PURPOSE: To investigate the change of retinal volume according to anterior segment refractive power using contact lens by spectral domain optical coherence tomography (SD-OCT). METHODS: The retinal volume was measured using a SD-OCT (Heidelberg retinal angiography Spectralis + OCT, Heidelberg Engineering, Heidelberg, Germany) in 60 subjects without any underlying disease. The same examiner performed a 31-section macular volume-scan at 240 µm intervals, re-measured the same area by changing the refractive power of the anterior segment by wearing soft contact lenses of +6.0 diopters and −6.0 diopters. By using the ImageJ software to calculate the cross-sectional area and of the cross-sectional area and the volume was measured. RESULTS: The mean age of the participants was 25.6 ± 1.5 years and the mean axial length was 25.7 ± 1.57 mm. The volume of the posterior pole retina measured without the contact lens was 13.48 ± 0.05 and the mean volume of the retina measured with +6.0 diopter and −6.0 diopter contact lens in the same patient was 13.47 ± 0.07 mm³ and 13.48 ± 0.05 respectively. The mean volume was significantly lower(p = 0.036) in the measurement with the +6.0 diopter lens than in the measurement without the lens, and the mean volume was significantly higher in the measurement with the +6.0 diopter lens (p = 0.042). The change in retinal thickness was increased with longer axial length (r = 0.32, p < 0.05), but the central foveal thickness did not correlate with anterior corneal power (p = 0.463). CONCLUSIONS: The volume of the retina measured using the SD-OCT is affected by the refractive power of the anterior segment and the axial length. Therefore, it is necessary to consider the change of refractive index because it can change the retinal volume measured by SD-OCT.
Angiography ; Contact Lenses, Hydrophilic ; Humans ; Refractometry ; Retina ; Retinaldehyde ; Tomography, Optical Coherence

PURPOSE: We explored changes in photoreceptor function and histology in an iodoacetic acid (IAA)-induced model of feline retinal degeneration. METHODS: From January to October 2014, we studied 11 adult felines (22 eyes) over 2 years of age divided into two groups (two in a control and nine in an IAA group). The mean body weights of these two groups were 1.75 ± 0.35 and 1.61 ± 0.19 kg, and the male:female sex ratios 1:1 and 2:7, respectively. Electroretinograms (ERGs) were obtained before injection and at 1–4 week post-injection (20 mg/kg IAA). Standard paraffin retinal sections were stained with hematoxylin/eosin and other sections subjected to immunohistochemistry. We histologically evaluated the outer nuclear layer, and photoreceptor cone and rod cells. RESULTS: In ERGs of the IAA group, both the rod and cone mean b wave amplitudes decreased significantly from week 1 to week 4 after injection (27.43, 29.41, 64.17, and 56.03; and 61.04, 51.25, 131.36, and 136.68 µV, respectively) compared to baseline (322.48 and 610.00 µV respectively) (p < 0.01). Optical microscopy revealed a significant decrease in the cell count of the outer nuclear retinal layer (16.83 ± 0.89 in the control and 11.98 ± 3.55 in the IAA groups, p < 0.01). Fluorescence microscopy revealed a significant reduction in the mean area per unit length of the rod cell layer (35,225.67 ± 2,477.02 and 14,903.62 ± 2,319.65 in the control and IAA groups, p < 0.01), but not in the cone cell count (26.16 ± 1.34 and 23.98 ± 6.16 in the control and IAA groups, p = 0.075). CONCLUSIONS ERGs revealed that functional b wave amplitudes fell after IAA-induce retinal degeneration in felines; histology showed that this was accompanied by reductions in the numbers of outer nuclear layers and rod cells. IAA induces photoreceptor degeneration in felines; further study is necessary.

BACKGROUND: Inorganic arsenic trioxide (As2O3) has emerged as a new drug of choice for refractory acute promyelocytic leukemia (APL). But, the curable disease spectrum and the arsenic resistance in association with the expression of multidrug resistance (MDR) proteins are not yet to be established. METHODS: Five de novo APL and 20 refractory acute leukemia cases were selected. Leukemic cells were cultured for 24 hr in media with various As2O3 concentrations. Apoptotic cells or damaged cells were measured by a morphologic examination after Wright stain and flow cytometry using annexin V/propidium iodide (PI) stain. The lowest concentration of As2O3 at which greater than 90% of leukemic cells were damaged morphologically was defined as the morphologic arsenic sensitivity of leukemic cells. MDR protein markers including multidrug resistance associated protein (MRP), lung resistance protein (LRP), P-glycoprotein (PGP) and glutathinoe-S-transferase (GST) were analyzed by flow cytometry. RESULTS: The leukemic cells from de novo APLs (in 3 of 5) were sensitive to arsenic trioxide, compared to refractory acute leukemia (only 1 of 20). Of the five MDR proteins examined, only PGP was expressed more in the arsenic resistant cases (in 8 of 21) than in the sensitive cases (none of 4) (P=.032). CONCLUSIONS: Refractory acute leukemia had a variable arsenic sensitivity, but were more resistant than de novo APL. The arsenic resistance seems to be related to PGP expression.
Arsenic ; Drug Resistance, Multiple ; Flow Cytometry ; Leukemia* ; Leukemia, Promyelocytic, Acute* ; Lung ; Multidrug Resistance-Associated Proteins ; P-Glycoprotein

BACKGROUND: Most laboratories in Korea have been used kinetic Jaffe method for creatinine measurement. However, kinetic Jaffe method is interfered by hyperbilirubinemia, which causes creatinine decrement. In this study, we evaluated the usefulness of deproteinization by trichloroacetic acid (TCA) in eliminating negative interference of bilirubin for accurate creatinine measurement. METHODS: We evaluated the correction effect of serum creatinine levels by deproteinization using 0.55 mol/L TCA in 43 samples with various total bilirubin levels. For 26 samples of them we measured creatinine using the enzymatic method for evaluating accuracy of TCA correction. Creatinine was measured by using the Toshiba 200-FR automated analyzer and the HiSense CREA reagents. RESULTS: After TCA treatment, 22 to the total 43 samples with more than 10 mg/dL of total bilirubin, revealed statistically higher creatinine concentration (P=0.0002) and the difference of creatinine results is mean 0.53 mg/dL (0.15-1.92 mg/dL). Also, 19 of them (86.4%) revealed 20% or more difference of creatinine results before and after TCA treatment and the negative interference of bilirubin increased in proportion to the rise in total bilirubin concentration (r=0.870). There was no significant difference of creatinine results between kinetic Jaffe method with 0.55 mol/L TCA treatment and enzymatic method (P=0.216). CONCLUSIONS: TCA deproteinization is simple and very efficient method for estimating accurate creatinine level by using kinetic Jaffe method in a patient with hyperbilirubinemia.
Bilirubin ; Creatinine ; Humans ; Hyperbilirubinemia ; Korea ; Trichloroacetic Acid

BACKGROUND: Most laboratories in Korea have been used kinetic Jaffe method for creatinine measurement. However, kinetic Jaffe method is interfered by hyperbilirubinemia, which causes creatinine decrement. In this study, we evaluated the usefulness of deproteinization by trichloroacetic acid (TCA) in eliminating negative interference of bilirubin for accurate creatinine measurement. METHODS: We evaluated the correction effect of serum creatinine levels by deproteinization using 0.55 mol/L TCA in 43 samples with various total bilirubin levels. For 26 samples of them we measured creatinine using the enzymatic method for evaluating accuracy of TCA correction. Creatinine was measured by using the Toshiba 200-FR automated analyzer and the HiSense CREA reagents. RESULTS: After TCA treatment, 22 to the total 43 samples with more than 10 mg/dL of total bilirubin, revealed statistically higher creatinine concentration (P=0.0002) and the difference of creatinine results is mean 0.53 mg/dL (0.15-1.92 mg/dL). Also, 19 of them (86.4%) revealed 20% or more difference of creatinine results before and after TCA treatment and the negative interference of bilirubin increased in proportion to the rise in total bilirubin concentration (r=0.870). There was no significant difference of creatinine results between kinetic Jaffe method with 0.55 mol/L TCA treatment and enzymatic method (P=0.216). CONCLUSIONS: TCA deproteinization is simple and very efficient method for estimating accurate creatinine level by using kinetic Jaffe method in a patient with hyperbilirubinemia.
Bilirubin ; Creatinine ; Humans ; Hyperbilirubinemia ; Korea ; Trichloroacetic Acid

The 5th year KONSAR surveillance in 2001 was based on routine test data at 30 participating hospitals. It was of particular interest to find a trend in the resistances of enterococci to vancomycin, of Enterobacteriaceae to the 3rd generation cephalosporin and fluoroquinolone, and of Pseudomonas aeruginosa and acinetobacters to carbapenem. Resistance rates of Gram-positive cocci were: 70% of Staphylococcus aureus to oxacillin; 88% and 16% of Enterococcus faecium to ampicillin and vancomycin, respectively. Seventy-two percent of pneumococci were nonsusceptible to penicillin. The resistance rates of Enterobacteriaceae were: Escherichia coli, 28% to fluoroquinolone; Klebsiella pneumoniae, 27% to ceftazidime, and 20% to cefoxitin; and Enterobacter cloacae, > or =40% to cefotaxime and ceftazidime. The resistance rates of P. aeruginosa were 21% to ceftazidime, 17% to imipenem, and those of the acinetobacters were > or =61% to ceftazidime, aminoglycosides, fluoroquinolone and cotrimoxazole. Thirty-five percent of non-typhoidal salmonellae were ampicillin resistant, and 66% of Haemophilus influenzae were -lactamase producers. Notable changes over the 1997-2001 period were: increases in vancomycin-resistant E. faecium, and amikacin- and fluoroquinolone-resistant acinetobacters. With the increasing prevalence of resistant bacteria, nationwide surveillance has become more important for optimal patient management, for the control of nosocomial infection, and for the conservation of the newer antimicrobial agents.
Anti-Bacterial Agents/*pharmacology ; Cephalosporins/pharmacology ; *Drug Resistance, Microbial ; Enterococcus faecium/metabolism ; Human ; Imipenem/pharmacology ; Klebsiella pneumoniae/metabolism ; Korea ; Pseudomonas aeruginosa/metabolism ; Time Factors ; Vancomycin/*pharmacology

We report a patient diagnosed with a germ-cell tumor presenting with spinal muscular atrophy with lower limb predominance (SMA-LED) caused by a DYNC1H1 genetic variant. His clinical and electrophysiologic phenotype was compatible with SMA-LED. We identified a heterozygous missense variant (c.1793G>T) of DYNC1H1. This report expands the clinical spectrum of DYNC1H1-related disorders, and reinforces the importance of DYNC1H1 in both central and peripheral neuronal functions. We suggest that germ-cell tumors should be considered as a possible phenotype of DYNC1H1-related disorders.

We report a patient diagnosed with a germ-cell tumor presenting with spinal muscular atrophy with lower limb predominance (SMA-LED) caused by a DYNC1H1 genetic variant. His clinical and electrophysiologic phenotype was compatible with SMA-LED. We identified a heterozygous missense variant (c.1793G>T) of DYNC1H1. This report expands the clinical spectrum of DYNC1H1-related disorders, and reinforces the importance of DYNC1H1 in both central and peripheral neuronal functions. We suggest that germ-cell tumors should be considered as a possible phenotype of DYNC1H1-related disorders.

We report a patient diagnosed with a germ-cell tumor presenting with spinal muscular atrophy with lower limb predominance (SMA-LED) caused by a DYNC1H1 genetic variant. His clinical and electrophysiologic phenotype was compatible with SMA-LED. We identified a heterozygous missense variant (c.1793G>T) of DYNC1H1. This report expands the clinical spectrum of DYNC1H1-related disorders, and reinforces the importance of DYNC1H1 in both central and peripheral neuronal functions. We suggest that germ-cell tumors should be considered as a possible phenotype of DYNC1H1-related disorders.