Magnetic and Ferroelectric Manipulation of Valley Physics in Janus Piezoelectric Materials.

The realization of multiferroic materials offers the possibility of multifunctional electronic device design. However, the coupling between the multiferroicity and piezoelectricity in Janus materials is rarely reported. In this study, we propose a mechanism for manipulating valley physics by magnetization reversing and ferroelectric switching in multiferroic and piezoelectric material. The ferromagnetic VSiGeP4 monolayer exhibits a large valley polarization up to 100 meV, which can be effectively operated by reversing magnetization. Interestingly, the antiferromagnetic VSiGeP4 bilayers with AB and BA stacking configurations allow the coexistence of valley polarization and ferroelectricity, supporting the proposed strategy for manipulating valley physics via ferroelectric switching and interlayer sliding. In addition, the VSiGeP4 monolayer contains remarkable tunable piezoelectricity regulated by electron correlation U. This study proposes a feasible idea for regulating valley polarization and a general design idea for multifunctional devices with multiferroic and piezoelectric properties, facilitating the miniaturization and integration of nanodevices.

Plant begomoviruses subvert ubiquitination to suppress plant defenses against insect vectors.

Most plant viruses are vectored by insects and the interactions of virus-plant-vector have important ecological and evolutionary implications. Insect vectors often perform better on virus-infected plants. This indirect mutualism between plant viruses and insect vectors promotes the spread of virus and has significant agronomical effects. However, few studies have investigated how plant viruses manipulate plant defenses and promote vector performance. Begomoviruses are a prominent group of plant viruses in tropical and sub-tropical agro-ecosystems and are transmitted by whiteflies. Working with the whitefly Bemisia tabaci, begomoviruses and tobacco, we revealed that C2 protein of begomoviruses lacking DNA satellites was responsible for the suppression of plant defenses against whitefly vectors. We found that infection of plants by tomato yellow leaf curl virus (TYLCV), one of the most devastating begomoviruses worldwide, promoted the survival and reproduction of whitefly vectors. TYLCV C2 protein suppressed plant defenses by interacting with plant ubiquitin. This interaction compromised the degradation of JAZ1 protein, thus inhibiting jasmonic acid defense and the expression of MYC2-regulated terpene synthase genes. We further demonstrated that function of C2 protein among begomoviruses not associated with satellites is well conserved and ubiquitination is an evolutionarily conserved target of begomoviruses for the suppression of plant resistance to whitefly vectors. Taken together, these results demonstrate that ubiquitination inhibition by begomovirus C2 protein might be a general mechanism in begomovirus, whitefly and plant interactions.

PI3K/AKT/mTOR signaling participates in insulin-mediated regulation of pathological myopia-related factors in retinal pigment epithelial cells.

BACKGROUND: Insulin positively correlates with the length of the eye axis and is increased in the vitreous and serum of patients with pathological myopia (PM). How insulin influences the physiological process of retinal pigment epithelial (RPE) cells in PM remains unclear. This study aimed to explore the effect of insulin on the ultrastructure and function of RPE cells and the role of PI3K/AKT/mTOR signaling involved in the development of PM. METHODS: The ARPE-19 cells were treated with different concentrations of insulin to analyze the cell morphology, cell viability, the protein level of insulin receptor ß, and the mRNA and protein levels of and PM-related factors (TIMP-2, MMP-2, bFGF, and IGF-1). The ultrastructure of APRE-19 cells was also observed after insulin treatment. Besides, the PI3K/AKT/mTOR signaling was studied with or without the PI3K inhibitor LY294002 in ARPE-19 cells. RESULTS: Insulin enhanced the cell viability of ARPE-19 cells and caused the endoplasmic reticulum to expand and vesiculate, suggesting increased secretion of growth factors and degeneration in ARPE-19 cells. Furthermore, the insulin receptor ß was stimulated with insulin treatment, subsequently, the phosphorylation of AKT and mTOR was positively activated, which was adversely suppressed in the presence of LY294002. The secretion of TIMP-2 and bFGF was significantly decreased, and the secretion of MMP-2 and IGF-1 was highly elevated with insulin treatment depending on the concentration in ARPE-19 cells. Furthermore, the effect of insulin on PM-related proteins was restored with the addition of LY294002. CONCLUSIONS: Our results indicated that insulin regulated the secretion of PM-related factors via the PI3K/AKT/mTOR signaling pathway in retinal pigment epithelial cells, and thus probably promoted the development of PM through transducing regulation signals from retina to choroid and sclera.

[Polarized activation affects iron metabolism in macrophages].

The aim of this study was to investigate the effects of polarization program on the ability of macrophages to regulate iron metabolism. M1 and M2 macrophages were propagated in vitro from porcine alveolar macrophages 3D4/2 and polarized by cytokines. The 3D4/2 macrophages were treated with 20 ng/mL interferon gamma (IFN-γ) and 10 ng/mL interleukin-4 (IL-4) combined with 10 ng/mL macrophage colony-stimulating factor (M-CSF) to induce polarization to M1 and M2, respectively. After incubation for 24 h, the expression levels of inflammatory factors and iron-metabolism genes were determined using real-time qPCR, Western bot and immunofluorescence. The M1/M2 macrophages culture media supernatant was collected and used to treat porcine intestinal epithelial cells IPEC-J2. The proliferation ability of IPEC-J2 was detected using CCK-8 assay kit. Following exogenous addition of ammonium ferric citrate (FAC) to M1/M2 macrophages, the phagocytic function of macrophages was detected using fluorescein isothiocyanate-dextran (FITC-dextran) and flow cytometry. The results showed that, compared with control, M1 macrophages had higher mRNA levels of iron storage proteins (ferritin heavy and light polypeptide, i.e. FtH and FtL), hepcidin and lipocalin-2, as well as iron content. Moreover, iron enhanced the ability of M1 macrophages to phagocytize FITC-dextran. There was no significant change in these mRNA expression levels in M2 macrophages, but the mRNA expression levels of ferroportin and transferrin receptor were up-regulated. In addition, the conditioned media supernatant from M2 macrophages promoted cell proliferation of IPEC-J2. These findings indicate that M1 macrophages tend to lock iron in the cell and reduce extracellular iron content, thereby inhibiting the proliferation of extracellular bacteria. While M2 macrophages tend to excrete iron, which contributes to the proliferation of surrounding cells and thus promotes tissue repair.

Three-Dimensional Analysis of Chloroplast Structures Associated with Virus Infection.

Chloroplasts are multifunctional organelles whose morphology is affected by environmental stresses. Although the three-dimensional (3D) architecture of thylakoid membranes has been reported previously, a 3D visualization of chloroplast under stress has not been explored. In this work, we used a positive-strand RNA ((+)RNA) virus, barley stripe mosaic virus (BSMV) to observe chloroplast structural changes during infection by electron tomography. The analyses revealed remodeling of the chloroplast membranes, characterized by the clustering of outer membrane-invaginated spherules in inner membrane-derived packets. Diverse morphologies of cytoplasmic invaginations (CIs) were evident with spherules at the periphery and different sized openings connecting the CIs to the cytoplasm. Immunoelectron microscopy of these viral components verified that the aberrant membrane structures were sites for BSMV replication. The BSMV αa replication protein localized at the surface of the chloroplasts and played a prominent role in eliciting chloroplast membrane rearrangements. In sum, our results have revealed the 3D structure of the chloroplasts induced by BSMV infection. These findings contribute to our understanding of chloroplast morphological changes under stress conditions and during assembly of plant (+)RNA virus replication complexes.

Visible-Light Direct Conversion of Ethanol to 1,1-Diethoxyethane and Hydrogen over a Non-Precious Metal Photocatalyst.

Converting renewable biomass and their derivatives into chemicals and fuels has received much attention to reduce the dependence on fossil resources. Photocatalytic ethanol dehydrogenation-acetalization to prepare value-added 1,1-diethoxyethane and H2 was achieved over non-precious metal CdS/Ni-MoS2 catalyst under visible light. The system displays an excellent production rate and high selectivity of 1,1-diethoxyethane, 52.1 mmol g-1 h-1 and 99.2 %, respectively. In-situ electron spin resonance, photoluminescence spectroscopy and transient photocurrent responses were conducted to investigate the mechanism. This study provides a promising strategy for a green application of bioethanol.

De novo genome assembly of endophytic fungus Nemania diffusa strain YAFEF818, isolated from Artemisia argyi.

Here, we report a draft genome sequence of endophytic fungus Nemania diffusa YAFEF818, isolated from Artemisia argyi. Oxford Nanopore Technologies PromethION and Illumina NovaSeq sequence reads were assembled using NECAT and polished using pilon to yield a 55.63 Mb genome.

Quantitative analysis of anthocyanins and flavonoids in purple and green leaves of Eleutherococcus senticosus by UPLC-MS/MS techniques.

Ultra performance liquid chromatography-high resolution mass spectrometry (UPLC-MS/MS) were used to target quantitative determination anthocyanins and flavonoids in the fresh leaves (purple and green) of Eleutherococcus senticosus. The results showed that the content of total anthocyanins was 99.68 µg/g (Fresh Weight, FW) in purple leaves and 29.12 µg/g in green leaves. Cyanidin-3-O-galactoside and delphinidin were the main anthocyanins compound in purple and green leaves, and the content of the both declined sharply in green leaves. The content of cyanidin-3-O-galactoside reached 616.23 ng/100 mg in purple leaves and was only fifth in green leaves. The total flavonoids content was 4.90 mg/g in purple leaves and 2.23 mg/g in green leaves. Quercetin-3-ß-D-glucoside (236.96 ng/mg) and kaempferol-3-O-glucoside (145.27 ng/mg) were the main flavonoids compound in purple leaves. Besides the two main flavonoids, large quantities of rutin (269.11 ng/mg) was detected in green leaves of E. senticosus.

Quercetin Regulates Microglia M1/M2 Polarization and Alleviates Retinal Inflammation via ERK/STAT3 Pathway.

Retinal inflammation is a pivotal characteristic observed in various retinal degenerative disorders, notably age-related macular degeneration (AMD), primarily orchestrated by the activation of microglia. Targeting the inhibition of microglial activation has emerged as a therapeutic focal point. Quercetin (Qu), ubiquitously present in dietary sources and tea, has garnered attention for its anti-neuroinflammatory properties. However, the impact of Qu on retinal inflammation and the associated mechanistic pathways remains incompletely elucidated. In this study, retinal inflammation was induced in adult male C57BL/6 J mice through intraperitoneal administration of LPS. The results revealed that Qu pre-treatment induces a phenotypic shift in microglia from M1 phenotype to M2 phenotype. Furthermore, Qu attenuated retinal inflammation and stabilized the integrity of the blood-retina barrier (BRB). In vitro experiments revealed that Qu impedes microglial activation, proliferation, and migration, primarily via modulation the ERK/STAT3 signaling pathway. Notably, these actions of Qu significantly contributed to the preservation of photoreceptors. Consequently, Qu pre-treatment holds promise as an effective strategy for controlling retinal inflammation and preserving visual function.

TNFSF15 inhibits progression of diabetic retinopathy by blocking pyroptosis via interacting with GSDME.

Diabetic retinopathy is a common microvascular complication of diabetes and a leading cause of blindness. Pyroptosis has emerged as a mechanism of cell death involved in diabetic retinopathy pathology. This study explored the role of GSDME-mediated pyroptosis and its regulation by TNFSF15 in diabetic retinopathy. We found GSDME was upregulated in the progression of diabetic retinopathy. High glucose promoted GSDME-induced pyroptosis in retinal endothelial cells and retinal pigment epithelial cells, attributed to the activation of caspase-3 which cleaves GSDME to generate the pyroptosis-executing N-terminal fragment. TNFSF15 was identified as a binding partner and inhibitor of GSDME-mediated pyroptosis. TNFSF15 expression was increased by high glucose but suppressed by the caspase-3 activator Raptinal. Moreover, TNFSF15 protein inhibited high glucose- and Raptinal-induced pyroptosis by interacting with GSDME in retinal cells. Collectively, our results demonstrate TNFSF15 inhibits diabetic retinopathy progression by blocking GSDME-dependent pyroptosis of retinal cells, suggesting the TNFSF15-GSDME interaction as a promising therapeutic target for diabetic retinopathy.

Differentiation of intestinal stem cells toward goblet cells under systemic iron overload stress are associated with inhibition of Notch signaling pathway and ferroptosis.

Iron overload can lead to oxidative stress and intestinal damage and happens frequently during blood transfusions and iron supplementation. However, how iron overload influences intestinal mucosa remains unknown. Here, the aim of current study was to investigate the effects of iron overload on the proliferation and differentiation of intestinal stem cells (ISCs). An iron overload mouse model was established by intraperitoneal injection of 120 mg/kg body weight iron dextran once a fortnight for a duration of 12 weeks, and an iron overload enteroid model was produced by treatment with 3 mM or 10 mM of ferric ammonium citrate for 24 h. We found that iron overload caused damage to intestinal morphology with a 64 % reduction in villus height/crypt depth ratio, and microvilli injury in the duodenum. Iron overload mediated epithelial function by inhibiting the expression of nutrient transporters and enhancing the expression of secretory factors in the duodenum. Meanwhile, iron overload inhibited the proliferation of ISCs and regulated their differentiation into secretory mature cells, such as goblet cells, through inhibiting Notch signaling pathway both in mice and enteroid. Furthermore, iron overload caused oxidative stress and ferroptosis in intestinal epithelial cells. In addition, ferroptosis could also inhibit Notch signaling pathway, and affected the proliferation and differentiation of ISCs. These findings reveal the regulatory role of iron overload on the proliferation and differentiation of ISCs, providing a new insight into the internal mechanism of iron overload affecting intestinal health, and offering important theoretical basis for the scientific application of iron nutrition regulation.

Molecular evidence for natural hybridization in the mangrove fern genus Acrostichum.

BACKGROUND: Natural hybridization is prevalent in ferns, and plays an important role in fern evolution and speciation. In the Indo West-Pacific region, the mangrove fern genus Acrostichum consists of two largely sympatric species, A. aureum and A. speciosum. Although there has been no report of interspecific hybridization before, we found some individuals morphologically intermediate between them in Guangdong and Hainan, China, for the first time, which were suspected to be hybrids. In this study, we aimed to test the hypothesis of natural hybridization between A. aureum and A. speciosum in Guangdong and Hainan using three low-copy nuclear genes. A chloroplast intergenic spacer was used to infer the hybridization direction once the hybrid status was confirmed. In addition, we examined spore shapes and germination for these taxa. RESULTS: Both A. aureum and A. speciosum showed a low level of polymorphism at all three nuclear genes; however, they were well separated at these loci. At both locations, each individual of the putative hybrid showed additivity in chromatograms at all sites where the two species showed fixed differences. Haplotype analysis at all three nuclear genes indicated that each individual of the putative hybrid possessed two haplotypes, matching with those of A. aureum and A. speciosum, respectively. Sequencing of the chloroplast trnV-trnM regions showed that A. aureum differed from A. speciosum by eleven nucleotide substitutions and three indels (insertions/deletions), and all sampled individuals of the putative hybrid had the identical sequences with A. speciosum. Compared with A. aureum and A. speciosum, the putative hybrid had much reduced spore germination rate. CONCLUSIONS: Sequence data of the three nuclear genes provide compelling evidence for natural hybridization between A. aureum and A. speciosum, and all the hybrid individuals are likely F1s. The hybridization is unidirectional and A. speciosum is the maternal parent of the hybrid based on the assumption of maternal inheritance of chloroplast DNA. Human disturbance on mangrove habitats may facilitate the establishment of hybrids of Acrostichum.

NbPHAN, a MYB transcriptional factor, regulates leaf development and affects drought tolerance in Nicotiana benthamiana.

MYB transcriptional factors, characterized by the presence of conserved DNA-binding domains (BDs) (MYB domain), are involved in diverse processes including plant growth, development, metabolic and stress responses. In this study, a new R2R3-type MYB gene, NbPHAN (Nicotiana benthamiana PHANTASTICA), was identified in N. benthamiana. The NbPHAN encodes a protein of 362 amino acids and shares high sequence identities with the AS1-RS2-PHANs (ARPs) from other plant species. The NbPHAN protein targets to and forms homodimers in the nucleus. The MYB domain and C-terminal region of NbPHAN determine its subcellular localization and homodimerization, respectively. Using virus-induced gene silencing, we showed that the NbPHAN-silenced leaves exhibited severe downward curling and abnormal growth of blades along the main veins through suppressing the expression of the NTH20 gene. In addition, we found NbPHAN plays an important role in drought tolerance. The NbPHAN-silenced plants exhibited severe wilting and increased rate of water loss than that found in the non-silenced plants when growing under the water deficit condition. Although abscisic acid accumulation was not altered in the NbPHAN-silenced plants as compared with that in the non-silenced plants, several other stress-inducible genes were clearly repressed under the water deficit condition. Our results provide strong evidence that other than controlling leaf development, the ARP genes can also regulate plant tolerance to drought stress.

Efficacy of subthreshold micropulse laser photocoagulation therapy versus anti-vascular endothelial growth factor therapy for refractory macular edema secondary to non-ischemic branch retinal vein occlusion.

OBJECTIVE: To assess the efficacy of subthreshold micropulse laser photocoagulation (SMLP) therapy versus anti-vascular endothelial growth factor (anti-VEGF) therapy in patients with refractory macular edema (ME) secondary to non-ischemic branch retinal vein occlusion (BRVO). METHODS: This single-center, prospective, nonrandomized, case-control trial involved patients with refractory ME that responded poorly to three or more initial anti-VEGF injections. The patients were examined and divided into two groups according to their chosen treatment: the intravitreal ranibizumab (IVR) group and the SMLP group. Both groups were followed up monthly for 12 months. Therapeutic efficacy and safety were assessed throughout the follow-up period. RESULTS: The IVR group comprised 49 eyes, and the SMLP group comprised 45 eyes. The improvements in the optical coherence tomography findings and visual acuity were comparable between the two groups at the final follow-up. The total number of injections was significantly lower in the SMLP than IVR group. No serious adverse events occurred during the study period. CONCLUSIONS: SMLP therapy is better for patients with central macular thickness (CMT) of ≤400 µm. For patients with CMT of >400 µm, we advise continuation of anti-VEGF agents to reduce ME followed by application of SMLP therapy when CMT has decreased to ≤400 µm.

Heme oxygenase-1 increases intracellular iron storage and suppresses inflammatory response of macrophages by inhibiting M1 polarization.

Heme oxygenase-1 (HO-1) catalyzes the first and rate-limiting enzymatic step of heme degradation, producing carbon monoxide, biliverdin, and free iron. Most iron is derived from aged erythrocytes by the decomposition of heme, which happened mainly in macrophages. However, the role of HO-1 on iron metabolism and function of macrophage is unclear. The present study investigated the effect of HO-1 on iron metabolism in macrophages, and explored the role of HO-1 on inflammatory response, polarization, and migration of macrophages. HO-1 inducer Hemin or HO-1 inhibitor zinc protoporphyrin was intravenously injected to C57BL/6 J mice every 4 d for 28 d. We found that HO-1 was mainly located in the cytoplasm of splenic macrophages of mice. Activation of HO-1 by Hemin significantly increased iron deposition in the spleen, up-regulated the gene expression of ferritin and ferroportin, and down-regulated gene expression of divalent metal transporter 1 and hepcidin. Induced HO-1 by Hemin treatment increased intracellular iron levels of macrophages, slowed down the absorption of extracellular iron, and accelerated the excretion of intracellular iron. In addition, activation of HO-1 significantly decreased the expression of pro-inflammatory cytokines including interleukin (IL)-6, IL-1ß, and inducible nitric oxide synthase, but increased the expression of anti-inflammatory cytokines such as IL-10. Furthermore, activation of HO-1 inhibited macrophages to M1-type polarization, and increased the migration rate of macrophages. This study demonstrated that HO-1 was able to regulate iron metabolism, exert anti-inflammatory effects, and inhibit macrophages polarization to M1 type.

miR-96-5p Induces Orbital Fibroblasts Differentiation by Targeting Smad7 and Promotes the Development of Thyroid-Associated Ophthalmopathy.

Background: Recent evidence shows that adipogenic differentiation of orbital fibroblasts (OFs) promotes the development of thyroid-associated ophthalmopathy (TAO), an organ-specific immune disease. Furthermore, miR-96-5p has been linked to adipogenic differentiation of C2C12 myoblasts and is significantly correlated with the severity of TAO. The purpose of this study is to look into the role of miR-96-5p in the adipogenesis of OFs with TAO. Methods: The orbital tissues from TAO patients and non-TAO participants were collected, and primary OFs were isolated and cultured for further analysis. miR-96-5p expression was examined using qRT-PCR. The adipogenic differentiation of OFs was then studied. Results: Orbital fibroblasts isolated from adipose tissues of TAO patients (t-OFs) demonstrated greater adipogenic differentiation ability than OFs isolated from adipose tissues of non-TAO participants. miR-96-5p was found to be overexpressed in the orbital tissues of TAO patients and t-OFs. Further research revealed that miR-96-5p, by targeting Smad7, could exacerbate PPAR-γ/C/EBPα signaling-induced adipogenic differentiation of t-OFs. However, inhibiting miR-96-5p could block t-OFs adipogenic differentiation-mediated adipogenesis via Smad7/PPAR-γ/C/EBPα. Conclusions: miR-96-5p plays a critical regulatory role in the development of TAO by targeting Smad7 and promoting adipogenic differentiation of OFs.

Active Asymmetric Electron-Transfer Effect on the Enhanced Piezoelectricity in MoTO (T = S, Se, or Te) Monolayers and Bilayers.

Development of piezoelectric materials is limited partly due to the incompleteness of internal mechanism and the lack of vertical piezoelectricity. Herein, we theoretically identify the stable MoTO (T = S, Se, or Te) monolayers and bilayers. When two elements are given but another element can be changed, the larger the electronegativity difference ratio Rratio is, the stronger the piezoelectricity will be. Vertical piezoelectric coefficient d33 of the MoTeO bilayer reaches 38.907 pm/V, which is 12 times larger than that of the bulk GaN. The "active asymmetric electron-transfer" strategy mainly contributes to the spontaneous remarkable piezoelectricity of MoTO. Importantly, we proposed the new method for calculating the piezoelectric coefficients of two-dimensional (2D) materials, which corresponds to the fact that 2D materials have a certain thickness. This study not only provides novel extraordinary candidates for energy conversion and touch-sensor nanodevices but also promotes a deeper understanding of piezoelectricity of 2D materials.

Nucleolar GTPase Bms1 displaces Ttf1 from RFB-sites to balance progression of rDNA transcription and replication.

18S, 5.8S, and 28S ribosomal RNAs (rRNAs) are cotranscribed as a pre-ribosomal RNA (pre-rRNA) from the rDNA by RNA polymerase I whose activity is vigorous during the S-phase, leading to a conflict with rDNA replication. This conflict is resolved partly by replication-fork-barrier (RFB)-sites sequences located downstream of the rDNA and RFB-binding proteins such as Ttf1. However, how Ttf1 is displaced from RFB-sites to allow replication fork progression remains elusive. Here, we reported that loss-of-function of Bms1l, a nucleolar GTPase, upregulates rDNA transcription, causes replication-fork stall, and arrests cell cycle at the S-to-G2 transition; however, the G1-to-S transition is constitutively active characterized by persisting DNA synthesis. Concomitantly, ubf, tif-IA, and taf1b marking rDNA transcription, Chk2, Rad51, and p53 marking DNA-damage response, and Rpa2, PCNA, Fen1, and Ttf1 marking replication fork stall are all highly elevated in bms1l mutants. We found that Bms1 interacts with Ttf1 in addition to Rc1l. Finally, we identified RFB-sites for zebrafish Ttf1 through chromatin immunoprecipitation sequencing and showed that Bms1 disassociates the Ttf1‒RFB complex with its GTPase activity. We propose that Bms1 functions to balance rDNA transcription and replication at the S-phase through interaction with Rcl1 and Ttf1, respectively. TTF1 and Bms1 together might impose an S-phase checkpoint at the rDNA loci.

Protective effects of human umbilical cord blood stem cell intravitreal transplantation against optic nerve injury in rats.

BACKGROUND: The majority of studies addressing traumatic optic neuropathy (TON) have focused on drugs, proteins, cytokines, and various surgical techniques. A recent study reported that transplantation of human umbilical cord blood stem cells (hUCBSCs) achieved therapeutic effects on TON, but the exact effects on optic nerve injury are still unknown, and the mechanisms underlying nerve protection remain poorly understood. METHODS: A total of 135 healthy Sprague-Dawley adult rats were randomly assigned to three groups: sham-surgery, model and transplantation, with 45 rats in each group. TON was induced in the model and transplantation groups via optic nerve crush injury. The crush injury was not performed in the sham-surgery group. Seven days after the injury, 10(6) hUCBSCs were injected into the rat vitreous cavity of transplantation group, and an equal volume of physiological saline was administered to the model and sham-surgery groups. Pathological observation of rat retina tissues was performed by hematoxylin-eosin (H&E) staining at days 3, 7, 14, 21 and 28 post-surgery. The number of retinal ganglion cells (RGCs) and mRNA expression levels of brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) were assessed by the Fluorogold (FG) retrograde labeling and reverse transcriptase-polymerase chain reaction (RT-PCR) methods, respectively. RESULTS: The number of labeled RGCs and the expression of BDNF and GDNF mRNA obviously increased, and pathological injury was significantly ameliorated in the transplantation group compared to the model group (P < 0.05). CONCLUSIONS: Via intravitreal transplantation, the hUCBSCs resulted in a significant increase in the survival of the RGCs, and improved pathological changes in the rat retina, following TON. The protective mechanism is correlated with the continuous secretion of BDNF and GDNF in vivo of retina in optic nerve injury rats by the transplanted hUCBSCs.

Two cases of primary intraocular lymphoma: fine needle aspiration diagnosis and intravitreal methotrexate treatment.

We described clinical process of two cases of intraocular lymphoma in aspects of early diagnosis by fine needle aspiration (FNA) and biopsy and treatment by intravitreal methotrexate (MTX). Two patients were suspected to have primary intraocular lymphoma (PIOL) with geographic yellow-white infiltrates and vitreous opacity. FNA confirmed malignant intraocular lymphoma in one patient and failed in the other patient due to complication of vitreous hemorrhage. Subsequent vitreous biopsy confirmed malignant intraocular lymphoma in the other patient. Both patients were treated by intravitreal methotrexate. In case 1 the tumor had complete remission and follow-up of 12 months had not found any signs of recurrence. In case 2 the patient died of brain metastasis 22 months after the ocular biopsy. Our findings demonstrate that although cytological examination of vitrectomy specimens remains the gold standard in diagnosis of PIOL, examination of FNA and biopsy increases the reliability of early diagnosing or excluding a PIOL. Individualized intravitreal methotrexate can be used to effectively treat PIOL. More effective integrated program treating primary central nervous system lymphoma/PIOL is worthy of looking forward to.