Selective Adsorption of Dyes and Fe3+ Sensing via Tb3+ Incorporation in an Anionic Cadmium-Organic Framework.

A three-dimensional (3D) anionic cadmium-organic framework, namely [(CH3)2NH2][Cd1.5(DMTDC)2] ⋅ 2DMA ⋅ 0.5H2O (Cd-MOF; DMA=N,N-dimethylacetamide), was successfully synthesized under solvothermal conditions by using a linear thienothiophene-containing dicarboxylate ligand, 3,4-dimethylthieno [2,3-b]-thiophene-2,5-dicar-boxylic acid (H2DMTDC). Single-crystal X-ray diffraction analysis reveals that Cd-MOF exhibits a 3D anionic framework with pcu α-Po topology, featuring rectangle and rhombus-shaped channels along b- and c- axis direction. Cd-MOF demonstrates selective adsorption of cationic dyes over anionic and neutral dyes. Additionally, Tb3+-loaded Cd-MOF serves as a fast-response fluorescence sensor for the sensitive detection of Fe3+ ions with a low limit of detection (8.90×10-7 M) through fluorescence quenching.

Non-alcoholic Fatty Liver Disease Is Associated With Aortic Calcification: A Cohort Study With Propensity Score Matching.

Objectives: Non-alcoholic fatty liver disease (NAFLD) greatly affects cardiovascular disease, but evidence on the associations between NAFLD and markers of aortic calcification is limited. We aim to evaluate the association between NAFLD and aortic calcification in a cohort of Chinese adults using propensity score-matching (PSM) analysis. Methods: This prospective cohort study involved adults who underwent health-screening examinations from 2009 to 2016. NAFLD was diagnosed by abdominal ultrasonography at baseline, and aortic calcification was identified using a VCT LightSpeed 64 scanner. Analyses included Cox proportional-hazards regression analysis and PSM with predefined covariates (age, gender, marital and smoking status, and use of lipid-lowering drugs) to achieve a 1:1 balanced cohort. Results: Of the 6,047 eligible participants, 2,729 (45.13%) were diagnosed with NAFLD at baseline, with a median age of 49.0 years [interquartile range, 44.0-55.0]. We selected 2,339 pairs of participants with and without NAFLD at baseline for the PSM subpopulation. Compared with those without NAFLD, patients with NAFLD were at a higher risk of developing aortic calcification during follow-up; significant results were observed before and after matching, with the full-adjusted hazard ratios and corresponding 95% confidence intervals being 1.19 (1.02-1.38) and 1.18 (1.01-1.38), respectively (both p < 0.05). In subgroup analyses, no interaction was detected according to age, gender, smoking status, body mass index, total cholesterol, low-density lipoprotein cholesterol, use of lipid-lowering drugs, hypertension, or type 2 diabetes. Conclusions: NAFLD may be independently associated with aortic calcification. Further studies are warranted to elucidate the possible underlying mechanisms.

Effect of femtosecond laser-assisted steepest-meridian clear corneal incisions on preexisting corneal regular astigmatism at the time of cataract surgery.

AIM: To investigate the clinical efficacy and safety of femtosecond laser-assisted steepest-meridian clear corneal incisions for correcting preexisting corneal astigmatism performed at the time of cataract surgery. METHODS: This prospective case series study comprised consecutive age-related cataract patients with corneal regular astigmatism (range: +0.75 to +2.50 D) who had femtosecond laser-assisted steepest-meridian clear corneal incisions (single or paired). Corneal astigmatism was performed with the Pentacam preoperatively and 3mo postoperatively. Total corneal astigmatism and steepest-meridian measured in the 3-mm central zone were used to guide the location, size and number of clear corneal incision. The vector analysis of astigmatic change was performed using the Alpins method. RESULTS: Totally 138 eyes of 138 patients were included. The mean preoperative corneal astigmatism was 1.31±0.41 D, and was significantly reduced to 0.69±0.34 D (equivalent to difference vector) after surgery (P<0.01). The surgically-induced astigmatism was 1.02±0.54 D. The correction index (ratio of target induced astigmatism and surgically-induced astigmatism: 0.72±0.36) as well as the magnitude of error (difference between surgically-induced astigmatism and target induced astigmatism: -0.29±0.51) represented a slight under correction. For angle of error, the arithmetic mean was 1.11±13.70, indicating no significant systematic alignment errors. CONCLUSION: Femtosecond-assisted steepest-meridian clear corneal incision is a fast, customizable, adjustable, precise, and safe technique for the reduction of low to moderate corneal astigmatism during cataract surgery.

Notch1-Nrf2 signaling crosstalk provides myocardial protection by reducing ROS formation.

Both the Notch1 and Keap1-Nrf2 signaling pathways have cardioprotective effects, but the role of Notch1-Nrf2 crosstalk in myocardial ischemia-reperfusion injury is unclear. In this study, we established hypoxia-reoxygenation in neonate rat myocardial cells and employed γ-secretase inhibitor and curcumin to inhibit and activate the Notch1 and Keap1-Nrf2 signaling pathways, respectively. We found that the combined action of the Notch1 and Keap1-Nrf2 signaling pathways significantly increased cardiomyocyte viability, inhibited cardiomyocyte apoptosis, reduced the formation of reactive oxygen species, and increased antioxidant activities. In conclusion, these findings suggest that Notch1-Nrf2 crosstalk exerts myocardial protection by reducing the formation of reactive oxygen species.

Notch1 protects against myocardial ischaemia-reperfusion injury via regulating mitochondrial fusion and function.

Mitochondrial fusion and fission dynamic are critical to the myocardial protection against ischaemia-reperfusion injury. Notch1 signalling plays an important role in heart development, maturation and repair. However, the role of Notch1 in the myocardial mitochondrial fusion and fission dynamic remains elusive. Here, we isolated myocardial cells from rats and established myocardial ischaemia-reperfusion injury (IRI) model. We modulated Notch1, MFN1 and DRP1 expression levels in myocardial cells via infection with recombinant adenoviruses. The results showed that Notch1 improves the cell viability and mitochondrial fusion in myocardiocytes exposed to IRI. These improvements were dependent on the regulation of MFN1 and DRP1. On the mechanism, we found that MNF1 is transcriptionally activated by RBP-Jk in myocardiocytes. Notch1 also improves the mitochondrial membrane potential in myocardiocytes exposed to IRI. Moreover, we further confirmed the protection of the Notch1-MFN1/Drp1 axis on the post-ischaemic recovery of myocardial performance is associated with the preservation of the mitochondrial structure. In conclusion, this study presented a detailed mechanism by which Notch1 signalling improves mitochondrial fusion during myocardial protection.

[2 + 2] cycloaddition reaction and luminescent sensing of Fe3+ and Cr2O72- ions by a cadmium-based coordination polymer.

A new cadmium-based coordination polymer (CP), [Cd3(bpe)2(ceba)2(fa)2(H2O)2]n (1; fa = formate anions), was constructed by solvothermal reactions of cadmium nitrates with trans-1,2-bis(4'-pyridyl)ethylene ligand (bpe) and 4-(1-carboxy-ethoxy)-benzoic acid (H2ceba). The [2 + 2] photodimerization reaction of CP 1 under UV irradiation generated the corresponding photoproduct [Cd3(rctt-tpcb)(ceba)2(fa)2(H2O)2]n (1a; rctt-tpcb = tetrakis(4-pyridyl)-cyclobutane) via a single-crystal-to-single-crystal (SCSC) transformation. Single crystal X-ray diffraction unveiled that CPs 1 and 1a have similar 2D layered structures, except that rctt-tpcb replaced a pair of bpe ligands in the latter. Furthermore, CPs 1 and 1a are good bifunctional luminescent sensors that can detect Fe3+ and Cr2O72- ions in a mixed medium of water and DMF and display high sensitivity, selectivity, and anti-jamming capability for the recognition of Fe3+ and Cr2O72- ions. Moreover, we also examine in detail the possible luminescent quenching mechanisms of 1 and 1a toward Fe3+ and Cr2O72- ions.

NSD2 silencing alleviates pulmonary arterial hypertension by inhibiting trehalose metabolism and autophagy.

Nuclear receptor binding SET domain 2 (NSD2)-mediated metabolic reprogramming has been demonstrated to regulate oncogenesis via catalyzing the methylation of histones. The present study aimed to investigate the role of NSD2-mediated metabolic abnormality in pulmonary arterial hypertension (PAH). Monocrotaline (MCT)-induced PAH rat model was established and infected with adeno-associated virus carrying short hairpin RNA (shRNA) targeting NSD2. Hemodynamic parameters, ventricular function, and pathology were evaluated by microcatheter, echocardiography, and histological analysis. Metabolomics changes in lung tissue were analyzed by LC-MS. The results showed that silencing of NSD2 effectively ameliorated MCT-induced PAH and right ventricle dysfunction, and partially reversed pathological remodeling of pulmonary artery and right ventricular hypertrophy. In addition, the silencing of NSD2 markedly reduced the di-methylation level of H3K36 (H3K36me2 level) and inhibited autophagy in pulmonary artery. Non-targeted LC-MS based metabolomics analysis indicated that trehalose showed the most significant change in lung tissue. NSD2-regulated trehalose mainly affected ABC transporters, mineral absorption, protein digestion and absorption, metabolic pathways, and aminoacyl-tRNA biosynthesis. In conclusion, we reveal a new role of NSD2 in the pathogenesis of PAH related to the regulation of trehalose metabolism and autophagy via increasing the H3K36me2 level. NSD2 is a promising target for PAH therapy.

Notch1 provides myocardial protection by improving mitochondrial quality control.

Mitochondrial quality control is a new target for myocardial protection. Notch signaling plays an important role in heart development, maturation, and repair. However, the role of Notch in the myocardial mitochondrial quality control remains elusive. In this study, we isolated myocardial cells from rats and established myocardial ischemia reperfusion injury (IRI) model. We modulated Notch1 expression level in myocardial cells via infection with recombinant adenoviruses Ad-N1ICD and Ad-shN1ICD. We found that IR reduced myocardial cells viability, but Notch1 overexpression increased the viability of myocardial cells exposed to IRI. In addition, Notch1 overexpression improved ATP production, increased mitochondrial fusion and decreased mitochondrial fission, and inhibited mitophagy in myocardial cells exposed to IRI. However, N1ICD knockdown led to opposite effects. The myocardial protection role of Notch1 was related to the inhibition of Pink1 expression and Mfn2 and Parkin phosphorylation. In conclusion, Notch1 exerts myocardial protection and this is correlated with the maintenance of mitochondrial quality control and the inhibition of Pink1/Mfn2/Parkin signaling.

NSD2 promotes ventricular remodelling mediated by the regulation of H3K36me2.

Histone lysine methylation plays an important role in the regulation of ventricular remodelling. NSD2 is involved in many types of tumours through enhancing H3K36me2 expression. However, the role of NSD2 in the regulation of histone lysine methylation during ventricular remodelling remains unclear. In this study, we established cardiac hypertrophy model in C57BL/6 mice by transverse aortic constriction and found that histone lysine methylation participated in ventricular remodelling regulation via the up-regulation of H3K27me2 and H3K36me2 expression. In addition, we constructed transgenic C57BL/6 mice with conditional knockout of NSD2 (NSD2-/- ) in the myocardium. NSD2-/- C57BL/6 mice had milder ventricular remodelling and significantly improved cardiac function compared with wild-type mice, and the expression of H3K36me2 but not H3K27me2 was down-regulated. In conclusion, NSD2 promotes ventricular remodelling mediated by the regulation of H3K36me2.

Notch signaling inhibits cardiac fibroblast to myofibroblast transformation by antagonizing TGF-ß1/Smad3 signaling.

PURPOSE: During myocardial infarction (MI), cardiac fibroblasts (CFs) transform into myofibroblast (CMT). This study aimed to investigate the crosstalk of Notch1 and transforming growth factor-ß1 (TGF-ß1)/Smad3 signaling in the regulation of CMT and myocardial fibrosis. METHODS: Primary CFs were isolated from young rats and treated with TGF-ß1 or adenovirus to overexpress or knockdown Notch1 intracellular domain (N1ICD) or Smad3. RESULTS: TGF-ß1 decreased the expression of fibroblast markers but increased the expression of myofibroblast markers in rat CFs. TGF-ß1 increased the proliferation, invasion, and adhesion, and the secretion of collagen I of CFs, and these effects were inhibited by N1ICD overexpression. Moreover, endogenous Smad3 phosphorylation in CFs was enhanced by N1ICD knockdown, whereas TGF-ß1 induced Smad3 phosphorylation was antagonized by the N1ICD overexpression. Conversely, endogenous N1ICD activation in CFs was antagonized by Smad3, whereas TGF-ß1 induced N1ICD inactivation was antagonized by Smad3 knockdown. Coimmunoprecipitation showed that N1ICD interacted with Smad3 and immunostaining revealed the colocalization of N1ICD and Smad3 in the nuclei of CFs. Moreover, we demonstrated the functional antagonism of N1ICD and Smad3 on the phenotypes of CFs. Finally, TGF-ß1/Smad3 signaling promoted whereas Notch signaling inhibited myocardial fibrosis in rat MI model. CONCLUSION: Notch signaling inhibits CMT by antagonizing TGF-ß1/Smad3 signaling. Notch signaling activators and TGF-ß1/Smad3 signaling inhibitors could be exploited for therapeutic intervention to inhibit myocardial fibrosis after MI.

miR-21 promotes cardiac fibroblast-to-myofibroblast transformation and myocardial fibrosis by targeting Jagged1.

Myocardial fibrosis after myocardial infarction (MI) is a leading cause of heart diseases. MI activates cardiac fibroblasts (CFs) and promotes CF to myofibroblast transformation (CMT). This study aimed to investigate the role of miR-21 in the regulation of CMT and myocardial fibrosis. Primary rat CFs were isolated from young SD rats and treated with TGF-ß1, miR-21 sponge or Jagged1 siRNA. Cell proliferation, invasion and adhesion were detected. MI model was established in male SD rats using LAD ligation method and infected with recombinant adenovirus. The heart function and morphology was evaluated by ultrasonic and histological analysis. We found that TGF-ß1 induced the up-regulation of miR-21 and down-regulation of Jagged1 in rat CFs. Luciferase assay showed that miR-21 targeted 3'-UTR of Jagged1 in rat CFs. miR-21 sponge inhibited the transformation of rat CFs into myofibroblasts, and abolished the inhibition of Jagged1 mRNA and protein expression by TGF-ß1. Furthermore, these effects of miR-21 sponge on rat CFS were reversed by siRNA mediated knockdown of Jagged1. In vivo, heart dysfunction and myocardial fibrosis in MI model rats were partly improved by miR-21 sponge but were aggravated by Jagged1 knockdown. Taken together, these results suggest that miR-21 promotes cardiac fibroblast-to-myofibroblast transformation and myocardial fibrosis by targeting Jagged1. miR-21 and Jagged1 are potential therapeutic targets for myocardial fibrosis.

Oridonin Suppresses Proliferation of Human Ovarian Cancer Cells via Blockage of mTOR Signaling.

Oridonin, an ent-kaurane diterpenoid compound isolated from the traditional Chinese herb Rabdosia rubescens, has shown various pharmacological and physiological effects such as anti-tumor, anti-bacterial, and anti-inflammatory properties. However, the effect of oridonin on human ovarian cancer cell lines has not been determined. In this study, we demonstrated that oridonin inhibited ovarian cancer cell proliferation, migration and invasion in a dose-dependent manner. Furthermore, we showed oridonin inhibited tumor growth of ovarian cancer cells (SKOV3) in vivo. We then assessed mechanisms and found that oridonin specifically abrogated the phosphorylation/activation of mTOR signaling. In summary, our results indicate that oridonin is a potential inhibitor of ovarian cancer by blocking the mTOR signaling pathway.

[Prevalence and surgical status of cataract among adults aged 50 years or above in rural Jiangsu Province].

OBJECTIVE: To survey the prevalence, operative status, surgical coverage rate and social burden rate of cataract blindness among older adults aged 50 years or above in 2 typical counties (district) of Jiangsu Province, China in 2010. METHODS: Cluster sampling was used in randomly selected 12 867 individuals aged 50 years or above in 58 clusters in Funing County of Northern Jiangsu and Binhu District of Southern Jiangsu. Among them, 12 053 individuals received visual acuity and eye examinations (response rate 93.8%). Lens and cataract operative status were evaluated by slit-lamp biomicroscope. Data bank was established by Epidata3.0 Software. Statistical analyses were performed with Stata/SE Statistical Software, version 10.0. Confidence intervals and P values (significant at P < 0.05) for prevalence of cataract, surgical coverage rate of cataract, social burden rate and surgical outcomes of cataract blindness were calculated with adjustment for clustering effects and stratification associated with the sampling design. RESULTS: Among 12 503 individuals, there were 2208 cases of cataract with a prevalence of 18.3%. The prevalence of cataract was higher in the aged, female and lower-income persons (P < 0.05). Among 2208 cataract patients, cataract surgery was performed in 263 cases (11.9%). The surgical coverage rate of cataract was 59.7% and the social burden rate of cataract blindness 1.93%. The social burden rate of cataract blindness was higher in the aged persons (P < 0.01). In 357 eyes with cataract surgery, the rate of intraocular lens implantation was 85.7%. At Binhu, 71.0% of eyes with cataract surgery underwent phacoemulsification. At Funing, 73.6% of eyes underwent modern extra-capsular surgery respectively. Post-operative presenting and best corrected visual acuity over 0.7 was 11.2% and 19.6% of operated eyes respectively. The main causes of post-operative eyes with worse visual acuity (< 0.3) were post-capsular opacity and retinal disorders. CONCLUSION: Cataract is the most common and important eye disease that may lead into blindness and severe visual impairment among older adults aged 50 years or above. The coverage rate of cataract surgery is higher in Jiangsu province than in other provinces. The visual outcomes of surgery is less than ideal. An important task in blindness prevention of Jiangsu province still is the elimination of cataract blindness and the improvement of visual outcomes for cataract surgery in the future.

[Cataract surgery rate and its impacting factors in Jiangsu Province in 2012].

OBJECTIVE: To survey the cataract surgery rate (CSR) according to the report data and its influencing factors of Jiangsu Province in 2012 so as to further improve CSR in China. METHODS: Through government websites in 2012, gross domestic product (GDP) and GDP per capital of 13 cities in Jiangsu Province and 7 counties of Nantong City reported to the Ministry of Health in China were collected to calculate CSR. The relationship between GDP and CSR of Jiangsu Province and Nantong City were analyzed with Spearman's rank correlation, and the differences in the proportion of cataract surgery between government and private hospitals were analyzed by Chi-square test. RESULTS: CSR in Jiangsu Province in 2012 was 939 cases per million population per year. Nantong City had the highest CSR (1362 cases per million population per year) and Suqian City the lowest (129 cases per million population per year). The GDP of 13 cities in Jiangsu Province had a positive correlation with CSR (spearman r = 0.59, P = 0.03), but there was no significant correlation with GDP per capital (spearman r = 0.50, P = 0.08). No significant correlation existed between GDP, GDP per capital and CSR of 7 counties of Nantong City (spearman r = -0.04, P = 0.94; spearman r = -0.29, P = 0.53). The proportion of private hospitals of Nantong was 33.3% and surgery cases were 4557 (45.9%). The CSR of Rugao County in 2012 was 3317 cases per million population per year. CONCLUSION: Socioeconomic level may be related with CSR. Providing village cataract screening services and lowering surgical costs help to boost CSR in China.

pH-sensitive strontium carbonate nanoparticles as new anticancer vehicles for controlled etoposide release.

Strontium carbonate nanoparticles (SCNs), a novel biodegradable nanosystem for the pH-sensitive release of anticancer drugs, were developed via a facile mixed solvent method aimed at creating smart drug delivery in acidic conditions, particularly in tumor environments. Structural characterization of SCNs revealed that the engineered nanocarriers were uniform in size and presented a dumbbell-shaped morphology with a dense mass of a scale-like spine coating, which could serve as the storage structure for hydrophobic drugs. Chosen as a model anticancer agent, etoposide was effectively loaded into SCNs based on a simultaneous process that allowed for the formation of the nanocarriers and for drug storage to be accomplished in a single step. The etoposide-loaded SCNs (ESCNs) possess both a high loading capacity and efficient encapsulation. It was found that the cumulative release of etoposide from ESCNs is acid-dependent, and that the release rate is slow at a pH of 7.4; this rate increases significantly at low pH levels (5.8, 3.0). Meanwhile, it was also found that the blank SCNs were almost nontoxic to normal cells, and ESCN systems were evidently more potent in antitumor activity compared with free etoposide, as confirmed by a cytotoxicity test using an MTT assay and an apoptosis test with fluorescence-activated cell sorter (FACS) analysis. These findings suggest that SCNs hold tremendous promise in the areas of controlled drug delivery and targeted cancer therapy.

One-step bulk preparation of calcium carbonate nanotubes and its application in anticancer drug delivery.

Bulk fabrication of ordered hollow structural particles (HSPs) with large surface area and high biocompatibility simultaneously is critical for the practical application of HSPs in biosensing and drug delivery. In this article, we describe a smart approach for batch synthesis of calcium carbonate nanotubes (CCNTs) based on supported liquid membrane (SLM) with large surface area, excellent structural stability, prominent biocompatibility, and acid degradability. The products were characterized by transmission electron micrograph, X-ray diffraction, Fourier transform infrared spectra, UV-vis spectroscopy, zeta potential, and particle size distribution. The results showed that the tube-like structure facilitated podophyllotoxin (PPT) diffusion into the cavity of hollow structure, and the drug loading and encapsulation efficiency of CCNTs for PPT are as high as 38.5 and 64.4 wt.%, respectively. In vitro drug release study showed that PPT was released from the CCNTs in a pH-controlled and time-dependent manner. The treatment of HEK 293T and SGC 7901 cells demonstrated that PPT-loaded CCNTs were less toxic to normal cells and more effective in antitumor potency compared with free drugs. In addition, PPT-loaded CCNTs also enhanced the apoptotic process on tumor cells compared with the free drugs. This study not only provides a new kind of biocompatible and pH-sensitive nanomaterial as the feasible drug container and carrier but more importantly establishes a facile approach to synthesize novel hollow structural particles on a large scale based on SLM technology.

A fibronectin scaffold approach to bispecific inhibitors of epidermal growth factor receptor and insulin-like growth factor-I receptor.

Engineered domains of human fibronectin (Adnectins™) were used to generate a bispecific Adnectin targeting epidermal growth factor receptor (EGFR) and insulin-like growth factor-I receptor (IGF-IR), two transmembrane receptors that mediate proliferative and survival cell signaling in cancer. Single-domain Adnectins that specifically bind EGFR or IGF-IR were generated using mRNA display with a library containing as many as 10 ( 13) Adnectin variants. mRNA display was also used to optimize lead Adnectin affinities, resulting in clones that inhibited EGFR phosphorylation at 7 to 38 nM compared to 2.6 µM for the parental clone. Individual, optimized, Adnectins specific for blocking either EGFR or IGF-IR signaling were engineered into a single protein (EI-Tandem Adnectin). The EI-Tandems inhibited phosphorylation of EGFR and IGF-IR, induced receptor degradation, and inhibited down-stream cell signaling and proliferation of human cancer cell lines (A431, H292, BxPC3 and RH41) with IC 50 values ranging from 0.1 to 113 nM. Although Adnectins bound to EGFR at a site distinct from those of anti-EGFR antibodies cetuximab, panitumumab and nimotuzumab, like the antibodies, the anti-EGFR Adnectins blocked the binding of EGF to EGFR. PEGylated EI-Tandem inhibited the growth of both EGFR and IGF-IR driven human tumor xenografts, induced degradation of EGFR, and reduced EGFR phosphorylation in tumors. These results demonstrate efficient engineering of bispecific Adnectins with high potency and desired specificity. The bispecificity may improve biological activity compared to monospecific biologics as tumor growth is driven by multiple growth factors. Our results illustrate a technological advancement for constructing multi-specific biologics in cancer therapy.

Expression of antibodies using single-open reading frame vector design and polyprotein processing from mammalian cells.

We describe a novel polyprotein precursor-based approach to express antibodies from mammalian cells. Rather than expressing heavy and light chain proteins from separate expression units, the antibody heavy and light chains are contained in one single-open reading frame (sORF) separated by an intein gene fused in frame. Inside mammalian cells this ORF is transcribed into a single mRNA, and translated into one polypeptide. The antibody heavy and light chains are separated posttranslationally, assembled into the functional antibody molecule, and secreted into culture medium. It is demonstrated that Pol I intein from P. horikoshii mediates protein splicing and cleavage reactions in mammalian cells, in the context of antibody heavy and light chain amino acid sequences. To allow the separation of antibody heavy chain, light chain, and the intein, we investigated a number of intein mutations designed to inhibit intein-mediated splicing but preserve cleavage reactions. We have also designed constructs in which the signal peptide downstream from intein has altered hydrophobicity. The use of some of these mutant constructs resulted in more efficient antibody secretion, highlighting areas that can be further explored in improving such an expression system. An antibody secreted using one of the sORF constructs was characterized. This antibody has correct N-terminal sequences for both of its heavy and light chains, correct heavy and light chain MW as well as intact MW as measured by mass spectrometry. Its affinity to antigen, as measured by surface plasmon resonance (SPR), is indistinguishable from that of the same antibody produced using conventional method.

[A case-control study of factors associated with primary angle-closure glaucoma].

OBJECTIVE: To understand the risk factors of primary angle-closure glaucoma. METHODS: One to one matched case-control study was conducted in this study. One hundred and ninety two PACG cases and 192 controls, matched by age and gender, were collected from Department of Ophthalmology, Affiliated Hospital of Nantong University. All of the participants were investigated for their demographic information, behavioral habits, disease history, glaucoma family history and received clinical ocular examinations. The difference between these two groups was analyzed. RESULTS: Several factors, including hypertension (OR = 2.004, P = 0.009), glaucoma family history (OR = 6.726, P = 0.003), presbyopia (OR = 3.192, P = 0.031), shallow anterior chamber (OR = 12.804, P = 0.000) and high cup-to-disc ratio (OR = 9.401, P = 0.007) were associated with PACG by multiply Logistic regression. The results did not support that smoking, drinking, myopia, diabetes mellitus and blood style were related to PACG. CONCLUSION: Follow up the populations with glaucoma family history, shallow anterior chamber or high cup-to-disc ratio are the main procedures for the decrease of incidence of PACG.

[Pathological study on effects of preservative-free 1% lidocaine on lens epithelial cells of patients with age-related cataract].

OBJECTIVE: To assess whether preservative-free 1% lidocaine is capable of destroying the LECs in age-related cataract (ARC) in order to provide scientific basis for pursuing safe and effective drugs to eliminate LECs in cataract surgery. METHODS: Lens anterior capsule (LAC) specimens were collected from 75 patients (82 eyes) with age-related cataract (ARC), including forty males (44 eyes) and thirty-five females (38 eyes). The age range was 41 - 85 years, the mean age was 67.97 years. There were 34 cortical cataracts, 22 nuclear cataracts and 26 subcapsular cataracts. Capsule specimens were divided into 4 groups: balanced salt solution (BSS) group I and group II (exposed to BSS for 1 minute), lidocaine group (exposed to preservative-free 1% lidocaine for 1 minute) and the control group. Specimens were stained with trypan blue and alizarin red. Photomicrographs of each capsule were taken to observe the viability of LECs and to count the number of necrosis LECs. The pathologic changes of LECs were evaluated by histological methods (11 LAC, 22 pieces) as well as transmission and scanning electron microscopes (5 LAC, 10 pieces). In the control and BSS group I (23 LAC), one half of each capsule specimen was used for the control group and the other half was used for BSS group I. In lidocaine group and BSS group II (43 LAC), one half of each capsule specimen was used for lidocaine group and the other half was used for BSS group II. RESULTS: The rate of necrosis LECs of the anterior capsules in the control group and BSS group I was (56.19 +/- 2.71)% and (57.23 +/- 1.98)%, respectively. The rate of necrosis LECs of the capsules in lidocaine group and BSS group II was (99.86 +/- 8.22)% and (57.64 +/- 7.00)%, respectively. Matching t-test showed that the rate of necrosis LECs in lidocaine group was greater than that in the BSS group II (t = 27.6781, P = 0.0000). There was no significant difference in the number of necrosis LECs between the control group and BSS group I (t = 2.0693, P = 0.0505). There was also no significant difference between males and females; between different cataract, types and between varying age groups (P > 0.05). After irrigated with lidocaine, LECs showed vacuoles and detached from the capsule, and many cavities appeared between the LECs and the capsule. The capsules of BSS and control group showed a normal layer of LECs attached to the capsule. Under transmission and scanning electron microscopes, in lidocaine group, the junction between the LECs and between the cells and the capsule were destroyed; many cells detached from the capsule and the rest arranged loosely. Some LECs dented and many vacuoles emerged, resulting in destruction of the cellular structures. CONCLUSION: Preservative-free 1% lidocaine may loose the junction between LECs and between the cells and the capsule, and also destroy cellular structures, resulting in degeneration and necrosis of the LECs.