A prospective randomized clinical trial of laser in situ keratomileusis with two different lasers.
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Biomedical subjects
Publications and source records attributed to J T Lin.
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PURPOSE: To develop formulae for the refractive state ratios, axial length growth and the age of onset (A*) of myopia. Calculated results are compared with measurements. METHODS: Using an image equation, the axial length in the ametropic state (L) is related to the length in the emmetropic state (L*) and refractive error (D) by a rate of change M (D mm(-1)). Three refractive state ratios are defined: C1 = L/r1, C2 = L/L* and C3 = L/H, where r1 and H are the anterior surface radius of the cornea and the transverse dimension of the eye, respectively. The age of onset A* is calculated by the rate of change of refractive error (M) and the axial growth rates N and N* in the ametropic and emmetropic states, respectively. RESULTS: The three ratios C1, C2 and C3 are increasing function of the myopia power, for example, C1 = 3.4, 3.1, 2.9 for D = -8, 0, +4 dioptres, respectively. The calculated C1* (for the emmetropic state) varies between 3.08 and 3.14, depending on corneal shape, and C3 = 0.985, 1.0, 1.04 for D = +3, 0, -3 dioptres: these values are consistent with measured data. For a typical system with effective focal length F = 22.25 mm, L* = 24.2 mm and L = 23.4, 24.9, 25.9 mm for D = +2, -2, -5 dioptres, respectively. The calculated rates of change of refractive error M = 2.3-2.9 D mm(-1) for F = 22-23 mm are also consistent with measured values 2.4-2.7 D mm(-1). The age of onset A* is calculated to be proportional to 1/(M dN), where dN = N-N* is the axial growth rate difference between the ametropic and emmetropic states and may be used as a better predictor for myopia onset than the conventional ratio L/r1. The A* is given by the crossing of L and L* curves, in which myopia onset occurs earlier for larger M dN. CONCLUSION: The theory provides formulae to calculate various refractive state ratios, which are consistent with measurements. By defining two rate functions, M and N, the onset of myopia can be predicted.
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Osteoporotic vertebral fractures represent the most common type of osteoporotic fracture. They can cause significant morbidity and mortality, including physical, functional, and psychosocial impairments. Screening using fracture risk assessments can identify those at greatest risk. Medical and non-medical comprise appropriate, comprehensive treatment programs. The minimally invasive spine procedures vertebroplasty and kyphoplasty can help to significantly reduce pain and deformity in patients with severe pain and deformity from vertebral fracture.
PURPOSE: High-grade mucosa-associated lymphoid tissue (MALT) lymphomas of the stomach are generally believed to be Helicobacter pylori-independent, autonomously growing tumors. However, anecdotal cases of regression of high-grade lymphomas after the cure of H pylori infection had been described. The present prospective study was conducted to evaluate the effect of anti-H pylori therapy in stage I(E) high-grade gastric MALT lymphomas. PATIENTS AND METHODS: Sixteen patients with H pylori infection and stage I(E) gastric high-grade MALT lymphoma consented to a brief antibiotic therapy as first-line treatment from June 1995 through April 2000. Then, patients underwent intensive endoscopic follow-up examinations (+/- endoscopic ultrasonography) with biopsy to evaluate tumor response. Patients with significant improvement of gross lesions that accompanied regression of large cells were followed up without additional treatment. Patients without significant improvement were immediately referred to systemic chemotherapy. RESULTS: Eradication of H pylori was achieved in 15 patients and was accompanied by rapid gross tumor regression and disappearance of large cells in 10. All 10 of these patients with early response had subsequent complete histologic remission of lymphoma. The complete remission rate was 62.5% (95% confidence interval, 35.8% to 89.1%). The response rate was not affected by the tumor grading (proportion of large blast cells within the tumor) but was adversely affected by the depth of tumor invasion. At a median follow-up of 43.5 months (range, 21.1 to 67.4 months), all 10 of these patients remained lymphoma-free. The median duration of complete response was 31.2 months (range, 14.4 to 49.1 months). CONCLUSION: These results suggest that high-grade transformation is not necessarily associated with the loss of H pylori dependence in early-stage MALT lymphomas of the stomach.
In order to define potential interaction sites of SGLT1 with the transport inhibitor phlorizin, mutagenesis studies were performed in a hydrophobic region of loop 13 (aa 604-610), located extracellularly, close to the C-terminus. COS 7 cells were transiently transfected with the mutants and the kinetic parameters of alpha-methyl-D-glucopyranoside (AMG) uptake into the cells were investigated. Replacement of the respective amino acids with lysine reduced the maximal uptake rate: Y604K showed 2.2%, L606K 48.4%, F607K 15.1%, C608K 13.1%, G609K 14.1%, and L610K 17.2% of control. In all mutants the apparent K(i) for phlorizin increased at least by a factor of 5 compared to the wild-type K(i) of 4.6 +/- 0.7 micromol/l; most striking changes were observed for Y604K (K(i) = 75.3 +/- 19.0 micromol/l) and C608K (K(i) = 83.6 +/- 13.9 micromol/l). Replacement of these amino acids with a nonpolar amino acid instead of lysine such as in Y604F, Y604G and C608A showed markedly higher affinities for phlorizin. In cells expressing the mutants the apparent affinity of AMG uptake for the sugar was not statistically different from that of the wild type (Km = 0.8 +/- 0.2 mmol/l). These studies suggest that the region between amino acids 604 and 610 is involved in the interaction between SGLT1 and phlorizin, probably by providing a hydrophobic pocket for one of the aromatic rings of the aglucone moiety of the glycoside.
Stable carbazole derivatives that contain peripheral diarylamines at the 3- and 6-positions and an ethyl or aryl substituent at the 9-position of the carbazole moiety have been synthesized via palladium-catalyzed C-N bond formation. These new carbazole compounds (carbs) are amorphous with high glass transition temperatures (T(g), 120-194 degrees C) and high thermal decomposition temperatures (T(d) > 450 degrees C). The compounds are weakly to moderately luminescent in nature. The emission wavelength ranges from green to blue and is dependent on the substituent at the peripheral nitrogen atoms. Two types of light-emitting diodes were constructed from carb: (I) ITO/carb/TPBI/Mg:Ag and (II) ITO/carb/Alq(3)/Mg:Ag, where TPBI and Alq(3) are 1,3,5-tris(N-phenylbenzimidazol-2-yl)benzene and tris(8-hydroxyquinoline) aluminum, respectively. In type I devices, the carb functions as the hole-transporting as well as emitting material. In type II devices, either carb, or Alq(3) is the light-emitting material. Several green light-emitting devices exhibit exceptional maximum brightness, and the physical performance appears to be better than those of typical green light-emitting devices of the structure ITO/diamine/Alq(3)/Mg:Ag. The relation between the LUMO of the carb and the performance of the light-emitting diode is discussed.
Autoimmune hepatitis (AIH) in humans arises spontaneously in genetically susceptible individuals and is associated with the presence of Th1 cells in the liver. The understanding of AIH has advanced more slowly than that of other organ-specific autoimmune diseases, however, largely because of the lack of an appropriate animal model. We now describe a new mouse model characterized by spontaneous development of necroinflammatory hepatitis that is restricted by genetic background. Mice deficient in the immunomodulatory cytokine TGF-beta1 were extensively back-bred to the BALB/c background. The BALB/c background dramatically modified the phenotype of TGF-beta1(-/-) mice: specifically, BALB/c-TGF-beta1(-/-) mice developed a lethal necroinflammatory hepatitis that was not observed in TGF-beta1(-/-) mice on a different genetic background. BALB/c background TGF-beta1(-/-) livers contained large numbers of activated CD4(+) T cells that produced large quantities of IFN-gamma, but little IL-4, identifying them as Th1 cells. BALB/c background TGF-beta1(-/-)/IFN-gamma(-/-) double knockout mice, generated by cross-breeding, did not develop necroinflammatory hepatitis, demonstrating that IFN-gamma is mechanistically required for its pathogenesis. This represents the first murine model of hepatitis that develops spontaneously, is restricted by genetic background, and is dependent upon the Th1 cytokine IFN-gamma, and that thus recapitulates these important aspects of AIH.
The sodium-D-glucose cotransporter (SGLT1) was expressed in a yeast mutant strain NY 17 (sec6-4) that accumulates secretory vesicles at a nonpermissive temperature because of a block in the delivery of these vesicles to the plasma membrane. By differential centrifugation a microsomal fraction enriched in secretory vesicles was prepared with a high specific activity of the vanadate-sensitive H+-ATPase and invertase. In this membrane fraction one protein band of an apparent molecular weight of 55 kDa representing the nonglycosylated SGLT1 protein could be detected by immunochemical analysis. In addition, higher molecular weight protein bands probably representing dimers and aggregates were found. In transport studies with the microsomes D-glucose fluxes showed asymmetric properties: efflux experiments revealed the typical properties of the SGLT1 such as sodium dependence, inhibition by phlorizin and potential dependence. Influx of D-glucose showed no dependence on sodium and was not inhibited by phlorizin. Furthermore, the transporter exhibited a striking asymmetry with regard to the D-glucose affinity and the sugar specificity. These results suggest that the orientation of the SGLT1 expressed in yeast secretory vesicles is, indeed, inverted with regard to its configuration in the plasma membrane of epithelial cells. Moreover, there are striking functional differences between the periplasmic and cytoplasmic face of the transporter.
To characterize phenotypic and genotypic changes in gastric cancer (GC), DNA copy number aberrations (CNAs) were assessed in 53 tumors using comparative genomic hybridization (CGH) and correlated with clinicopathologic characteristics and status of TP53 and replication error (RER). The number of CNAs per tumor was 6.8 (gain 5.3, loss 1.5), and the number of changes was significantly higher in tumors with advanced stage, TP53 mutation, and without RER than in those with early stage (7.7 vs. 3.0), no TP53 mutations (12.4 vs. 4.8) or RER phenotype (8.2 vs. 2.6). Frequent abnormalities included gains on chromosomal arms 8q (43%), 6q (26%), 11q (26%), 13q (24%), 7p (23%), 17q (23%), and 20q (23%), and losses on chromosomal arms 16q (26%), 19p (23%), 5q (19%), 3p (15%), 4q(15%), and 1p (15%). Advanced GC demonstrated a higher prevalence of gains of 8q (51% vs. 10%, P < 0.05) and loss of 16q (33% vs. 0%, P < 0.05) than early GC. Gains on 8q (64% vs. 20%, P < 0.05), 17q (39% vs. 4%, P < 0.05) and losses on 3p (25% vs. 4%, P = 0.05) and 5q (32% vs. 4%, P < 0.05) were higher in intestinal GC than in diffuse GC. On the other hand, gains on 13q were more common in the diffuse type (40% vs. 11%, P < 0.05). As compared with noncardia cancer, cardia cancer showed more gains on 7p (58% vs. 12%, P < 0.05) and 20q (58% vs. 12%, P < 0.05) and more losses on 4q (50% vs. 5%, P < 0.05). The finding of histology-related aberrations and the combination of CGH and molecular data thus provide additional evidence suggesting genetic heterogeneity of GC.