The distribution of white blood cell fat oxidation in health and disease.

Fat oxidation is important for maintaining health and for supplying energy for exercise. We have proposed that the predisposition for individual rates of fat oxidation is determined genetically but may be modulated by acute exercise or exercise training. The purpose of this study was to examine cellular fat oxidation in white blood cells (WBC) using [9,10-3H]palmitic acid. Sedentary controls free of symptoms (SED-C, n=32), were compared with known carnitine palmitoyltransferase (CPT) II-deficient patients (n =2), patients with fatiguing diseases (chronic fatigue syndrome, CFS, n=6; multiple sclerosis, MS, n=31), obesity (OB, n=5), eating disorders (ED, n=16), sedentary individuals prior to and after exercise (SED-Ex, n=12), exercise-trained sedentary individuals (SED-Tr, n=12), and elite runners (ER, n=5). Fat oxidation in WBC for all subjects was normally distributed (mean=0.270 +/- 0.090 nmol/h per 10(9) WBC) and ranged from 0.09 nmol/h per 10(9) WBC in CPT II-deficient patients to 0.59 nmol/h per 10(9) WBC in ER. There were no significant sex or acute exercise effects on WBC fat oxidation. Patients with MS, OB or ED were not different from SED-C; however, in CPT II-deficient patients, fat oxidation was low, while that of CFS patients was high. Exercise training in SED-C resulted in a 16% increase in fat oxidation but in ER it was still 97% higher than in SED-C. We propose that while WBC fat oxidation is not significantly affected by sex or acute exercise, and only by 15-20% with training, genetic factors play a role in determining both high and low fat oxidation in certain groups of individuals. The genetic predisposition for individual rates of fat oxidation may be easily measured using WBC fat oxidation, as has been shown for CPT II-deficient patients and for elite runners. Ranges of WBC fat oxidation that are abnormally low (<20 nmol/h per 10(9) WBC, normal 20-35) or high (>35 nmol/h per 10(9) WBC) are proposed based on genetic factors evaluated in this study.

Corneal topography of small-beam tracking excimer laser photorefractive keratectomy.

PURPOSE: To evaluate the topographic characteristic of photorefractive keratectomy (PRK) for low myopia performed with a small-beam (0.9 mm) tracking excimer laser. SETTING: Department of Ophthalmology, LSU Eye Center, Louisiana State University Medical Center School of Medicine in New Orleans, and the Refractive Surgery Center of the South at the Eye, Ear, Nose, & Throat Hospital, New Orleans, Louisiana, USA. METHODS: Sixty-seven eyes of 47 patients had PRK with a small-beam tracking laser. Of these, 49 eyes had data permitting evaluation of ablation centration; usable data for topographic analysis were available for 59 eyes preoperatively, 54 eyes at 1 month, 42 eyes at 3 months, and 25 eyes at 6 months, permitting measurement of various topographic parameters, including the cylinder (CYL), average corneal power (ACP), surface regularity index (SRI), surface asymmetry index (SAI), corneal eccentricity index (CEI), and coefficient of variation of corneal power (CVP). RESULTS: Preoperatively, all eyes were topographically normal. Postoperatively, no eye exhibited a "central island" by even the least-restrictive definition, and all eyes had best spectacle-corrected visual acuities (BSCVAs) of 20/20 or better at all follow-ups. Mean decentration of the ablations from the pupil centers was 0.42 mm +/- 0.28 (SD) (n = 49). There was no correlation between measured decentration and BSCVA (P = .46). The central cornea was flattened (decreased ACP; P < .001) and made oblate (decreased CEI; P < .001) as expected. There was no increase in SRI or SAI (irregular astigmatism) at 6 months compared with preoperative values (P = .91); however, CYL and CVP (varifocality) increased slightly (P = .04 and .02, respectively). CONCLUSION: The absence of significant regular or irregular astigmatism 6 months after PRK with the small-beam laser is an improvement over published results achieved with wide-beam lasers and is consistent with the excellent visual acuity results in this cohort.

Normal human corneal cell populations evaluated by in vivo scanning slit confocal microscopy.

PURPOSE: To analyze cellular populations in healthy human corneas. METHODS: The study group consisted of 58 eyes of 45 patients with normal corneas. The age distribution was 45 +/- 17 years (mean +/- SD; range, 20-84). Scanning slit confocal microscopy of the central corneas was performed. The images were analyzed visually for cell morphology, and the densities and areas of cells were measured. RESULTS: No statistically significant differences were measured in cell densities or cell areas of any corneal layer between female and male patients (p = 0.22-0.50) nor between right and left eyes (p = 0.16-0.45). The area of superficial epithelial cells was 913 +/- 326 microm2 (mean +/- SD; range, 518-2,112), and the superficial epithelial cell density was 1,213 +/- 370 cells/mm2 (mean +/- SD; range, 473-1,929). The area of basal epithelial cells was 177 +/- 19 microm2 (mean +/- SD; range, 138-242), and the basal epithelial cell density was 5,699 +/- 604 cells/mm2 (mean +/- SD; range, 4,135-7,267). The average apparent keratocyte density was 1,058 +/- 217 cells/mm2 (mean +/- SD; range, 604-1,599) in the anterior stroma, and 771 +/- 135 cells/mm2 (mean +/- SD; range, 493-1,145) in the posterior stroma. The difference in apparent keratocyte densities between the anterior and posterior stroma was statistically significant (p < 0.001). The average endothelial cell area was 334 +/- 51 microm2 (range, 273-553), and the cell density was 3,055 +/- 386 cells/mm2 (mean +/- SD; range, 1,809-3,668). The endothelial cell density had a negative, statistically significant correlation with age (r = -0.68, p < 0.001). The densities of the other corneal cell layers did not have a statistically significant correlation with age. CONCLUSION: In vivo scanning slit confocal microscopy is a useful tool for studying corneal cell populations. Central corneal cell densities were found to decrease significantly with age only in the endothelium. For the first time in human corneas using in vivo confocal microscopy, this study statistically confirms a higher apparent number of keratocytes in the anterior stroma than in the posterior stroma.

In vivo confocal microscopy of Fuchs' endothelial dystrophy.

PURPOSE: The purpose of this study is to analyze in vivo confocal microscopic findings of corneas with Fuchs' endothelial dystrophy. METHODS: Central corneas of 17 eyes of 11 patients aged 41-86 years were examined using in vivo scanning slit confocal microscopy after being diagnosed with Fuchs' endothelial dystrophy. The cellular structure of the corneas was analyzed morphologically and quantitatively and compared to control results from 22 healthy corneas. RESULTS: Bullae were detected in the basal epithelial layer of one eye. Eight of 17 eyes (47%) exhibited an abnormal Bowman's layer: diffuse bright reflection and absence of nerves. Eleven eyes (65%) exhibited abnormal anterior stroma: lacunae and diffuse increased light reflection due to edema. In 12 eyes (71%), lacunae or dark bands 5-20 microm wide against increased background reflection were noted in the posterior stroma. Descemet's membrane was thickened in all eyes. Dark bands were detected in six eyes (35%). Guttae (137-1,231/mm2) 20-40 microm in diameter were found in every endothelial cell layer. The mean endothelial cell count was 1,202 +/- 850 (cells/mm2 +/- SD; range, 0-2,735). There was a positive correlation between endothelial cell counts obtained by specular microscopy and those obtained by confocal microscopy (r = 0.95). CONCLUSION: In vivo confocal microscopic findings of Fuchs' endothelial dystrophy are described for the first time in a series of cases. Pathological changes in Fuchs' dystrophy were detected in all corneal layers, more frequently in the posterior layers. Endothelial cell counts obtained with confocal microscopy were statistically similar to those obtained with standard specular microscopy.