Lipoprotein‐associated phospholipase A2 levels are associated with erectile dysfunction in patients without known coronary artery disease

Endothelial dysfunction and microvascular damage play a crucial role in the pathogenesis of erectile dysfunction (ED). Lp‐PLA2 is a calcium‐independent member of the phospholipase A2 family and hydrolyses oxidised phospholipids on low‐density lipoprotein (LDL) particles that plays a pivotal role in ox‐LDL‐induced endothelial dysfunction. The purpose of the current study was to determine the association between Lp‐PLA2 levels and ED in patients without known coronary artery disease (CAD). All patients were evaluated for ED and divided into two groups: 88 patients suffering from ED for >1 year were enrolled as an experimental group and 88 patients without ED were enrolled as a control group in this study. Diagnosis of ED was based on the International Index of Erectile Function Score‐5. Levels of Lp‐PLA2 were measured in serum by colorimetric assay. The relationship between Lp‐PLA2 levels and ED in patients was evaluated statistically. The mean age of patients with ED group was 59.4 ± 11.32 and 55.8 ± 9.67 in the control group. Plasma Lp‐PLA2 levels were significantly higher in ED than in the control group (220.3 ± 66.90 and 174.8 ± 58.83 pg ml^?1, respectively, P < 0.001). The Lp‐PLA2 levels were negatively correlated with score of ED (r = ?0.482, P < 0.05). In logistic regression analysis, enhanced plasma Lp‐PLA2 levels result in approximately 1.2‐fold increase in ED [1.22 (1.25–2.76)]. In this study, serum Lp‐PLA2 levels were found to be associated with endothelial dysfunction predictive of ED. Serum Lp‐PLA2 level appears to be a specific predictor of ED, and it may be used in early prediction of ED in the male population.     

Association and meta‐analysis of HLA and non‐obstructive azoospermia in the Han Chinese population

The exact aetiology and pathogenesis of most non‐obstructive azoospermia (NOA) are still unknown. The previous two genomewide association studies (GWASs) have identified three different loci within the HLA region for NOA in the Han Chinese population, including rs3129878, rs498422 and rs7194. To further validate the risk of three GWAS‐linked loci for NOA, we conducted a case–control study of these three risk loci in an independent Han Chinese male population, with 603 NOA patients and 610 controls. Furthermore, we also performed a meta‐analysis of five studies on these three NOA‐risk loci. The case–control study strongly suggested a significant association between loci rs3129878, rs498422 and rs7194 and NOA (P = 6.75 × 10^?21 (OR = 2.2586), P = 0.0060 (OR = 1.4013) and P = 0.0128 (OR = 1.2626) respectively). Our meta‐analyses also supported the susceptibility of these three risk loci to NOA (P < 0.01). The risk variants within the HLA region potentially have a strong effect on males at risk of NOA, and may serve as diagnostic markers for male infertility. However, considering genetic difference between different populations, future validating studies in larger independent samples and animal experiments are suggested.     

Terazosin‐induced alterations in catalase expression and lipid peroxidation in the rat seminal vesicles

Previous studies have shown that alpha1‐adrenergic receptor antagonists may alter seminal vesicle contractility and impair fertility in male rats. This study was designed to investigate the effects of terazosin on the catalase expression in the seminal vesicles and the lipid peroxidation of the seminal fluid in normal adult rats. Wistar rats were treated with terazosin (1.2 mg kg^?1 body weight, given orally every second day) for 120 days. Catalase expression was assessed immunohistochemically in tissue sections of the seminal vesicles, and lipid peroxidation was estimated by measuring the malondialdehyde (MDA) levels in the seminal vesicles' fluid. The seminal vesicles in terazosin‐treated rats were particularly distended in comparison with those of controls, and their secreting epithelium was suppressed. Cytoplasmic catalase expression in the secreting epithelial cells (% of cells) was increased in terazosin‐treated specimens in comparison with controls (76.1 ± 17.1 versus 51.3 ± 25.1, P = 0.005). MDA levels (μm ) were also higher in samples from treated subjects in comparison with controls (2.67 ± 1.19 versus 1.39 ± 0.19, P = 0.01). Although the direct effect of terazosin treatment on the seminal vesicles is that of impaired contractility, an indirect effect is that on fertility by increasing lipid peroxidation in the seminal fluid and/or through degrading of hydrogen peroxide that is essential for sperm capacitation.     

Hypoxia‐induced apoptosis and mechanism of epididymal dysfunction in rats with left‐side varicocele

To investigate the relationship between hypoxia and epididymal dysfunction and the mechanism of epididymal dysfunction in rats with left‐side varicocele, a total of 45 male Wistar rats were randomly divided into three groups in average. The expression of hypoxia‐inducible factor‐1α (HIF‐1α) was detected by Western blot and immunohistochemical analysis respectively. HIF‐1α was expressed in the experimental group, and the positive rate was significantly higher than that of either the sham or the control group (P < 0.05). The apoptosis index (AI) of epididymal epithelium was higher in the experimental group (7.25 ± 2.56) than that in either the sham (0.52 ± 0.57, P < 0.01) or the control group (0.08 ± 0.13, P < 0.01). Additionally, the levels of sialic acid and carnitine were lower in the experimental group than that in either the sham or the control group (P < 0.05) and were significantly negatively correlated with HIF‐1α expression (r = ?0.620, P = 0.014, and r = ?0.610, P = 0.016 respectively). It is concluded that left‐side varicocele could cause epididymal hypoxia and epididymal dysfunction. Moreover, HIF‐1α maybe act as useful factor to predict germ cell apoptosis in varicocele.     

Hypoadiponectinemia,elevated iron and high‐sensitivity C‐reactive protein levels and their relation with prostate size in benign prostatic hyperplasia

Elevated iron, high‐sensitivity C‐reactive protein (CRP) and hypoadiponectinemia are known to initiate tumour development. There is paucity of data regarding the above‐mentioned parameters and their relation with prostate size in benign prostatic hyperplasia (BPH). The present study was designed to assess the levels of iron, hs‐CRP and adiponectin levels and their association with prostate size in BPH patients. A total of 37 BPH cases and 36 controls were enrolled in the study. Iron, hs‐CRP and adiponectin were estimated in both the groups. Iron and hs‐CRP were significantly increased and adiponectin was significantly reduced in BPH cases when compared with controls. Iron (r = .397, p = .015), hs‐CRP (r = .341, p = .039) and adiponectin (r = ?.464, p = .004) were significantly associated with prostate size in BPH cases. Multivariate linear regression analysis showed that iron acts as predictor of prostate size in BPH (R² = 0.395, β = 0.526, p = .001). We conclude that iron and hs‐CRP are elevated and adiponectin is reduced in BPH cases and associated with prostate size.     

The effects of reactive hyperemia on stimulation of endothelium-derived nitric oxide in on-pump and off-pump coronary artery bypass surgeries

The purpose of this study is to compare the effects of cardiopulmonary bypass (CPB) on the endothelium‐derived nitric oxide (NO) levels in on‐pump and off‐pump coronary artery bypass surgeries. Forty consecutive patients were divided randomly into two groups depending on use of CPB in coronary artery bypass graft surgery (group 1: n = 20, off‐pump, and group 2: n = 20, on‐pump). The plasma endothelium‐derived NO levels were determined at baseline and after reactive hyperemia before and after surgery. Reactive hyperemia was induced by inflating a blood pressure cuff placed on the upper forearm, for 5 min at 250 mm Hg followed by a rapid deflation. Blood was collected at 1 min after cuff deflation from the radial artery on the same side. Preoperative use of all medications was recorded. The baseline plasma NO levels before operation were 17.10 ± 7.58 in group 1 and 15.49 ± 5.26 nmol/L in group 2. Before operation after reactive hyperemia, the plasma NO levels were 26.97 ± 11.49 in group 1 and 26.57 ± 12.87 nmol/L in group 2. Two hours after surgery, the plasma NO levels at baseline and after reactive hyperemia were not significantly different from each other (group 1: 18.03 ± 6.37 and group 2: 19.89 ± 9.83 nmol/L; group 1: 27.89 ± 18.36 and group 2: 39.13 ± 23.60 nmol/L, respectively; P > 0.05). A positive correlation was shown between preoperative nitroglycerine use and the postoperative plasma NO levels after reactive hyperemia (r = 0.51, P = 0.001). Linear regression analysis was performed (F = 4.10, R = 0.56, R² = 0.32, P = 0.008) and the only independent parameter that had an effect on postoperative plasma NO levels after reactive hyperemia was found to be preoperative nitroglycerine use (t = 3.68, P = 0.001). Coronary artery bypass surgery with CPB does not have significant effect on plasma endothelial derived NO levels. The postoperative plasma NO levels after reactive hyperemia significantly correlated with preoperative nitroglycerine use.     

Toxic effects of arsenic on semen and hormonal profile and their amelioration with vitamin E in Teddy goat bucks

The present environmental study has been planned to investigate the toxic effects of arsenic on reproductive functions of Teddy bucks as well as to examine whether these toxic effects are ameliorated by vitamin E. Sixteen adult Teddy bucks were divided randomly into four equal groups A, B, C and D with following treatment: A (control), B (sodium arsenite 5 mg kg^?1 BW day^?1), C (vit E 200 mg kg^?1 BW day^?1 + Arsenic 5 mg kg^?1 BW day^?1) and D (vit E 200 mg kg^?1 BW day^?1). This treatment was continued for 84 days. Semen quality parameters were evaluated weekly. Male testosterone, luteinising hormone (LH), follicle‐stimulating hormone (FSH) and cortisol levels were measured through enzyme‐linked immunosorbent assay (ELISA) after every 2 weeks. The data were subjected to two‐way analysis of variance followed by Duncan test for multiple comparisons. Semen evaluation parameters were reduced significantly (P < 0.05) in arsenic‐treated animals. The serum hormonal profile of testosterone, LH and FSH was reduced significantly (P < 0.05) in arsenic group, while the serum level of cortisol was increased. Vitamin E alleviated the toxic effects of arsenic on semen and hormonal parameters. It may be concluded from this study that sodium arsenite causes major toxicity changes in semen and hormonal profile in Teddy goat bucks and vitamin E has ameliorative effects on these toxic changes.     

Sperm abnormalities induced by pre‐pubertal exposure to cyclophosphamide are effectively mitigated by Moringa oleifera leaf extract

Moringa oleifera L. is a medicinal plant with potential antioxidant property. This study was aimed at investigating the chemoprotective effect of Moringa oleifera leaf extract (MOE) on cyclophosphamide (CP)‐induced testicular toxicity. Two‐week‐old male Swiss albino mice were intraperitoneally injected with phosphate‐buffered saline, 50 mg kg^?1 of CP and 25 mg kg^?1 of MOE. In combination treatment, mice were injected with 25 mg kg^?1 of MOE 24 h prior to CP injection, 24 h prior and post‐CP injection and 24 h post‐CP injection for 5 consecutive days (10 mg kg^?1). Six weeks later, mice were sacrificed to assess epididymal sperm parameters. MOE alone did not have any significant effect on sperm parameters. However, acute injection of CP resulted in significant decline in motility (P < 0.001), increase in head abnormality (P < 0.01) and DNA damage (P < 0.05). Combining MOE with CP increased the sperm density, motility and reduced head defect and DNA damage, irrespective of the schedule and dosage of MOE. Administration of MOE prior to CP significantly elevated the level of superoxide dismutase and catalase with concomitant decrease in lipid peroxidation in the testicular tissue. In conclusion, MOE may have potential benefit in reducing the loss of male gonadal function following chemotherapy.     

Saturated,omega‐6 and omega‐3 dietary fatty acid effects on the characteristics of fresh,frozen–thawed semen and blood parameters in rams

The aim of this study was to investigate the effects of several dietary fatty acids (FAs) on semen quality and blood parameters in rams. We gave diet‐supplemented treatments (35 g day^?1 ram^?1) by C16:0 (palm oil), C18:2 [sunflower oil (SO)] and an n‐3 source [fish oil (FO)] to 12 rams, who were fed for 15 weeks during their breeding season. Semen was collected once per week. Semen samples were extended with Tris‐based cryoprotective diluents, then cooled to 5 °C and stored in liquid nitrogen. Positive responses were seen with FO after 4 weeks. The mean prefreezing semen characteristics improved with the intake of FO (P < 0.05). Interestingly, maximum sperm output in FO was achieved 7.5 × 10⁹ when compared to palm oil 5.3 × 10⁹. Rams that received FO had the highest total testosterone concentrations (11.3 ng ml^?1 for FO, 10.8 ng ml^?1 for SO and 10.2 ng ml^?1 for palm oil) during the experiment (P < 0.05). FO also improved the rams' sperm characteristics after thawing (P < 0.05). Although C16:0 is a major saturated FA in ram sperm and all rams have been fed isoenergetic rations, the unique FAs of FO improved fresh semen quality and freezing ability compared to other oils.     

Cryoprotective effect of l‐carnitine on motility,vitality and DNA oxidation of human spermatozoa

Successful cryopreservation for human spermatozoa markedly influences the reproductive outcomes of assisted reproductive technologies. But in spite of its usefulness, cryopreservation significantly decreases sperm quality. l ‐carnitine has been found to improve the quality of spermatozoa in selected cases with male infertility. Here, we examined the efficacy of l ‐carnitine in improving sperm motility and vitality and reducing sperm DNA oxidation during cryopreservation. Semen samples from infertile patients (n = 22) were collected and analysed. Cryopreservation medium supplemented with l ‐carnitine was mixed with the semen at a ratio of 1 : 1 (v/v). The final l ‐carnitine concentration in each cryovial was 0.5 mg ml^?1 per 5 × 10⁶ cell ml^?1. Controls were cryopreserved without addition of l ‐carnitine. After 24 h of cryopreservation, thawed sperm samples were analysed for motility, vitality and DNA oxidation. Sperm vitality was assessed by the eosin–nigrosin test, while sperm DNA oxidation was measured by flow cytometry. Addition of l ‐carnitine significantly improved sperm motility and vitality (P < 0.05) compared with the control. The flow cytometry experiment showed no statistical difference (P > 0.05) in the levels of DNA oxidation between samples and controls. In conclusion, l ‐carnitine improves human sperm motility and vitality, but has no effect on sperm DNA oxidation after cryopreservation.     

Changes in bone microarchitecture following kidney transplantation—Beyond bone mineral density

Bone disease in kidney transplant recipients (KTRs) is characterized by bone mineral density (BMD) loss but bone microarchitecture changes are poorly defined. In this prospective cohort study, we evaluated bone microarchitecture using non‐invasive imaging modalities; high‐resolution magnetic resonance imaging (MRI), peripheral quantitative computed tomography (pQCT), dual energy X‐ray absorptiometry (DXA), and the trabecular bone score (TBS) following kidney transplantation. Eleven KTRs (48.3 ± 11.2 years) underwent MRI (tibia), pQCT (radius) and DXA at baseline and 12 months post–transplantation. Transiliac bone biopsies, performed at transplantation, showed 70% of patients with high/normal bone turnover. Compared with baseline, 12‐month MRI showed deterioration in indices of trabecular network integrity—surface to curve ratio (S/C; ?15%, P = 0.03) and erosion index (EI; +19%, P = 0.01). However, cortical area increased (+10.3%, P = 0.04), with a non‐significant increase in cortical thickness (CtTh; +7.8%, P = 0.06). At 12 months, parathyroid hormone values (median 10.7 pmol/L) correlated with improved S/C (r = 0.75, P = 0.009) and EI (r = ?0.71, P = 0.01) while osteocalcin correlated with CtTh (r = 0.72, P = 0.02) and area (r = 0.70, P = 0.02). TBS decreased from baseline (?5.1%, P = 0.01) with no significant changes in BMD or pQCT. These findings highlight a post–transplant deterioration in trabecular bone quality detected by MRI and TBS, independent of changes in BMD, underlining the potential utility of these modalities in evaluating bone microarchitecture in KTRs.     

Long‐term outcomes and transmission rates in hepatitis C virus‐positive donor to hepatitis C virus‐negative kidney transplant recipients: Analysis of United States national data

The use of kidneys from hepatitis C virus (HCV)‐positive (D+) deceased donors for HCV‐negative recipients (R?) might increase the donor pool. We analyzed the national Organ Procurement and Transplant Network (OPTN) registry from 1994 to 2014 to compare the outcomes of HCV D+/R? (n = 421) to propensity‐matched HCV‐negative donor (D?)/R? kidney transplants, as well as with waitlisted patients who never received a transplant, in a 1:5 ratio (n = 2105, per matched group). Both 5‐year graft survival (44% vs 66%; P < .001) and patient survival (57% vs 79%; P < .001) were inferior for D+/R? group compared to D?/R?. Nevertheless, 5‐year patient survival from the time of wait listing was superior for D+/R? when compared to waitlisted controls (68% vs 43%; P < .001). Of the 126 D+/R? with available post‐transplant HCV testing, HCV seroconversion was confirmed in 62 (49%), likely donor‐derived. Five‐year outcomes were similar between D+/R? that seroconverted vs D+/R? that did not (n = 64). Our analysis shows inferior outcomes for D+/R? patients although detailed data on pretransplant risk factors was not available. Limited data suggest that HCV transmission occurred in half of HCV D+/R? patients, although this might not have been the primary factor contributing to the poor observed outcomes.     

Relationship between nuclear DNA fragmentation,mitochondrial DNA damage and standard sperm parameters in spermatozoa of fertile and sub‐fertile men before and after freeze‐thawing procedure

The aim of this study was to assess the stability of nuclear and mitochondrial DNA (n‐DNA and mt‐DNA) of spermatozoa under freeze‐thawing and to find out the correlation between them and their association with standard sperm parameters. Forty‐three semen samples were collected from fertile (G.1; n = 29) and sub‐fertile (G.2; n = 14). N‐DNA fragmentation was determined by TUNEL assay and mt‐DNA using caspase 3 staining. Each semen sample was frozen at ?196°C by the programmed freezer. Freeze‐thawing decrease vitality, total motility and membrane integrity from (43.02 ± 22.74%; 31.63 ± 18.15%; 51.5 ± 24.82%) to (22.71 ± 17.3%; 9.21 ± 6.61%; 34.64 ± 19.92% respectively [p < .001]). G.1 native spermatozoa stained positive with TUNEL and caspase 3 were (14.85 ± 17.6% and 5.8 ± 11.59%) and increased after freeze‐thawing to 27.54 ± 19.74% (p = .004) and 7.3 ± 6.13% (p = .01) respectively. In G.2, TUNEL and caspase 3 were (19.84 ± 17.52% and 7.53 ± 8.56%) and increased to (29.48 ± 16.97% [p = .03] and 10.21 ± 11.73%). In conclusion, freeze‐thawing process affects not only semen parameters but also n‐DNA and mt‐DNA. Therefore, n‐DNA and mt‐DNA could be used as sensitive parameters for assessment of the cryodamage of human spermatozoa.     

In vivo effects of Eurycoma longifolia Jack (Tongkat Ali) extract on reproductive functions in the rat

An aqueous extract of Eurycoma longifolia (Tongkat Ali; TA) roots is traditionally used to enhance male sexuality. Because previous studies are limited to only few sperm parameters or testosterone concentration, this study investigated the in vivo effects of TA on body and organ weight as well as functional sperm parameters in terms of safety and efficacy in the management of male infertility. Forty‐two male rats were divided into a control, low‐dose (200 mg kg^?1 BW) and high‐dose (800 mg kg^?1 BW) group (n = 14). Rats were force‐fed for 14 days and then sacrificed. Total body and organ weights of the prostate, testes, epididymides, gastrocnemius muscle and the omentum were recorded. Moreover, testosterone concentration, sperm concentration, motility, velocity, vitality, acrosome reaction and mitochondrial membrane potential (MMP) were assessed. Whilst TA decreased BW by 5.7% (P = 0.0276) and omentum fat by 31.9% (P = 0.0496), no changes in organ weights were found for the prostate, testes and epididymides. Testosterone concentration increased by 30.2% (P = 0.0544). Muscle weight also increased, yet not significantly. Whilst sperm concentration, total and progressive motility and vitality increased significantly, MMP improved markedly (P = 0.0765) by 25.1%. Because no detrimental effect could be observed, TA appears safe for possible treatment of male infertility and ageing male problems.     

Hypogonadal men with psoriasis benefit from long‐term testosterone replacement therapy – a series of 15 case reports

Psoriasis is increasingly recognised as a skin disease with far‐reaching systemic effects, associated with a high prevalence of comorbid disease such as cardiometabolic dysfunction, shifting the focus from a single organ disease confined to the skin to a systemic inflammatory condition. Chronic and systemic inflammation plays a major role in the development of these diseases, and there are striking similarities between the molecular and inflammatory pathways in psoriasis and atherosclerosis. In a single‐centre, cumulative, prospective registry study of 347 hypogonadal men (total testosterone ≤12.1 nmol l^?1), fifteen men with psoriasis could be studied. Upon testosterone administration, the skin disease improved considerably. Scores on the Psoriasis Area and Severity Index and Physician Global Assessment for Psoriasis showed significant improvement for the first 24 months. Thereafter, these improvements were sustained. Upon testosterone treatment, C‐reactive protein declined significantly. There were significant improvements of obesity and of lipid profiles. Adipose tissue is now regarded as a source of inflammatory factors. These preliminary results deserve to be studied in a specifically designed study to investigate the effects of testosterone on psoriasis and its associated immunopathology.     

The association between thrombotic and inflammatory biomarkers and lower‐extremity peripheral artery disease

Lower‐extremity peripheral artery disease (LEAD) is associated with increased rates of mortality and morbidity. The aim of this study was to evaluate the associations among inflammatory and thrombotic markers and lower‐extremity peripheral disease. A total of 280 patients were enrolled in this study. Of these patients, 152 patients had LEAD on peripheral angiography that was performed because of suspected lower‐extremity peripheral disease based on history, physical examination, and non‐invasive tests. The control group consisted of 128 patients without LEAD on peripheral angiography. Patients with LEAD were classified according to trans‐atlantic inter‐society consensus (TASC) II classification. Subsequently, patients in TASC A to B were defined as having mild to moderate peripheral artery disease, and those in TASC C to D were defined as having advanced peripheral artery disease. Thrombotic and inflammatory markers, such as the neutrophil‐to‐lymphocyte ratio (NLR), the high‐sensitivity C (hs‐C) reactive protein level, the monocyte‐to‐high‐density lipoprotein‐cholesterol ratio, the fibrinogen to albumin ratio (FAR), and whole‐blood viscosity at high shear rate (HSR) and low shear rate (LSR), were evaluated in this population. The NLR, the monocyte‐to‐high‐density lipoprotein‐cholesterol ratio, the FAR, and whole‐blood viscosity, both at a LSR and a HSR, were significantly higher in patients with lower‐extremity peripheral disease compared with patients without lower‐extremity peripheral disease. We determined that lower‐extremity peripheral disease severity was correlated with the NLR, monocyte‐to‐high‐density lipoprotein‐cholesterol ratio, FAR, whole‐blood viscosity at LSR, and whole‐blood viscosity at HSR (r = 0.719, P = .004; r = 0.25, P = .008; r = 0.691, P = .002; r = 0.546, P < .001; and r = 0.448, P = .001, respectively). However hs‐C reactive protein levels were similar between patients with or without LEAD (2.47 ± 1.32 1.61 ± 0.91 P = .685). In addition, there was no correlation between the severity of LEAD and hs‐C reactive levels. In this study, we determined that the levels of inflammatory and thrombotic biomarkers are elevated in peripheral artery disease, and these levels predict disease severity.     

Recovery of lead‐induced suppressed reproduction in male rats by testosterone

The objective of the present study was to investigate the effects of testosterone in recuperation of lead‐induced suppressed reproduction in adult male rats. Lead acetate was administered orally to adult male rats (95 ± 5 days) at dosage level of 0.05 and 0.15% for 55 days through drinking water and injected intraperitoneally with either testoviron depot at a dose of 4.16 mg kg^?1 body weight or vehicle alone on days 1, 7 and 14 respectively. At the end of treatment, control and treated males were cohabited with untreated normal‐cycling females. After cohabitation for 5 days, all the male rats were killed and weights of reproductive organs were determined. Significant increase in the indices of testis, epididymis, seminal vesicles, vas deferens and prostate glands was observed in testosterone (T)‐treated rats when compared to those of lead‐exposed rats. Testosterone treatment significantly increased epididymal sperm count, motile spermatozoa, viable spermatozoa and HOS tail‐coiled spermatozoa and also the activity levels of testicular 3β‐ and 17β‐hydroxysteroid dehydrogenases when compared to those of lead‐exposed males. From the results, it can be hypothesised that supplementation of testosterone mitigated lead‐induced suppressed reproduction in male rats.     

Preventive effect of Pueraria mirifica on testosterone‐induced prostatic hyperplasia in Sprague Dawley rats

Pueraria mirifica (PM) extract contains phytoestrogen daidzein and genistein. In this study, we investigated the protective effect of PM extract, daidzein and genistein on a testosterone‐induced prostatic hyperplasia in rats. Testosterone was administered at 3 mg kg^?1 to rats followed by the PM extract, daidzein and genistein for a period of 30 days with finasteride as positive control. The testosterone level was increased, indicating inhibition of 5α‐reductase converting testosterone to dihydrotestosterone. This was confirmed by prostate‐specific antigen level that significantly decreased when treated with PM extract, daidzein and genistein. The PM extract, daidzein and genistein reduced the increase in the prostate/body weight ratio in testosterone‐induced rats. This gives indication that PM extract, daidzein and genistein possessed protective activity for the treatment of benign prostatic hyperplasia. The analysis of histoarchitechture of the prostate has also shown that there was a significant improvement in prostatic cells of the testosterone‐induced rats when treated with PM extract, daidzein and genistein.     

Testosterone and trenbolone enanthate increase mature myostatin protein expression despite increasing skeletal muscle hypertrophy and satellite cell number in rodent muscle

The androgen‐induced alterations in adult rodent skeletal muscle fibre cross‐sectional area (fCSA), satellite cell content and myostatin (Mstn) were examined in 10‐month‐old Fisher 344 rats (n = 41) assigned to Sham surgery, orchiectomy (ORX), ORX + testosterone (TEST; 7.0 mg week^?1) or ORX + trenbolone (TREN; 1.0 mg week^?1). After 29 days, animals were euthanised and the levator ani/bulbocavernosus (LABC) muscle complex was harvested for analyses. LABC muscle fCSA was 102% and 94% higher in ORX + TEST and ORX + TREN compared to ORX (p < .001). ORX + TEST and ORX + TREN increased satellite cell numbers by 181% and 178% compared to ORX, respectively (p < .01), with no differences between conditions for myonuclear number per muscle fibre (p = .948). Mstn protein was increased 159% and 169% in the ORX + TEST and ORX + TREN compared to ORX (p < .01). pan‐SMAD2/3 protein was ~30–50% greater in ORX compared to SHAM (p = .006), ORX + TEST (p = .037) and ORX + TREN (p = .043), although there were no between‐treatment effects regarding phosphorylated SMAD2/3. Mstn, ActrIIb and Mighty mRNAs were lower in ORX, ORX + TEST and ORX + TREN compared to SHAM (p < .05). Testosterone and trenbolone administration increased muscle fCSA and satellite cell number without increasing myonuclei number, and increased Mstn protein levels. Several genes and signalling proteins related to myostatin signalling were differentially regulated by ORX or androgen therapy.     

Impact of de novo donor‐specific HLA antibodies detected by Luminex solid‐phase assay after transplantation in a group of 88 consecutive living‐donor renal transplantations

De novo donor‐specific HLA antibodies (DSA) after renal transplantation are known to be correlated with poor graft outcome and the development of acute and chronic rejection. Currently, data for the influence of de novo DSA in patient cohorts including only living‐donor renal transplantations (LDRT) are limited. A consecutive cohort of 88 LDRT was tested for the occurrence of de novo DSA by utilizing the highly sensitive Luminex solid‐phase assay for antibody detection. Data were analyzed for risk factors for de novo DSA development and correlated with acute rejection (AR) and graft function. Patients with de novo DSA [31 (35%)] showed a trend for inferior graft function [mean creatinine change (mg/dL/year) after the first year: 0.15 DSA (+) vs. 0.02 DSA (?) (P = 0.10)] and a higher rate of AR episodes, especially in case of de novo DSA of both class I and II [6 (55%), (P = 0.05)]. Antibody‐mediated rejection (AMR) appeared in five patients and was significantly correlated with de novo DSA (P = 0.05). Monitoring for de novo DSA after LDRT may help to identify patients at risk of declining renal function. Especially patients with simultaneous presence of de novo DSA class I and class II are at a high risk to suffer AR episodes.