Visual axis opacification after AcrySof intraocular lens implantation in children

PURPOSE: To evaluate visual axis opacification after AcrySof intraocular lens (IOL) (Alcon) implantation in pediatric eyes. SETTING: Iladevi Cataract and IOL Research Centre, Ahmedabad, India. METHODS: This prospective study evaluated 103 consecutive eyes of 72 children with congenital cataract. Two groups were formed based on age at surgery: Group 1, younger than 2 years, and Group 2, older than 2 years. All eyes in Group 1 (n = 37) had primary posterior continuous curvilinear capsulorhexis (PCCC) with anterior vitrectomy. In Group 2 (n = 66), management of the posterior capsule was assigned randomly to no PCCC (Group 2A, n = 37) or PCCC (Group 2B, n = 29). The PCCC group was further randomized into 2 subgroups: no vitrectomy (Group 2BN, n = 14) or vitrectomy (Group 2BV, n = 15). The primary outcome measures were visual axis opacification and the resulting need for a secondary procedure. Statistical analysis was performed using SPSS for Windows (version 11.0.1). RESULTS: The mean age of the patients was 5.2 years +/- 5.0 (SD) (range 0.2 to 16.0 years) and the mean follow-up, 2.3 +/- 0.9 years (range 1.0 to 4.0 years). Overall, 41 eyes (39.8%) developed visual axis opacification and 14 (13.6%) required secondary intervention. In Group 1, 4 eyes (10.8%) developed visual axis opacification and 3 (8.1%) had a secondary pars plana vitrectomy. In Group 2A, 31 eyes (83.8%) developed posterior capsule opacification (PCO) and 10 eyes (27.7%) had secondary intervention. Children 8 years or younger at the time of surgery developed significantly greater PCO than older children (P =.01). Five eyes (37.5%) in Group 2BN had opacification of the anterior vitreous face, 1 of which required a secondary procedure. One eye (6.7%) in Group 2BV had visual axis opacification that did not require a secondary procedure. CONCLUSIONS: AcrySof IOL implantation with appropriate management of the posterior capsule maintained a clear visual axis in 60.2% of eyes. Of the 39.8% of eyes with visual axis opacification, 13.6% had visually significant opacification and required a secondary procedure.     

Growth inhibition of human colon cancer cells by nitric oxide (NO)-donating aspirin is associated with cyclooxygenase-2 induction and beta-catenin/T-cell factor signaling, nuclear factor-kappaB, and NO synthase 2 inhibition: implications for chemoprevention

Nitric oxide (NO)-releasing aspirin (ASA), consisting of a traditional ASA molecule to which a NO-donating moiety is covalently bound, is a promising colon cancer chemopreventive agent. NO-ASA inhibits colon cancer cell growth more potently than ASA by inhibiting cell proliferation and enhancing cell killing. We examined in cultured human colon cancer cells the effect of NO-ASA on the beta-catenin/T-cell factor signaling pathway, nuclear factor-kappaB, and NO synthase 2 and on cyclooxygenase (COX) expression, all presumed to participate in colon carcinogenesis. Besides inhibiting cell growth, NO-ASA inhibited the beta-catenin/T-cell factor signaling pathway (IC(50), 1.1 microM), nuclear factor-kappaB DNA binding (IC(50), 7.5 microM), and NO synthase 2 expression (IC(50), 2 microM). Interestingly, NO-ASA induced COX-2 expression, although it had no effect on COX-1. COX-2 induction was accompanied by increased prostaglandin E(2) production. These effects occurred at NO-ASA concentrations below or near its IC(50) for cell growth (IC(50), 2-50 microM). The metabolism of NO-ASA by these cells is characterized by a rapid deacetylation step and the formation of a conjugate with glutathione. NO-ASA had no effect on intracellular cyclic GMP concentrations. We propose a model incorporating the pleiotropic effects of NO-ASA on cell signaling and postulate that collectively these effects may contribute to its strong chemopreventive effect.     

Reactive oxygen species and acute renal failure

Acute renal failure is commonly due to acute tubular necrosis (ATN), the latter representing an acute, usually reversible loss of renal function incurred from ischemic or nephrotoxic insults occurring singly or in combination. Such insults instigate a number of processes-hemodynamic alterations, aberrant vascular responses, sublethal and lethal cell damage, inflammatory responses, and nephron obstruction-that initiate and maintain ATN. Eventually, reparative and regenerative processes facilitate the resolution of renal injury and the recovery of renal function. Focusing mainly on ischemic ATN, this article reviews evidence indicating that the inordinate or aberrant generation of reactive oxygen species (ROS) may contribute to the initiation and maintenance of ATN. This review also discusses the possibility that ROS may instigate adaptive as well as maladaptive responses in the kidney with ATN, and raises the possibility that ROS may participate in the recovery phase of ATN.     

Renal response to repetitive exposure to heme proteins: chronic injury induced by an acute insult

BACKGROUND: Renal diseases are conventionally classified into acute and chronic disorders. We questioned whether acute, reversible, renal insults may be induced to incite a chronic scarring process, employing as an acute insult the glycerol model of heme protein-induced renal injury. METHODS: Rats were subjected to weekly injections of hypertonic glycerol for up to six months. Renal function was serially determined, and the effect of such insults on renal histology and renal expression of collagen and fibrogenic cytokines was assessed. RESULTS: After the first injection of glycerol, which, expectedly, induced a prompt fall in the glomerular filtration rate (GFR), subsequent injections encountered a remarkable renal resistance in that the fall in GFR was markedly blunted. This resistance to acute decline in renal function in rats subjected to repetitive injections of glycerol was accompanied by less necrosis and apoptosis of renal tubular epithelial cells after such injections. The attenuation in the fall in GFR in response to repetitive exposure to glycerol-induced heme protein injury was maintained for up to six months. A progressive decline in GFR appeared after three months and was accompanied by histologic tubulointerstitial injury, the latter assessed at six months. These kidneys demonstrated up-regulation of collagen I, III, and IV in conjunction with increased expression of the oxidant-inducible, chemotactic cytokine, monocyte chemoattractant protein-1 (MCP-1), and the oxidant-inducible, fibrogenic cytokine, transforming growth factor-beta1 (TGF-beta1). The exposure of the kidney to a single injection of hypertonic glycerol increased the expression of both cytokines some three to five days following this exposure, while the exposure of NRK 49F cells in culture to an iron-dependent model of oxidative stress also increased expression of TGF-beta1 and collagen mRNAs. CONCLUSIONS: We conclude that this nephrotoxic insult, repetitively administered, encounters a resistance in the kidney such that the expected fall in GFR does not occur. However, with time, such resistance is accompanied by a decrease in GFR, the latter associated with chronic tubulointerstitial disease. Thus, a long-term cost is exacted, either along with, or as a consequence of, such resistance. We suggest that chronic up-regulation of such oxidant-inducible genes such as TGF-beta1 and MCP-1 contributes to tubulointerstitial disease, and iron-mediated oxidative stress may directly induce TGF-beta1.     

Temporosphenoid giant cell tumour

Only a few cases of Giant Cell tumours of temporal and sphenoid bones have been documented in English literature. Concurrent temporoshenoid location is extremely rare for a Giant Cell Tumour. These locally aggressive bonedestructive tumours usually have a fairly predictable pat-tern of spread. We present here a case of Temporosphenoid Giant Cell Tumour that exhibited an unusual pattern of spread. This tumour was removed in a single stage without any untoward sequelae. A brief review of literature is included.