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Vitreous Humor (vitreous + humor)

Distribution by Scientific Domains
Chemistry66%
Medical Sciences33%

Selected Abstracts

Relationships Between Concentrations of Cocaine and Its Hydrolysates in Peripheral Blood, Heart Blood, Vitreous Humor and Urine

JOURNAL OF FORENSIC SCIENCES, Issue 2 2006
Wayne C. Duer Ph.D.
ABSTRACT: Cocaine is known to degrade in vivo and in vitro by several hydrolytic mechanisms. A previous study found that the initial amount of cocaine added to plasma could be accounted for by summing the molar concentrations of cocaine's hydrolysis products and the cocaine remaining after hydrolysis. The present study was undertaken to investigate whether or not relationships might exist between such molar concentration sums for different postmortem bodily fluids. Determinations of cocaine, benzoylecgonine, ecgonine methyl ester, and ecgonine were performed using liquid chromatography/mass spectrometry (LC/MS/MS) with heart blood, femoral blood, vitreous humor (VH), and urine (UR). The results demonstrate a strong correlation between blood and VH concentrations (correlation coefficients of 0.88,0.94), weak correlation between the UR and blood concentrations (correlation coefficients of 0.61,0.64), and weak correlation between UR and VH concentrations (correlation coefficient of 0.59). The results demonstrate that ecgonine is a significant hydrolysate with concentrations on the same order of magnitude as benzoylecgonine. The results are consistent with rapid distribution of the parent drug and its hydrolysates in the blood and VH. The strong correlation between the blood and VH demonstrates that VH is an important medium for toxicology testing when attempting to make a determination of cocaine intoxication. [source]

Profiling of vitreous proteomes from proliferative diabetic retinopathy and nondiabetic patients

PROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 22 2007
Taeoh Kim
Abstract Diabetes can lead to serious microvascular complications like proliferative diabetic retinopathy (PDR), which is the leading cause of blindness in adults. The proteomic changes that occur during PDR cannot be measured in the human retina for ethical reasons, but could be reflected by proteomic changes in vitreous humor. Thus, we considered that comparisons between the proteome profiles of the vitreous humors of PDR and nondiabetic controls could lead to the discovery of novel pathogenic proteins and clinical biomarkers. In this study, the authors used several proteomic methods to comprehensively examine vitreous humor proteomes of PDR patients and nondiabetic controls. These methods included immunoaffinity subtraction (IS)/2-DE/MALDI-MS, nano-LC-MALDI-MS/MS, and nano-LC-ESI-MS/MS. The identified proteins were subjected to the Trans-Proteomic Pipeline validation process. Resultantly, 531 proteins were identified, i.e., 415 and 346 proteins were identified in PDR and nondiabetic control vitreous humor samples, respectively, and of these 531 proteins, 240 were identified for the first time in this study. The PDR vitreous proteome was also found to contain many proteins possibly involved in the pathogenesis of PDR. The proteins described provide the most comprehensive proteome listing in the vitreous humor samples of PDR and nondiabetic control patients. [source]

Lornoxicam pharmacokinetics in the vitreous humor of albino rabbits

ACTA OPHTHALMOLOGICA, Issue 2009
C TSIKA
Purpose To assess the elimination half-life of intravitreal lornoxicam, a non-steroidal anti-inflammatory drug (NSAID). Methods Both eyes of 15 rabbits were intravitreally injected with 250 ,g of commercially available lornoxicam (for intravenous/intramuscular use, Xefo® 8 IV/IM Injection, Nycomed Hellas S.A.). Six eyes were enucleated at time points 0, 1, 2, 6 and 24 hours after the injection was performed. The eyes were immediately frozen at -80°C. The vitreous was eviscerated from the eye and the drug was liquid-liquid extracted from a 0.4 ml sample. Lornoxicam was isolated by a reversed-phase High Performance Liquid Chromatography (HPLC) method at retention time 10.7 min and detected at 372 nm. The data were statistically analyzed in order to evaluate the pharmacokinetic parameters of the drug. Results The recovery of lornoxicam after liquid-liquid extraction was calculated at 69.6% and the limit of determination was 0.1 ,g/ml. Statistical analysis revealed that lornoxicam concentrations followed first-order kinetics with an elimination rate constant of 0.235h-1 and a half-life of 3.0 h. Conclusion The determination of the pharmacokinetic characteristics of intravitreal lornoxicam allows the possibility for further investigation of the drug's intraocular behaviour and therapeutic potential. [source]

Profiling of vitreous proteomes from proliferative diabetic retinopathy and nondiabetic patients

PROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 22 2007
Taeoh Kim
Abstract Diabetes can lead to serious microvascular complications like proliferative diabetic retinopathy (PDR), which is the leading cause of blindness in adults. The proteomic changes that occur during PDR cannot be measured in the human retina for ethical reasons, but could be reflected by proteomic changes in vitreous humor. Thus, we considered that comparisons between the proteome profiles of the vitreous humors of PDR and nondiabetic controls could lead to the discovery of novel pathogenic proteins and clinical biomarkers. In this study, the authors used several proteomic methods to comprehensively examine vitreous humor proteomes of PDR patients and nondiabetic controls. These methods included immunoaffinity subtraction (IS)/2-DE/MALDI-MS, nano-LC-MALDI-MS/MS, and nano-LC-ESI-MS/MS. The identified proteins were subjected to the Trans-Proteomic Pipeline validation process. Resultantly, 531 proteins were identified, i.e., 415 and 346 proteins were identified in PDR and nondiabetic control vitreous humor samples, respectively, and of these 531 proteins, 240 were identified for the first time in this study. The PDR vitreous proteome was also found to contain many proteins possibly involved in the pathogenesis of PDR. The proteins described provide the most comprehensive proteome listing in the vitreous humor samples of PDR and nondiabetic control patients. [source]

Local environmental influences on uveal melanoma

CANCER, Issue 8 2008
Vitreous humor promotes uveal melanoma invasion, whereas the aqueous can be inhibitory
Abstract BACKGROUND Uveal melanomas of the choroid and ciliary body are aggressive tumors causing the death of approximately 50% of patients. In contrast, iris melanomas only infrequently metastasize; why these differences exist is not known. The local environment can regulate cancer growth and development, and it is probable the aqueous and vitreous humors have an important role in regulating uveal melanoma behavior. METHODS To explore this possibility cultures of uveal melanoma were exposed to aqueous and vitreous and the effects investigated using invasion and proliferation assays. ChemiArrays (Chemicon International, Temecula, Calif) were performed to determine which regulatory factors might influence the process. RESULTS The vitreous universally promoted uveal melanoma invasion, whereas the aqueous mainly had no effect or was inhibitory. Tumor location, and the baseline invasion of the melanoma, affected the ability of aqueous and vitreous from different patients to regulate invasive behavior. Proliferation was not significantly altered as a result of exposure to the aqueous or vitreous. The ability of the humors to regulate uveal melanomas may involve TIMP-2, TIMP-3, and TGF-,2, as high expression was found by ChemiArray analysis and there were differences in the levels of the regulators in the aqueous compared with the vitreous. CONCLUSIONS The findings suggest that in situ uveal melanoma development reflects an interaction between the tumor and the environment of the eye. Exposure to the aqueous would therefore contribute to the benign nature of iris melanomas, whereas potential interaction with the vitreous appears to promote the aggressive behavior of posterior uveal melanomas. Cancer 2008. © 2008 American Cancer Society. [source]