PURPOSE: Keratoconus is a bilateral noninflammatory ecstatic disease of cornea. Clinical manifestations and treatments are well-described , but the exact pathophysiology has many debates. There are many reports on pathologic abnormalities of keratoconus, but few reports on epithelial adhesion complex. The authors investigated the abnormalities in epithelial adhesion complex of keratoconus. METHODS: Using 4 corneas from 4 recipients of penetrating keratoplasty, examination was done with transmission electron microscope (Hitachi-600, Japan) after proper fixation and staining. Central and peripheral portion of each corneal tissues were examined. RESULTS: In two tissues, severe degeneration of basement membrane and Bowman's layer were found. Some degree of abnormalities was found in other tissues, which had minimal change. Some of hemidesmosomes, the most distinct part of adhesion complex, were found only in well-maintained tissue but the distribution was abnormal. CONCLUSIONS: The fact that basal plasma membrane had selectively more degenerations and changes than intercellular plasma membrane implies pathophysiology of keratoconus on adhesion complex, basal plasma membrane, basement membrane and Bowman's layer. Further study on this issue will reveal more information as to its pathophysiology.
Basement Membrane ; Cell Membrane ; Cornea ; Hemidesmosomes ; Keratoconus* ; Keratoplasty, Penetrating

PURPOSE: This study aimed to investigate the microscopic findings of characteristic epithelial herpes simplex keratitis (HSK) and the changes of those findings over time. METHODS: Sixteen rabbits were inoculated with the Kos-stain of herpes simplex virus (HSV) type 1 in both eyes. Two rabbits each were enucleated on the 2nd, 3rd, 4th, 5th, 6th, 7th, and 9th day after viral inoculation and were observed with a scanning electron microscope (S-2380n, Hitachi, Japan). RESULTS: Corneas showed dendritic epithelial desquamation, changes in epithelial microvilli, and changes in intercellular adhesion. With progression, the basement membrane and basal cells were exposed, intercellular spaces were broadened, and the adhesion of basal cells to basement membrane and the intercellular adhesion were loosened. Later, infiltrations of some inflammatory cells were found. Until the last day there was no destruction of basement membrane or an exposure of stroma. CONCLUSIONS: Though it was impossible to follow up a lesion throughout the experiment because of the necessity of enucleation, and in addition, the findings could not be generalized to all the strains, this study provides a better understanding of HSK. Further studies on various manifestations of HSK from other strains of HSV are needed in the future.
Basement Membrane ; Cornea ; Extracellular Space ; Follow-Up Studies ; Keratitis* ; Keratitis, Herpetic ; Microscopy, Electron, Scanning ; Microvilli ; Rabbits* ; Simplexvirus

Urinary incontinence (UI), affecting 3%-11% of males and 25%-45% of females globally, is expected to rise with an aging population. It significantly impacts mental health, causing depression, stress, and reduced quality of life. UI can exacerbate psychiatric conditions, affecting treatment compliance and effectiveness. Itis categorized into transient and chronic types. Transient UI, often reversible, is caused by factors summarized in the acronym DIAPPERS: Delirium, Infection, Atrophic urethritis/vaginitis, Psychological disorders, Pharmaceuticals, Excess urine output, Restricted mobility, Stool impaction. Chronic UI includes stress, urge, mixed, overflow, functional, and persistent incontinence. Drug-induced UI, a transient form, is frequently seen in psychiatric treatment. Antipsychotics, antidepressants, and other psychiatric medications can cause UI through various mechanisms like affecting bladder muscle tone, altering nerve reflexes, and inducing other conditions like diabetes or epilepsy. Specific drugs like lithium and valproic acid have also been linked to UI, though mechanisms are not al-ways clear. Managing UI in psychiatric patients requires careful monitoring of urinary symptoms and judiciousmedication management. If a drug is identified as the cause, options include discontinuing, reducing, or adjusting the dosage. In cases where medication continuation is necessary, additional treatments like desmopressin, oxybutynin, trihexyphenidyl, or amitriptyline may be considered.

Objective: This study investigates NOX4, an enzyme producing hydrogen peroxide, in endochondral ossification and bone remodeling. NOX4’s role in osteoblast formation and osteogenic signaling pathways is explored. Methods: Using NOX4-deficient (NOX4−/− ) and ovariectomized (OVX) mice, we identify NOX4’s potential mediators in bone maturation. Results: NOX4−/− mice displayed significant differences in bone mass and structure.Compared to the normal Control and OVX groups. Hematoxylin and eosin staining showed NOX4−/− mice had the highest trabecular bone volume, while OVX had the lowest. Proteomic analysis revealed significantly elevated MPO and OPN levels in bone marrow-derived cells in NOX4−/− mice. Immunohistochemistry confirmed increased MPO, OPN, and collagen II (COLII) near the epiphyseal plate. Collagen and chondrogenesis analysis supported enhanced bone development in NOX4−/− mice. Conclusions and Relevance: Our results emphasize NOX4’s significance in bone morphology, mesenchymal stem cell proteomics, immunohistochemistry, collagen levels, and chondrogenesis. NOX4 deficiency enhances bone development and endochondral ossification, potentially through increased MPO, OPN, and COLII expression. These findings suggest therapeutic implications for skeletal disorders.

Objective: This study investigates NOX4, an enzyme producing hydrogen peroxide, in endochondral ossification and bone remodeling. NOX4’s role in osteoblast formation and osteogenic signaling pathways is explored. Methods: Using NOX4-deficient (NOX4−/− ) and ovariectomized (OVX) mice, we identify NOX4’s potential mediators in bone maturation. Results: NOX4−/− mice displayed significant differences in bone mass and structure.Compared to the normal Control and OVX groups. Hematoxylin and eosin staining showed NOX4−/− mice had the highest trabecular bone volume, while OVX had the lowest. Proteomic analysis revealed significantly elevated MPO and OPN levels in bone marrow-derived cells in NOX4−/− mice. Immunohistochemistry confirmed increased MPO, OPN, and collagen II (COLII) near the epiphyseal plate. Collagen and chondrogenesis analysis supported enhanced bone development in NOX4−/− mice. Conclusions and Relevance: Our results emphasize NOX4’s significance in bone morphology, mesenchymal stem cell proteomics, immunohistochemistry, collagen levels, and chondrogenesis. NOX4 deficiency enhances bone development and endochondral ossification, potentially through increased MPO, OPN, and COLII expression. These findings suggest therapeutic implications for skeletal disorders.

Objective: This study investigates NOX4, an enzyme producing hydrogen peroxide, in endochondral ossification and bone remodeling. NOX4’s role in osteoblast formation and osteogenic signaling pathways is explored. Methods: Using NOX4-deficient (NOX4−/− ) and ovariectomized (OVX) mice, we identify NOX4’s potential mediators in bone maturation. Results: NOX4−/− mice displayed significant differences in bone mass and structure.Compared to the normal Control and OVX groups. Hematoxylin and eosin staining showed NOX4−/− mice had the highest trabecular bone volume, while OVX had the lowest. Proteomic analysis revealed significantly elevated MPO and OPN levels in bone marrow-derived cells in NOX4−/− mice. Immunohistochemistry confirmed increased MPO, OPN, and collagen II (COLII) near the epiphyseal plate. Collagen and chondrogenesis analysis supported enhanced bone development in NOX4−/− mice. Conclusions and Relevance: Our results emphasize NOX4’s significance in bone morphology, mesenchymal stem cell proteomics, immunohistochemistry, collagen levels, and chondrogenesis. NOX4 deficiency enhances bone development and endochondral ossification, potentially through increased MPO, OPN, and COLII expression. These findings suggest therapeutic implications for skeletal disorders.

Objective: This study investigates NOX4, an enzyme producing hydrogen peroxide, in endochondral ossification and bone remodeling. NOX4’s role in osteoblast formation and osteogenic signaling pathways is explored. Methods: Using NOX4-deficient (NOX4−/− ) and ovariectomized (OVX) mice, we identify NOX4’s potential mediators in bone maturation. Results: NOX4−/− mice displayed significant differences in bone mass and structure.Compared to the normal Control and OVX groups. Hematoxylin and eosin staining showed NOX4−/− mice had the highest trabecular bone volume, while OVX had the lowest. Proteomic analysis revealed significantly elevated MPO and OPN levels in bone marrow-derived cells in NOX4−/− mice. Immunohistochemistry confirmed increased MPO, OPN, and collagen II (COLII) near the epiphyseal plate. Collagen and chondrogenesis analysis supported enhanced bone development in NOX4−/− mice. Conclusions and Relevance: Our results emphasize NOX4’s significance in bone morphology, mesenchymal stem cell proteomics, immunohistochemistry, collagen levels, and chondrogenesis. NOX4 deficiency enhances bone development and endochondral ossification, potentially through increased MPO, OPN, and COLII expression. These findings suggest therapeutic implications for skeletal disorders.

Background/Aims: Drugs with anticholinergic properties (DAPs) are associated with adverse health outcomes in older patients. The objective of this study was to evaluate the factors that determine the prescribing of more DAPs in long-term care hospitals (LTCHs) in Korea. In addition, the current patterns of DAP prescription were explored using a novel platform, which can collect data from LTCHs. Methods: This was a Health-RESPECT (integrated caRE Systems for elderly PatiEnts using iCT) sub-study, which is a pragmatic, cluster-randomized, controlled trial. The Health-RESPECT platform was used to collect prescribed medication data of 466 patients (aged ≥ 65 years) from seven LTCHs. DAPs were identified using the Korean Anticholinergic Burden Scale (KABS). Physical frailty, cognitive function, functional status, and quality of life were evaluated. Results: Among 466 LTCH patients, 88.8% (n = 414) were prescribed DAPs, and the prevalence of high KABS (≥ 3) was 70.4% (n = 328). The drugs that contributed most to the total KABS were quetiapine (20.7%), chlorpheniramine (19.5%), tramadol (9.8%), cimetidine (5.8%), and furosemide (3.6%). Polypharmacy, higher body mass index, less dependence, better communication and cognitive functions, and poorer quality of life were associated with high KABS. Conclusions Although the patients with a high burden of DAPs were less dependent and had better cognitive and communication functions, they had poorer quality of life. DAP use in LTCH patients should be monitored carefully, and the risk/ benefit relationship for their use should be considered.