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Biomedical subjects

A Negi

Publications and source records attributed to A Negi.

At least 19 recordsLinked to original sources
PubMed2006

The -174G/C interleukin-6 promoter polymorphism influences the development of macular oedema following uncomplicated phacoemulsification surgery.

AIM: To determine whether the functional -174 G/C interleukin-6 gene polymorphism is a risk factor for the development of cystoid macular oedema (CMO) following routine uncomplicated phacoemulsification surgery in patients with no established risk factors. METHODS: A total of 40 patients who underwent routine phacoemulsification surgery as part of a randomised controlled trial comparing the use of postoperative steroid drops against a single sub-tenon injection of triamcinolone were genotyped for the IL-6 -174G/C polymorphism. All patients underwent fluorescein angiography at 30 days and anterior chamber flare measurements pre-operatively and at day 1, 7, and 30. RESULTS: Angiographic CMO developed in 14 patients of the 40 studied. 9 out of the 14 patients carried the GG genotype (Fisher's exact test P=0.05, Hazard ratio for GG genotype; 4.05 (1.02-16.00)). There was no difference in flare measurements between the GG and Non-GG (GC/CC) group. The two groups were otherwise well matched in terms of age, sex, phacoemulsification energy used intraoperatively, and proportion of patients receiving postoperative triamcinolone or steroid drops. CONCLUSION: The -174G/C interleukin-6 promoter gene variant appears to modulate the response to phacoemulsification surgery and to influence the development of postoperative CMO. These data suggest a genetic predisposition to this complication.

Aged↗
PubMed2006

Different transitions of multifocal electroretinogram recordings between patients with age-related macular degeneration and polypoidal choroidal vasculopathy after photodynamic therapy.

AIM: To compare and evaluate the transitions in retinal function after photodynamic therapy (PDT) between age-related macular degeneration (AMD) and polypoidal choroidal vasculopathy (PCV) using multifocal electroretinograms (mfERGs). METHODS: 10 eyes with choroidal neovascularisation (CNV) secondary to AMD and 11 eyes with CNV secondary to PCV were included in the study. mfERGs were recorded before PDT, and 1 week and 3 months after PDT. mfERG recordings were acquired by a Veris system (V.3.1.3) using a 103 hexagon stimulus. The first-order kernel was used to calculate amplitudes and latencies. Mean amplitudes and latencies from two central rings rated 0-4 degrees of visual angle were analysed and compared with each disease. RESULTS: In AMD, the mean first negative peak (N1) amplitudes tended to decrease, and the mean first positive peak (N1P1) amplitudes reduced to significant levels (p = 0.047) 1 week after PDT. 3 months after PDT, there were no significant differences in the mean N1 and N1P1 amplitudes compared with pre-PDT values. In PCV, there were no significant changes in the mean N1 and N1P1 amplitudes 1 week after treatment. However, 3 months after PDT, mean amplitudes showed significant increases in N1 (p = 0.008) and N1P1 (p = 0.006) amplitudes compared with pre-PDT values. CONCLUSIONS: mfERG recording transitions are different between patients with AMD and those with PCV. In patients with AMD, these results may show transient impairments in retinal function 1 week after PDT, but in those with PCV, the efficacy of PDT is superior to the impairment after PDT.

Aged↗
PubMed2006

Intravitreal triamcinolone will cause posterior subcapsular cataract in most eyes with diabetic maculopathy within 2 years.

PURPOSE: To determine the incidence of cataract following intravitreal triamcinolone (IVTA) for diabetic macular oedema. METHODS: Prospective, non-randomised, interventional cohort case series. A total of 27 eyes of 27 patients with diabetic macular oedema received an intravitreal injection of 4 mg (0.1 ml) of triamcinolone acetonide inferotemporally through the pars plana under direct vision. In 20 patients the fellow eye served as control, whereas seven patients had both eyes injected (not simultaneously). Seven patients had a repeat (second) injection in the same eye. The main outcome measures were cataract and intraocular pressure (IOP) rise of at least 5 mmHg (IOP responder). RESULTS: The mean follow-up time was 18.9 months (range 13-29 months). A total of 22 (81%) of 27 eyes developed cataract during the follow-up period, of which 20 (74%) were posterior subcapsular in nature. None of the 20 uninjected fellow eyes developed posterior subcapsular cataract. Mean time to cataract formation was 16.2 months. In the seven patients who had both eyes injected, mean time to cataract formation was 16.5 and 17.1 months in the first and second eye, respectively. Mean time to cataract formation in seven eyes receiving a repeat second injection was 17.9 months. There was no significant difference in cataract formation between IOP responders (85%) and non-responders (79%) (P=1.00, Fisher's exact test). Uneventful cataract surgery was performed in six eyes of five patients. CONCLUSION: This study demonstrates that given appropriate long-term follow-up, the majority of patients, even after a single IVTA injection, will go on to develop cataract, of which posterior subcapsular will be by far the most common.

Adult↗
PubMed2005

Macular thickness reduction in eyes with unilateral optic atrophy detected with optical coherence tomography.

AIMS: To assess the changes in macular and peripapillary retinal nerve fibre layer (RNFL) thickness in eyes with unilateral optic atrophy and to evaluate the relationship between retinal thickness and visual function. METHODS: Enrolled were 22 patients with unilateral optic atrophy. Macular thickness at the divided nine areas and peripapillary RNFL thickness in quadrantic sections were measured by optical coherence tomography. Thickness values in the affected eyes were compared with those in the contralateral unaffected eyes. The correlation of foveal thickness with best-corrected visual acuity (BCVA) was evaluated. The correlation between retinal thickness and the remaining visual field area circumscribed with I-4-e isopter in superior and inferior hemifield was assessed. RESULTS: Macular thinning was observed in all areas (P < 0.001 in each area) other than the fovea (P = 0.068). Peripapillary RNFL thickness decreased in all quadrantic sections (P < 0.001 in each section). The affected to unaffected eye ratio of retinal thickness was more than 0.6 in each area. BCVA did not correlate with foveal thickness (correlation coefficient = 0.094, P = 0.668). Although not statistically significant (P = 0.281, superior hemifield; P = 0.053, inferior hemifield), there was a tendency that eyes with severe visual field loss show more marked retinal thinning. CONCLUSIONS: Macular thinning with the preserved foveal thickness is a hallmark of eyes with optic atrophy. Together with no correlation between foveal thickness and BCVA, this finding would help in differential diagnosis of macular and optic nerve diseases.

Adult↗
PubMed2005

Is poor life expectancy a predictive factor in the progression of primary open angle glaucoma?

AIM: To investigate the disease progression and final visual outcome of glaucoma patients with poor life expectancy, compared to matched patients with a longer life expectancy. METHOD: Visual fields at diagnosis and at the last ophthalmic appointment before death were analysed for glaucoma patients referred between 1991 and 1995, and deceased before the end of 2001. These patients were matched to the patients living beyond 2001. Functional vision was also assessed, and classified as better than the NHS partial sighted criteria. RESULTS: A total of 61 deceased patients were identified, resulting in 40 matched pairs. In all, 6.5% of the patients with poor life expectancy progressed from functional vision to beyond partial sighted criteria, and none of the matched patients progressed to this extent. At final assessment an association between poor life expectancy and progression beyond functional vision was found existing (P = 0.02), with a lesser association at diagnosis (P = 0.06). Visual field scores of the matched pairs who had test results available for both initial and final assessment (n = 23 pairs) showed no statistically significant difference between the two groups at diagnosis (P = 0.52); However, a significant difference at final the assessment did exist (P = 0.042). No difference between the initial (off medication) intraocular pressures (IOPs) was found (P = 0.82). At the final assessment a significant difference existed (P = 0.025), with the surviving group having a higher final mean pressure (15.9 mmHg, SD 2.8, vs 18.3 mmHg, SD 4.9). CONCLUSION: Patients with poor life expectancy progressed more than the matched surviving patients, when measured from an initially similar position, despite better IOP control.

Aged↗
PubMed2005

Improved visual acuity and macular thickness 1 week after intravitreal triamcinolone for diabetic macular oedema.

PURPOSE: To evaluate the clinical and volumetric improvement 1 week after an injection of intravitreal triamcinolone acetonide in eyes with diabetic macular oedema. METHODS: Seven phakic eyes of seven diabetic patients diagnosed with clinically significant macular oedema were treated with a single 4-mg intravitreal injection of triamcinolone acetonide (0.1 ml). LogMAR best corrected visual acuity (logMAR BCVA), best corrected reading ability (RA), and central macular thickness (CMT) with optical coherence tomography (OCT) were assessed prior and 1 week subsequent to treatment. RESULTS: Mean improvement in logMAR BCVA was 0.146 (P=0.03). Mean reduction in CMT was 150.9 mum (P=0.02, Wilcoxon signed-rank test). Mean improvement in RA was 3 lines. CONCLUSION: Reduction in macular oedema was demonstrated on OCT at 1 week, in most cases associated with improvement in central visual function, in particular, reading ability. Total resolution of diabetic macular oedema may occur at 1 week following intravitreal steroid injection.

Aged↗
PubMed2001

Humoral immune response directed against LEDGF in patients with VKH.

Vogt-Koyanagi-Harada disease is an autoimmune systemic disorder. In Vogt-Koyanagi-Harada disease, inflammatory disorders occur in multiple organs containing melanocytes, including uvea (resulting in acute bilateral panuveitis), skin (resulting in vitiligo and alopecia), central nervous system (resulting in meningitis) and inner ears (resulting in hearing loss and tinnitus). These inflammatory aspects are attributed to the destruction of melanocytes through immunological mechanisms. Studies have been carried out to elucidate the exact etiology and target autoantigen in Vogt-Koyanagi-Harada disease, but much remains to be investigated. Identification of target autoantigen is important to understand the etiology of autoimmune diseases, and for development of antigen-specific immuno-modulation therapy. To identify the target autoantigens in Vogt-Koyanagi-Harada disease, we made use of an immunoscreening of a bovine uveal cDNA expression library with serum samples obtained from patients with Vogt-Koyanagi-Harada disease. We identified an immunoreactive cDNA clone that encodes bovine lens epithelium derived growth factor. mRNA of human lens epithelium derived growth factor was determined by reverse transcription-polymerase chain reaction and it was expressed in human uvea, retina and melanocytes. Immunoglobulin G (IgG) autoantibodies were quantitated in an enzyme-linked immunosorbent assay, using recombinant human lens epithelium derived growth factor. The prevalence of IgG anti-lens epithelium derived growth factor autoantibodies in patients with Vogt-Koyanagi-Harada disease was significantly higher than that in healthy controls (66.7% versus 21.6%, P<0.001). On the other hand, the prevalence of the autoantibody in patients with panuveitis of other etiology, Behçet's disease and sarcoidosis, was almost same as that in healthy controls. These results suggest that the humoral immune response agonist lens epithelium derived growth factor is not a mere secondary phenomena caused by uveal tissue damage.

Adult↗
PubMed2001

Identification of a novel autoantigen UACA in patients with panuveitis.

To identify the target autoantigens in Vogt-Koyanagi-Harada disease, we made use of an immunoscreening of a bovine uveal cDNA expression library with serum samples obtained from patients with Vogt-Koyanagi-Harada disease. We identified a novel bovine antigen and homologous human autoantigen and designated it as UACA (uveal autoantigen with coiled coil domains and ankyrin repeats). mRNA of human UACA is expressed most abundantly in skeletal muscles and in various human tissues, including choroid, retina, and epidermal melanocytes. IgG autoantibodies were quantitated in an ELISA, using recombinant C-terminal 18.0% fragment of human UACA. The prevalence of IgG anti-UACA autoantibodies in patients with panuveitis (Vogt-Koyanagi-Harada disease, Behçet's disease, sarcoidosis) was significantly higher than that in healthy controls (19.6-28.1% vs 0%, P < 0.05) indicating that autoimmunity directed against UACA is a common phenomenon in these diseases.

Adolescent↗
PubMed2001

Starch and protein digestibility of newly released moth bean cultivars: Effect of soaking, dehulling, germination and pressure cooking.

Effect of soaking (12 h), soaking (12 h) dehulling, germination (60 h) and pressure cooking on starch and protein digestibility of four varieties of moth bean, one Local commonly used by the farmers of the area and three newly released high yielding varieties, Jwala, RMO 225 and RMO 257, was studied. The starch digestibility of raw unprocessed moth bean cultivars differed significantly (P < 0.05) from 25.4-28.2 mg maltose released/g flour being the highest and lowest in RMO 257 and RMO 225, respectively. The protein digestibility differed significantly from 70.3-74.6 per cent among all the unprocessed varieties of moth bean. All the processing treatments namely soaking, dehulling, germination and pressure cooking brought about appreciable enhancement in protein digestibility (1-19%) over the control and starch digestibility (19-115%) of all the four moth bean cultivars. However, out of all the processing treatments, germination (60 h) of soaked seeds (12 h) was the most effective in bringing about improvement in digestibility of starch and protein followed by dehulling and soaking (12 h).

Cooking↗
PubMed2001

Matrix metalloproteinases induction by pseudomonal virulence factors and inflammatory cytokines in vitro.

The pathogenesis of pseudomonal keratitis was investigated by focusing on induction and activation of matrix metalloproteinases (MMPs) by pseudomonal virulence factors and proinflammatory cytokines. Corneal lesions and MMP induction in vivo were evaluated in rabbit corneas infected with a clinical isolate of Pseudomonas aeruginosa. Effects of pseudomonal virulence factors [elastase, alkaline protease, exotoxin A and lipopolysaccharide (LPS)], tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta on MMP induction and activation were further examined in vitro in rabbit corneal fibroblasts (RCF) and human fibrosarcoma (HT1080) cells using reverse transcriptase-polymerase chain reaction (RT-PCR), zymography and immunoblotting. Corneal ulcers with typical ring abscesses were observed 12-24 h after infection, and MMPs, particularly MMP-9, were upregulated in infected corneas. Pseudomonal elastase caused the most extensive damage to both cell types. RCF treated with pseudomonal exoproteases or LPS expressed and secreted MMP-9. Exotoxin A had no effect on MMP expression. Both IL-1beta and TNF-alpha augmented MMP-9 expression in HT1080 cells. Pseudomonal elastase proteolytically activated MMP-2 and MMP-9 released from the cells. In conclusion, corneal destruction seen with P. aeruginosa infections may result from enhanced expression of MMPs by corneal stromal cells stimulated with pseudomonal exoproteases and proinflammatory cytokines and the proteolytic activation of MMPs by pseudomonal elastase.

ADP Ribose Transferases↗
PubMed2001

Fundus changes corresponding to visual field defects after vitrectomy for macular hole.

OBJECTIVE: Visual field defects are one of the complications of macular hole surgery, and mechanical retinal damage induced by infusion air is a proposed causative factor of this complication. In this study, we examined the fundus to see whether the changes observed corresponded to postoperative visual field defects. DESIGN: Observational case series. PARTICIPANTS: Seventeen eyes of 17 patients who had postoperative visual field defects after vitrectomy for idiopathic macular hole were examined. METHODS: The fundus was examined by ophthalmoscopy and by fluorescein and indocyanine green angiography. MAIN OUTCOME MEASURES: Fundus changes corresponding to postoperative visual field defects. RESULTS: In eight eyes, detectable fundus changes were observed, including regional mottling and degeneration of the retinal pigment epithelium, filling delay of the choroidal circulation, subretinal fibrosis, and epiretinal membrane formation. These findings corresponded exactly to the visual field defects observed. Although the visual field defects had been detected shortly after surgery, fundus changes were detected, on average, more than 8 months after surgery. CONCLUSIONS: Fundus changes become apparent after surgery, and they are progressive. Therefore, it is important to examine eyes with visual field defects for a follow-up period of several years.

Aged↗
PubMed2001

N-(2-Chloroethyl)-N-ethyl-2-bromobenzylamine reduces intracellular calcium response to noradrenaline in rat visual cortex.

Using the fluorescent indicator Fura-2, we investigated the effects of N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4), a noradrenergic neurotoxin, on intracellular calcium responses to noradrenaline, N-methyl-D-aspartate, and carbamylcholine chloride in brain slices of the rat visual cortex. Noradrenergic depletion in the visual cortex of young rats was induced by DSP-4, and its selectivity was confirmed by two different methods, i.e., immunostaining with anti-dopamine-beta-hydroxylase antibody and biochemical analysis by high-performance liquid chromatography. The treatment with DSP-4 (25 mg/kg i.p., x2) caused disruption of noradrenergic fibers throughout all cortical layers, and reduced the content of noradrenaline to 6.4% of that in the normal control. In the normal cortex, bath-applied noradrenaline (100 microM) increased the intracellular calcium to 123% of the control in terms of the F(340)/F(380) ratio of Fura-2 fluorescence. Quantitative analysis of the F(340)/F(380) ratio was performed in layers II to IV, since the increase was mainly observed in these layers. The intracellular calcium response to noradrenaline was significantly (P<0.0001) reduced in the DSP-4-treated animals to 63.2% of that in the normal control. The response to N-methyl-D-aspartate (100 microM) was also reduced, whereas the response to carbamylcholine chloride, a muscarinic cholinergic agonist (100 microM), was not affected by the DSP-4 treatment. From these findings we suggest that noradrenergic denervation by DSP-4 reduces the intracellular calcium response to noradrenaline through changes in the intracellular signal transduction.

Adrenergic Agents↗
PubMed2001

Selective reduction of the S-cone component of the electroretinogram in Posner-Schlossman syndrome.

PURPOSE: The changes in short wavelength sensitive (S-) cone electroretinograms (ERGs) to ganzfeldt flash stimuli were examined in patients with Posner-Schlossman syndrome to study the differences in S-cone action in both the acute attack phase and the remission phase. METHODS: Ganzfeldt colour flashes under bright white background illumination were used to elicit short wavelength (S-), and mixed long- (L) and middle- (M) wavelength sensitive cone ERGs. Three subjects with unilateral Posner-Schlossman syndrome and 18 age-matched normal controls were compared. To compare the media opacity we obtained the L,M-cone balance, namely, the log density units of the neutral density filter required to produce the L,M-cone b-wave elicited with red stimuli which is identical to those with blue stimuli. RESULTS: Selective reduction of the S-cone ERG b-wave in acute attacks of Posner-Schlossman syndrome was found. Two of three cases showed the recovery of the S-cone b-wave with a decrease in the intraocular pressure. With regard to the implicit time, significant delay of the S-cone b-wave could not be detected in all subjects. CONCLUSION: Selective reduction of the S-cone component of the ERG during raised intraocular pressure was found. The S-cone pathway is thought to be more vulnerable to damage than the L,M-cone systems following elevations of intraocular pressure.

Acute Disease↗