Acinic cell carcinoma of the parotid gland: Auckland experience and literature review

Acinic cell carcinoma is an uncommon malignancy of the salivary glands and as such it has been difficult to accurately delineate its natural history. The aim of this study is to assess the behaviour of acinic cell salivary cancer of the parotid gland presenting to a single head and neck surgical unit in Auckland. The study is a structured review of cases of acinic cell carcinoma of the parotid gland presenting from 2000 to 2006 to the Head and Neck Unit at Auckland Hospital, those identified from the pathology database and the Otobase head and neck database. Case records and pathology reports were reviewed. Fifteen patients were identified, 9 men and 6 women. The mean age was 67.2 years, with range 50-85 years. The mean follow up was 4.4 years and range 1.1-7 years. There was one case of local recurrence during study period and no deaths. Five of 15 patients received postoperative radiotherapy. Postoperative complications consisted of one wound haematoma and two cases of marginal mandibular weakness (one transient and one permanent). Current management strategies are obtaining appropriate rates of recurrence and postoperative complications within the Auckland population.     

Pinocembrin triggers Bax-dependent mitochondrial apoptosis in colon cancer cells

Bioflavanoids are the major pigments in plants with multitude of biological activities including inhibition of proliferation or induction of apoptosis in tumor cells. Even though the safety records of most flavanoids are exceptional, its therapeutic use is still in its infancy. We have isolated pinocembrin (5,7-dihydroxyflavanone) from Alpinia galanga that showed cytotoxicity against a variety of cancer cells including normal lung fibroblasts with relative nontoxicity to human umbilical cord endothelial cells. The compound induced loss of mitochondrial membrane potential with subsequent release of cytochrome c and processing of caspase-9 and -3 in colon cancer cell line HCT 116. Processing of caspase-8 was minimal. The initial trigger for mitochondrial apoptosis appears to be by the translocation of cytosolic Bax protein to mitochondria. Overexpression of proapoptotic Bax protein sensitized the colon cancer cells to pinocembrin-induced apoptosis and Bax knockout cells were resistant to pinocembrin-induced apoptosis. Antiapoptotic protein Bcl-X(L) only partially prevented apoptosis induced by this compound. The Bax-dependent cell death involving classical cytochrome c release and processing of caspase-9 and -3 suggests that pinocembrin is a classical mitochondrial apoptosis inducer. But the failure of Bcl-X(L) overexpression to completely prevent apoptosis induced by this compound suggests that pinocembrin is capable of triggering mitochondrial-independent cell death that needs to be clarified. The existence of cell death upon Bcl-X(L) overexpression is a promising feature of this compound that can be exploited against drug resistant forms of cancer cells either alone or in combination with other drugs.     

Reversible hemiparesis associated with the use of topiramate.

We report a case of a 5-year-old boy with intractable partial seizures who developed a transient hemiparesis, worsening of the electroencephalogram (EEG) and a change in his seizure pattern with increased seizure frequency after receiving topiramate (TPM). Symptoms resolved within a month after TPM was discontinued. Clinicians need to be aware that TPM use may occasionally be associated with focal motor weakness and exacerbation of seizures.     

Pressure sore risk assessment in palliative care

Pressure sore prevention in palliative care is recognized as being an essential element of holistic care, with the primary goal of promoting quality of life for patient and family. Little is known about the incidence of pressure sore development and the use of pressure sore risk assessment tools in palliative care settings. The development of a risk assessment tool specifically for palliative care patients in a 41-bedded specialist palliative care unit is described. The risk assessment tool was developed as part of a tissue viability practice development initiative. The approach adopted in the validation of the Hunters Hill Marie Curie Centre pressure sore risk assessment tool was the comparative analysis of professional judgment of experienced palliative care nurses with the numerical scores achieved during the assessment of risk on 291 patients (529 risk assessment events). This comparative analysis identified the threshold for different degrees of risk for the patient group involved: low risk, medium risk, high risk and very high risk. Further work is being undertaken to evaluate the inter-rater reliability of the new tool. A number of issues are explored in this paper in relation to pressure sore prevention in palliative care: the role of risk assessment tools, the sometimes conflicting aims of trying to ensure comfort and prevent pressure sore damage, and the uncertainties faced by palliative care nurses when they are trying to maintain quality of life for the dying.     

Neuroanatomical distribution of abnormal prion protein in naturally occurring atypical scrapie cases in Great Britain

Mucopolysaccharidoses (MPS) are inherited disorders caused by the deficiency of lysosomal enzymes. Sanfilippo syndrome (MPS III) and Hunter syndrome (MPS II) are characterized by severe and mild neurological disorders, respectively, in which the neurodegenerative mechanisms remain to be clarified. We immunohistochemically examined the involvement of tauopathy/synucleinopathy, cell death and oxidative damage in the brains of three cases each of MPS IIIB and MPS II and age-matched controls. In cases of MPS IIIB, the density of GABAergic interneurons in the cerebral cortex immunoreactive for calbindin-D28K and parvalbumin was markedly reduced when compared with age-matched controls. The swollen neurons showed immunoreactivity for phosphorylated α-synuclein but not for phosphorylated tau protein or β-amyloid protein; those in the cerebral cortex demonstrated nuclear immunoreactivity for TUNEL, single-stranded DNA and 8-OHdG. Neither lipid peroxidation nor protein glycation was marked in MPS cases. The expression levels of superoxide dismutases (Cu/ZnSOD and MnSOD) and glial glutamate transporters (EAAT1 and EAAT2) were reduced in two MPS II cases. The disturbance of GABAergic interneurons can be related to mental disturbance, while synucleinopathy and/or DNA impairment may be implicated in the neurodegeneration of swelling neurons due to storage materials in MPS IIIB cases. These findings suggest the possibility of neuroprotective therapies other than enzyme replacement in MPS patients.