PURPOSE: To report a case of irregular astigmatism caused by a free flap during laser-assisted in situ keratomileusis (LASIK) surgery that was treated with a flap rotation based on postoperative topography. CASE SUMMARY: A 21-year-old female underwent LASIK, which was complicated by a free cap on her right eye. Because the gentian violet markings were no longer present, the exact orientation of the cap was unknown. At 3 months after surgery, the astigmatism of the right eye was −3.00 diopters (D) with an uncorrected visual acuity (UCVA) of 0.4, and the astigmatism of the left eye was −0.75 D with an UCVA of 1.0. The corneal topography was analyzed in order to return to the existing position. Free cap repositioning was performed and irregular astigmatism was corrected to improve the UCVA to 1.0. CONCLUSIONS: If the preoperative markings cannot be identified on a free flap during LASIK, secondary postoperative corneal topographic analysis can be performed to restore the corneal free flap to its original position to minimize astigmatism with good visual outcomes.
Astigmatism ; Corneal Topography ; Female ; Free Tissue Flaps ; Gentian Violet ; Humans ; Keratomileusis, Laser In Situ ; Visual Acuity ; Young Adult

Motor neuron diseases (MNDs) refer to a heterogeneous group of progressive neurologic disorders caused by degeneration of motor neurons. The diseases affect either the upper motor neurons, lower motor neurons, or both, and are characterized by weakness, atrophy, fasciculation, spasticity, and respiratory failure. We report a case of a 61-year-old male patient with no past history of cardiovascular or pulmonary disease, who presented with only dyspnea, and no indication of any other symptom such as muscle weakness, atrophy, or bulbar dysfunction. Neuromuscular conduction study, including a study of the phrenic nerve, confirmed the diagnosis of MND. The patient greatly improved giving respiratory assistance at night, using a noninvasive ventilator. This case indicates that MNDs should be considered as differential diagnoses for patients showing acute respiratory failure of unknown causes. This report will aid in the prompt diagnosis and treatment of MNDs.
Atrophy ; Diagnosis ; Diagnosis, Differential ; Dyspnea ; Fasciculation ; Humans ; Lung Diseases ; Male ; Middle Aged ; Motor Neuron Disease* ; Motor Neurons* ; Muscle Spasticity ; Muscle Weakness ; Nervous System Diseases ; Phrenic Nerve ; Respiration, Artificial ; Respiratory Insufficiency* ; Ventilators, Mechanical

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.

Mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) is one of the mitochondrial disorders that can present as a stroke-like episode or seizure. Although the pathophysiology of MELAS remains inconclusive, the main possibilities are thus far thought to be mitochondrial cytopathy and angiopathy. This case report describes a 61-year-old woman diagnosed with MELAS who presented simultaneously with vascular hyperemia and crossed cerebellar diaschisis.
Acidosis, Lactic ; Female ; Humans ; Hyperemia ; Kearns-Sayre Syndrome ; Mitochondrial Diseases ; Mitochondrial Encephalomyopathies ; Mitochondrial Myopathies ; Seizures

Mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) is one of the mitochondrial disorders that can present as a stroke-like episode or seizure. Although the pathophysiology of MELAS remains inconclusive, the main possibilities are thus far thought to be mitochondrial cytopathy and angiopathy. This case report describes a 61-year-old woman diagnosed with MELAS who presented simultaneously with vascular hyperemia and crossed cerebellar diaschisis.
Acidosis, Lactic ; Female ; Humans ; Hyperemia ; Kearns-Sayre Syndrome ; Mitochondrial Diseases ; Mitochondrial Encephalomyopathies ; Mitochondrial Myopathies ; Seizures

Callosal anomalies are frequently associated with other central nervous system (CNS) and/or somatic anomalies. We retrospectively analyzed the clinical features of corpus callosal agenesis/hypoplasia accompanying other CNS and/or somatic anomalies. We reviewed the imaging and clinical information of patients who underwent brain magnetic resonance imaging in our hospital, between 2005 and 2012. Callosal anomalies were isolated in 13 patients, accompanied by other CNS anomalies in 10 patients, associated with only non-CNS somatic anomalies in four patients, and with both CNS and non-CNS abnormalities in four patients. Out of 31 patients, four developed normally, without impairments in motor or cognitive functions. Five of nine patients with cerebral palsy were accompanied by other CNS and/or somatic anomalies, and showed worse Gross Motor Function Classification System scores, compared with the other four patients with isolated callosal anomaly. In addition, patients with other CNS anomalies also had a higher seizure risk.
Adolescent* ; Brain ; Central Nervous System ; Cerebral Palsy ; Child* ; Classification ; Humans ; Magnetic Resonance Imaging ; Retrospective Studies ; Seizures

Objectives: This study aimed to analyze the outcomes of the Comprehensive Health and Social Need Assessment (CHSNA) system, which identifies community residents’ health and social needs, and to link these needs with the International Classification of Functioning, Disability, and Health (ICF). Methods: Adult community residents in a metropolitan city in Korea were recruited. They were asked to assess their health and social needs via the CHSNA system, which was integrated into an online community-care platform. Three assessment steps (basic health assessment, needs for activities of daily living, and in-depth health assessment) associated with five ICF components were used to evaluate physical health impairment, difficulties in activities and participation, and environmental problems. The final list of health and social needs was systematically linked to the domains and categories of the ICF. Only data from participants who completed all three assessment steps were included. Results: Wide ranges of impairments and difficulties regarding the daily living activities, physical health, and environmental status of the community were recorded from 190 people who completed assessments of their health and social needs by the CHSNA system. These participants reported various health and social needs for their community life; common needs corresponded to the ICF components of body functions and activities/participation. Conclusions The ICF may be suitable for determining the health-related problems and needs of the general population. Possible improvements to the present system include providing support for completing all assessment steps and developing an ICF core set for an enhanced understanding of health and social needs.