Analysis of network expression and immune infiltration of disulfidptosis-related genes in chronic obstructive pulmonary disease.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a globally prevalent respiratory disease, and programmed cell death plays a pivotal role in the development of COPD. Disulfidptosis is a newly discovered type of cell death that may be associated with the progression of COPD. However, the expression and role of disulfidptosis-related genes (DRGs) in COPD remain unclear. METHODS: The expression of DRGs was identified by analyzing RNA sequencing (RNA-seq) data in COPD. Further, COPD patients were classified into two subtypes by unsupervised cluster analysis to reveal their differences in gene expression and immune infiltration. Meanwhile, hub genes associated with disulfidptosis were screened by weighted gene co-expression network analysis. Subsequently, the hub genes were validated experimentally in cells and animals. In addition, we screened potential therapeutic drugs through the hub genes. RESULTS: We identified two distinct molecular clusters and observed significant differences in immune cell populations between them. In addition, we screened nine hub genes, and experimental validation showed that CDC71, DOHH, PDAP1, and SLC25A39 were significantly upregulated in cigarette smoke-induced COPD mouse lung tissues and bronchial epithelial cells (BEAS-2B) treated with cigarette smoke extract. Finally, we predicted 10 potential small molecule drugs such as Atovaquone, Taurocholic acid, Latamoxef, and Methotrexate. CONCLUSION: We highlighted the strong association between COPD and disulfidptosis, with DRGs demonstrating a discriminative capacity for COPD. Additionally, the expression of certain novel genes, including CDC71, DOHH, PDAP1, and SLC25A39, is linked to COPD and may aid in the diagnosis and assessment of this condition.

Tibial transverse transport induces mobilization of endothelial progenitor cells to accelerate angiogenesis and ulcer wound healing through the VEGFA/CXCL12 pathway.

BACKGROUND: Tibial transverse transport (TTT) can promote the healing of chronic foot ulcers, but the specific cellular and molecular mechanisms by which TTT promotes wound healing remain unclear. METHODS: New Zealand White rabbits were selected to induce foot ulcer models. The treatment included unilateral TTT surgery and bilateral TTT surgery. Observation of tissue neovascularization structure by HE staining and CD31 immunofluorescence detection. Collagen fiber formation was detected through the Masson staining. The mobilization of endothelial progenitor cell (EPCs) were analyzed by VEGFR2 immunofluorescence detection and flow cytometry detection of the number of VEGFR2/Tie-2-positive cells in peripheral blood. ELISA and qPCR assay were performed to detect VEGFA and CXCL12 levels. RESULTS: The complete healing time of ulcer surfaces in sham, unilateral and bilateral TTT groups was about 22 days, 17 days and 13 days, respectively. TTT treatment significantly increased the deposition of granulation tissue and epithelialization of wounds. It also led to an increase in collagen fiber content and the level of the microvascular marker CD31. Furthermore, TTT treatment upregulated the levels of VEGFA and CXCL12 in peripheral blood and wound tissues, as well as increased the expression of VEGFR2 in wound tissues and the proportion of VEGFR2/Tie-2 in peripheral blood. Moreover, these effects of TTT treatment in the bilateral group was more significant than that in the unilateral group. CONCLUSIONS: TTT may facilitate wound fibroblasts to release VEGFA and CXCL12, causing EPC mobilization, thus promoting angiogenesis and ulcer wound healing.

FOXC1 Promotes Osteoblastic Differentiation of Bone Marrow Mesenchymal Stem Cells via the Dnmt3b/CXCL12 Axis.

Bone defects have remained a clinical problem in current orthopedics. Bone marrow mesenchymal stem cells (BM-MSCs) with multi-directional differentiation ability have become a research hotspot for repairing bone defects. In vitro and in vivo models were constructed, respectively. Alkaline phosphatase (ALP) staining and alizarin red staining were performed to detect osteogenic differentiation ability. Western blotting (WB) was used to detect the expression of osteogenic differentiation-related proteins. Serum inflammatory cytokine levels were detected by ELISA. Fracture recovery was evaluated by HE staining. The binding relationship between FOXC1 and Dnmt3b was verified by dual-luciferase reporter assay. The relationship between Dnmt3b and CXCL12 was explored by MSP and ChIP assays. FOXC1 overexpression promoted calcium nodule formation, upregulated osteogenic differentiation-related protein expression, promoted osteogenic differentiation, and decreased inflammatory factor levels in BM-MSCs, and promoted callus formation, upregulated osteogenic differentiation-related protein expression, and downregulated CXCL12 expression in the mouse model. Furthermore, FOXC1 targeted Dnmt3b, with Dnmt3b knockdown decreasing calcium nodule formation and downregulating osteogenic differentiation-related protein expression. Additionally, inhibiting Dnmt3b expression upregulated CXCL12 protein expression and inhibited CXCL12 methylation. Dnmt3b could be binded to CXCL12. CXCL12 overexpression attenuated the effects of FOXC1 overexpression and inhibited BM-MSCs osteogenic differentiation. This study confirmed that the FOXC1-mediated regulation of the Dnmt3b/CXCL12 axis had positive effects on the osteogenic differentiation of BM-MSCs.

Efflux pump Rv1258c activates novel functions of the oxidative stress and via the VII secretion system ESX-3-mediated iron metabolic pathway in Mycobacterium tuberculosis.

Oxidative stress and iron metabolism are essential for Mycobacterium tuberculosis (M.tb) survival in host cells. The efflux pump Rv1258c belongs to the major facilitator superfamily (MFS) and can actively pump drugs to promote certain drug resistance in M.tb. In this study, we compared H37RvΔRv1258c with wild-type (WT) M.tb H37Rv. The qRT-PCR results suggested that Rv1258c is potentially involved in the iron metabolic pathway by regulating the expression of ESX-3, which is required for iron uptake. Protein-Protein Affinity Predictor (PPA-Pred2) and the artificial intelligence program AlphaFold 2 were used for prediction and showed that Rv1258c has direct interactions with PPE4 and EccD3 but weak interactions with EccB3. This was further determined via protein-protein interaction analysis of the yeast two-hybrid expression system. By comparing mutant H37RvΔRv1258c strains with WT strains, we discovered that the absence of Rv1258c led to elevated intracellular H+ potential and NAD+/NADH ratios in M.tb, thereby resulting in oxidative stress. We hypothesize that the efflux pump Rv1258c not only has the function of regulating drug resistance in M.tb but also has a novel function in activating oxidative stress and regulating ESX-3-associated iron metabolism in M.tb.

Study on the Action Mechanism of Dkk-1, TGF-ß1 and TNF-α Expression Levels in Dupuytren's Contracture.

BACKGROUND: The biological mechanism of Dupuytren's contracture needs to be further studied in order to minimize postoperative recurrence and provide a pathological basis for the development of new therapeutic targets. METHODS: HE staining, immunohistochemistry, PCR and western blotting were performed in pathological palmar aponeurosis specimens and normal palmar aponeurosis tissues for comparative study. RESULTS: (1) TNF-α expression was up-regulated: TNF-α mRNA was more highly expressed in the pathological tissues of DD patients than in the CT group, P < 0.05, and the difference between the two groups was statistically significant; (2) Dkk-1 expression was down-regulated: Dkk-1 mRNA was lower expressed in the pathological tissues of DD patients than in the CT group, P < 0.05, and the difference between the two groups was statistically significant; (3) TGF-ß1 expression was up-regulated: TGF-ß1 mRNA was higher expressed in the pathological tissues of DD patients than in the CT group, P < 0.05, and the difference between the two groups was statistically significant; (4) Pearson correlation analysis suggested that TNF-α expression was positively correlated with TGF-ß1 expression, TNF-α expression was negatively correlated with DKK-1 expression, and TGF-ß1 expression was negatively correlated with DKK-1 expression. CONCLUSION: TNF-α, DKK-1 and TGF-ß1 may play a role in the pathogenesis of palmar aponeurosis contracture, and there is a relationship between them. The study of the relationship between the three and their related signaling pathways provides a therapeutic target and a basis for the prevention and early treatment of palmar aponeurotic contracture.

The Treatment Experience of Different Types of Flaps for Repairing Soft Tissue Defects of the Heel.

OBJECTIVE: To summarize the clinical application effects of three different types of flaps for repairing soft tissue defects of the heel, and to discuss the importance of tissue repair and heel reconstruction. METHODS: A total of 46 cases with skin tissue defects of the heel with deep tissue exposure were treated. The reasons for the defect were trauma (n = 26), burns and electric shocks (n = 12), chronic ulcers (n = 2), postoperative infection of the calcaneus and Achilles tendon (n = 5), and tumor resection (n = 1). The scope of wound defect was 2.0×2.5 to approximately 15.0×20.0 cm. The flaps used were medial plantar island flaps (n = 9), distal pedicled sural neurovascular island flaps (n = 23), and free anterolateral thigh (perforator) flaps (n = 14). The flap cutting range was 3.0×3.5 to approximately 16.0×22.0 cm. RESULTS: After surgery, all 46 flaps survived. In two cases, patients experienced partial epidermal necrosis at the distal end of the flap that healed after local dressing exchange, and after this treatment, the complete skin grafts survived. Follow-up was conducted in 40 cases, with an average follow-up duration of 8.2 months (3-44 months) and the two-point discrimination of 5-14 mm. The average American Orthopaedic Foot and Ankle Society scale was 89.2 points with good flap color and texture, satisfactory appearance, and normal gait. CONCLUSION: The repair method should be selected according to the"5-zone method": The plantar medial island flap is suitable for small area (<5 cm) of medial, posterior and plantar defects. The distal pedicled sural neurovascular flap is suitable for lateral, posterior, and medium-range (6-10 cm) joint area defects. The free anterolateral thigh perforator flap is suitable for large-scale (>10 cm) joint area defects.

Recent advances in functionalized upconversion nanoparticles for light-activated tumor therapy.

Upconversion nanoparticles (UCNPs) are a class of optical nanocrystals doped with lanthanide ions that offer great promise for applications in controllable tumor therapy. In recent years, UCNPs have become an important tool for studying the treatment of various malignant and nonmalignant cutaneous diseases. UCNPs convert near-infrared (NIR) radiation into shorter-wavelength visible and ultraviolet (UV) radiation, which is much better than conventional UV activated tumor therapy as strong UV-light can be damaging to healthy surrounding tissue. Moreover, UV light generally does not penetrate deeply into the skin, an issue that UCNPs can now address. However, the current studies are still in the early stage of research, with a long way to go before clinical implementation. In this paper, we systematically analysed recent advances in light-activated tumor therapy using functionalized UCNPs. We summarized the purpose and mechanism of UCNP-based photodynamic therapy (PDT), gene therapy, immunotherapy, chemo-therapy and integrated therapy. We believe the creation of functional materials based on UCNPs will offer superior performance and enable innovative applications, increasing the scope and opportunities for cancer therapy in the future.

Clinical Differences between Eosinophilic and Noneosinophilic Acute Exacerbation of Chronic Obstructive Pulmonary Disease: A Multicenter Cross-Sectional Study.

METHODS: A total of 643 AECOPD patients were enrolled in this multicenter cross-sectional study. Finally, 455 were included, 214 in the normal-eosinophil AECOPD (NEOS-AECOPD) group, 63 in the mild increased-eosinophil AECOPD (MEOS-AECOPD) group, and 138 in the severe increased-eosinophil AECOPD (SEOS-AECOPD) group. Demographic data, underlying diseases, symptoms, and laboratory findings were collected. Multiple logistic regression analysis was performed to identify the independent factors associated with blood eosinophils (EOS). Correlations between blood EOS and its associated independent factors were evaluated. RESULTS: The significant differences in 19 factors, including underlying diseases, clinical symptoms, and laboratory parameters, were identified by univariate analysis. Subsequently, multiple logistic regression analysis revealed that lymphocyte%, neutrophil% (NS%), procalcitonin (PCT), and anion gap (AG) were independently associated with blood EOS in AECOPD. Both blood EOS counts and EOS% were significantly correlated with lymphocyte%, NS%, PCT, and AG. CONCLUSIONS: Collectively, blood EOS was independently associated with lymphocyte%, NS%, PCT, and AG in AECOPD patients. Lymphocyte% was lower, and NS%, PCT, and AG were higher in eosinophilic AECOPD. Our results indicate that viral-dominant infections are the probable major etiologies of eosinophilic AECOPD. Noneosinophilic AECOPD is more likely associated with bacterial-dominant infections. The systemic inflammation in noneosinophilic AECOPD was more severe.

LncRNA H19 Regulates BMP2-Induced Hypertrophic Differentiation of Mesenchymal Stem Cells by Promoting Runx2 Phosphorylation.

OBJECTIVES: Bone morphogenetic protein 2 (BMP2) triggers hypertrophic differentiation after chondrogenic differentiation of mesenchymal stem cells (MSCs), which blocked the further application of BMP2-mediated cartilage tissue engineering. Here, we investigated the underlying mechanisms of BMP2-mediated hypertrophic differentiation of MSCs. MATERIALS AND METHODS: In vitro and in vivo chondrogenic differentiation models of MSCs were constructed. The expression of H19 in mouse limb was detected by fluorescence in situ hybridization (FISH) analysis. Transgenes BMP2, H19 silencing, and overexpression were expressed by adenoviral vectors. Gene expression was determined by reverse transcription and quantitative real-time PCR (RT-qPCR), Western blot, and immunohistochemistry. Correlations between H19 expressions and other parameters were calculated with Spearman's correlation coefficients. The combination of H19 and Runx2 was identified by RNA immunoprecipitation (RIP) analysis. RESULTS: We identified that H19 expression level was highest in proliferative zone and decreased gradually from prehypertrophic zone to hypertrophic zone in mouse limbs. With the stimulation of BMP2, the highest expression level of H19 was followed after the peak expression level of Sox9; meanwhile, H19 expression levels were positively correlated with chondrogenic differentiation markers, especially in the late stage of BMP2 stimulation, and negatively correlated with hypertrophic differentiation markers. Our further experiments found that silencing H19 promoted BMP2-triggered hypertrophic differentiation through in vitro and in vivo tests, which indicated the essential role of H19 for maintaining the phenotype of BMP2-induced chondrocytes. In mechanism, we characterized that H19 regulated BMP2-mediated hypertrophic differentiation of MSCs by promoting the phosphorylation of Runx2. CONCLUSION: These findings suggested that H19 regulates BMP2-induced hypertrophic differentiation of MSCs by promoting the phosphorylation of Runx2.

Recombinant adenovirus (AdEasy system) mediated exogenous expression of long non-coding RNA H19 (lncRNA H19) biphasic regulating osteogenic differentiation of mesenchymal stem cells (MSCs).

BACKGROUND: We previously constructed AdEasy system for rapid generation of recombinant adenovirus expressing coding genes. However, it is unclear if AdEasy system could be used for exogenously expression of long noncoding RNAs (lncRNAs). Here we investigated how to overexpress lncRNA H19 with AdEasy system and identified the effect of overexpression H19 on mesenchymal stem cells (MSCs) osteogenic differentiation. METHODS: H19 fragment 1 and H19 fragment 2 were amplified from mouse genomic DNA separately and then connected for full-length H19. H19 was firstly subcloned to homemade pMOK plasmid, then H19 was cut off from pMOK-H19 and subcloned to recombinant adenovirus plasmid. After homologous recombination in AdEasier cells (BJ5183 cell), packing in mammalian packaging cell line and amplification in 293pTP cells, high titer AdH19 was obtained. Immortalized mouse adipose-derived progenitors (iMADs) were infected by AdH19 with different infection rate, the expression of H19, H19 related microRNAs (miRs) and osteogenic differentiation markers were determined by TqPCR. Alkaline phosphatase (ALP) activities and matrix mineralization were determined by ALP assays and Alizarin red S staining respectively. RESULTS: AdEasy system was suitable for rapid generation and production of H19, AdH19 can effectively overexpress H19 and serve as functional lncRNA in mesenchymal stem cells (MSCs). Higher dosage of AdH19 inhibited osteogenic differentiation of MSCs, however, lower dosage of AdH19 promoted osteogenic differentiation of MSCs. CONCLUSIONS: We firstly reported the method for the generation of functional lncRNA with AdEasy system, and identified the biphasic effect of H19 on MSCs osteogenic differentiation.

BMP9 exhibits dual and coupled roles in inducing osteogenic and angiogenic differentiation of mesenchymal stem cells.

Bone morphogenetic protein (BMP) 9 (BMP9) is one of most potent BMPs in inducing osteogenic differentiation of mesenchymal stem cells (MSCs). Recently, evidence has shown that osteogenesis and angiogenesis are coupled, however, it is unclear whether BMP9 induces MSC differentiation into endothelial-like cells and further promotes blood vessel formation. In the present study, we explored the potential of BMP9-induced angiogenic differentiation of MSCs, and the relationship between BMP9-induced osteogenic and angiogenic differentiation of MSCs. Osteogenic activities and angiogenic differentiation markers were analyzed at mRNA and protein levels. In vivo osteogenic and angiogenic differentiation of MSCs were tested by the ectopic bone formation model. We identified that adenoviral vectors effectively transduced in immortalized mouse embryonic fibroblasts (iMEFs) and expressed BMP9 with high efficiency. We found that BMP9 induces early and late osteogenic differentiation, and it up-regulated osteogenic marker expression in MSCs. Meanwhile, BMP9 induces angiogenic differentiation of MSCs via the expression of vascular endothelial growth factor a (VEGFa) and CD31 at both mRNA and protein levels. CD31-positive cells were also increased with the stimulation of BMP9. The ectopic bone formation tests found that BMP9-induced trabecular bone formation was coupled with the expression of blood vessel formation markers and sinusoid capillary formation. These findings suggest that BMP9 exhibits dual and coupled roles in inducing osteogenic and angiogenic differentiation of MSCs.

Three-dimensional silk fibroin scaffolds enhance the bone formation and angiogenic differentiation of human amniotic mesenchymal stem cells: a biocompatibility analysis.

Silk fibroin (SF) is a fibrous protein with unique mechanical properties, adjustable biodegradation, and the potential to drive differentiation of mesenchymal stem cells (MSCs) along the osteogenic lineage, making SF a promising scaffold material for bone tissue engineering. In this study, hAMSCs were isolated by enzyme digestion and identified by multiple-lineage differentiation. SF scaffold was fabricated by freeze-drying, and the adhesion and proliferation abilities of hAMSCs on scaffolds were determined. Osteoblast differentiation and angiogenesis of hAMSCs on scaffolds were further evaluated, and histological staining of calvarial defects was performed to examine the cocultured scaffolds. We found that hAMSCs expressed the basic surface markers of MSCs. Collagen type I (COL-I) expression was observed on scaffolds cocultured with hAMSCs. The scaffolds potentiated the proliferation of hAMSCs and increased the expression of COL-I in hAMSCs. The scaffolds also enhanced the alkaline phosphatase activity and bone mineralization, and upregulated the expressions of osteogenic-related factors in vitro. The scaffolds also enhanced the angiogenic differentiation of hAMSCs. The cocultured scaffolds increased bone formation in treating critical calvarial defects in mice. This study first demonstrated that the application of 3D SF scaffolds co-cultured with hAMSCs greatly enhanced osteogenic differentiation and angiogenesis of hAMSCs in vitro and in vivo. Thus, 3D SF scaffolds cocultured with hAMSCs may be a better alternative for bone tissue engineering.

Theoretical analysis for spherical aberration induction with low-order correction in refractive surgery.

A theoretical foundation for the analysis of ocular aberration correction is developed. It enables a comparative study for two different refractive surgical approaches, namely, the conventional and the Q-preserved treatment modalities. A refractive surgical factor is identified that leads to a simple cubic function for the postoperative asphericity factor for the conventional treatment. A formulation is developed that paves the way for the calculation of the induction of spherical aberration for low-order aberration correction in refractive surgery. Opposite to the general belief, the Munnerlyn shape makes myopic LASIK more prolate, not oblate. A Monte Carlo simulation was conducted for 1000 eyes for these two refractive surgical modalities. It was found that, although the postoperative spherical aberration is similar for these surgical modalities, for the induction of spherical aberration from the ablation target shape, the conventional modality appears to be slightly more predictable.

Validity of scaling zernike coefficients to a larger diameter for refractive surgery.

PURPOSE: To investigate the validity of a Zernike rescaling algorithm to a larger wavefront diameter. METHODS: Using 4256 preoperative wavefront examinations, the variability of inter-examination wavefront root-mean-square (RMS) was compared to the error induced due to scaling Zernike coefficients to a larger diameter. The validity of scaling Zernike coefficients was set when the error due to the scaling was the same as the variability of the inter-examination wavefronts. The inter-examination variability was calculated from eyes having at least 3 same-day, preoperative examinations over the same diameters. Error from scaling Zernike coefficients to a larger diameter was calculated by comparing the wavefront for a (scaled-up) set of Zernike coefficients to the wavefront of the average of Zernike coefficient sets at a larger diameter for the same eye. Wavefront diameters of 5, 5.5, 6, 6.5, and 7 mm were considered. RESULTS: No significant difference was found for the variability for different pupil sizes. The error due to scaling Zernike coefficients to a larger pupil size was generally smaller than the inter-examination variability when the new diameter was 0.25 mm larger than the original diameter. The error was comparable to the inter-examination variability when the new diameter was 0.5 mm larger. The error became larger when the new diameter was >0.75 mm larger than the original diameter. CONCLUSIONS: Rescaling Zernike coefficients from a smaller diameter to a larger one has practical applications in optical zone extension for wavefront-guided refractive surgery.

Spherical aberrations of human astigmatic corneas.

PURPOSE: To evaluate whether the average spherical aberration of human astigmatic corneas is statistically equivalent to human nonastigmatic corneas. METHODS: Spherical aberrations of 445 astigmatic corneas prior to laser vision correction were retrospectively investigated to determine Zernike coefficients for central corneal areas 6 mm in diameter using CTView (Sarver and Associates). Data were divided into groups according to cylinder power (0.01 to 0.25 diopters [D], 0.26 to 0.75 D, 0.76 to 1.06 D, 1.07 to 1.53 D, 1.54 to 2.00 D, and >2.00 D) and according to age by decade. Spherical aberrations were correlated with age and astigmatic power among groups and the entire population. Statistical analyses were conducted, and P<.05 was considered statistically significant. RESULTS: Mean patient age was 42.6±11 years. Astigmatic corneas had an average astigmatic power of 0.78±0.58 D and mean spherical aberration was 0.25±0.13 µm for the entire population and approximately the same (0.27 µm) for individual groups, ranging from 0.23 to 0.29 µm (P>.05 for all tested groups). CONCLUSIONS: Mean spherical aberration of astigmatic corneas was not correlated significantly with cylinder power or age (P>.05). Spherical aberrations are similar to those of nonastigmatic corneas, permitting the use of these additional data in the design of aspheric toric intra-ocular lenses.

Wavefront propagation from one plane to another with the use of Zernike polynomials and Taylor monomials.

In wavefront-driven vision correction, ocular aberrations are often measured on the pupil plane and the correction is applied on a different plane. The problem with this practice is that any changes undergone by the wavefront as it propagates between planes are not currently included in devising customized vision correction. With some valid approximations, we have developed an analytical foundation based on geometric optics in which Zernike polynomials are used to characterize the propagation of the wavefront from one plane to another. Both the boundary and the magnitude of the wavefront change after the propagation. Taylor monomials were used to realize the propagation because of their simple form for this purpose. The method we developed to identify changes in low-order aberrations was verified with the classical vertex correction formula. The method we developed to identify changes in high-order aberrations was verified with ZEMAX ray-tracing software. Although the method may not be valid for highly irregular wavefronts and it was only proven for wavefronts with low-order or high-order aberrations, our analysis showed that changes in the propagating wavefront are significant and should, therefore, be included in calculating vision correction. This new approach could be of major significance in calculating wavefront-driven vision correction whether by refractive surgery, contact lenses, intraocular lenses, or spectacles.

Comparison of wavefront reconstructions with Zernike polynomials and Fourier transforms.

PURPOSE: To make a direct comparison between Fourier and Zernike reconstructions of ocular wavefronts using a newly available analytical theory by which Fourier coefficients can be converted to Zernike coefficients and vice versa. METHODS: Noise-free random wavefronts were simulated with up to the 15th order of Zernike polynomials. For each case, 100 random wavefronts were simulated separately. These wavefronts were smoothed with a low-pass Gaussian filter to remove edge effects. Wavefront slopes were calculated, and normally distributed random noise was added within the circular area to simulate realistic Shack-Hartmann spot patterns. Three wavefront reconstruction methods were performed. The wavefront surface error was calculated as the percentage of the input wavefront root mean square. RESULTS: Fourier full reconstruction was more accurate than Zernike reconstruction from the 6th to the 10th orders for low-to-moderate noise levels. Fourier reconstruction was found to be approximately 100 times faster than Zernike reconstruction. Fourier reconstruction always makes optimal use of information. For Zernike reconstruction, however, the optimal number of orders must be chosen manually. The optimal Zernike order for Zernike reconstruction is lower for smaller pupils than larger pupils. CONCLUSIONS: Fourier full reconstruction is faster and more accurate than Zernike reconstruction, makes optimal use of slope information, and better represents ocular aberrations of highly aberrated eyes.

Optical surface optimization for the correction of presbyopia.

Presbyopia, the gradual loss of accommodation that accompanies aging, can be corrected by creating asphericity in the optical path of the eye. Bifocal and aspheric contact lenses, intraocular lenses, spectacle lenses, and laser refractive surgery are all widely used to alleviate the symptoms of presbyopia. These types of corrective surfaces try to concentrate vision in limited peaks over the full range of vergences. The methodology described in this paper is designed to correct presbyopia by optimizing vision over the entire target range of near to distant. A corrective surface was created by employing an iterative function minimization algorithm to optimize an optical metric. In most cases, it is possible to obtain an optical surface that will optically compensate for presbyopia.

System performance evaluation of refractive surgical lasers: a mathematical approach.

A study was conducted for the purpose of improving the designs of the next generation of refractive surgical laser systems. Two common refractive laser systems, variable-spot scanning (type A) and small-spot scanning (type B), are discussed by identifying sources of error that could adversely affect the capability of these lasers to accurately produce complex, customized wavefront guided ablations. A mathematical model was used to construct a laser simulator that models the two common laser systems in terms of the root-mean-square error. Error sources from ablation profile fitting, ablation registration, eye tracking, and the laser delivery system are compared, and the relative contribution of each to the overall system error is analyzed. This system-level analysis can be helpful to the improvement of both laser systems.