Abstract:A clinical guideline and algorism for interstitial cystitis and hypersensitive bladder syndrome has been developed by a group of East Asian urologists as a revised form of the Japanese guideline for interstitial cystitis. The guideline defines interstitial cystitis (IC) as a disease of the urinary bladder diagnosed by 3 requirements; 1) a characteristic complex of lower urinary tract symptoms, 2) bladder pathology such as Hunner's ulcer and bladder bleeding after overdistension, and 3) exclusions of confusable diseases. The characteristic symptom complex is termed as hypersensitive bladder syndrome (HBS), which is defined as bladder hypersensitivity, usually associated with urinary frequency, with or without bladder pain. For the definite diagnosis of IC, cytoscopy or hydrodistension is crutial; HBS is the diagnosis when IC is suspected but not confirmed by the 3 requirements. Numerous therapeutic options are available; however, most of them lack in high level of evidence, leaving a few as recommended therapies. Etiology of IC are multifactorial; the interaction among nervous, immune and endocrine factors forms a vicious cycle, provocating and maintaining inflammatory reactions in the bladder. The inclusion and efficacy criteria for clinical trials should be standardized to enhance the clinical research for this disabling disease, which has proved to be more prevalent than previously believed.

The clinical guidelines for interstitial cystitis and related symptomatic conditions were revised by updating our previous guidelines. The current guidelines define interstitial cystitis/bladder pain syndrome as a condition with chronic pelvic pain, pressure or discomfort perceived to be related to the urinary bladder accompanied by other urinary symptoms, such as persistent urge to void or urinary frequency in the absence of confusable diseases. The characteristic symptom complex is collectively referred as hypersensitive bladder symptoms. Interstitial cystitis/bladder pain syndrome is divided into Hunner‐type interstitial cystitis and bladder pain syndrome; Hunner‐type interstitial cystitis and bladder pain syndrome represent interstitial cystitis/bladder pain syndrome with Hunner lesions and interstitial cystitis/bladder pain syndrome without Hunner lesions, respectively. So‐called non‐Hunner‐type interstitial cystitis featured by glomerulations or bladder bleeding after distension is included in bladder pain syndrome. The symptoms are virtually indistinguishable between Hunner‐type interstitial cystitis and bladder pain syndrome; however, Hunner‐type interstitial cystitis and bladder pain syndrome should be considered as a separate entity of disorder. Histopathology totally differs between Hunner‐type interstitial cystitis and bladder pain syndrome; Hunner‐type interstitial cystitis is associated with severe inflammation of the urinary bladder accompanied by lymphoplasmacytic infiltration and urothelial denudation, whereas bladder pain syndrome shows little pathological changes in the bladder. Pathophysiology would also differ between Hunner‐type interstitial cystitis and bladder pain syndrome, involving interaction of multiple factors, such as inflammation, autoimmunity, infection, exogenous substances, urothelial dysfunction, neural hyperactivity and extrabladder disorders. The patients should be treated differently based on the diagnosis of Hunner‐type interstitial cystitis or bladder pain syndrome, which requires cystoscopy to determine the presence or absence Hunner lesions. Clinical studies are to be designed to analyze outcomes separately for Hunner‐type interstitial cystitis and bladder pain syndrome.

Reduction of thermal conductivity κ while preserving high electrical conductivity σ in materials continues to be a vital goal in thermoelectric study for the reuse of exhaust heat energy. In the use of an eco-friendly and ubiquitous element, Si as thermoelectric material, high κ value in bulk Si is the essential bottleneck to achieve high dimensionless figure of merit. This is a motivation for many recent studies on reducing κ in Si, by nanostructuring, e.g., using grains/wires with size smaller than the phonon mean free path. However, κ reduction that can be achieved tends to be saturated presumably due to an amorphous limit. Here, we present a nanoarchitecture for defeating the κ amorphous limit while preserving bulk-like σ. This new nanoarchitecture is an assembly of Si nanocrystals with oriented crystals separated by a 1-monolayer amorphous layer with well-controlled nanoscale shaped interfaces. At these interfaces, novel phonon scattering occurs resulting in κ reduction below the amorphous limit. Preservation of bulk-like σ results from the coherency of the carrier wavefunctions among the oriented nanocrystals separated by the ultrathin amorphous layer.

Aims of Study:The Bladder Pain Syndrome Committee of the International Consultation on Incontinence was assigned the task by the consultation of reviewing the syndrome, formerly known as interstitial cystitis, in a comprehensive fashion. This included the topics of definition, nomenclature, taxonomy, epidemiology, etiology, pathology, diagnosis, symptom scales, outcome assessment, principles of management, specific therapies, and future directions in research. Study Design, Materials, Methods: The emphasis was on new information developed since the last consultation 4 years previously. Where possible, existing evidence was assessed and a level of recommendation was developed according to the Oxford system of classification. Results: The consultation decided to refer to the condition as ''bladder pain syndrome'' (BPS) because the designation is more descriptive of the clinical condition and better fits standard classification taxonomy. Reasonable definitions of BPS include the definition of the ESSIC European group and a slight modification made at a SUFU sponsored Miami meeting in early 2008. Males or females with pain, pressure, or discomfort that they perceive to be related to the bladder with at least one urinary symptom, such as frequency not obviously related to high fluid intake, or a persistent urge to void should be evaluated for possible BPS. The initial assessment consists of a frequency/volume chart, focused physical examination, urinalysis, and urine culture. Urine cytology and cystoscopy are recommended if clinically indicated. Treatment progresses from conservative management through various oral and intravesical therapies, with most surgical therapies reserved for unresponsive cases. Pain management is critical throughout the treatment process. The consultation believes that the disorder is best viewed as one of a group of chronic pain syndromes, rather than as primarily an inflammatory bladder disorder. Recommendations for future research pathways are suggested.

We have isolated a new cell division cycle gene (resl+) required for entry into S phase, as a multicopy dual suppressor of the paut and cdclO mutants of the fission yeast Schizosaccharomyces pombe. The resi+ gene specifies a 72 kDa protein with two copies of the cdclO/SWI6 motif. A disruptant of resl+ grows poorly at 30°C with severe heat-and cold-sensitivities, and completely arrests in G1 at 36°C and 23°C. The arrested disruptant retains a full conjugation ability. In addition to the cdclO/SWI6 motif, Resl and SWI4 proteins share a remarkable homology in their aminoterminal region, whereas CdclO and SWI6 do so in their carboxy-terminal region. Moreover, the amino-terminal region is essential for the function of Resl as it is for the function of SWI4. Furthermore, analogous to the relationship of SWI4 to SWI6, the resl+ gene effectively rescues cdclO mutants, but the cdclO+ gene cannot rescue the resl-phenotype. Thus, striking similarities exist in both structural and functional relationships between Resl and SWI4, and between CdclO and SWI6. In view of the fact that SWI4 and SWI6 form a transcription factor complex and activate promoters containing the SWI4/SWI6 dependent cell-cycle box, Resl might be a putative association partner of CdclO which appears to be involved at least in the activation of promoters containing a MluI cell-cycle box.

Bladder dysfunction, characterized by loss of sensation, increased capacity and decreased contractility, was the main observation of diabetic cystopathy regardless of the duration or severity of the disease. The association of bladder dysfunction and autonomic neuropathy detected by the sympathetic skin response might indicate that diabetic cystopathy is a manifestation of peripheral neuropathy induced by diabetes.

These findings suggest that ACE inhibitors augment reactive hyperemia, an index of endothelium-dependent vasorelaxation, in patients with essential hypertension. This augmentation may be due to increases in NO.

Clinical guidelines for interstitial cystitis and hypersensitive bladder have been updated as of 2015. The guidelines define interstitial cystitis by the presence of hypersensitive bladder symptoms (discomfort, pressure or pain in the bladder usually associated with urinary frequency and nocturia) and bladder pathology, after excluding other diseases explaining symptoms. Interstitial cystitis is further classified by bladder pathology; either Hunner type interstitial cystitis with Hunner lesions or non-Hunner type interstitial cystitis with mucosal bleeding after distension in the absence of Hunner lesions. Hypersensitive bladder refers to a condition, where hypersensitive bladder symptoms are present, but bladder pathology or other explainable diseases are unproven. Interstitial cystitis and hypersensitive bladder severely affect patients' quality of life as a result of disabling symptoms and/or comorbidities. Reported prevalence suggestive of these disorders varies greatly from 0.01% to >6%. Pathophysiology would be an interaction of multiple factors including urothelial dysfunction, inflammation, neural hyperactivity, exogenous substances and extrabladder disorders. Definite diagnosis of interstitial cystitis and hypersensitive bladder requires cystoscopy with or without hydrodistension. Most of the therapeutic options lack a high level of evidence, leaving a few as recommended therapeutic options.