced BM-MSCs differentiation into ECs. However, the molecular functions and biological roles of lncRNA MIAT in ED remained unclear. METHODS: The rat model of ED was established. Quantitative real-time PCR (qRT-PCR) and western blotting were used to detect the expression of lncRNA MIAT, von Willebrand factor (vWF), vascular endothelial cadherin (VE-cadherin), endothelial NO synthase (eNOS) and VEGF following BM-MSCs transfection. Erectile function was evaluated by intra-cavernous pressure/mean artery pressure (ICP/MAP). Furthermore, RNA immunoprecipitation (RIP) assay and RNA pull down as well as luciferase reporter assay were carried out to examine the interaction among lncRNA MIAT, miR-200a and VEGF. RESULTS: BM-MSCs restored ED by upregulating lncRNA MIAT. LncRNA MIAT was upregulated in a time-dependent manner during BM-MSCs differentiation into ECs. LncRNA MIAT regulated VEGF via targeting miR-200a, thereby promoting BM-MSCs differentiation into ECs. LncRNA MIAT knockdown in vivo abolished the effect of BM-MSCs on ED. CONCLUSION: LncRNA MIAT promoted BM-MSCs differentiation into ECs and restored ED via miR-200a.

Comparison of intrafascial and non-intrafascial radical prostatectomy for low risk localized prostate cancer.

In this meta-analysis study, we compared the oncological and functional outcomes of intrafascial radical prostatectomy (IFRP) with non-intrafascial radical prostatectomy (NIFRP) in the treatment of patients with low risk localized prostate cancer (PCa). Relevant articles were identified by searching PubMed, EMBASE, Cochrane Library, Ovid, and the ISI Web of Knowledge databases. A total of 2096 patients were included from 7 eligible studies. Results of the pooled data showed that the oncological outcomes including gleason score, positive surgical margin and biochemical free survival rates were similar between the two groups. IFRP was superior to NIFRP with lower postoperative complication rates (RR 0.57, 95% CI 0.38, 0.85, p = 0.006), higher continence rates at 3 months post-operation (RR: 1.14; 95% CI, 1.04, 1.26; p = 0.006), and higher potency rates at 6 months (RR: 1.53; 95% CI, 1.07, 2.18; p = 0.02) and 12 months post-operation (RR: 1.38; 95% CI, 1.11, 1.73; p = 0.005). Additionally, there was a tendency towards higher potency rate in patients ≤65 years old compared with patients >65 years old after IFRP. Overall, these findings suggest that IFRP in young patients with low risk localized PCa had less postoperative complications, shortened time to return to continence and improved potency rate without compromising complete tumor control.

Cavernous nerve reconstruction with autologous vein graft and platelet-derived growth factors.

In this study, we investigated the feasibility of using autologous vein graft and platelet-derived growth factors to bridge transected cavernous nerve in a rat model. A short defect in the bilateral cavernous nerve was created and repaired with vein graft from the right jugular vein or vein graft plus platelet-derived growth factors. The 32 rats were divided into four groups, namely Group 1 - no repair as a negative control, Group 2 - vein graft alone, Group 3 - vein graft plus platelet-derived growth factors, and Group 4 - sham operation as a positive control. We evaluated nerve regeneration and functional recovery using retrograde tracing study with FluoroGold, Toluidine blue staining of cavernous nerve, and the intracavernous pressure at 3 months. Three months after surgery, rich FluoroGold-positive cells were observed in the sham and vein graft plus platelet-derived growth factors group, but very few were found in the no repair group. The number of myelinated axons of regenerated cavernous nerve and intracavernous pressure were increased obviously in the two vein graft groups, especially in the vein graft plus platelet-derived growth factors group. These findings confirm the feasibility of using autologous vein as guides for cavernous nerve regeneration, and the regeneration can be further enhanced when the vein is filled with platelet-derived growth factors.

[Estradiol stimulates proliferation of prostatic smooth muscle cells via estrogen receptor alpha and IGF1].

OBJECTIVE: To investigate the effects of estrogen receptor alpha (ERa) and insulin-like growth factor 1 (IGF1) on the proliferation of prostatic smooth muscle cells (PSMCs) in vitro. METHODS: The ERalpha shRNA expression frame was subcloned to the pGSadeno adenovirus vector by homologous recombination technology to construct the pGSaaeno-ERalpha vector. After the mouse PSMCs were transfected in vitro by pGSaaeno-ERalpha, the mRNA and protein expression levels of ERalpha were detected by RT-PCR and Western blot respectively. The expression of IGF1 in the ERa-reduced cells was determined by Western blot 6 hours after treatment with 17beta-estradiol (E2) at 10(-8) mol/L. The post-transfection activity of estrogen or exogenous IGF1 in the proliferation of PSMCs was evaluated by MTT chlormetric analysis. RESULTS: After treatment with E2, the proliferation of PSMCs and the expression of the IGF1 gene were significantly increased in the normal control group (P <0.05), but not obviously changed in the ERalpha-siRNA group (P> 0.05). And exogenous IGF1 failed to induce the proliferation of the ERalpha-reduced PSMCs. CONCLUSION: E2 induces the expression of IGF1 via ERalpha, and IGFl, with the interaction of ERalpha, promotes the proliferation of PSMCs.

Estrogen receptor alpha is essential for the proliferation of prostatic smooth muscle cells stimulated by 17ß-estradiol and insulin-like growth factor 1.

Estradiol (E2) and its receptor estrogen receptor alpha (ERα) are implicated in the pathology of stromal-predominant benign prostatic hyperplasia (BPH). Insulin-like growth factor 1(IGF1) is produced primarily by stromal cells in the prostate. Recent study showed that E2-mediated regulation of IGF1 in mouse uterus requires the DNA binding ability of ERα. However, the crosstalk between ERα and IGF1 in the prostate has not been addressed yet. Therefore, in this study we employed mouse prostatic smooth muscle cells (PSMCs) as a model to demonstrate that E2 stimulated the proliferation of PSMCs and up-regulated the expression of IGF1 and its receptor IGF1R as well as cyclin D1 in PSMCs, all of which could be inhibited by shRNA-mediated knockdown of ERα. Furthermore, we found that exogenous IGF1 could not promote cell proliferation and cyclin D1 expression in PSMCs subjected to shRNA-mediated knockdown of ERα. Interestingly, blockage of IGF1R by antibody could inhibit E2-stimulated PSMCs proliferation. Altogether our present study provides the first line of evidence that there is crosstalk between ERα and IGF1 signaling in PSMCs proliferation in which ERα up-regulates the expression of IGF1 and IGF1R, and IGF1 signaling is indispensable to mediate downstream effects of E2 and ERα.

The effect of platelet-rich plasma on cavernous nerve regeneration in a rat model.

The aim of this study was to investigate the effect of platelet-rich plasma (PRP) on cavernous nerve (CN) regeneration and functional status in a nerve-crush rat model. Twenty-four Sprague-Dawley male rats were randomly divided into three equal groups: eight had a sham operation, eight underwent bilateral nerve crushing with no further intervention and eight underwent bilateral nerve crushing with an immediate application of PRP on the site of injury. Erectile function was assessed by CN electrostimulation at 3 months and nerve regeneration was assessed by toluidine blue staining of CN and nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase staining of penile tissue. Three months after surgery, in the group that underwent bilateral nerve crushing with no further intervention, the functional evaluation showed a lower mean maximal intracavernous pressure (ICP) and maximal ICP per mean arterial pressure (MAP) with CN stimulation than those in the sham group. In the group with an immediate application of PRP, the mean maximal ICP and maximal ICP/MAP were significantly higher than those in the injured control group. Histologically, the group with the application of PRP had more myelinated axons of CNs and more NADPH-diaphorase-positive nerve fibres than the injured control group but fewer than the sham group. These results show that the application of PRP to the site of CN-crush injury facilitates nerve regeneration and recovery of erectile function. Our research indicates that clinical application of PRP has potential repairing effect on CN and peripheral nerves.

[Effect of platelet rich plasma on the regeneration of cavernous nerve: experiment with rats].

OBJECTIVE: To investigate the effect of platelet rich plasma (PRP) on the regeneration of injured cavernous nerve (CN). METHODS: Blood was collected from the hearts of 6 SD rats to prepare PRP. 24 male adult rats were randomly divided into 3 equal groups: pure suture group undergoing bilateral CN transaction and pure suture immediately, PRP group undergoing bilateral CN transaction + suture + PRP 200 microl to the site of suture, and sham operation group. 3 months later intracavernous pressure (ICP) was measured by CN electrostimulation and then samples of CN were obtained to undergo pathological examination. RESULTS: 3 months later after surgery, the ICP of the pure suture group was (46 +/- 8) cm H2O, significantly lower than that of the sham group [(109 +/- 13) cm H2O, P < 0.01], and that of the PRP group was (94 +/- 13) cm H2O, significantly higher than that of the pure sutured group (P < 0.01), however, still significantly lower than that of the sham operation group (P < 0.05). The number of axons of CN in the PRP group was (121 +/- 16), significantly higher than that of the pure sutured group (70 +/- 14, P < 0.01); however, still significantly lower than that of the sham operation group (181 +/- 21, P < 0.01). CONCLUSION: PRP can promote the regeneration of injured CN and the recovery of erectile function.