SUMMARYRetrieval of spermatozoa is unfortunately still only successful in a subset of patients suffering from non-obstructive azoospermia (NOA) by conventional testicular sperm extraction (TESE). Microdissection TESE may have some theoretical benefits over conventional TESE, but uncertainty exists about its superiority. The objective of this systematic review was therefore to compare the efficacy and safety of microTESE with conventional TESE in men with NOA. The systematic review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis statement. Literature was searched for studies comparing outcome of conventional TESE with microdissection TESE. Primary outcome was sperm retrieval rate (SRR). Secondary outcomes were clinical predictors of sperm retrieval as well as complication rate. Of 62 articles, a total of seven studies were included in the final analysis. Overall SRR was significantly higher in the microTESE group in comparison with conventional TESE in five of these studies. Overall sperm retrieval ranged from 16.7 to 45% in the conventional TESE vs. 42.9 to 63% in the microTESE group. A sub-analysis of the SRR according to testicular histology was available in four of the selected articles. MicroTESE in men with Sertoli cell only syndrome and hypospermatogenesis carried a small but significant more favourable outcome according to, respectively, two and one of the studies. Correlation of serum follicle stimulating hormone and testicular volume with positive outcome was variable. Fewer complications were observed on ultrasound examination after microTESE procedure. Clinical randomized studies comparing microTESE with conventional TESE in NOA are still lacking to date. Pseudo-randomized prospective data, however, show more favourable sperm retrieval in NOA for microTESE, especially in histological patterns of patchy spermatogenesis such as Sertoli cell only syndrome. However, in patients with uniform histological patterns such as maturation arrest outcome of microTESE seems less favourable.

Brief cold stimuli applied to the skin can evoke a sudden desire to urinate, which can be highly bothersome in patients with overactive bladder. We developed an animal model to study this phenomenon, and found that it depends on a specific molecular cold sensor, transient receptor potential M8 (TRPM8). Pharmacological inhibition of TRPM8 may alleviate acute cold-induced urinary urgency in humans.

We demonstrate that the sensory protein transient receptor potential vanilloid 4 (TRPV4) can be targeted to improve bladder function in animals that have iatrogenic injury to the nerves innervating the bladder. Further research is required to determine whether these results can be translated to patients with an underactive bladder.

Transient receptor potential (TRP) channels belong to the most intensely pursued drug targets of the last decade. These ion channels are considered promising targets for the treatment of pain, hypersensitivity disorders and lower urinary tract symptoms (LUTS). The aim of the present review is to discuss to what extent TRP channels have adhered to their promise as new pharmacological targets in the lower urinary tract (LUT) and to outline the challenges that lie ahead.• TRP vanilloid 1 (TRPV1) agonists have proven their efficacy in the treatment of neurogenic detrusor overactivity (DO), albeit at the expense of prolonged adverse effects as pelvic 'burning' pain, sensory urgency and haematuria.• TRPV1 antagonists have been very successful in preclinical studies to treat pain and DO. However, clinical trials with the first generation TRPV1 antagonists were terminated early due to hyperthermia, a serious, on-target, side-effect.• TRP vanilloid 4 (TRPV4), TRP ankyrin 1 (TRPA1) and TRP melastatin 8 (TRPM8) have important sensory functions in the LUT. Antagonists of these channels have shown their potential in pre-clinical studies of LUT dysfunction and are awaiting clinical validation.

Objectives To create a rat model for neurogenic detrusor underactivity (DU) by bilateral pelvic nerve crush injury (BPNI) and to study temporal changes in detrusor contractility and morphology. Materials and Methods Male Sprague‐Dawley rats were subjected to BPNI or sham surgery and evaluated at 1, 3 and 9 weeks after surgery. Bladder function was determined in vivo by awake cystometry, micturition pattern analysis, and 24‐h urine collection. Bladders were harvested for in vitro pharmacological investigation by isometric tension recording. Bladders and major pelvic ganglia were investigated by quantitative reverse transcription‐polymerase chain reaction and histochemistry. Results Overflow incontinence was observed at 1 week after BPNI. At 3 and 9 weeks after BPNI, rats showed a bladder phenotype characteristic for DU with increased post‐void residual urine volumes, reduced voiding efficiencies, and lower maximum pressures. In isolated bladder strips, contractile responses to KCl, carbachol, and α,β‐methylene adenosine 5′‐triphosphate (α,β‐mATP) were preserved. On the other hand, neural‐induced contractility was reduced after BPNI, in line with reduced expression of protein gene product 9.5 and choline acetyltransferase in the major pelvic ganglion at 1 week after BPNI. The bladder‐to‐body weight ratio and detrusor thickness increased after BPNI, indicating detrusor hypertrophy to compensate for the reduced neural input. Conclusions BPNI induces a rat model for neurogenic DU. In this model, the detrusor maintains its contractility but denervation of the detrusor was observed.