Anterior segment optical coherence tomography for superficial keratectomy.

PURPOSE: To report the use of anterior segment optical coherence tomography (AS-OCT) for superficial keratectomy (SK) in anterior corneal opacity. METHODS: The characteristics of 43 eyes (39 patients) with various lesions responsible for anterior corneal opacity were included in this retrospective non-comparative study. AS-OCT was performed on all eyes before surgery. The thickness of corneal opacity and the underlying healthy stroma were measured. SK was performed on each individual. RESULTS: Four types of anterior corneal opacity were evaluated, including corneal degeneration (26/43), Reis-Bücklers corneal dystrophy (8/43), alkali burn (1/43) and corneal tumors (8/43). Based on AS-OCT images, all eyes showed abnormal hyper-reflective signals in the superficial cornea to less than one-third of the normal corneal thickness in the deepest corneal opacity. All 43 eyes underwent an SK procedure. In addition, 1 eye with alkali burns and 7 eyes with corneal tumors were combined with amniotic membrane transplantation. All eyes restored transparency without significant complications. CONCLUSION: AS-OCT is a valuable method for objective preoperative and noninvasive assessments of anterior corneal opacities and is useful for guiding SK.

Comparison of photodynamic therapy with two different parameters combined with subconjunctival injection of bevacizumab for corneal neovascularization.

BACKGROUND: To the best of our knowledge, no studies have been performed to determine the optimal parameters of photodynamic therapy (PDT) combined with subconjunctival injection of bevacizumab for corneal neovascularization. This study aimed to compare the effect of photodynamic therapy with two different sets of parameters combined with subconjunctival injection of bevacizumab for corneal neovascularization. METHODS: Patients with stable corneal neovascularization (CNV) unresponsive to conventional treatment (topical steroid) were included in this study. Patients were divided into two groups, receiving PDT with two different sets of parameters (group 1 receiving fluence of 50 J/cm2 at 15 min after intravenous injection of verteporfin with, group 2 receiving fluence of 150 J/cm2 at 60 min after intravenous injection of verteporfin with). Subconjunctival injection of bevacizumab was performed immediately after PDT. All patients were followed for 6 months. Best-corrected visual acuity and intraocular pressure were evaluated, and slit-lamp biomicroscopy as well as digital photography were performed. Average diameter and cumulative length of corneal neovascular were measured to evaluate the corneal neovascularization. RESULTS: Seventeen patients (20 eyes) were included in this study. At the last visit, the vision was improved in 12 eyes (60 %), steady in 4 eyes (20 %) and worsen in 4 eyes (20 %). The intraocular pressure (IOP) of all patients remained in normal range. A significant decrease in corneal neovascularization was showed in all the eyes after treatment. At 6 months after the combined treatment, the average diameter and cumulative length of vessels significantly decreased to 0.041 ± 0.023 mm (P < 0.05) and 18.78 ± 17.73 mm (P < 0.05), respectively, compared with the pretreatment data (0.062 ± 0.015 mm, 31.48 ± 18.21 mm). The reduction was more remarkable in group 2 compared to group 1.In group 1, the average diameter was 0.062 ± 0.013mm before and 0.056 ± 0.017mm after, the cumulative length of vessels was 38.66 ± 22.55mm before and 31.21 ± 17.30 after. In group 2, the date were 0.061 ± 0.016mm before and 0.029 ± 0.020mm after, 25.60 ± 8.95 mm before and 8.61 ± 8.26 mm. The reported complications included epithelial defect in four eyes, small white filaments in two eyes and corneal epithelial erosion in two eyes. CONCLUSION: The PDT combined with subconjunctival injection of bevacizumab was effective for the chronic corneal neovascularization. A more promising treatment outcome was observed when PDT was performed at 60 min after intravenous injection of verteporfin with fluence of 150 J/cm2. No serious complications or systemic events were observed throughout the follow-up period.

Circ_0030042 inhibits trophoblast cell growth, invasion and epithelial-mesenchymal transition process in preeclampsia via miR-942-5p/LITAF.

BACKGROUND: There is increasing evidence that circular RNAs (circRNAs) are involved in the processes of preeclampsia (PE). Circ_0030042 was found to be abnormally expressed in PE patients. However, the role and molecular mechanism of circ_0030042 in PE progression remains unclear. METHODS: Quantitative real-time PCR was used for determining the expression of circ_0030042, microRNA (miR)- 942-5p and lipopolysaccharide induced TNF-α factor (LITAF). Trophoblast cell functions were determined using cell counting kit 8 assay, EdU assay, flow cytometry and transwell assay. The protein levels of epithelial-mesenchymal transition (EMT)-related markers and LITAF were examined using western blot analysis. Dual-luciferase reporter assay and RNA pull-down assay were used to verify RNA interaction. RESULTS: Circ_0030042 had an elevated expression in PE patients, and its overexpression inhibited trophoblast cell growth, invasion, and EMT process. Circ_0030042 served as miR-942-5p sponge, and miR-942-5p inhibitor also reversed the regulation of circ_0030042 on trophoblast cell growth, invasion and EMT process. LITAF was targeted by miR-942-5p, and its knockdown abolished the inhibition effect of miR-942-5p on trophoblast cell growth, invasion, and EMT process. Also, circ_0030042 regulated LITAF expression via sponging miR-942-5p. CONCLUSION: Circ_0030042 regulated trophoblast cell growth, invasion, and EMT process via the miR-942-5p/LITAF axis, providing a novel insight for PE treatment.

Puerarin prevents sepsis-associated encephalopathy by regulating the AKT1 pathway in microglia.

BACKGROUND: Previous studies have reported that puerarin possesses cardioprotective, vasodilatory, anti-inflammatory, anti-apoptotic, and hypoglycemic properties. However, the impact of puerarin on sepsis-associated encephalopathy (SAE) remains unexplored. In this study, we explored whether puerarin can modulate microglia-mediated neuroinflammation for the treatment of SAE and delved into the underlying mechanisms. METHODS: We established a murine model of SAE through intraperitoneal injection of lipopolysaccharide (LPS). The puerarin treatment group received pretreatment with puerarin. For in vitro experiments, BV2 cells were pre-incubated with puerarin for 2 h before LPS exposure. We employed network pharmacology, the Morris Water Maze (MWM) test, Novel Object Recognition (NOR) test, immunofluorescence staining, enzyme-linked immunosorbent assay (ELISA), Western blotting, and quantitative real-time PCR (qRT-PCR) to elucidate the molecular mechanism of underlying puerarin's effects in SAE treatment. RESULTS: Our findings demonstrate that puerarin significantly reduced the production of inflammatory cytokines (TNF-α and IL-6) in the peripheral blood of LPS-treated mice. Moreover, puerarin treatment markedly ameliorated sepsis-associated cognitive impairment. Puerarin also exhibited inhibitory effects on the release of TNF-α and IL-6 from microglia, thereby preventing hippocampal neuronal cell death. Network pharmacology analysis identified AKT1 as a potential therapeutic target for puerarin in SAE treatment. Subsequently, we validated these results in both in vitro and in vitro experiments. Our study conclusively demonstrated that puerarin reduced LPS-induced phosphorylation of AKT1, with the AKT activator SC79 reversing puerarin's anti-inflammatory effects through the activation of the AKT1 signaling pathway. CONCLUSION: Puerarin exerts an anti-neuroinflammatory effect against SAE by modulating the AKT1 pathway in microglia.

Successful regression of newly formed corneal neovascularization by subconjunctival injection of bevacizumab in patients with chemical burns.

Purpose: To investigate the effect and timing of subconjunctival bevacizumab injection on inhibiting corneal neovascularization (CorNV) in patients after chemical burns. Methods: Patients with CorNV secondary to chemical burns were involved. Two subconjunctival injections of bevacizumab (2.5 mg/0.1 mL per involved quadrant) with an interval of 4 weeks were administered, and followed up a year. The area occupied by neovascular vessels (NA), accumulative neovascular length (NL), mean neovascular diameter (ND), best-corrected visual acuity (BCVA) and intraocular pressure (IOP) were evaluated. Complication was also recorded. Results: Eleven patients with CorNV were involved. Eight patients had a history of surgery (four had amniotic grafts, one had keratoplasty, and three had amniotic grafts and keratoplasty). Decreasing in NA, NL, and ND were statistically significant at each time point compared to the baseline (p < 0.01). CorNV that developed within 1 month was considerably regressed, and vessels with fibrovascular membranes were found to be narrower and shorter than pretreatment. BCVA improved in five patients (from one to five lines), remained unchanged in five patients, and decreased in one patient compared to pretreatment. Conclusion: Subconjunctival bevacizumab injection has a particular potential for the regression of CorNV, especially newly formed within 1 month in patients after chemical burns.

PABPN1 aggregation is driven by Ala expansion and poly(A)-RNA binding, leading to CFIm25 sequestration that impairs alternative polyadenylation.

Poly(A)-binding protein nuclear 1 (PABPN1) is an RNA-binding protein localized in nuclear speckles, while its alanine (Ala)-expanded variants accumulate as intranuclear aggregates in oculopharyngeal muscular dystrophy. The factors that drive PABPN1 aggregation and its cellular consequences remain largely unknown. Here, we investigated the roles of Ala stretch and poly(A) RNA in the phase transition of PABPN1 using biochemical and molecular cell biology methods. We have revealed that the Ala stretch controls its mobility in nuclear speckles, and Ala expansion leads to aggregation from the dynamic speckles. Poly(A) nucleotide is essential to the early-stage condensation that thereby facilitates speckle formation and transition to solid-like aggregates. Moreover, the PABPN1 aggregates can sequester CFIm25, a component of the pre-mRNA 3'-UTR processing complex, in an mRNA-dependent manner and consequently impair the function of CFIm25 in alternative polyadenylation. In conclusion, our study elucidates a molecular mechanism underlying PABPN1 aggregation and sequestration, which will be beneficial for understanding PABPN1 proteinopathy.

Activated AMPK-mediated glucose uptake and mitochondrial dysfunction is critically involved in the glutamate-induced oxidative injury in HT22 cell.

BACKGROUND: Accumulation of glutamate damages neurons via the reactive oxygen species (ROS) injury, which was involved in the development of neurodegenerative diseases. However, the mechanism of neuronal oxidative stress damage caused by glutamate and the intervention targets still needs to be further studied. This study explored whether 5' adenosine monophosphate-activated protein kinase (AMPK)-induced glucose metabolic and mitochondrial dysfunction were related to glutamate-dependent ROS injury of the neuron. METHODS: Neuronal oxidative stress injury was induced by glutamate treatment in HT-22 cells. Western blotting was used to evaluate the phosphorylation of the AMPK. The XF24 Flux Analyzer was used to measure the effect of glutamate and Compound C (a well-known pharmacological inhibitor of AMPK phosphorylation) on the cellular oxygen consumption rate (OCR) of HT-22 cells. Glucose uptake, intracellular ROS, mitochondrial potential, apoptosis and cell viability were quantified using biochemical assays. RESULTS: Glutamate caused the phosphorylation of AMPK and subsequently promoted the glucose uptake. Furthermore, AMPK-mediated glucose uptake enhanced OCR and increased the intracellular ROS levels in neurons. The pharmacological inhibition of AMPK phosphorylation by Compound C attenuated glutamate-induced toxicity in HT22 cells by regulating the glucose uptake/mitochondrial respiration/ROS pathway. CONCLUSIONS: The AMPK phosphorylation/glucose uptake/mitochondrial respiration/ROS pathway was involved in glutamate-induced excitotoxic injury in HT22 cells. The inhibition of AMPK phosphorylation may be a potential target for the development of therapeutic agents for treating the glutamate-induced neurotoxicity.

Chemerin promotes the pathogenesis of preeclampsia by activating CMKLR1/p-Akt/CEBPɑ axis and inducing M1 macrophage polarization.

A higher ratio of M1/M2 macrophages and an elevated chemerin level are both related to increased risk of preeclampsia. However, the crosstalk between these two events and their collective contribution to preeclampsia are not well understood. In this study, we assessed the impacts of chemerin chemokine-like receptor 1 (CMKLR1)/p-Akt/CEBPα axis in regulating macrophage polarization and mediating the pathogenic effects of chemerin on preeclampsia. We showed that chemerin, in a dose- and time-dependent manner, stimulated M1 macrophage polarization, inhibited macrophage-induced trophoblast invasion and migration, and suppressed macrophage-mediated angiogenesis. All these chemerin-induced phenotypes are essentially mediated by sequentially CMKLR1, Akt activation, and CEBPα. Mechanistically, CEBPα acted as a transcriptional activator for both IRF8 and chemerin. In vivo, chemerin aggravated preeclampsia, while α-NETA, an inhibitor for CMKLR1, significantly suppressed M1 macrophage polarization and alleviated preeclampsia. In summary, chemerin, by activating CMKLR1/Akt/CEBPα axis, forms a positive feedback loop, promotes M1 macrophage polarization, suppresses trophoblast migration/invasion and angiogenesis, and contributes to preeclampsia. Therefore, targeting chemerin signaling may benefit the prevention and/or treatment of preeclampsia.

Ferroptosis, a New Insight Into Acute Lung Injury.

Acute lung injury (ALI), a common and critical illness with high morbidity and mortality, is caused by multiple causes. It has been confirmed that oxidative stress plays an important role in the development of ALI. Ferroptosis, a newly discovered programmed cell death in 2012, is characterized by iron-dependent lipid peroxidation and involved in many diseases. To date, compelling evidence reveals the emerging role of ferroptosis in the pathophysiological process of ALI. Here, we review the role of ferroptosis in the pathogenesis of ALI and its therapeutic potential in ALI.

Xuanbai Chengqi decoction plus Western Medicine in treatment of severe pneumonia with symptom pattern of phlegm-heat obstructing lung: a Meta-analysis.

OBJECTIVE: To evaluate the effectiveness and safety of Xuanbai Chengqi decoction (, XBCQD) plus Western Medicine (WM) in treatment of severe pneumonia with symptom pattern of phlegm-heat obstructing lung. METHODS: Randomized controlled trials (RCTs) investigating the effect of XBCQD on severe pneumonia with symptom pattern of phlegm-heat obstructing lung, were included in this study. Seven electronic databases were searched up to March 2019. Meta-analysis was conducted by Review Manager 5.3 software. Risk ratio (RR) and mean difference (MD) with 95% confidence interval (CI) were used as effect estimation. RESULTS: Eleven RCTs were included, involving 992 participants. Meta-analysis showed that XBCQD combined with WM achieved better effectiveness than WM alone in terms of total effective rate [RR = 1.23, 95%CI (1.16, 1.30)], clinical pulmonary infection score [CPIS, MD = -2.02, 95%CI (-2.42, -1.63)], acute physiology and chronic health evaluation Ⅱ [APACHEⅡ, MD = -6.81, 95% CI (-8.26, 5.37)], mechanical ventilation time [MD = -101.41, 95%CI (-140.47, -62.34)], and lactic acid content in arterial blood [MD = -2.41, 95%CI (-2.64, -2.18)]. CONCLUSION: XBCQD combined with WM had better benefit than WM alone to the patients of severe pneumonia with the symptom pattern of phlegm-heat obstructing lung. However, due to low quality of the included studies, more rigorously designed studies were required to further evaluate the effectiveness and safety of XBCQD in the treatment of severe pneumonia with symptom pattern of phlegm-heat obstructing lung.

Early Application of Bevacizumab After Sclerocorneal Grafting for Patients With Severe Late-Stage Ocular Chemical Burns.

PURPOSE: To investigate whether subconjunctival bevacizumab help prevent corneal graft neovascularization and prolong the graft survival of patients with chemical burns. METHODS: We performed a prospective nonrandomized comparative case series study. Twenty-six eyes received subconjunctival bevacizumab (10 mg/0.4 mL) once and topical immunosuppressive agents after sclerocorneal lamellar keratoplasty as the treatment, and 13 eyes received a topical immunosuppressant alone and served as the control group. The main outcomes were a cumulative probability of graft survival, development of corneal neovascularization, and complications. RESULTS: The postoperative follow-up time was 14.3 months (range, 2-62 mo). The cumulative graft survival time was significantly longer in the treatment group than that in the control group (42.9 ± 5.9 vs. 4.8 ± 0.7 mo; log rank < 0.001). In the treatment group, 19 of the 26 grafts (73.1%) survived as transparent with a mean follow-up of 18.7 ± 3.0 months. At the end of the follow-up, 4 grafts remained free of neovascularization, 2 developed edema without neovascularization, and 15 remained transparent with a stable ocular surface and some neovascular vessels in the peripheral transplant interface. The other 5 grafts became opaque and neovascularized. In the control group, all grafts became opaque and neovascularized within the follow-up period (5.5 ± 0.7 mo). During the follow-up, a corneal epithelial defect developed in 9 eyes in the treatment group and 7 in the control group. CONCLUSIONS: Early application of subconjunctival bevacizumab after sclerocorneal lamellar keratoplasty can significantly prevent corneal neovascularization and promote graft survival for severe late-stage ocular chemical burns.

Visual Acuity and Size of Choroidal Neovascularization in Highly Myopic Eyes with a Dome-Shaped Macula.

INTRODUCTION: A dome-shaped macula (DSM) is an inward convexity or anterior deviation of the macular area. DSM is believed as a protective factor in maintaining visual acuity in highly myopic eyes. OBJECTIVE: To investigate the correlation between best-corrected visual acuity (BCVA), choroidal neovascularization (CNV), and a dome-shaped macula (DSM) in highly myopic eyes. METHODS: In this retrospective and observational case series study, BCVA tests and optical coherence tomography (OCT) were performed in a total of 472 highly myopic eyes (refractive error ≥6.5 diopters or axial length ≥26.5 mm). CNV was detected by fundus fluorescein angiography (FFA), and the CNV area was measured by ImageJ software. BCVA, central retinal thickness (CRT), and the CNV area were compared between highly myopic eyes with and without DSM. RESULTS: The data revealed 13 eyes with DSM complicated by CNV, for an estimated prevalence of 25%. The eyes with CNV in the DSM group showed worse BCVA than those in the non-DSM group (1.59 ± 0.69 and 0.63 ± 0.64, respectively, p < 0.05), and the CNV area in the DSM group was larger than that in the non-DSM group (2793.91 ± 2181.24 and 1250.71 ± 1210.36 pixels, respectively, p < 0.05). After excluding the eyes with CNV, the DSM group had better BCVA than the non-DSM group (0.33 ± 0.17 and 0.44 ± 0.48, respectively, p < 0.05); however, no significant difference was observed in the CRT of eyes with CNV between the DSM group and the non-DSM group. CONCLUSION: These results show that DSM might be a protective mechanism for visual acuity, but its protective capability is limited. DSM eyes have better visual acuity within the protective capability. If a more powerful pathogenic factor exceeding the protective capability is present, then the eye will have more severe CNV and worse visual acuity.

A case report of ocular tuberculosis in a patient with membranous nephropathy.

RATIONALE: Membranous nephropathy (MN), a chronic kidney disease (CKD), due to hypoproteinemia, malnutrition, anemia, long-term intake of immunosuppressive agents, changes in cellular immune state, and decrease in antimicrobial peptides, is a high risk for Mycobacterium tuberculosis (MTB) infection, which can cause tuberculosis (TB). TB manifests by various clinical symptoms. Ocular symptoms is a rare presentation of TB. Here, we describe a case of ocular tuberculosis in a patient with MN. PATIENT CONCERNS: A 63-year-old man with membranous nephropathy (MN) history presented with ocular symptoms. DIAGNOSES: According to the pathological manifestations of ocular tissue biopsy and a positive polymerase chain reaction (PCR) on samples from sputum and bronchoalveolar lavage fluid (BALF), we elicited a diagnosis of disseminated tuberculosis. INTERVENTION: The patient received antituberculous therapy and immunosuppressive therapy. OUTCOMES: The clinical manifestations significantly improved. LESSONS: Clinicians should be aware of the possibility of TB in cases of immunocompromised patients and perform an appropriate diagnostic work-up for TB.

Serum chemerin level in women with PCOS and its relation with the risk of spontaneous abortion.

BACKGROUND AND AIM: Insulin resistance (IR) was recognized as a risk factor for the occurrence of abortion in patients with polycystic ovary syndrome (PCOS). Chemerin was an adipokine which could induce IR and associated with reproductive process closely. However, few studies have inquired the relativity between chemerin and the occurrence of abortion in patients with PCOS. The aim of this study was to evaluate the relationship between serum chemerin and the occurrence of abortion in women with PCOS. METHODS: We recruited 198 women with PCOS to participate in our study. On the third day of menstrual cycle or a random day in women with amenorrhea, we obtained their venous blood and measured the fasting insulin, fasting plasma glucose, total cholesterol, high density lipoprotein cholesterol, triglyceride, chemerin, and hormones including FSH, E2, P, PRL, LH, and T. Additionally, BMI, HOMA-IR and LH/FSH of each subject were calculated. Finally, 58 of them were included in the study, in which 30 of them had normal pregnancy and the other 28 had an early miscarriage. We compared the biochemical characteristics between the normal pregnancy group and abortion group by independent-samples t test. RESULTS: In our study, those with a normal pregnancy had a lower level of BMI, FINs, HOMA-IR, and chemerin compared to abortion patients (p < .05). After adjusted for BMI, only chemerin was associated with the occurrence of abortion in PCOS patients (p < .05). CONCLUSIONS: Serum chemerin level is associated with the occurrence of abortion in patients with PCOS. Thus, serum chemerin may serve as a biomarker to identify pregnant women with PCOS who are at particular risk for later abortion, and who may benefit from prevention strategies.

Role of chemerin/CMKLR1 in the maintenance of early pregnancy.

Chemerin is a cytokine that attracts much attention in the reproductive process. This study aimed to explore the effects of chemerin and its receptor chemokine-like receptor 1 (CMKLR1) on the maintenance of early pregnancy. The expression levels of chemerin and CMKLR1 in the decidua tissues of 20 early normal pregnant women and 20 early spontaneous abortion women were examined by Western blot and real-time polymerase chain reaction analyses. CMKLR1 receptor antagonist (α-NETA) was then intrauterinely injected into normal pregnant mice model to assess its effect on the outcome of pregnancy and the phosphorylation rate of ERK1/2 in decidua tissues.We found that the expression level of chemerin in women who had experienced early spontaneous abortion was lower than in those who had experienced normal early pregnancy (P < 0.01); conversely, CMKLR1 expression was higher in the former than in the latter (P < 0.01). In a pregnant-mouse model, the embryo resorption rate of α-NETA group was higher than that in the negative control group (61.5% vs. 10.8%) (P < 0.001). Compared with the control group, ERK1/2 phosphorylation in decidua tissues decreased in the α-NETA-treated group (P < 0.01). These results suggested that the inhibition of the chemerin/CMKLR1 signaling pathway can lead to the abortion of mouse embryos, and that chemerin/CMKLR1 may play an important role in the maintenance of early pregnancy possibly by regulating ERK1/2 phosphorylation.

Case report of ocular Kaposi's sarcoma.

BACKGROUND: Kaposi's sarcoma (KS) is generally considered a neoplastic disorder of vascular origin and occurs in patients with acquired immunodeficiency syndrome (AIDS) or who have received immunosuppressive treatments after an organ transplant (Soulier et al., Blood 86(4):1276-80, 1995; Viejo-Borbolla and Schulz, AIDS Rev 5(4):222-9, 2003; Schulz, J Antimicrob Chemother 45(Suppl T3):15-27, 2000; Aversa et al. Crit Rev Oncol Hematol 53(3):253-65, 2005; Mbulaiteye and Engels, Int J Cancer 119(11):2685-91, 2006; Tessari et al., Eur J Dermatol 16(5):553-7, 2006). Several Kaposi's sarcoma case reports involving eyelids and conjunctiva have been published (Bavishi et al., Int J STD AIDS 23(3):221-2, 2012; Baumann et al., Ger J Ophthalmol 4(4):239-45, 1995). CASE PRESENTATION: we report a 13 years old asian male patient rare case of ocular KS that was initiated from the sclera and progressed into the cornea and conjunctiva without an human Immunodeificiency Virus (HIV) or HHV-8 infection after a peripheral blood stem cells transplantation. In this case, anti- vascular endothelial growth factor (VEGF) therapy was attempted to stop the advance of ocular lesions and failed. Eventually, the KS was cured by a limbo-corneal lamellar graft, an amniotic membrane and scleral allograft transplantation plus intraoperative mitomycin C(MMC) after the complete excision of the tumors. CONCLUSION: A compete surgical excision combined with the intraoperative application of MMC, as well as grafts to repair the scleral, conjunctival, and corneal surfaces, could prevent a recurrence of KS.

Serum chemerin level during the first trimester of pregnancy and the risk of gestational diabetes mellitus.

OBJECTIVE: To investigate the association between chemerin level in the first trimester of pregnancy and the risk of gestational diabetes mellitus. METHODS: The blood samples of 212 women at 8-12 weeks of gestation were collected. After screening for gestational diabetes mellitus (GDM), 19 women with GDM and 20 women randomly selected from 144 women with normal glucose tolerance (NGT) were included in the study. Blood samples were collected from these women. Triglycerides, glucose, total cholesterol, and HDL cholesterol, LDL cholesterol, insulin and chemerin were measured. Gestational weight gain and body mass index was assessed. RESULTS: Serum levels of chemerin were significantly elevated during late gestation, and the risk of GDM was positively associated with maternal serum chemerin in the first trimester. CONCLUSION: Serum chemerin level during the first trimester of pregnancy has the potential to predict risk of GDM.

Limbal conjunctival versus amniotic membrane in the intraoperative application of mitomycin C for recurrent pterygium: a randomized controlled trial.

PURPOSE: This study compared the outcomes of a limbal conjunctival autograft (LCAG) with those of an amniotic membrane graft (AMG) followed by intraoperative 0.02 % mitomycin C (MMC) to treat recurrent pterygium. METHODS: In this randomized controlled trial, ninety-six eyes with recurrent pterygium were enrolled and randomly allocated into two groups using a computer-generated random number table. Pterygium removal was followed by intraoperative 0.02 % MMC for 3 min and then either LCAG or AMG transplantation. The major outcomes were recurrence rate, conjunctival inflammation grade, healing time of the corneal epithelial defect, eye-movement amplitude (EMA), uncorrected distance visual acuity (UDVA), and complications. RESULTS: A follow-up of 12 months was conducted for 93 eyes of 82 patients. Grade D (recurrence) presented in one eye of the LCAG group and five eyes of the AMG group, with no between-group difference (p = 0.196). However, Grades A, B, and C presented in 46, zero and zero eyes of the LCAG group respectively, and in 37, two and two eyes of the AMG group respectively, with the surgical bed generally showing a better appearance in the LCAG group than in the AMG group (p = 0.008). Compared with baseline values, the postoperative EMA improved significantly in both groups (p < 0.001 for the LCAG group; p = 0.001 for the AMG group), as did UDVA (p = 0.005 for the LCAG group; p = 0.012 for the AMG group). No between-group differences were found in terms of the healing time for epithelial defect, conjunctival inflammation grade, or the frequency of complications such as punctate epithelial keratitis, episcleral melting, corneal pannus, and delayed corneal epithelium healing. CONCLUSIONS: LCAG transplantation with intraoperative 0.02 % MMC is as efficacious in treating recurrent pterygium as AMG transplantation with MMC. The former procedure results in an attractive cosmetic appearance but might result in limbal damage in some eyes. The surgeon's familiarity with these procedures should determine the method of treatment.

Two mutations G335D and Q343R within the amyloidogenic core region of TDP-43 influence its aggregation and inclusion formation.

TDP-43 is a DNA/RNA binding protein associated with TDP-43 proteinopathies. Many mutations have been identified in the flexible C-terminal region, which is implicated in the disease pathology. We investigated four point mutations in the amyloidogenic core region (residues 311-360) of TDP-43 by biochemical and spectroscopic methods. We found that the G335D mutation enhances the aggregation and inclusion formation of TDP-43 and this mutant in TDP-35 (the C-terminal fragment of 35 kDa) exaggerates the antagonist effect on RNA processing by endogenous TDP-43; whereas Q343R gives an opposite effect. As a comparison, M337V and Q331K have very little impact on the aggregation and inclusion formation of TDP-43 or TDP-35. NMR structural analysis showed that the G335D mutant in the core region forms a loop linker between the two α-helices and promotes α-to-ß transition, but Q343R loses the second helix and consequently the structural transformation. Thus, the propensity of structural transformation in the amyloidogenic core of TDP-43 determines its aggregation and inclusion formation. This study may provide a molecular mechanism of the TDP-43 proteinopathies caused by genetic mutations.

Micellar electrokinetic chromatographic determination of triazine herbicides in water samples.

Dispersive liquid-liquid microextraction combined with online sweeping preconcentration in micellar electrokinetic chromatography was developed for the simultaneous determination of five triazine herbicides (atrazine, simazine, propazine, prometon and simetryn) in water samples. Several experimental parameters affecting the extraction efficiencies such as the type and volume of both the extraction and dispersive solvents, the addition of salt to sample solution, the extraction time and the pH of the sample solution were investigated. Under optimum conditions, the linearity of the method was good in the range from 0.33 to 20 ng mL(-1) for simazine, propazine, atrazine and simetryn, and from 0.17 to 20 ng mL(-1) for prometon, respectively. The sensitivity enrichment factors were in the range from 1750 to 2100, depending on the compound. The limit of detection (S/N = 3) ranged from 0.05 to 0.10 ng mL(-1). The developed method was successfully applied to the analysis of the five triazines in river, ground and well waters.