Purpose: We present a case of malignant glaucoma following cataract surgery in a nanophthalmic eye.Case summary: A 74-year-old woman with a nanophthalmic right eye (axial length 20.51 mm) underwent cataract surgery at a local hospital. One week postoperatively, she presented with a dislocated intraocular lens (IOL) and a shallow anterior chamber. Malignant glaucoma was suspected, and the patient underwent pars plana vitrectomy followed by neodymium-doped yttrium aluminum garnet laser posterior capsulotomy. Despite these interventions, the IOL remained anteriorly displaced, prompting referral to our institution for further management. Upon presentation, the patient exhibited an intraocular pressure (IOP) of 38 mmHg despite maximal medical therapy; spherical equivalent (SE) was -3.88 diopters. To differentiate pupillary block and establish a definitive diagnosis, laser iridotomy was performed; this resulted in a significant reduction in IOP to 10 mmHg and deepening of the anterior chamber. However, 19 days post-iridotomy, the IOP again increased to 39 mmHg; the SE worsened to -4.88 diopters. Slit-lamp examination and ultrasound biomicroscopy revealed a transparent membrane obstructing the iridotomy site behind the iris, consistent with a complex of disrupted ciliary zonules and the anterior hyaloid. Subsequently, photodisruption of this membrane was performed through the existing iridotomy. This intervention deepened the anterior chamber and achieved a wide-open iridocorneal angle. At the last follow-up, the patient had maintained an IOP of 10 mmHg without glaucoma medication. Furthermore, SE improved to -0.38 diopters, resulting in a best-corrected visual acuity of 1.0. Conclusions Our case demonstrates the development of malignant glaucoma following cataract surgery and subsequent total vitrectomy and laser posterior capsulotomy in a nanophthalmic eye. Thorough irido-zonulo-hyaloidotomy demonstrated to be an effective approach for achieving significant IOP reduction.

Purpose: We present a case of malignant glaucoma following cataract surgery in a nanophthalmic eye.Case summary: A 74-year-old woman with a nanophthalmic right eye (axial length 20.51 mm) underwent cataract surgery at a local hospital. One week postoperatively, she presented with a dislocated intraocular lens (IOL) and a shallow anterior chamber. Malignant glaucoma was suspected, and the patient underwent pars plana vitrectomy followed by neodymium-doped yttrium aluminum garnet laser posterior capsulotomy. Despite these interventions, the IOL remained anteriorly displaced, prompting referral to our institution for further management. Upon presentation, the patient exhibited an intraocular pressure (IOP) of 38 mmHg despite maximal medical therapy; spherical equivalent (SE) was -3.88 diopters. To differentiate pupillary block and establish a definitive diagnosis, laser iridotomy was performed; this resulted in a significant reduction in IOP to 10 mmHg and deepening of the anterior chamber. However, 19 days post-iridotomy, the IOP again increased to 39 mmHg; the SE worsened to -4.88 diopters. Slit-lamp examination and ultrasound biomicroscopy revealed a transparent membrane obstructing the iridotomy site behind the iris, consistent with a complex of disrupted ciliary zonules and the anterior hyaloid. Subsequently, photodisruption of this membrane was performed through the existing iridotomy. This intervention deepened the anterior chamber and achieved a wide-open iridocorneal angle. At the last follow-up, the patient had maintained an IOP of 10 mmHg without glaucoma medication. Furthermore, SE improved to -0.38 diopters, resulting in a best-corrected visual acuity of 1.0. Conclusions Our case demonstrates the development of malignant glaucoma following cataract surgery and subsequent total vitrectomy and laser posterior capsulotomy in a nanophthalmic eye. Thorough irido-zonulo-hyaloidotomy demonstrated to be an effective approach for achieving significant IOP reduction.

Purpose: We present a case of malignant glaucoma following cataract surgery in a nanophthalmic eye.Case summary: A 74-year-old woman with a nanophthalmic right eye (axial length 20.51 mm) underwent cataract surgery at a local hospital. One week postoperatively, she presented with a dislocated intraocular lens (IOL) and a shallow anterior chamber. Malignant glaucoma was suspected, and the patient underwent pars plana vitrectomy followed by neodymium-doped yttrium aluminum garnet laser posterior capsulotomy. Despite these interventions, the IOL remained anteriorly displaced, prompting referral to our institution for further management. Upon presentation, the patient exhibited an intraocular pressure (IOP) of 38 mmHg despite maximal medical therapy; spherical equivalent (SE) was -3.88 diopters. To differentiate pupillary block and establish a definitive diagnosis, laser iridotomy was performed; this resulted in a significant reduction in IOP to 10 mmHg and deepening of the anterior chamber. However, 19 days post-iridotomy, the IOP again increased to 39 mmHg; the SE worsened to -4.88 diopters. Slit-lamp examination and ultrasound biomicroscopy revealed a transparent membrane obstructing the iridotomy site behind the iris, consistent with a complex of disrupted ciliary zonules and the anterior hyaloid. Subsequently, photodisruption of this membrane was performed through the existing iridotomy. This intervention deepened the anterior chamber and achieved a wide-open iridocorneal angle. At the last follow-up, the patient had maintained an IOP of 10 mmHg without glaucoma medication. Furthermore, SE improved to -0.38 diopters, resulting in a best-corrected visual acuity of 1.0. Conclusions Our case demonstrates the development of malignant glaucoma following cataract surgery and subsequent total vitrectomy and laser posterior capsulotomy in a nanophthalmic eye. Thorough irido-zonulo-hyaloidotomy demonstrated to be an effective approach for achieving significant IOP reduction.

Objective: Despite the increasingly widespread adoption of unilateral biportal endoscopic (UBE) decompressive laminectomy for lumbar spinal stenosis, the learning curve for surgeons new to endoscopic techniques remains a significant barrier. This study aimed to quantify this learning curve and identify strategies to expedite proficiency, focusing on reducing operative times and complications. Methods: The cumulative summation test was used to evaluate the learning curves for both the operative time and the degree of intraoperative dural tear occurrence. Moreover, clinical outcomes and postoperative complications were compared between the cranial and caudal approaches, depending on the direction of ligamentum flavum removal. Results: In total, 54 patients were included, with 22 in the cranial group and 32 in the caudal group. The operative time was notably shorter in the caudal group (cranial group, 110.86±32.63 minutes; caudal group, 79.56±24.21 minutes; p<0.01), and the complication rate was considerably lower (cranial group, 40%; caudal group, 15%; p=0.04). Twenty-six patients and 29 patients were needed to overcome the learning curves for operative time and intraoperative dural tear occurrence, respectively. Conclusion Although UBE surgery has a short learning curve, a considerable number of cases (26 and 29, respectively) were needed to achieve competency in terms of operative time and intraoperative dural tear occurrence. We highlight the caudal-to-cranial direction of ligamentum flavum dissection and removal as a way to decrease the number of dural tears and shorten the operative time.

BACKGROUND/OBJECTIVES: Accurate estimation of nutrient intake from food consumption requires reliable food composition data. However, since nutrient content changes during cooking, the application of raw ingredient composition may lead to overestimation, particularly for energy and fat in meat dishes. In this study, the suitability of applying cooked food codes for meat dishes to improve the validity of recipe-based nutrient content estimation was evaluated.MATERIALS/METHODS: Pork (thin-sliced and thick-cut belly and shoulder butt) and beef (tenderloin, loin, rib meat, and brisket point) were examined for cooking yield after grilling and their nutrient contents were estimated. Each cut was portioned to 100 g of raw meat and cooked in triplicate. Nutrient content was calculated using both raw and cooked meat codes from the Korean Standard Food Composition Table, and differences in energy, fat, and protein content were compared. RESULTS: When grilled under standardized conditions, the average cooking yield was approximately 65% for pork and 80% for beef (P < 0.0001). Thin slices of pork belly had a lower yield (62.6%) than thicker cuts (68.0%), while beef brisket point had the lowest yield among beef cuts (63.6%). Applying cooked meat codes and measured cooking yields resulted in overall decreases in energy (−10% to −50%) and fat (−20% to −60%) content, with slight increase in protein (up to +34%, P < 0.0001). For beef tenderloin, additional comparisons using matched raw and grilled data from the United States Department of Agriculture SR Legacy Database showed smaller percent differences in energy, fat, and protein than those obtained from the Korean database. CONCLUSION Incorporating measured cooking yields and corresponding cooked meat codes into recipe-based databases can improve the accuracy of nutrient intake estimation. The development of nutrient databases that reflect differences in cooking conditions—including temperature, duration, and doneness—should be prioritized to enhance the validity of national dietary surveys.

Chronic obstructive pulmonary disease (COPD), a leading cause of morbidity and mortality throughout the world, is a highly complicated disease that includes chronic airway inflammation, airway remodeling, emphysema, and mucus hypersecretion.For respiratory function, an intact lung structure is required for efficient air flow through conducting airways and gas exchange in alveoli. Structural changes in small airways and inflammation are major features of COPD. At present, mechanisms involved in the genesis and development of COPD are poorly understood. Currently, there are no effective treatments for COPD. To develop better treatment strategies, it is necessary to study mechanisms of COPD using proper experimental models that can recapitulate distinctive features of human COPD. Therefore, this review will discuss representative established mouse models to investigate inflammatory processes and basic mechanisms of COPD. In addition, human COPD-mimicking human lung organoid models are introduced to help researchers overcome limits of mouse COPD models.

In this study, we explored the impact of systemic inflammation on initial brain injury and repair processes, including neurite extension and synapse formation. For this purpose, we established a brain injury model by administering adenosine triphosphate (ATP), a component of damage-associated molecular patterns (DAMPs), through stereotaxic injection into the striatum of mice. Systemic inflammation was induced by intraperitoneal injection of lipopolysaccharide (LPS-ip). Bulk RNA-sequencing (RNA-seq) analyses and immunostaining for microtubule-associated protein 2 (MAP2) and tyrosine hydroxylase (TH) showed that LPS-ip led to a reduction in initial brain injury, but inhibited neurite extension into the damaged brain. LPS-ip upregulated expression of defense response genes and anti-apoptotic genes, but decreased expression of genes associated with repair and regeneration. In addition, LPS-ip reduced levels of vGlut1 and PSD95 (markers for excitatory pre and post synapses, respectively), but had little effect on vGAT and gephyrin (markers for inhibitory pre and post synapses, respectively). Taken together, these findings suggest that systemic inflammation reduce initial damage but impede subsequent repair process.

Chronic obstructive pulmonary disease (COPD), a leading cause of morbidity and mortality throughout the world, is a highly complicated disease that includes chronic airway inflammation, airway remodeling, emphysema, and mucus hypersecretion.For respiratory function, an intact lung structure is required for efficient air flow through conducting airways and gas exchange in alveoli. Structural changes in small airways and inflammation are major features of COPD. At present, mechanisms involved in the genesis and development of COPD are poorly understood. Currently, there are no effective treatments for COPD. To develop better treatment strategies, it is necessary to study mechanisms of COPD using proper experimental models that can recapitulate distinctive features of human COPD. Therefore, this review will discuss representative established mouse models to investigate inflammatory processes and basic mechanisms of COPD. In addition, human COPD-mimicking human lung organoid models are introduced to help researchers overcome limits of mouse COPD models.

In this study, we explored the impact of systemic inflammation on initial brain injury and repair processes, including neurite extension and synapse formation. For this purpose, we established a brain injury model by administering adenosine triphosphate (ATP), a component of damage-associated molecular patterns (DAMPs), through stereotaxic injection into the striatum of mice. Systemic inflammation was induced by intraperitoneal injection of lipopolysaccharide (LPS-ip). Bulk RNA-sequencing (RNA-seq) analyses and immunostaining for microtubule-associated protein 2 (MAP2) and tyrosine hydroxylase (TH) showed that LPS-ip led to a reduction in initial brain injury, but inhibited neurite extension into the damaged brain. LPS-ip upregulated expression of defense response genes and anti-apoptotic genes, but decreased expression of genes associated with repair and regeneration. In addition, LPS-ip reduced levels of vGlut1 and PSD95 (markers for excitatory pre and post synapses, respectively), but had little effect on vGAT and gephyrin (markers for inhibitory pre and post synapses, respectively). Taken together, these findings suggest that systemic inflammation reduce initial damage but impede subsequent repair process.

In this study, we explored the impact of systemic inflammation on initial brain injury and repair processes, including neurite extension and synapse formation. For this purpose, we established a brain injury model by administering adenosine triphosphate (ATP), a component of damage-associated molecular patterns (DAMPs), through stereotaxic injection into the striatum of mice. Systemic inflammation was induced by intraperitoneal injection of lipopolysaccharide (LPS-ip). Bulk RNA-sequencing (RNA-seq) analyses and immunostaining for microtubule-associated protein 2 (MAP2) and tyrosine hydroxylase (TH) showed that LPS-ip led to a reduction in initial brain injury, but inhibited neurite extension into the damaged brain. LPS-ip upregulated expression of defense response genes and anti-apoptotic genes, but decreased expression of genes associated with repair and regeneration. In addition, LPS-ip reduced levels of vGlut1 and PSD95 (markers for excitatory pre and post synapses, respectively), but had little effect on vGAT and gephyrin (markers for inhibitory pre and post synapses, respectively). Taken together, these findings suggest that systemic inflammation reduce initial damage but impede subsequent repair process.