Bilateral macular haemorrhages secondary to hepatitis-associated aplastic anaemia, treated with Nd:YAG laser posterior hyaloidotomy.

Hepatitis-associated aplastic anaemia (HAAA) is an uncommon but distinct variant of aplastic anaemia in which pancytopenia and bone marrow failure appears 2-3 months after an acute attack of hepatitis. Although bilateral vision loss may rarely be the initial presentation of aplastic anaemia, no such report is known in HAAA. Here the authors report such a case presenting with large premacular subhyaloid haemorrhages secondary to severe anaemia and thrombocytopenia.

Acute bilateral ophthalmoparesis with pupilary areflexical mydriasis in miller-fisher syndrome treated with intravenous immunoglobulin.

Miller-Fisher syndrome (MFS) is a rare condition characterized by the classical triad of ophthalmoplegia, ataxia, and areflexia (Fisher, 1956). It is considered a variant of Guillain-Barré syndrome (GBS) with which it may overlap, or it can occur in more limited forms. We report a case of a thirty-five-year-old male who presented with a six-day history of diplopia, following a recent chest infection.

Evaluation of shear bond strength of microwaveable acrylic resins in denture repair: a comparative study.

Objective: Acrylic denture base fracture is a common mode of failure. Heat-cured, auto-polymerized, visible light-cured, and microwaveable acrylic resins have been used as repair materials. The aim of this study was to evaluate the shear bond strength of two microwaveable resins (Acron MC and Justi) and one auto-polymerizing acrylic resin (ProBase Cold) as denture repair materials as opposed to a heat-cured one using the non-flasking procedure after thermocycling and photoaging.

Inactivating mutations targeting the chfr mitotic checkpoint gene in human lung cancer.

A hallmark of cancer is inactivation of cell cycle checkpoints. However, very few mutations targeting mitotic checkpoint genes have been described, and in those instances, a wild-type copy of the gene was retained. chfr is a mitotic checkpoint gene that functions in early prophase delaying chromosome condensation in response to microtubule poisons.

p53 activates ICAM-1 (CD54) expression in an NF-kappaB-independent manner.

Intercellular adhesion molecule-1 (ICAM-1) is a crucial receptor in the cell-cell interaction, a process central to the reaction to all forms of injury. Its expression is upregulated in response to a variety of inflammatory/immune mediators, including cellular stresses. The NF-kappaB signalling pathway is known to be important for activation of ICAM-1 transcription.

The complement inhibitor CD59 and the lymphocyte function-associated antigen-3 (LFA-3, CD58) genes possess functional binding sites for the p53 tumor suppressor protein.

p53 is an oncosuppressor protein, which acts via transcriptional and non-transcriptional mechanisms. The transcriptional function of p53 is mediated by specific responsive elements. In the present study we found active responsive elements, specific for the p53 within the 5'flanking region and within the first intron of the gene encoding for the CD59 membrane inhibitor of reactive lysis, and within the first intron of the gene encoding for the CD58 membrane protein (LFA-3).

Transcription factor E2F-1 acts as a growth-promoting factor and is associated with adverse prognosis in non-small cell lung carcinomas.

Numerous upstream stimulatory and inhibitory signals converge to the pRb/E2F pathway, which governs cell-cycle progression, but the information concerning alterations of E2F-1 in primary malignancies is very limited. Several in vitro studies report that E2F-1 can act either as an oncoprotein or as a tumour suppressor protein. In view of this dichotomy in its functions and its critical role in cell cycle control, this study examined the following four aspects of E2F-1 in a panel of 87 non-small cell lung carcinomas (NSCLCs), previously analysed for defects in the pRb-p53-MDM2 network: firstly, the status of E2F-1 at the protein, mRNA and DNA levels; secondly, its relationship with the kinetic parameters and genomic instability of the tumours; thirdly, its association with the status of its transcriptional co-activator CBP, downstream target PCNA and main cell cycle regulatory and E2F-1-interacting molecules pRb, p53 and MDM2; and fourthly, its impact on clinical outcome.

Vascular endothelial growth factor (VEGF) is expressed by neoplastic Hodgkin-Reed-Sternberg cells in Hodgkin's disease.

Vascular endothelial growth factor (VEGF) is involved in tumour angiogenesis, an important process for the growth and metastatic potential of solid tumours. Numerous studies have demonstrated up-regulation of VEGF at both mRNA and protein level in various tumours and a correlation with advanced stage and prognosis has been demonstrated in some cases. Limited information exists about its role in lymphoid malignancies and in particular, Hodgkin's disease.