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.

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.

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.