Our comprehension of interstitial cystitis/painful bladder syndrome (IC/PBS) has evolved over time. The term painful bladder syndrome, preferred by the International Continence Society, is characterized as “a syndrome marked by suprapubic pain during bladder filling, alongside increased daytime and nighttime frequency, in the absence of any proven urinary infection or other pathology.” The diagnosis of IC/PBS primarily relies on symptoms of urgency/frequency and bladder/pelvic pain. The exact pathogenesis of IC/PBS remains a mystery, but it is postulated to be multifactorial. Theories range from bladder urothelial abnormalities, mast cell degranulation in the bladder, bladder inflammation, to altered bladder innervation. Therapeutic strategies encompass patient education, dietary and lifestyle modifications, medication, intravesical therapy, and surgical intervention. This article delves into the diagnosis, treatment, and prognosis prediction of IC/PBS, presenting the latest research findings, artificial intelligence technology applications in diagnosing major diseases in IC/PBS, and emerging treatment alternatives.

Our understanding of interstitial cystitis/bladder pain syndrome (IC/BPS) has evolved over time. The diagnosis of IC/BPS is primarily based on symptoms such as urgency, frequency, and bladder or pelvic pain. While the exact causes of IC/BPS remain unclear, it is thought to involve several factors, including abnormalities in the bladder’s urothelium, mast cell degranulation within the bladder, inflammation of the bladder, and altered innervation of the bladder. Treatment options include patient education, dietary and lifestyle modifications, medications, intravesical therapy, and surgical interventions. This review article provides insights into IC/BPS, including aspects of treatment, prognosis prediction, and emerging therapeutic options. Additionally, it explores the application of deep learning for diagnosing major diseases associated with IC/BPS.

Artificial intelligence (AI) is being used in many areas of healthcare, including disease diagnosis and personalized treatment and rehabilitation management. Medical AI research and development has primarily focused on diagnosis, prediction, treatment, and management as an aid to patient care. AI is being utilized primarily in the areas of personal healthcare and diagnostic imaging. In the field of urology, significant investments are being made in the development of urination monitoring systems in the field of personal healthcare and ureteral stricture and urinary stone diagnosis solutions in the field of diagnostic imaging. In addition, AI technology is also being applied in the field of neurogenic bladder to develop risk monitoring systems based on video and audio data. This paper examines the application of AI to urological diseases and discusses the current trends and future prospects of AI research.

Background: Inflammatory bowel disease (IBD), including both Crohn’s disease and ulcerative colitis, are chronic human diseases that are challenging to cure and are often unable to be resolved. The inbred mouse strain C57BL/ 6 N has been used in investigations of IBD as an experimental animal model. The purpose of the current study was to compare the inflammatory responsiveness of C57BL/6NKorl mice, a sub-strain recently established by the National Institute of Food and Drug Safety Evaluation (NIFDS), with those of C57BL/6 N mice from two different sources using a dextran sulfate sodium (DSS)-induced colitis model. Results: Male mice (8 weeks old) were administered DSS (0, 1, 2, or 3%) in drinking water for 7 days. DSS significantly decreased body weight and colon length and increased the colon weight-to-length ratio. Moreover, severe colitisrelated clinical signs including diarrhea and rectal bleeding were observed beginning on day 4 in mice administered DSS at a concentration of 3%. DSS led to edema, epithelial layer disruption, inflammatory cell infiltration, and cytokine induction (tumor necrosis factor-α, interleukin-6, and interleukin-1β) in the colon tissues. However, no significant differences in DSS-promoted abnormal symptoms or their severity were found between the three sub-strains. Conclusions These results indicate that C57BL/6NKorl mice responded to DSS-induced colitis similar to the generally used C57BL6/N mice, thus this newly developed mouse sub-strain provides a useful animal model of IBD.

Background: Inflammatory bowel disease (IBD), including both Crohn’s disease and ulcerative colitis, are chronic human diseases that are challenging to cure and are often unable to be resolved. The inbred mouse strain C57BL/ 6 N has been used in investigations of IBD as an experimental animal model. The purpose of the current study was to compare the inflammatory responsiveness of C57BL/6NKorl mice, a sub-strain recently established by the National Institute of Food and Drug Safety Evaluation (NIFDS), with those of C57BL/6 N mice from two different sources using a dextran sulfate sodium (DSS)-induced colitis model. Results: Male mice (8 weeks old) were administered DSS (0, 1, 2, or 3%) in drinking water for 7 days. DSS significantly decreased body weight and colon length and increased the colon weight-to-length ratio. Moreover, severe colitisrelated clinical signs including diarrhea and rectal bleeding were observed beginning on day 4 in mice administered DSS at a concentration of 3%. DSS led to edema, epithelial layer disruption, inflammatory cell infiltration, and cytokine induction (tumor necrosis factor-α, interleukin-6, and interleukin-1β) in the colon tissues. However, no significant differences in DSS-promoted abnormal symptoms or their severity were found between the three sub-strains. Conclusions These results indicate that C57BL/6NKorl mice responded to DSS-induced colitis similar to the generally used C57BL6/N mice, thus this newly developed mouse sub-strain provides a useful animal model of IBD.

Acetaminophen (APAP) is the most common antipyretic analgesic worldwide. However, APAP overdose causes severe liver injury, especially centrilobular necrosis, in humans and experimental animals. At therapeutic dosage, APAP is mainly metabolized by sulfation and glucuronidation, and partly by cytochrome P450–mediated oxidation. However, APAP overdose results in production of excess reactive metabolite, N-acetyl-p-benzoquinone imine (NAPQI), by cytochromes P450; NAPQI overwhelms the level of glutathione (GSH), which could otherwise detoxify it. NAPQI binds covalently to proteins, leading to cell death. A number of studies aimed at the prevention and treatment of APAP-induced toxicity are underway. Rats are more resistant than mice to APAP hepatotoxicity, and thus mouse models are mainly used. In the present study, we compared the toxic responses induced by APAP overdose in the liver of ICR mice obtained from three different sources and evaluated the usability of the Korl:ICR stock established by the National Institute of Food and Drug Safety Evaluation in Korea. Administration of APAP (300 mg/kg) by intraperitoneal injection into male ICR mice enhanced CYP2E1 protein expression and depleted hepatic GSH level 2 h after treatment accompanied with significantly increased level of hepatic malondialdehyde, a product of lipid peroxidation. Regardless of the source of the mice, hepatotoxicity, as evidenced by activity of serum alanine aminotransferase, increased from 8 h and peaked at 24 h after APAP treatment. In summary, hepatotoxicity was induced after the onset of oxidative stress by overdose of APAP, and the response was the same over time among mice of different origins.
Acetaminophen ; Alanine Transaminase ; Animals ; Cell Death ; Cytochrome P-450 CYP2E1 ; Cytochromes ; Glutathione ; Humans ; Injections, Intraperitoneal ; Korea ; Lipid Peroxidation ; Liver ; Male ; Malondialdehyde ; Mice ; Mice, Inbred ICR ; Necrosis ; Oxidative Stress ; Rats

Non-alcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease worldwide. It is characterized by the accumulation of lipids without alcohol intake and often progresses to non-alcoholic steatohepatitis (NASH), liver fibrosis, and end-stage liver diseases such as cirrhosis or cancer. Although animal models have greatly contributed to the understanding of NAFLD, studies on the disease progression in humans are still limited. In this study, we used the recently reported high-fat L-methionine-defined and choline-deficient (HFMCD) diet to rapidly induce NASH and compared the responses to HFMCD in ICR mice from three different countries: Korea (supplied by the National Institute of Food and Drug Safety Evaluation), USA, and Japan during 6 weeks. Feeding HFMCD did not cause significant differences in weight gain in comparison with mice fed control diet. Relative weight of the liver increased gradually, while the relative weight of the kidneys remained unchanged. The parameters of liver injury (serum activities of alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase) increased rapidly from 1 week and remained elevated for as long as 6 weeks. Histopathological analysis showed that the accumulation of hepatic lipids induced by HFMCD was prominent at 1 week after diet supplementation and increased further at 6 weeks. Inflammatory markers were significantly increased in a time-dependent manner by HFMCD. The mRNA levels of TNF-α and IL-6 were elevated approximately 15-fold relative to control diet and that of IL-1β was increased more than 20-folds at 6 week after the onset of HFMCD intake. In addition, mRNA expression of fibrosis markers such as α-SMA, TGFβ1, and Col1a1 were also significantly increased at 6 week. In summary, the responses of Korl:ICR mice by intake of HFMCD diet were similar to those of ICR mice from other sources, which suggests that Korl:ICR mice is also a useful resource to study the pathogenesis of diet-induced NAFLD.

OBJECTIVE: This retrospective case series study of the effectiveness of electroconvulsive therapy (ECT) augmentation on clozapine-resistant schizophrenia was conducted by EMR review. METHODS: Clozapine-resistance was defined as persistent psychotic symptoms despite at least 12 weeks of clozapine administration with blood levels over 350 ng/mL in order to rule out pseudo-resistance. Seven in-patients who were taking clozapine and treated with ECT were selected. We analyzed the psychopathology and subscales changed by ECT. RESULTS: The average number of ECT sessions was 13.4 (±4.6). Total Positive and Negative Syndrome Scale (PANSS) score was significantly reduced by 17.9 (±12.8) points (p=0.0384) on average, which represented a reduction of 25.5% (±14.3). 71.4% (5/7) of patients were identified as clinical remission, with at least a 20% reduction in PANSS score. PANSS reduction was associated with number of ECT sessions, stimulus level in the final session, and blood clozapine levels before ECT. However, the negative subscale on the PANSS were not reduced by ECT in any patient. We did not observe any persistent adverse cognitive effects. CONCLUSION: This study supports that ECT augmentation on clozapine-resistant schizophrenia reveals clinically effective and safe. Further research should be done involving a larger number of patients to investigate the effectiveness of clozapine/ECT combination therapy.
Clozapine ; Electroconvulsive Therapy* ; Humans ; Psychopathology ; Retrospective Studies ; Schizophrenia*

Regional anesthesia for non-obstetric surgery in parturients is a method to decrease patient and fetal risk during general anesthesia. Thoracic interfascial nerve block can be used as an analgesic technique for surgical procedures of the thorax. The Pecs II block is an interfascial block that targets not only the medial and lateral pectoral nerves, but also the lateral cutaneous branch of the intercostal nerve. Pecto-intercostal fascial block (PIFB) targets the anterior cutaneous branch of the intercostal nerve. The authors successfully performed a modified Pecs II block and PIFB without complications in a parturient who refused general anesthesia for breast surgery.
Anesthesia, Conduction ; Anesthesia, General ; Breast* ; Female ; Humans ; Intercostal Nerves ; Methods ; Nerve Block* ; Pregnant Women* ; Thoracic Nerves ; Thorax

Regional anesthesia for non-obstetric surgery in parturients is a method to decrease patient and fetal risk during general anesthesia. Thoracic interfascial nerve block can be used as an analgesic technique for surgical procedures of the thorax. The Pecs II block is an interfascial block that targets not only the medial and lateral pectoral nerves, but also the lateral cutaneous branch of the intercostal nerve. Pecto-intercostal fascial block (PIFB) targets the anterior cutaneous branch of the intercostal nerve. The authors successfully performed a modified Pecs II block and PIFB without complications in a parturient who refused general anesthesia for breast surgery.
Anesthesia, Conduction ; Anesthesia, General ; Breast* ; Female ; Humans ; Intercostal Nerves ; Methods ; Nerve Block* ; Pregnant Women* ; Thoracic Nerves ; Thorax