Confusion around Certification of Vision Impairment (CVI) and registration processes-are patients falling through the cracks?

BACKGROUND: In the UK, the Certificate of Vision Impairment (CVI) certifies a person as sight impaired (partially sighted) or severely sight impaired (blind). This is completed by ophthalmologists and passed with the patient's consent to their GP, their local authority, and The Royal College of Ophthalmologists Certifications office. Once a person is certified, they can be registered by their local authority which is voluntary but enables the person to access rehabilitation or habitation services, financial concessions, welfare benefits and other services provided by local authorities. METHODS: We conducted semi-structured individual interviews with 17 patients with a diagnosed eye condition, 4 Eye Clinic Liaison Officers (ECLO) and 4 referring optometrists around their experiences around CVI and registration processes. Analysis of themes was conducted with results synthesised in a narrative analysis. RESULTS: Patients reported lack of clarity around the processes of certification and registration, benefits of certification and what happens beyond certification, the type of support that they are entitled to, delays in accessing support. Optometrists appear not to engage with the process much, especially if the patient is being treated by the hospital eye service. CONCLUSION: Vision loss can be a devastating experience for the patient. There is a lack of information and confusion around the process. The lack of a joined-up process between certification and registration needs to be addressed if we are to provide the support that patients deserve in order to improve their quality of life and wellbeing.

The in vitro effects of interferon-gamma, alone or in combination with amphotericin B, tested against the pathogenic fungi Candida albicans and Aspergillus fumigatus.

OBJECTIVE: Recent studies into the antifungal activity of NK-cells against the Aspergillus fumigatus have presented differing accounts on their mode of antifungal activity. One of these mechanisms proposed that NK-cells may kill the fungus via the direct effects of exposure to Interferon gamma (IFN-γ). RESULTS: In this study we investigated the direct antifungal effects of recombinant human IFN-γ against a range of pathogenic fungi by measuring cellular damage using an XTT-based assay and cell viability through plate counts. It was found that 32 pg/ml of IFN-γ exhibited a significant but small antifungal effect on A. fumigatus (p = 0.02), Aspergillus flavus (p = 0.04) and Saccharomyces cerevisiae (p = 0.03), inhibiting growth by 6, 11 and 17% respectively. No significant inhibitory effects were observed in Candida species (p > 0.05 for all species tested) or Cryptococus neoformans (p = 0.98). Short term exposure (3 h) to a combination of amphotericin B (1 µg/ml) and IFN-γ (32 pg/ml) increased the effectiveness of amphotericin B against A. fumigatus and S. cerevisiae but not Candida albicans. These data suggest that IFN-γ does not possess strong antifungal activity but can enhance the effect of amphotericin B under some testing conditions against Aspergillus species.

The effects of phenoxodiol on the cell cycle of prostate cancer cell lines.

BACKGROUND: Prostate cancer is associated with a poor survival rate. The ability of cancer cells to evade apoptosis and exhibit limitless replication potential allows for progression of cancer from a benign to a metastatic phenotype. The aim of this study was to investigate in vitro the effect of the isoflavone phenoxodiol on the expression of cell cycle genes. METHODS: Three prostate cancer cell lines-LNCaP, DU145, and PC3 were cultured in vitro, and then treated with phenoxodiol (10 µM and 30 µM) for 24 and 48 h. The expression of cell cycle genes p21(WAF1), c-Myc, Cyclin-D1, and Ki-67 was investigated by Real Time PCR. RESULTS: Here we report that phenoxodiol induces cell cycle arrest in the G1/S phase of the cell cycle, with the resultant arrest due to the upregulation of p21(WAF1) in all the cell lines in response to treatment, indicating that activation of p21(WAF1) and subsequent cell arrest was occurring via a p53 independent manner, with induction of cytotoxicity independent of caspase activation. We found that c-Myc and Cyclin-D1 expression was not consistently altered across all cell lines but Ki-67 signalling expression was decreased in line with the cell cycle arrest. CONCLUSIONS: Phenoxodiol demonstrates an ability in prostate cancer cells to induce significant cytotoxicity in cells by interacting with p21(WAF1) and inducing cell cycle arrest irrespective of p53 status or caspase pathway interactions. These data indicate that phenoxodiol would be effective as a potential future treatment modality for both hormone sensitive and hormone refractory prostate cancer.

Cytotoxic effects of the novel isoflavone, phenoxodiol, on prostate cancer cell lines.

Phenoxodiol is an isoflavone derivative that has been shown to elicit cytotoxic effects against a broad range of human cancers. We examined the effect of phenoxodiol on cell death pathways on the prostate cell lines LNCaP, DU145 and PC3, representative of different stages of prostate cancer, and its effects on cell death pathways in these cell lines. Cell proliferation assays demonstrated a significant reduction in the rate of cell proliferation after 48 h exposure to phenoxodiol (10 and 30 µM). FACS analysis and 3'-end labelling indicated that all three prostate cancer cell lines underwent substantial levels of cell death 48 h after treatment. Mitochondrial membrane depolarization, indicative of early-stage cell death signalling, using JC-1 detection, was also apparent in all cell lines after exposure to phenoxodiol in the absence of caspase-3 activation. Caspase inhibition assays indicated that phenoxodiol operates through a caspase-independent cell death pathway. These data demonstrate that phenoxodiol elicits anti-cancer effects in prostate cancer cell lines representative of early and later stages of development through an as-yet-unknown cell death mechanism. These data warrant the further investigation of phenoxodiol as a potential treatment for prostate cancer.