Changes in High-order Aberrations after Phacotrabeculectomy Surgery

PURPOSE: To investigate changes in ocular high-order aberrations (HOAs) resulting from phacotrabeculectomy and phacoemulsification. METHODS: We retrospectively reviewed 38 eyes of 38 glaucoma and cataract patients who underwent mitomycin C (MMC) augmented trabeculectomy with phacoemulsification and 34 eyes of 34 cataract patients who underwent phacoemulsifiction. For all patients, we measured the best corrected visual acuity (BCVA), intraocular pressure (IOP), keratometry, and HOAs (iTrace, Tracey Technologies, Houston, TX, USA) both preoperatively and postoperatively. RESULTS: IOP was significantly decreased after surgery in the combined group (p < 0.001). Entire eye, coma-like, and spherical-like high-order aberrations from each entire eye, corneal aberrations, and internal-optics aberration were increased until after 2 weeks, which then decreased until 3 months after phacotrabeculectomy. In the phacoemulsification group, entire eye (each p = 0.006, p =0.006), coma-like (each p = 0.006 and p = 0.005), and spherical-like high-order aberrations (each p = 0.008, p = 0.005) from entire eye and internal-optics aberrations were decreased. CONCLUSIONS: After cataract surgery, entire eye, coma-like, and spherical-like high-order aberrations were significantly decreased while aberrations did not change after combined operation. These results suggest that a change in high-order aberrations of internal optics results in a decrease in postoperative HOAs. In addition, the baseline HOAs of the cataract group were higher than those of the combined surgery group, and the effect of trabeculectomy on HOAs may offset the impact of cataract surgery in the combined surgery group.

Acute Kidney Injury due to Rbadomyolysis Complicated with Zolpidem Overdose / 대한내과학회지

Zolpidem (Stilnox®, Handok, Seoul, Korea) is a hypnotic imidazopyridine that is often used to treat insomnia because it has less abuse and addiction potential than benzodiazepines. Its side effects include headache, dizziness, and nausea, but these are mild. Zolpidem intoxication rarely has severe complications. Here, we report a case of acute kidney injury due to rhabdomyolysis related to zolpidem. A 51-year-old man was admitted with drowsy mentality after taking an overdose of zolpidem in a suicide attempt. Laboratory findings showed a blood urea nitrogen of 59.9 mg/dL, serum creatinine of 5.8 mg/dL, and creatine phosphokinase of 16,210 IU/L. Acute kidney injury associated with rhabdomyolysis complicating zolpidem intoxication was diagnosed. The patient was managed with hemodialysis and recovered completely in terms of renal function and muscle enzyme levels.

A Case of Pigmentary Glaucoma Due to Multidrug-Resistant Tuberculosis Treatment

PURPOSE: To report a case of secondary pigmentary glaucoma due to clofazimine treatment for extensive drug-resistant tuberculosis. CASE SUMMARY: A 23-year-old man presented with blurred vision in both eyes. The patient started to take clofazimine for extensive drug-resistant tuberculosis six months prior, after which his facial skin color changed to a dark-brown. Intraocular pressure (IOP) was 50 mm Hg in the right eye and 48 mm Hg in the left eye. Slit lamp examination revealed corneal edema, opacity, and flare in the anterior chamber in both eyes. A color vision test revealed a mild color defect in both eyes. Visual field (VF) test revealed superior temporal VF loss in the left eye. Gonioscopy revealed open angles with high pigmentation in the trabecular meshwork in both eyes. The patient was diagnosed with pigmentary glaucoma, and maximum tolerated medical therapy was performed. However, the IOP was uncontrolled. Trabeculectomy was performed in both eyes. Postoperative IOP was measured to be 12 mm Hg in both eyes without medication, and visual acuity measured 20/22 in the right eye and 20/17 in the left eye. CONCLUSIONS: To the best of our knowledge, this report is the first case of clofazimine being a possible cause of pigmentary glaucoma in a patient with extensive drug-resistant tuberculosis.

Role of transcription factor acetylation in the regulation of metabolic homeostasis

Post-translational modifications (PTMs) of transcription factors play a crucial role in regulating metabolic homeostasis. These modifications include phosphorylation, methylation, acetylation, ubiquitination, SUMOylation, and O-GlcNAcylation. Recent studies have shed light on the importance of lysine acetylation at nonhistone proteins including transcription factors. Acetylation of transcription factors affects subcellular distribution, DNA affinity, stability, transcriptional activity, and current investigations are aiming to further expand our understanding of the role of lysine acetylation of transcription factors. In this review, we summarize recent studies that provide new insights into the role of protein lysine-acetylation in the transcriptional regulation of metabolic homeostasis.

Efficacy of Plasma Exchange Therapy for Steroid-Unresponsive Neuromyelitis Optica

PURPOSE: To report the therapeutic efficacy of plasma exchange therapy on steroid-unresponsive neuromyelitisoptica (NMO) patients. CASE SUMMARY: Three patients who had not achieved improvement of visual acuity and visual field after high steroid pulse therapy after optic neuritis visited our clinic with decreasing visual acuity combined with eye pain in the other eye. All patients were diagnosed as neuromyelitisoptica (NMO) based on the presence of NMO-IgG antibody and optic nerve enhancing in contrast-enhanced orbital magnetic resonance imaging (MRI). Recurrent optic neuritis was observed. Steroid pulse retreatment was started but visual acuity was not improved in all patients. The patients received plasma exchange therapy, followed by immune suppression therapy. All patients showed improved visual acuity and restored visual field promptly without recurrence of neuromyelitisoptica. CONCLUSIONS: In case of steroid-unresponsive neuromyelitisoptica, plasma exchange should be promptly considered as the treatment of choice.

A Case of Retinal Pigmentary Degeneration in PKAN

PURPOSE: Pantothenate kinase-associated neurodegeneration (PKAN), also known as neurodegeneration with brain iron accumulation is an extremely rare degenerative disease. The present study reports a case of retinal pigmentary changes in PKAN. CASE SUMMARY: A 6-year-old girl presented with night blindness and developmental delay. Neurologic examination revealed toe gait and dystonia. Ocular examination showed retinal pigmentary change in the entire retina without optic atrophy. Brain magnetic resonance imaging showed iron deposits in the basal ganglia, the so-called "eye of the tiger" sign. Genetic tests confirmed a mutation in the gene encoding pantothenate kinase 2. Electroretinography demonstrated severe loss of rod and cone responses, prominently reduced in the rod response. The patient was diagnosed with PKAN and pharmacologic treatment started. CONCLUSIONS: In the case of systemic neurological abnormalities with pigmentary retinal change, PKAN should be considered as a differential diagnosis.

Modulation of the Transcriptional Activity of Peroxisome Proliferator-Activated Receptor Gamma by Protein-Protein Interactions and Post-Translational Modifications

Peroxisome proliferator-activated receptor gamma (PPARgamma) belongs to a nuclear receptor superfamily; members of which play key roles in the control of body metabolism principally by acting on adipose tissue. Ligands of PPARgamma, such as thiazolidinediones, are widely used in the treatment of metabolic syndromes and type 2 diabetes mellitus (T2DM). Although these drugs have potential benefits in the treatment of T2DM, they also cause unwanted side effects. Thus, understanding the molecular mechanisms governing the transcriptional activity of PPARgamma is of prime importance in the development of new selective drugs or drugs with fewer side effects. Recent advancements in molecular biology have made it possible to obtain a deeper understanding of the role of PPARgamma in body homeostasis. The transcriptional activity of PPARgamma is subject to regulation either by interacting proteins or by modification of the protein itself. New interacting partners of PPARgamma with new functions are being unveiled. In addition, post-translational modification by various cellular signals contributes to fine-tuning of the transcriptional activities of PPARgamma. In this review, we will summarize recent advancements in our understanding of the post-translational modifications of, and proteins interacting with, PPARgamma, both of which affect its transcriptional activities in relation to adipogenesis.

Clinical Characteristics and Treatment of Esotropia Following Bare Sclera Pterygium Surgery

PURPOSE: The clinical features of esotropia after bare scleral pterygium surgery and dipolpia treatment results were evaluated in the present study. METHODS: Twenty eyes of 12 patients who had esotropia after bare sclera pterygium surgery from 2008 to 2011 were retrospectively investigated. RESULTS: Diplopia occurred at 2.8 +/- 1.6 months (1-6 months) after pterygium surgery. The mean pre-operative angle of esotropia was 19.4 +/- 8.9 PD (8-40 PD) at distance and 16 +/- 7.3 PD (0-30 PD) at near. All patients showed limitation of abduction in the pterygium operated eye. Two patients were prescribed prism glasses, 2 patients underwent conjunctiva surgery, and medial rectus recession with simultaneous intraoperative adjustment surgery was performed in 8 patients. An additional strabismus operation was required for 2 patients who received conjunctival surgery due to diplopia recurrence. Seven patients (70%) showed orthotropia at 3 months. CONCLUSIONS: In this study, diplopia following postoperative adhesion caused by bare sclera pterygium surgery technique was observed. Conjunctiva-perimuscular scar tissue removal and medial rectus recession were effective methods in eliminating diplopia.

Lysophosphatidylglycerol inhibits formyl peptide receptor like-1-stimulated chemotactic migration and IL-1beta production from human phagocytes

In this study, we observed that lysophosphatidylglycerol (LPG) completely inhibited a formyl peptide receptor like-1 (FPRL1) agonist (MMK-1)-stimulated chemotactic migration in human phagocytes, such as neutrophils and monocytes. LPG also dramatically inhibited IL-1beta production by another FPRL1 agonist serum amyloid A (SAA) in human phagocytes. However, LPG itself induced intracellular calcium increase and superoxide anion production in human phagocytes. Keeping in mind that phagocytes migration and IL-1beta production by FPRL1 are important for the induction of inflammatory response, our data suggest that LPG can be regarded as a useful material for the modulation of inflammatory response induced by FPRL1 activation.

Effect of Doxorubicin on Catecholamine Release in the Isolated Perfused Rat Adrenal Gland

The present study was undertaken to investigate the effect of doxorubicin (DX) on secretion of catecholamines (CA) evoked by ACh, high K+, DMPP and McN-A-343 from the isolated perfused rat adrenal gland and to establish the mechanism of its action. DX (10(-7)~10(-6) M) perfused into an adrenal vein for 60 min produced relatively dose- and time-dependent inhibition of CA secretory responses evoked by ACh (5.32 X 10(-3) M), DMPP (10(-4) M) and McN-A-343 (10(-4) M). However, lower dose of DX did not affect CA secretion by high K+ (5.6 X 10(-2) M), but its higher doses depressed time-dependently CA secretion evoked by high K+. DX itself did also fail to affect basal CA output. In adrenal glands loaded with DX (3 X 10(-7) M), CA secretory responses evoked by Bay-K-8644, an activator of L-type Ca2+ channels and cyclopiazonic acid, an inhibitor of cytoplasmic Ca2+-ATPase were time-dependently inhibited. Furthermore, daunorubicin (3 X 10(-7) M), given into the adrenal gland for 60 min, attenuated CA secretory responses evoked by ACh, high K+, DMPP and McN-A-343. Taken together, these results suggest that DX causes relatively dose- and time-dependent inhibition of CA secretory responses evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors from the isolated perfused rat adrenal gland. However, lower dose of DX did not affect CA secretion by high K+, and higher doses of DX reduced time-dependently CA secretion of high K+. It is thought that these effects of DX may be mediated by inhibiting both influx of extracellular calcium into the rat adrenomedullary chromaffin cells and intracelluar calcium release from the cytoplasmic store. Also, there was no difference in the mode of action between DX and daunorubicin in rat adrenomedullary CA secretion.