Classification of Homo sapiens gene behavior using linear discriminant analysis fused with minimum entropy mapping.

Classification of Homo sapiens gene behavior employing computational biology is a recent research trend. But monitoring gene activity profile and genetic behavior from the alphabetic DNA sequence using a non-invasive method is a tremendous challenge in functional genomics. The present paper addresses such issue and attempts to differentiate Homo sapiens genes using linear discriminant analysis (LDA) method. Annotated protein coding sequences of Homo sapiens genes, collected from NCBI, are taken as test samples. Minimum entropy-based mapping (MEM) technique assists to extract highest information from the numerical DNA sequences. The proposed LDA technique has successfully classified Homo sapiens genes based on the following features: composition of hydrophilic amino acids, dominance of arginine amino acid, and magnitude and size of individual amino acids. The proposed algorithm is successfully tested on 84 Homo sapiens healthy and cancer genes of the prostate and breast cells. Classification performance of the proposed LDA technique is judged by sensitivity (89.12%), specificity (91.9%), accuracy (90.87%), F1 score (92.03%), Matthews' correlation coefficients (81.04%), and miss rate (9.12%), and it outperforms other four existing classifiers. The results are cross-validated through Rayleigh PDF and mutual information technique. Fisher test, 2-sample T-test, and relative entropy test are considered to verify the efficacy of the present classifier.

Incidence of spontaneous intestinal perforations exceeds necrotizing enterocolitis in extremely low birth weight infants fed an exclusive human milk-based diet: A single center experience.

BACKGROUND: Spontaneous intestinal perforation (SIP) and necrotizing enterocolitis (NEC) are complications of extremely low birth weight (ELBW, ≤1000 g) infants. ELBW infants at Texas Children's Hospital receive an exclusive human milk-based diet, which has been associated with a reduction of NEC. OBJECTIVES: 1) Assess incidence of SIP and NEC (Stage II or greater) in ELBW infants receiving 100% human milk-based diet, 2) Describe mortality rates of ELBW infants with SIP and NEC. METHODS: Prospective single-center observational cohort study of ELBW infants born between 2010 and 2014 with SIP or NEC (exclusion: congenital anomalies and death within 48 h). RESULTS: Of 379 ELBW infants, 345 were eligible. Of these, 28 (8.1%) had SIP and 8 (2.3%) had NEC (medical n = 1, surgical n = 7). SIP infant mortality was 32% (n = 9) compared to 63% (n = 5) for NEC patients. Of SIP infants with PD (n = 25), 52% required subsequent exploratory laparotomy (LAP). Of NEC infants with peritoneal drainage (PD) (n = 2), both required subsequent LAP. CONCLUSION: Using an exclusive human milk-based diet, the incidence of SIP exceeds NEC in ELBW infants at our institution. This shows a changing trend in the incidence of these two diagnoses in the era of human milk, as NEC had previously been more prevalent in ELBW infants. More than half of infants who initially received PD later required LAP. There were no differences in survival outcomes in both SIP and NEC groups based on surgical management.

Implications of Population Screening for Thalassemias and Hemoglobinopathies in Rural Areas of West Bengal, India: Report of a 10-Year Study of 287,258 Cases.

Thalassemia and hemoglobinopathies are the most common cause of high morbidity and mortality in India. Detection of carriers and premarital counseling play an important role in preventing the birth of a thalassemic child. The present study aimed to detect large numbers of asymptomatic carriers in rural areas of West Bengal, India. The present cross-sectional study was conducted over a period of 10 years. Thalassemia awareness programs and detection camps were organized at the community level. After signed written consent was obtained, the collected blood samples were subjected to a complete blood count (CBC) in an automated blood cell counter and then analyzed by high performance liquid chromatography (HPLC); in difficult cases, samples were sent to the reference laboratory for molecular characterization. Out of 287,258 samples collected, 32,921 (11.46%) cases revealed abnormal hemoglobins (Hbs); of these, 31,782 (11.06%) carried heterozygous states (carriers/traits), and the remainder were either homozygous or compound heterozygous for different hemoglobinopathies. Two common variants were revealed in the study, namely ß-thalassemia (ß-thal) (7.23%) and Hb E [ß26(B8)Glu→Lys, HBB: c.79G>A] (2.77%) traits. Among homozygous or compound heterozygous states, Hb E/ß-thal (0.14%) and ß-thal major (ß-TM) (0.12%) were predominant. In rural areas of West Bengal, the most common Hb variants detected were ß-thal and Hb E traits. In view of the high prevalence of hemoglobinopathies in this region, routine premarital screening and genetic counseling should be emphasized and encouraged to prevent the birth of a thalassemic child, and thus curtailing the burden on families and the health economy.

Identification of Homo sapiens cancer classes based on fusion of hidden gene features.

Classification of Homo sapiens cancer genes in molecular level is a challenging research issue as they are extremely pseudo random in nature. Signature gene features need to be exposed to distinctly identify the gene class. Tree-structured filter bank is chosen to perform feature extraction and dimension reduction of the genes. Extracted gene features are fused using Gaussian mixture probability distribution function and identify different cancer classes depending on amount of correlation and exploiting maximum likelihood function. The algorithm is tested on 161 sample gene data of 7 different cancer classes. Sensitivity, specificity, accuracy, precision and F-score are used as metrics to judge the performance of the system and ROC is plotted in comparison with existing electrical network model based classifier. The proposed classifier can identify more than stated number of cancer classes which is a major limitation of the existing electrical network based method. The proposed algorithm is validated by comparing the results with other seven existing image processing based methods.

The Cardioprotective Role of N-Acetyl Cysteine Amide in the Prevention of Doxorubicin and Trastuzumab-Mediated Cardiac Dysfunction.

BACKGROUND: In the breast cancer setting, anticancer therapies including doxorubicin (DOX) and trastuzumab (TRZ) are associated with a significantly increased risk of cardiotoxicity. Despite the increasing support for the role of oxidative stress (OS) in its pathophysiology, we still do not have an optimal antioxidant for the prevention of DOX + TRZ-mediated cardiac dysfunction. The objective of this study was to investigate whether the novel antioxidant N-acetylcysteine amide (NACA) can attenuate DOX + TRZ-induced heart failure in a murine model. METHODS: A total of 100 C57Bl/6 female mice received 1 of the following drug regimens: (1) saline, (2) NACA, (3) DOX, (4) TRZ, (5) DOX + TRZ, (6) NACA + DOX, (7) NACA + TRZ, and (8) NACA + DOX + TRZ. Serial echocardiography was performed over a 10-day study period, after which the mice were killed for histologic and biochemical analyses. RESULTS: In mice receiving DOX, the left ventricular ejection fraction (LVEF) decreased from 73% ± 4% to 43% ± 2% on day 10. In mice receiving DOX + TRZ, the LVEF decreased from 72% ± 3% to 32% ± 2% on day 10. Prophylactic administration of NACA to mice receiving DOX or DOX + TRZ was cardioprotective, with an LVEF of 62% ± 3% and 55% ± 3% on day 10, respectively. Histologic and biochemical analyses demonstrated a loss of cellular integrity, increased OS, and increased cardiac apoptosis in mice treated with DOX + TRZ, which was attenuated by the prophylactic administration of NACA. CONCLUSIONS: NACA attenuated the cardiotoxic side effects of DOX + TRZ in a murine model of chemotherapy-induced cardiac dysfunction by decreasing OS and apoptosis.

The utility of cardiac biomarkers and echocardiography for the early detection of bevacizumab- and sunitinib-mediated cardiotoxicity.

The recent introduction of novel anticancer therapies, including bevacizumab (BVZ) and sunitinib (SNT), is associated with an increased risk of cardiotoxicity. However, early identification of left ventricular (LV) systolic dysfunction may facilitate dose modification and avoid the development of advanced heart failure. Using a murine model of BVZ- and SNT-mediated cardiotoxicity, we investigated whether cardiac biomarkers and/or tissue velocity imaging (TVI) using echocardiography can detect early changes in cardiac function, before a decrease in LV ejection fraction is identified. A total of 75 wild-type C57Bl/6 male mice were treated with either 0.9% saline, BVZ, or SNT. Serial monitoring of blood pressure, high-sensitivity troponin I, and echocardiographic indexes were performed over a 14-day study period, after which the mice were euthanized for histological and biochemical analyses. Mice treated with either BVZ or SNT developed systemic hypertension as early as day 7, which increased by day 14. Cardiac biomarkers, specifically high-sensitivity troponin I, were not predictive of early LV systolic dysfunction. Although conventional LV ejection fraction values decreased at day 13 in mice treated with either BVZ or SNT, TVI confirmed early LV systolic dysfunction at day 8. Histological and biochemical analysis demonstrated loss of cellular integrity, increased oxidative stress, and increased cardiac apoptosis in mice treated with BVZ or SNT therapy at day 14. In a murine model of BVZ- or SNT-mediated cardiomyopathy, noninvasive assessment by TVI detected early LV systolic dysfunction before alterations in conventional echocardiographic indexes.

US-guided percutaneous liver biopsy in pediatric liver transplant recipients.

OBJECTIVES: The present study assesses the safety of ultrasound (US)-guided percutaneous liver biopsies (PLBs) within pediatric liver allograft recipients, describes the pathological results according to early (≤12 months) and late (>12 months) posttransplantation periods, and analyzes the value of liver function tests (LFTs) and Doppler US variables in determining these results. METHODS: A total of 219 US-guided PLBs in 85 pediatric patients with liver transplant (mean age 7 ±â€Š5 years, range: 6 months to 18 years) performed between March 2005 and May 2012 were retrospectively evaluated at a single institution. Doppler US and LFT evaluation (including total bilirubin, alanine aminotransferase, aspartate aminotransferase, γ-glutamyl transferase, alkaline phosphatase) occurred within 1 day of early (n = 92, 42%) and late term (n = 127, 58%) posttransplantation biopsies. RESULTS: The rate of major complications (hemorrhage requiring blood transfusion) was 0.91% (n = 2). The early versus late term biopsy results, respectively, included: cholestasis at 36% versus 18% (P = 0.003), minimal changes 16% versus 24% (not significant [NS]), acute rejection 13% versus 5% (P = 0.027), inflammatory diseases 15% versus 15% (NS), indeterminate acute rejection 11% versus 7% (NS), chronic rejection 4% versus 14% (P = 0.017), fibrotic diseases 4% versus 12% (NS), and other 0% versus 5% (NS). Neither LFT nor US variables were correlated with pathological outcomes. CONCLUSIONS: The rate of complications in pediatric patients after US-guided liver biopsy is low. A range of pathological results exists between early and late posttransplantation liver biopsies. LFT and Doppler US findings are not predictors of pathological results.

Modeling of molecular interaction between apoptin, BCR-Abl and CrkL--an alternative approach to conventional rational drug design.

In this study we have calculated a 3D structure of apoptin and through modeling and docking approaches, we show its interaction with Bcr-Abl oncoprotein and its downstream signaling components, following which we confirm some of the newly-found interactions by biochemical methods. Bcr-Abl oncoprotein is aberrantly expressed in chronic myelogenous leukaemia (CML). It has several distinct functional domains in addition to the Abl kinase domain. The SH3 and SH2 domains cooperatively play important roles in autoinhibiting its kinase activity. Adapter molecules such as Grb2 and CrkL interact with proline-rich region and activate multiple Bcr-Abl downstream signaling pathways that contribute to growth and survival. Therefore, the oncogenic effect of Bcr-Abl could be inhibited by the interaction of small molecules with these domains. Apoptin is a viral protein with well-documented cancer-selective cytotoxicity. Apoptin attributes such as SH2-like sequence similarity with CrkL SH2 domain, unique SH3 domain binding sequence, presence of proline-rich segments, and its nuclear affinity render the molecule capable of interaction with Bcr-Abl. Despite almost two decades of research, the mode of apoptin's action remains elusive because 3D structure of apoptin is unavailable. We performed in silico three-dimensional modeling of apoptin, molecular docking experiments between apoptin model and the known structure of Bcr-Abl, and the 3D structures of SH2 domains of CrkL and Bcr-Abl. We also biochemically validated some of the interactions that were first predicted in silico. This structure-property relationship of apoptin may help in unlocking its cancer-selective toxic properties. Moreover, such models will guide us in developing of a new class of potent apoptin-like molecules with greater selectivity and potency.

Role of MSK1 in the malignant phenotype of Ras-transformed mouse fibroblasts.

Activated by the RAS-MAPK signaling pathway, MSK1 is recruited to immediate-early gene (IEG) regulatory regions, where it phosphorylates histone H3 at Ser-10 or Ser-28. Chromatin remodelers and modifiers are then recruited by 14-3-3 proteins, readers of phosphoserine marks, leading to the occupancy of IEG promoters by the initiation-engaged form of RNA polymerase II and the onset of transcription. In this study, we show that this mechanism of IEG induction, initially elucidated in parental 10T1/2 murine fibroblast cells, applies to metastatic Hras1-transformed Ciras-3 cells. As the RAS-MAPK pathway is constitutively activated in Ciras-3 cells, MSK1 activity and phosphorylated H3 steady-state levels are elevated. We found that steady-state levels of the IEG products AP-1 and COX-2 were also elevated in Ciras-3 cells. When MSK1 activity was inhibited or MSK1 expression was knocked down in Ciras-3 cells, the induction of IEG expression and the steady-state levels of COX-2, FRA-1, and JUN were greatly reduced. Furthermore, MSK1 knockdown Ciras-3 cells lost their malignant phenotype, as reflected by the absence of anchorage-independent growth.

Estrogen regulated expression of the p21 Waf1/Cip1 gene in estrogen receptor positive human breast cancer cells.

The cyclin-dependent kinase inhibitor protein p21(Waf1/Cip1) is a potent tumor suppressor. Here, we demonstrate that estradiol regulates the p21(Waf1/Cip1) gene. Estradiol induces p21(Waf1/Cip1) mRNA expression within 30-60 min independent of new protein synthesis in the estrogen receptor alpha (ER alpha) positive human breast cancer cell line MCF-7. Similar to other estradiol responsive promoters, the p21(Waf1/Cip1) upstream promoter region has several estrogen response element (ERE) half-sites nestled in AP-1 binding sites, which are positioned upstream to Sp1 binding sites. Using the chromatin immunoprecipitation (ChIP) assay, we show that estradiol stimulation resulted in the recruitment of transcription factors ER alpha, Sp1, and Sp3 to the p21(Waf1/Cip1) upstream promoter element. The Sp1 inhibitor mithramycin A abrogated Sp1, and to a lesser extent Sp3 binding, and markedly reduced the estradiol stimulated p21(Waf1/Cip1) gene expression. However, ER alpha binding was not affected in the mithramycin A and estradiol treated cells. On closer examination of the half-site ERE/AP-1 sites upstream to the Sp1 sites in a separate ChIP experiment, we found a pronounced association of ER alpha upon estradiol treatment compared to almost negligible binding of Sp1 or Sp3. Together these studies provide evidence that ER alpha is recruited to the half-site ERE/AP-1 sites in the p21(Waf1/Cip1) upstream promoter element. Although Sp1/Sp3 is not involved in the recruitment of ER alpha to the promoter, Sp1 is necessary for estrogen-induced p21(Waf1/Cip1) promoter activity.

Rational drug design.

In this article, current knowledge of drug design is reviewed and an approach of rational drug design is presented. The process of drug development is challenging, expensive, and time consuming, although this process has been accelerated due to the development of computational tools and methodologies. The current target based drug design approach is incomplete because most of the drugs developed by structure guided approaches have been shown to have serious toxic side effects. Otherwise these drugs would have been an ideal choice for the treatment of diseases. Hence, rational drug design would require a multidisciplinary approach. In this regard, incorporation of gene expression technology and bioinformatics tools would be indispensable in the structure based drug design. Global gene expression data and analysis of such data using bioinformatics tools will have numerous benefits such as efficiency, cost effectiveness, time saving, and will provide strategies for combination therapy in addition to overcoming toxic side effects. As a result of incorporation of gene expression data, partial benefit of the structure based drug design is slowly emerging and rapidly changing the approach of the drug development process. To achieve the full benefit of developing a successful drug, multidisciplinary approaches (approaches such as computational chemistry and gene expression analysis, as discussed in this article) would be necessary. In the future, there is adequate room for the development of more sophisticated methodologies.

Effects of the in vivo supply of butyrate on histone acetylation of cecum in piglets.

BACKGROUND: In vitro, butyrate inhibits histone deacetylase and down-regulates expression of cyclin D1. We hypothesized that an increased entry rate of butyrate into the cecal lumen would have similar effects in vivo. METHODS: We used frozen cecal tissue and data from previous studies, one showing that lactulose supplementation caused an increased rate of cecal synthesis of butyrate and decreased cecal cell proliferation and density of clostridia and the other showing that cecal cell proliferation was increased by an exogenous cecal butyrate infusion at a comparable rate. The ratio of acetylated to total histones (AH ratio) and cyclin D1 mRNA expression were measured in cecal tissue. RESULTS: Lactulose supplementation caused a 189% increase in the AH ratio (p = .004), which inversely correlated with cecal cell proliferation (r = -0.782; p = .008). With cecal butyrate infusion, we observed a significant decrease in histone acetylation (p = .02), which also inversely correlated with cecal cell proliferation (r = -0.797; p = .002). Cyclin D1 expression was increased 6.5-fold by lactulose feeding (p = .02) but decreased 50% with cecal butyrate infusion (p = .004). CONCLUSIONS: The effects on histone acetylation of increased "endogenous" butyrate production produced by lactulose feeding, but not exogenous cecal infusion of butyrate, mirror those in vitro. Thus, bacterial production and exogenous infusion of butyrate have opposite effects on histone acetylation and cyclin D1 expression, suggesting that the composition of bacterial flora may play a role in butyrate's in vivo effects on the cell cycle.

An integrated analysis of genes and pathways exhibiting metabolic differences between estrogen receptor positive breast cancer cells.

BACKGROUND: The sex hormone estrogen (E2) is pivotal to normal mammary gland growth and differentiation and in breast carcinogenesis. In this in silico study, we examined metabolic differences between ER(+)ve breast cancer cells during E2 deprivation. METHODS: Public repositories of SAGE and MA gene expression data generated from E2 deprived ER(+)ve breast cancer cell lines, MCF-7 and ZR75-1 were compared with normal breast tissue. We analyzed gene ontology (GO), enrichment, clustering, chromosome localization, and pathway profiles and performed multiple comparisons with cell lines and tumors with different ER status. RESULTS: In all GO terms, biological process (BP), molecular function (MF), and cellular component (CC), MCF-7 had higher gene utilization than ZR75-1. Various analyses showed a down-regulated immune function, an up-regulated protein (ZR75-1) and glucose metabolism (MCF-7). A greater percentage of 77 common genes localized to the q arm of all chromosomes, but in ZR75-1 chromosomes 11, 16, and 19 harbored more overexpressed genes. Despite differences in gene utilization (electron transport, proteasome, glycolysis/gluconeogenesis) and expression (ribosome) in both cells, there was an overall similarity of ZR75-1 with ER(-)ve cell lines and ER(+)ve/ER(-)ve breast tumors. CONCLUSION: This study demonstrates integral metabolic differences may exist within the same cell subtype (luminal A) in representative ER(+)ve cell line models. Selectivity of gene and pathway usage for strategies such as energy requirement minimization, sugar utilization by ZR75-1 contrasted with MCF-7 cells, expressing genes whose protein products require ATP utilization. Such characteristics may impart aggressiveness to ZR75-1 and may be prognostic determinants of ER(+)ve breast tumors.

S100A7 (psoriasin) influences immune response genes in human breast cancer.

S100A7 (psoriasin) is highly expressed in preinvasive breast carcinomas and in a subset of poor prognosis invasive tumors. To determine the influence of S100A7 expression on ERalpha negative breast cancer, we profiled mRNA gene expression by Microarray and SAGE analysis, using the ERalpha negative MDA-MB-231 cell line model. Statistically significant transcripts of genes with very high differential expression were further validated by QPCR in both MDA-MB-231 and MDA-MB-468 cell lines expressing exogenous and endogenous S100A7. S100A7 expression correlated with increases in genes associated with MHC class II receptor activity, antigen processing and antigen presentation, and immune cell activation. The transcription factors (TFs) prediction tool CARRIE confirmed an association between TFs reported to be upregulated by S100A7 (NF-kappaB, AP-1, and HIF1) and the regulation of many genes in this dataset. The relationship between S100A7 up-regulation and the MHC class II and HLA-class II molecule coding gene CD74 was examined further in a cohort of ERalpha negative breast tumors by tissue microarray (TMA) and immunohistochemistry (IHC), confirming a significant association in vivo (p=0.042, n=149). These results are consistent with a role for S100A7 in modulating the immune response which may be a factor in early breast tumor progression.

A novel series of potent cytotoxic agents targeting G2/M phase of the cell cycle and demonstrating cell killing by apoptosis in human breast cancer cells.

Breast cancer, a leading cause of mortality in women, warrants the development and biological evaluation of new anticancer agents. A novel series of thiopyridine triazine derivatives was synthesized and investigated in the human breast cancer cell line, MDA-MB-468. SM40, the most potent derivative, induced a G2/M arrest and apoptosis with a possible involvement of p53. The cytotoxicity of SM40 was also examined against the NCI 60 cell line panel and its potency was rationalized using molecular modeling. Results suggest that SM40 is a promising cytotoxic agent.

A new platinum complex of triazine demonstrates G1 arrest with novel biological profile in human breast cancer cell line, MDA-MB-468.

A novel class of platinum(II) complexes of pyridine sulfide derivatives of triazine was synthesized, characterized, and investigated using the human breast cancer cell line, MDA-MB-468. S-30 was one of the most potent derivatives of its class (IC(50), 0.39 microM) eliciting the greatest biological response. S-30 induced arrest in the G1 phase and apoptosis (TUNEL assay) in a p53/p21(WAF1/CIP1)-consistent manner. Modeling and docking experiments were performed for three known targets for cisplatin, d(GpG), d(ApG), and a protein (Cu/Zn superoxide dismutase, SOD) from bovine origin. A Blast search of bovine SOD was performed to identify analogous human protein targets resulting in about 22 human proteins. A multi-sequence alignment of those targets showed >80% sequence identity and >88% similarity. One of them is SOD1 that is differentially expressed (based on global gene expression pattern) in various forms of cancer and other diseases. SOD1 controls apoptosis via p53/BAD/BAX/BCL2 in the amyotrophic lateral sclerosis (ALS) pathway and is also involved in various other KEGG's pathways. Results suggest that the S-30 is a potential cytotoxic agent.

Identification of myo-inositol 1,2-cyclic monophosphate by electrospray tandem mass spectrometry, a major constituent of EGF-stimulated phosphoinositide turnover in MDA 468 cells.

Epidermal growth factor (EGF) caused an increase in phosphoinositide (PI) turnover in MDA 468 cells. This EGF-stimulated effect was inhibited by the protein tyrosine kinase inhibitor lavendustin A (LA). MDA 468 cells generated an atypical PI turnover profile. Examination and quantitation of the PI metabolite profile showed that even control cells produced a metabolite which was acid-labile and which formed about 60% of the total PI metabolites. By using the technique of electrospray ionization tandem mass spectrometry, we were able to confirm the identity of this acid-labile metabolite through the specific fragmentation as compared with the standard. The precursor molecule fragmented into two distinct productions with molar masses identical to that of the standard myo-inositol 1,2-cyclic monophosphate (cInsP). Changes in the PI turnover profile could be accounted for by the alterations in myo-inositol 1,2-cyclic monophosphate generated in these cells. We thus conclude that, by some as-yet-unidentified mechanism, cyclic inositol monophosphate forms a major constituent of EGF-stimulated PI turnover in MDA 468 cells.

Mitomycin-C-augmented trabeculectomy for neovascular glaucoma. A preliminary report.

PURPOSE: This study aimed to investigate the safety and efficacy of trabeculectomy with intraoperative mitomycin C (MMC) in the management of eyes with neovascular glaucoma (NVG). METHODS: Fifteen eyes of 14 patients with NVG were included in the study. NVG was secondary to central retinal vein occlusion (3 eyes), hemiretinal vein occlusion (2 eyes), proliferative diabetic retinopathy (8 eyes), branch retinal vein occlusion (1 eye) and idiopathic (1 eye). Preoperative retinal ablation was performed in eyes with evidence of posterior segment ischaemia. Following this, all eyes underwent trabeculectomy with intraoperative MMC (0.4 mg/ml for 3 minutes). Clinical outcome assessment included visual acuity, intraocular pressure (IOP), bleb appearance, identification of complications and antiglaucoma medications required to control IOP. RESULTS: The mean IOP decreased from 38.6 +/- 12.9 mmHg (range, 15-64 mmHg) to 17.4 +/- 9.33 mmHg (range, 4-34 mmHg) (P = 0.001). Preoperative visual acuity ranged from light perception to 6/9 in the affected eye. Thirteen (86.6%) of 15 eyes improved vision or retained preoperative vision, one (6.7%) eye lost light perception and one (6.7%) eye developed tractional retinal detachment two years after trabeculectomy. Ten (66.7%) of 15 eyes were classified as surgical success with a mean follow-up of 28.6 +/- 26.3 months (range, 2-82 months). None of the patients developed choroidal haemorrhage, hypotony maculopathy, late onset bleb leak or endophthalmitis. CONCLUSION: Trabeculectomy with intraoperative MMC is a good treatment modality in the management of eyes with NVG.