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In a patient with tetralogy of Fallot (TOF) and pulmonary atresia, treating the cardiac problem or the associated congenital illness is always a challenge. We describe the challenges and successful initial management of bilateral cataract to prevent visual loss in an infant with TOF with pulmonary atresia.

Purpose: To determine the nature and the origin of metallic foreign particles appearing on the iris after phacoemulsification surgery., Setting: P.D. Hinduja Hospital and Medical Research Centre, Mumbai, Maharashtra, India., Design: Case series., Methods: Metallic foreign particles were observed on the iris surface and the pupillary border on the first postoperative visit after phacoemulsification. One metallic particle, which was stuck to the iris surface, was removed intraoperatively and sent for metal analysis along with the phaco needle, the wrench used to tighten the phaco needle to the phaco handpiece, and the anterior chamber maintainer used during phacoemulsification. The composition of the elements was studied by scanning electron microscopy (SEM) to determine the origin of the metallic particle., Results: Foreign particles were seen in 11 eyes. On SEM, 3 elements (carbon, magnesium, and silicone) were common in the metal particle and 4 elements (carbon, magnesium, silicone, and titanium) on the wrench. The elements in the phaco needle (titanium) and anterior chamber maintainer (manganese, iron, and nickel) did not match those in the metal particle., Conclusion: The metal contents of the metallic particle extracted from the eye matched some of the constituent metals of the wrench that was used to tighten the phaco needle on the handpiece just before surgery., Financial Disclosure: No author has a financial or proprietary interest in any material or method mentioned., (Copyright © 2013 ASCRS and ESCRS. Published by Elsevier Inc. All rights reserved.)

Hypoxia inducible factor-2α (HIF-2α) has a critical role in renal tumorigenesis. HIF-2α is stabilized in von Hippel-Lindau (VHL)-deficient renal cell carcinoma through mechanisms that require ongoing mRNA translation. Mammalian target of rapamycin (mTOR) functions in two distinct complexes: Raptor-associated mTORC1 and Rictor-associated mTORC2. Rictor-associated mTORC2 complex has been linked to maintaining HIF-2α protein in the absence of VHL; however, the mechanisms remain to be elucidated. Although Raptor-associated mTORC1 is a known key upstream regulator of mRNA translation, initiation and elongation, the role of mTORC2 in regulating mRNA translation is not clear. Complex assembly of the mRNA cap protein, eukaryotic translation initiation factor 4 (eIF4)E, with activators (eIF4 gamma (eIF4G)) and inhibitors (eIF4E-binding protein 1 (4E-BP1)) are rate-limiting determinants of mRNA translation. Our laboratory has previously demonstrated that reactive oxygen species, mediated by p22(phox)-based Nox oxidases, are enhanced in VHL-deficient cells and have a role in the activation of Akt on S473, a site phosphorylated by the mTORC2 complex. In this study, we examined the role of Rictor-dependent regulation of HIF-2α through eIF4E-dependent mRNA translation and examined the effects of p22(phox)-based Nox oxidases on TORC2 regulation. We demonstrate for the first time that mTORC2 complex stability and activation is redox sensitive, and further defined a novel role for p22(phox)-based Nox oxidases in eIF4E-dependent mRNA translation through mTORC2. Furthermore, we provide the first evidence that silencing of p22(phox) reduces HIF-2α-dependent gene targeting in vitro and tumor formation in vivo. The clinical relevance of these studies is demonstrated.

Two distinct sets of chiral-partner bands have been identified in the nucleus 133Ce. They constitute a multiple chiral doublet, a phenomenon predicted by relativistic mean field (RMF) calculations and observed experimentally here for the first time. The properties of these chiral bands are in good agreement with results of calculations based on a combination of the constrained triaxial RMF theory and the particle-rotor model.

Purpose: To compare the effect of phacoemulsification on the corneal endothelium using fortified balanced salt solution (BSS Plus) and Ringer lactate as the intraocular irrigating solution., Setting: P.D. Hinduja Hospital, Mumbai, India., Design: Prospective randomized controlled double-blinded clinical study., Methods: Patients with senile cataract up to nuclear grade III were randomized to have phacoemulsification with posterior chamber intraocular lens implantation performed using fortified balanced salt solution (Group A) or Ringer lactate (Group B) as the intraocular irrigating solution. The corneal endothelial cell density (primary outcome) and pachymetry were measured preoperatively and 1 week and 1 and 6 months postoperatively., Results: Each group comprised 35 eyes (35 patients). The postoperative percentage of endothelial cell loss was not significantly different between the 2 groups at 1 week (P=.582), 1 month (P=.668), or 6 months (5.03% and 8.35% in Group A and Group B, respectively) (P=.483) and was within the limits reported in the literature. The postoperative percentage change in pachymetry was not significantly different between the 2 groups at 1 week (P=.179) or 1 month (P=.170) but was significant at 6 months (P<.001) (-1.59% and 0.54% in Group A and Group B, respectively); however, the mean pachymetry value was near baseline in both groups at 6 months., Conclusion: Corneal endothelial cell loss after phacoemulsification with Ringer lactate was similar to that with fortified balanced salt solution over the long term., (Copyright © 2012 ASCRS and ESCRS. Published by Elsevier Inc. All rights reserved.)

Microbial carbon capture cells (MCCs) were constructed with cyanobacteria growing in a photo biocathode in dual-chambered flat plate mediator-less MFCs separated by an anion exchange membrane from the anode compartment containing Shewanella putrefaciens. The performance of the MCC with Anabaena sparged with CO(2)-air mixture was compared with that of a conventional cathode sparged with air only. The power densities achieved were 57.8 mW/m(2) for Anabaena sparged with a CO(2)-air mixture, 39.2 mW/m(2) for CO(2)-air mixture sparging only, 29.7 mW/m(2) for Anabaena sparged with air, and 19.6 mW/m(2) for air sparging only. The pH of the cathode containing Anabaena gradually increased from 7 to 9.12 and power generation decreased from 34.7 to 23.8 mW/m(2) 17 due to pH imbalance associated voltage losses without CO(2)-air mixture sparging. Sparging with a 5% CO(2)-air mixture produced maximum power of 100.1 mW/m(2). In addition, the power density of MCC increased by 31% when nitrate was added into the catholyte., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

This paper demonstrates replication of ultrafast laser-induced micro/nano surface textures on poly(dimethylsiloxane) (PDMS). The surface texture replication process reduces the processing steps for microtexturing while improving light trapping. Two methods are demonstrated to replicate surface microtexture, a simple mold method and an embossing method. The laser microtextured silicon and titanium surfaces with micro to nanoscale features have been successfully replicated. Optical characterization of the replicated microtextured PDMS surfaces is performed and the results agree with model predictions. The replicated microtextured PDMS film is applied on a silicon surface and optical characterization shows that surface reflectance can be suppressed over 55% compared to the control value.

A low-cost pulsed N(2)-laser has been used to successfully demonstrate the formation of self-organized conical microtexture in Si. The process is demonstrated in vacuum environment to avoid the use of SF(6) gas and sulfur incorporation. The microtexture is formed with an average structure height of ~15 um, base diameter ~10 μm, and tip-to-tip separation ~8 μm. Energy dispersive x-ray spectroscopy of individual conelike structure shows that the material remains free from impurity incorporation. We have shown that the laser-induced-damage-related absorption can be successfully restored after an hour annealing at 1000 °C, making the material an ideal candidate for photovoltaic and other photonic applications., (© 2012 Optical Society of America)

A femtosecond-laser-textured Si photodetector is reported. Broadband spectral optical response is detected from UV to NIR. A quantum efficiency of greater than 80% from 490  nm to 780  nm has been achieved. The quantum efficiency at 245  nm is 62%, which is comparable to UV-enhanced Si photodiodes. The bandwidth of a 250-μm-diameter device is 60  MHz.

We report a phenomenon of spontaneous formation of self-organized 2D periodic arrays of nanostructures (protrusions) by directly exposing a silicon surface to multiple nanosecond laser pulses. These self-organized 2D periodic nanostructures are produced toward the edge as an annular region around the circular laser spot. The heights of these nanostructures are around 500 nm with tip diameter ~100 nm. The period of the nanostructures is about 1064 nm, the wavelength of the incident radiation. In the central region of the laser spot, nanostructures are destroyed because of the higher laser intensity (due to the Gaussian shape of the laser beam) and accumulation of large number of laser pulses. Optical diffraction from these nanostructures indicates a threefold symmetry, which is in accordance with the observed morphological symmetries of these nanostructures.

The most successful metal implant materials currently have relatively smooth surfaces on the micron size scale, with most failures occurring after only 10 years. To move beyond this limiting time scale, texturing methods have been developed to modify the metal surface to enhance integration of the implant directly with surrounding bone. A flexible single-step ultrafast-laser texturing process has been developed that results in a surface texture that exhibits micron scale peaks and troughs with superimposed submicron and nano-scale features. The textured titanium samples remain completely hydrophilic with no measurable contact angle even after several weeks in normal atmosphere. An increase in mesenchymal stem cell number is observed over that on an untreated control titanium surface. Extensive formation of cellular bridges by stromal cells between pillars shows the favorable response of differentiated cells to the surface and the promotion of their attachment. Expression of the alkaline phosphatase and osteocalcin genes in human bone marrow cells were seen to increase on the textured surface. The development of this single-step method for creating micron, submicron, and nano-scale surface texture directly on metals makes a significant contribution to the goal of improving the integration and life span of joint replacement implants., (Copyright © 2011 Wiley Periodicals, Inc.)

The strength distributions of the giant monopole resonance (GMR) have been measured in the even-A Sn isotopes (A=112-124) with inelastic scattering of 400-MeV alpha particles in the angular range 0 degrees -8.5 degrees . We find that the experimentally observed GMR energies of the Sn isotopes are lower than the values predicted by theoretical calculations that reproduce the GMR energies in 208Pb and 90Zr very well. From the GMR data, a value of Ktau = -550 +/- 100 MeV is obtained for the asymmetry term in the nuclear incompressibility.

The objective of this study was to investigate whether exposure of human monocytes to a pulsed ultra-wideband electromagnetic field (EMF) of 1 kV/cm average peak power triggers a signaling pathway responsible for the transcriptional regulation of NFKB (NF-kappaB)-dependent gene expression. Human Mono Mac 6 (MM6) cells were exposed intermittently to EMF pulses for a total of 90 min. The pulse width was 0.79+/-0.01 ns and the pulse repetition rate was 250 pps. The temperature of the medium was maintained at 37 degrees C in both sham- and EMF-exposed flasks. Total NFKB DNA-binding activity was measured in the nuclear extracts by the electrophoretic mobility shift assay. Cells exposed to the EMFs and incubated for 24 h postexposure showed a 3.5+/-0.2-fold increase in the NFKB DNA-binding activity. Since activation of NFKB was observed, the possibility of kappaB-dependent gene expression in response to exposure to the EMFs was investigated using NFKB signal-specific gene arrays. The results revealed no difference in the NFKB-dependent gene expression profiles at 8 or 24 h postexposure, indicating that activated NFKB does not lead to the differential expression of kappaB-dependent target genes. To determine whether the absence of the kappaB-dependent gene expression was due to compromised transcriptional regulation of NFKB, the functional activity of NFKB was examined in cells transiently transfected with Mercury Pathway constructs containing 4x NFKB binding sites associated either with the luciferase reporter system or a control vector. Pulsed EMF exposure did not induce NFKB-driven luciferase activity in these cells, indicating that the activation of NFKB at 24 h after the 1 kV/cm EMF exposure is functionally inactive. From these results, it is clear that the EMF-induced NFKB activation is only a transient response, with minimal or no downstream effect.

Estrogen receptor-alpha (ERalpha) promotes proliferation of breast cancer cells, whereas tumor suppressor protein p53 impedes proliferation of cells with genomic damage. Whether there is a direct link between these two antagonistic pathways has remained unclear. Here we report that ERalpha binds directly to p53 and represses its function. The activation function-2 (AF-2) domain of ERalpha and the C-terminal regulatory domain of p53 are necessary for the interaction. Knocking down p53 and ERalpha by small interfering RNA elicits opposite effects on p53-target gene expression and cell cycle progression. Remarkably, ionizing radiation that causes genomic damage disrupts the interaction between ERalpha and p53. Ionizing radiation together with ERalpha knock down results in additive effect on transcription of endogenous p53-target gene p21 (CDKN1) in human breast cancer cells. Our findings reveal a novel mechanism for regulating p53 and suggest that suppressing p53 function is an important component in the pro-proliferative role of ERalpha.

High-spin states in 135Nd were populated with the 110Pd(30Si,5n)135Nd reaction at a 30Si bombarding energy of 133 MeV. Two DeltaI=1 bands with close excitation energies and the same parity were observed. These bands are directly linked by DeltaI=1 and DeltaI=2 transitions. The chiral nature of these two bands is confirmed by comparison with three-dimensional tilted axis cranking calculations. This is the first observation of a three-quasiparticle chiral structure and establishes the primarily geometric nature of this phenomenon.

Although it is clear that p53 plays a pivotal role in G1/G2 checkpoints to conserve genomic integrity, its role in S phase checkpoint is less well understood. Recently, it has been reported that p53 is transcriptionally impaired even though it is stabilized during replication blockade. However, the mechanisms underlying this phenomenon are not known. In the present study, it has been shown that p53 accumulates and transactivates its target genes such as p21, gadd45 and bax in response to replication blockade in normal and cancer cells. Lack of transcriptional activation under similar conditions in cells lacking p53 shows that p53-target gene activation during replication blockade is indeed p53-dependent. Further, transactivation of p21 in response to replication blockade by hydroxyurea and aphidicolin is similar to that in response to ionizing radiation except that the latter is more immediate compared to the response to replication blockade. These findings suggest that impairment of transcriptionally active p53 in response to replication blockade is not a general phenomenon.

We have determined the energy of the J(pi) = 1/2(+), T = 3/2 resonance in 32S(p,p) to be E(p) = 3374.7+/-0.8 keV. This disagrees with the previously accepted value of E(p) = 3370+/-1 keV by Abbondanno et al. [Nuovo Cimento 70A, 391 (1970)] and solves a problem raised by recent observations of unexpected deviations from the isobaric multiplet mass equation. This resonance is also important in calibrating the beta-delayed proton spectra from 33Ar and 32Ar, and our findings may modify previous conclusions.

The frequency of p53 mutations is low and there is evidence of p53 protein overexpression even without p53 mutations in cervical cancers. This suggests that alternative mechanisms other than p53 mutation could be responsible for tumourigenesis of the uterine cervix. Therefore, an attempt has been made in the present investigation to analyze mutation and rearrangement of p53 gene in primary cervical cancers. The results indicated absence of mutation and presence of rearrangement in about 35% of cervical cancer patients. However, p53 overexpression in 50% of patients was demonstrated by immunohistochemistry and Western blot analysis. Further, rearrangement of p53 has been correlated with p53 mRNA and p53 protein status. The results indicated presence of overexpressed p53 protein in the samples with rearranged p53 gene. Thus, it is presumed that rearrangement of p53 might lead to production of defective p53 protein by affecting the level of p53 protein and this might have a role in the process of tumourigenesis. This study reports for the first time rearrangement of p53 in cervical cancers.

Different transcription factors activate and repress the p53 gene expression. Recently, a tissue specific binding of NF1/YY1 to p53 promoter has been reported and further, it has been demonstrated that NF1/YY1 activates p53 promoter activity. The deregulated expression of p53 appears to be a central feature of malignant transformation and the basis of this deregulation is not well defined. Hence, an attempt has been made to know the binding of NF1/YY1 to p53 promoter taking breast tumour as a model system. Results have indicated a differential binding of NF1 to p53 promoter and a depletion or low level of NF1 in majority of breast tumour samples. Further, a correlation between NF1 and p53 has indicated the presence of p53 RNA even without NF1. Hence it is assumed that p53 expression is not NF1-dependent in breast tumours. However, the results clearly demonstrate a deregulation of NF1 transcription factor in breast tumours.

Few reports are available on mutations in the promoter of tumour suppressor genes like p16, WT1 and Rb in cancers. However, the involvement of p53 promoter in cancers is not clearly known. Further, methylation of CpG sites is a major contributor of mutations in several genes. So an attempt has been made to determine the mutation and methylation status of p53 promoter in breast tumours. Results have demonstrated absence of mutations and deletions in p53 promoter, leading us to conclude that mutation of p53 promoter is probably not a significant factor in breast tumorigenesis. Methylation analysis has shown that the CCGG sites in the p53 promoter are unmethylated unlike that of its exons. Further, it has been shown that there is no change in the methylation profile of the CCGG sites in breast tumours. However, such studies are to be conducted in different types of tumours to define the role of p53 promoter mutation and methylation in the process of tumorigenesis., (Copyright 1999 S. Karger AG, Basel)

Different postreplicative, transcriptional, and translational mechanisms responsible for p53 gene inactivation are slowly unfolding. Rearrangement of the p53 gene is a very rare event in human solid tumors and has been reported only in osteosarcomas. From our laboratory we have recently reported rearrangement only in the coding region of the p53 gene in breast tumors. In this report we have undertaken a systemic investigation of p53 in oral tumors. Results have shown rearrangement in the coding region of p53 in 20% of cases and in the 5' region of p53 gene in approximately 8% of cases. No allelic loss and amplification of p53 gene was observed in these tumor samples. In our earlier studies on breast tumors, we found no abnormality in the 5' region of p53. However, in the present study we report for the first time rearrangement in the 5' region of p53 in oral tumors. Correlation of p53 gene rearrangement with p53 expression of RNA and protein indicates that rearrangement in the 5' region of p53 might not have a role in p53 expression. However, rearrangement in the coding region of p53 might play a critical role in controlling p53 gene activity in the process of tumorigenesis.

Rearrangement of the p53 gene is frequent in virus transformed cell lines and in chronic myelogenous leukemia. It is a rare event in solid tumours and has been reported only in osteosarcomas. In this study we have examined rearrangement of the p53 gene in human breast tumours. We found rearrangement in 35% of the patients (7 of 20 tumours examined). Normal tissue from these patients had an unrearranged gene, indicating that the genetic abnormality in the tumour is acquired during the natural process of tumorigenesis. No intronic rearrangement or allelic loss of the p53 gene was found in the breast tumour samples studied. Further, rearrangement of the p53 gene has been correlated with the p53 transcriptional status. Only two patients with rearranged p53 showed a high level of p53 RNA as well as protein expression. Thus, for the first time we report the rearrangement of the p53 gene in breast tumours, which may play a role in the process of tumorigenesis.

It is well established that TP53 regulates the expression of many genes, but the regulation of expression of TP53 itself is poorly understood. Recently, it has been shown that there is a tissue-specific binding of nuclear proteins in the TP53 gene promoter. The aim of this study was to determine the nuclear proteins that bind to the TP53 promoter elements (between -104 and -458) in male breast cancer. The results of our study, using the electrophoretic mobility shift assay (EMSA) and Southwestern analysis, have showed: (1) nuclear proteins or factors other than p53 bind to the TP53 promoter; (2) the levels of at least four nuclear proteins vary between normal and tumour breast tissue; and (3) two newly discovered nuclear proteins bind to the TP53 promoter in tumour tissue but are absent in normal tissue. This differential binding of nuclear proteins to the TP53 gene promoter might play a critical role in TP53 transcription and cancer progression in male breast tumours.

The aim of this investigation was to study the prevalence of p53 gene mutations in male and female breast cancers and to find out the relationship between this event and p53 protein expression. Genomic p53 was amplified by polymerase chain reaction (PCR). Exons 5-8 were screened for mutations using single stranded conformation polymorphism (SSCP) analysis. P53 protein expression was detected by immunohistochemistry (IHC) with the monoclonal antibody DO-1. In female breast cancer, p53 gene mutation was detected in 33% cases in either exon 5 or 6. However, in male, mutation was detected only in exon 6 in 90% cases. On the other hand, p53 protein expression was observed in all of these cases. Moreover, p53 protein immunostaining was observed in some of those cancer tissues, where no mutation was detected in exons 5-8. P53 dysfunction, as indicated by mutation or increased protein expression, common in both male and female breast cancer, but rate of occurrence or site of mutation differ from each other. Our results in male breast tumors indicate a positive correlation between p53 mutation and p53 protein overexpression, whereas the results in female breast tumors indicate an overexpression of p53 protein even without p53 gene mutation. Therefore, it may be presumed that p53 protein accumulation can result primarily from mutation. In addition, stabilization of p53 through binding to other proteins is another possible reason of p53 overexpression.