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Background Ocular toxoplasmosis caused by Toxoplasma gondii is an infectious disease which is widely distributed around the world and can present with various clinic manifestations. We are here reporting an unusual case presented with epiretinal membrane (ERM), i.e., macular pucker. Case presentation A 16-year old male patient visited our outpatient clinic complaining of decreased vision for about 8 years in his left eye. The best-corrected visual acuity (BCVA) was 20/20 OD and 20/400 OS. There was sensory exotropia in his left eye. No inflammatory cells or flare were found in his anterior chamber or vitreous cavity OU. An ERM involving his left macular area was found on his dilated fundus exam, which was confirmed by Optical Coherence Tomography (OCT). The ERM was found to involve his left macular area with his foveal ellipsoid zone absent. The right eye was found to be within normal limit. After a thorough discussion with the patient and his parents about treatment options and surgical benefits, risks and alternatives, we performed vitrectomy, peeled off the ERM and collected the vitreous sample for parasite testing during the procedure. Patient’s blood also was drawn for serological testing. Vitreous sample analysis and serological tests confirmed ocular toxoplasmosis OS as his final diagnosis. Unfortunately, the BCVA of this patient was not improved after the surgery, but the exotropia disappeared. Conclusion ERM is an unusual clinical presentation of ocular toxoplasmosis. We may add Toxoplasma gondii infection as a differential diagnosis when encountering ERM cases.

The MEF2 (myocyte enhancer factor 2) family belongs to the MADS-box superfamily of eukaryotic transcription factors. The vertebrate genes compose four distinct subfamilies designated MEF2A, -B, -C, and -D. There are multiple mef2 genes in the common carp (Cyprinus carpio). So far, the embryonic expression patterns of these genes and the evolution of fish mef2 genes have been barely investigated. In this study, we completed the coding information of C. carpio mef2ca2 and mef2d1 genes via gene cloning and presented two mosaic mef2 sequences as evidence for recombination. We also analyzed the phylogenetic relationship and conserved synteny of mef2 genes and proposed a new evolutionary scenario. In our version, MEF2B and the other three vertebrate subfamilies were generated in parallel from the single last ancestor via two rounds of whole genome duplication events that occurred at the dawn of vertebrates. Moreover, we examined the expression patterns of C. carpio mef2 genes during embryogenesis, by using whole-mount in situ hybridization, and found the notochord to be a new expression site for these genes except for mef2ca1&2. Our results thus provide new insights into the evolution and expression of mef2 genes.

The purpose of this study is to compare the outcomes following femtosecond laser-assisted deep anterior lamellar keratoplasty (DALK) with 75% of stromal dissection (predescemetic group) and femtosecond laser-assisted DALK using big-bubble technique with total stromal resection (descemetic group) for the treatment of keratoconus. Twenty eyes of 17 patients with keratoconus were studied. There were 10 eyes of 9 patients in predescemetic group and 10 eyes of 8 patients in descemetic group. The postoperative best-corrected visual acuity (BCVA), manifest refraction, keratometry, endothelial cell density (ECD), and central corneal thickness (CCT) were analyzed. All surgeries were performed uneventfully. At 1 year after surgery, the BCVA, corneal astigmatism, keratometry, CCT, and ECD between two groups were not statistically significant (all P > 0.05). However, the mean manifest refraction was -9.43 ± 7.44 diopter (D) and -1.03 ± 1.13D in predescemetic and descemetic groups, respectively, which was statistically significant between two groups (P < 0.05). The results of BCVA and corneal astigmatism, keratometry, ECD, and CCT were comparable between two groups. However, the mean postoperative manifest refraction was lower in descemetic group.

Background To identify the genetic defects and investigate the possible mechanism of cataract genesis in a five-generation family with autosomal dominant congenital posterior polar cataracts. Methods Clinical data were collected, and the lens phenotypes of the affected members in this family were recorded by slit lamp photography. Genomic DNA was isolated from peripheral blood using QIAamp DNA Blood Mini Kits. Twenty-three mutational hot spots associated with autosomal dominant congenital posterior polar cataracts were screened by PCR-based DNA sequencing. Properties and structural models of wild-type and mutant alpha-B (αB)-crystallin (CRYAB) were generated and analyzed using SWISS-MODEL. Results All affected individuals in this family started to exhibit poor vision at the age of 8–10 years. The lens opacity consisted of a single, well-defined plaque, 0.5–3 mm in diameter, which was confined to the posterior pole of the lens. DNA sequencing analysis of the affected members showed a novel, heterozygous missense mutation c.59C > G (P20R) in exon 1 of the CRYAB gene. This mutation was not found in 10 unaffected family members, or in 200 unaffected and unrelated individuals, thereby excluding the possibility that it is a rare polymorphism. Data generated using the ProtScale and PyMOL programs revealed that the mutation altered the stability and solubility of the αB-crystallin protein. Conclusions This study reported a novel c.59C > G (P20R) missense mutation in CRYAB in a five-generation Chinese family with posterior polar cataract.

Purpose: To evaluate the optical quality and tear-film dynamics in patients with aqueous-deficient or evaporative subtype of dry eye disease (DED). Methods: Twenty-five aqueous-deficient dry eye (ADDE) patients, 25 DED patients with meibomian gland dysfunction (MGD), and 25 healthy subjects were included in this study. Vision-related health-targeted quality of life was evaluated using the Ocular Surface Disease Index (OSDI) questionnaire. Dynamic recording with a double-pass system (Optical Quality Analysis System [OQAS]) was performed in right eyes. Scattered light was measured as the objective scatter index (OSI) at 0.5-second intervals over 20 seconds without blinking. Then, we recorded OSI every 0.5 seconds within a 20-second period with the subjects asked to blink freely. Several parameters were established to evaluate the dynamic alterations of optical quality and the effects of blinks: OSI, OSI standard deviation (SD), ΔOSI, ΔOSI/time, blinking change (BC), and blinking frequency (BF). Additional clinical examination included tear film break-up time (BUT), Schirmer I test (SIT), fluorescein staining grade (FL), meibomian gland quality, meibomian gland expressibility, and meibomian gland drop-out. Results: The OSI, SD, ΔOSI, ΔOSI/time, BC, and BF were significantly higher in DED patients than controls (P < 0.01, respectively). The OSI, SD, ΔOSI, ΔOSI/time, BC, and BF were significantly higher in patients with MGD than patients with ADDE (P < 0.01). In the MGD group, BUT, FL staining score, lid abnormality, meibomian gland expressibility, and meibomian gland drop-out were correlated with Δ OSI and Δ OSI/time. Conclusion: Dry eye patients with MGD had significant alterations of optical quality compared with ADDE patients. The double-pass system has potential to be a useful quantitative method to evaluate the optical quality and tear-film dynamics in patients with dry eye.

Background Almost one-third of congenital cataracts are primarily autosomal dominant disorders, which are also called autosomal dominant congenital cataract, resulting in blindness and clouding of the lens. The purpose of this study was to identify the disease-causing mutation in a Chinese family affected by bilateral, autosomal dominant congenital cataract. Methods The detection of candidate gene mutation and the linkage analysis of microsatellite markers were performed for the known candidate genes. Molecular mapping and cloning of candidate genes were used in all affected family members to screen for potential genetic mutations and the mutation was confirmed by single enzyme digestion. Results The proband was diagnosed with isolated, congenital cataract without the typical clinical manifestations of cataract, which include diabetes, porencephaly, sporadic intracerebral hemorrhage, and glomerulopathy. A novel mutation, c.2345 G > C (Gly782Ala), in exon 31 of the collagen type IV αlpha1 ( COL4A1 ) gene, which encodes the collagen alpha-1(IV) chain, was found to be associated with autosomal dominant congenital cataract in a Chinese family. This mutation was not found in unaffected family members or in 200 unrelated controls. Sequence analysis confirmed that the Gly782 amino acid residue is highly conserved. Conclusions The novel mutation (c.2345 G > C) of the COL4A1 gene is the first report of a non-syndromic, autosomal dominant congenital cataract, thereby highlighting the important role of type IV collagen in the physiological and optical properties of the lens.

For a vessel flexure of measure ship under the influence of internal and external environmental factors, which resulting data errors of measuring equipment, the development of the \"Vessel Flexure System\" can solve the problem. The paper briefly describes the principle and hardware components of Vessel Flexure System, focuses on the application of digital image processing techniques used on linear CCD, put forward the interpretation method of gravity-center, which can determine the location of the center of facula accurately.

Aim： Polypeptide from Chlamysfarreri （PCF, molecular mass is 879） is a new marine polypeptide compound isolated from Chlamysfarreri. This study investigates the possible protective roles and the mechanism of PCF against ultraviolet B （UVB）-induced apoptosis in murine thymocytes. Methods： The rate of apoptosis and caspase-3 activation was measured by flow cytometry. The expression of stress-response genes c-fos and c-jun was observed by RT-PCR. Western blot analysis was performed to determine the release of cytochrome c. Results： It was found that UVB induced murine thymocyte death. The cells treated with UVB showed an increase in cytochrome c release, caspase-3 activity, as well as in the expression of c-fos and c-jun. In addition, all were involved in UVB-induced cell apoptosis. Conclusion： Our present observations pointed to the ability of PCF to avert UVB-induced apoptosis in thymocytes by modulating c-fos and c-jun expression, cytochrome c release, and the consequent activation of caspase-3, which were essential components of the UV-induced cell apoptotic pathway. The results suggested that PCF is a promising protective substance against UV radiation.

The major pathological changes in Alzheimer＇s disease are beta amyloid deposits and cognitive impairment. Calycosin is a typical phy- toestrogen derived from radix astragali that binds to estrogen receptors to produce estrogen-like effects. Radix astragali Calycosin has been shown to relieve cognitive impairment induced by diabetes mellitus, suggesting calycosin may improve the cognitive function of Alzhei- mer＇s disease patients. The protein kinase C pathway is upstream of the mitogen-activated protein kinase pathway and exerts a neuropro- tective effect by regulating Alzheimer＇s disease-related beta amyloid degradation. We hypothesized that calycosin improves the cognitive function of a transgenic mouse model of Alzheimer＇s disease by activating the protein kinase C pathway. Various doses of calycosin （10, 20 and 40 mg/kg） were intraperitoneally injected into APP/PS1 transgenic mice that model Alzheimer＇s disease. Calycosin diminished hippocampal beta amyloid, Tau protein, interleukin-lbeta, tumor necrosis factor-alpha, acetylcholinesterase and malondialdehyde levels in a dose-dependent manner, and increased acetylcholine and glutathione activities. The administration of a protein kinase C inhibitor, cal- phostin C, abolished the neuroprotective effects of calycosin including improving cognitive ability, and anti-oxidative and anti-inflammato- ry effects. Our data demonstrated that calycosin mitigated oxidative stress and inflammatory responses in the hippocampus of Alzheimer＇s disease model mice by activating the protein kinase C pathway, and thereby improving cognitive function.

miRNAlet-7al表达减少和IGF1R信号通路激活都与前列腺癌的发生发展密切相关，两者之间在肿瘤中的表达关系尚未明确。我们最近研究发现，在前列腺癌PC-3细胞中，let-7al可直接靶向调控IGFIR的表达，抑制细胞增殖。首先通过TargetScan分析，发现IGF1R是let-7al的靶基因之一，在它的3’非翻译区存在3个let-7al的靶点（T1、T2、T3）。采用实时定量PCR、免疫印迹和荧光素酶报告基因检测技术检测Pc．3细胞中let-7al对IGF1R基因表达的影响。结果显示，let-7al可直接作用于IGF1R mRNA的3’非翻译区中的T1和T2靶点，靶向抑fNIGFIR基因的表达。进一步采用RT-PCR、荧光素酶报告基因检测、MTT、流式细胞术和Hoechst 33342染色技术，检测let-7al导致的IGF1R表达下调对IGF1R信号通路的影响。结果表明，let-7al下调IGF1R表达可使E1k1活化减少、其靶基因c-los表达降低、细胞增殖抑制、凋亡增强和细胞周期阻滞；反之，抑制let-7al可使IGF1R表达上调，伴有E1k1活性增强、c-fos表达增加、细胞增殖加快。以上结果提示，miRNA let-7a有可能成为前列腺癌治疗的新靶点。