The urinary bladder (UB) serves as a storage and elimination organ for urine. UB dysfunction can cause multiple symptoms of failure to store urine or empty the bladder, e.g., incontinence, frequent urination, and urinary retention. Treatment of these symptoms requires knowledge on bladder function, which involves physiology, pathology, and even psychology. There is no ideal animal model for the study of UB function to understand and treat associated disorders, as the complexity in humans differs from that of other species. However, several animal models are available to study a variety of other bladder disorders. Such models include animals from rodents to nonhuman primates, such as mice, rats, rabbits, felines, canines, pigs, and mini pigs. For incontinence, vaginal distention might mimic birth trauma and can be measured based on leak point pressure. Using peripheral and central models, inflammation, bladder outlet obstruction, and genetic models facilitated the study of overactive bladder. However, the larger the animal model, the more difficult the study is, due to the associated animal ethics issues, laboratory facility, and budget. This review aims at facilitating adapted animal models to study bladder function according to facility, priority, and disease.

Objective: Renal colic caused by ureteral stone is commonly encountered in the emergency department (ED). This study was designed to measure meridian electrical conductance of patients with ureteral stone in emergency settings. Design: A cohort of patients who had ureteral calculus and acute renal colic and who had visited the ED was enrolled in this study. A device, the design of which is based on the Ryodoraku theory, was used to measure the meridian electrical conductance of patients in the ED. Sixty (60) patients (aged 42.0 ± 12.6 years) who had a primary ED diagnosis of ureteral calculus or renal colic were enrolled. Thirty (30) healthy volunteers (aged 40.8 ± 11.7 years) were recruited to serve as controls. Results: Statistical analysis showed that (1) the average electrical conductance of the patient group was statistically lower than that of the control group (p < 0.01), (2) the average index of sympathovagal balance of the patient group was statistically higher than that of the control group (p < 0.01), (3) the average coefficient of variation of the electrical conductance and index of sympathovagal balance in the patient group was statistically different from that in the control group (p < 0.01), and (4) the patients who needed intervention had a higher autonomic nervous imbalance than the patients who had spontaneous stone passage (p < 0.01). Conclusions: Measures of electrical conductance, especially the index of sympathovagal balance, may be used as valuable supplementary diagnostic methods for selective intervention in patients with acute renal colic.

The treatment of hyperuricemia and gout is mostly based on lowering serum uric acid levels using drugs, such as allopurinol, or increasing urinary excretion of uric acid. However, some patients still experience adverse reactions to allopurinol and turn to Chinese medicine as an alternative. Therefore, it is crucial to design a preclinical study to obtain more convincing data on the treatment of hyperuricemia and gout with Chinese medicine. This study aimed to explore the therapeutic effect of emodin, a Chinese herbal extract, in a rat model of hyperuricemia and gout. In this study, we used 36 Sprague–Dawley rats, which were randomly divided into six groups for experimentation. Hyperuricemia was induced in rats by intraperitoneal injections of potassium oxonate. The efficacy of emodin in reducing serum uric acid levels was demonstrated by comparing the positive control group with groups treated with three different concentrations of emodin. The inflammatory profiles, including interleukin (IL)-1β, IL-6, and tumor necrosis factor-α levels, were unaffected by emodin treatment. In the experimental results, it was observed that the serum uric acid concentration in the vehicle control group was 1.80 ± 1.14, while the concentrations in the moderate and high concentration emodin groups were 1.18 ± 0.23 and 1.12 ± 0.57, resulting in no significant difference in uric acid concentration between these treatment groups and the control group, indicating that emodin has a therapeutic effect on hyperuricemia. The increase in the fractional excretion of uric acid (FEUA) demonstrated that emodin promoted urinary uric acid excretion without significantly affecting the inflammatory profile. Thus, emodin reduced the serum uric acid concentration to achieve effective treatment of hyperuricemia and gout by increasing urinary excretion. These results were supported by the measured serum uric acid and FEUA levels. Our data have potential implications for the treatment of gout and other types of hyperuricemia in clinical practice.