Biography:

In the past Kenneth Opeskin has collaborated on articles with Kevin A.P. Lee and Carmela Ricciardelli. One of their most recent publications is Fatal alkali burns. Which was published in journal Forensic Science International.

More information about Kenneth Opeskin research including statistics on their citations can be found on their Copernicus Academic profile page.

Kenneth Opeskin's Articles: (7)

Fatal alkali burns

AbstractA case is reported of a worker in an aluminium plant who was found lying in a shallow pool of concentrated caustic solution, which had been heated to ~95 °C. He had been employed to operate a pump draining a sump. A pressurised ruptured airline lay nearby, this being the likely precipitating cause of an alkaline spray. The spray led to the deceased running towards the nearest safety shower, at the base of which he was subsequently found. This is a relatively uncommon form of death, resulting from contact with a hot concentrated alkali solution. Subsequent experimentation indicated that the deceased had been in contact with the fluid for a period of ~13 min.

Regular articleTumorigenesis and neoplastic progressionThe ADAMTS1 Protease Gene Is Required for Mammary Tumor Growth and Metastasis

A disintegrin and metalloprotease with thrombospondin motifs protein 1 (ADAMTS1) is a protease commonly up-regulated in metastatic carcinoma. Its overexpression in cancer cells promotes experimental metastasis, but whether ADAMTS1 is essential for metastatic progression is unknown. To address this question, we investigated mammary cancer progression and spontaneous metastasis in the MMTV-PyMT mouse mammary tumor model in Adamts1 knockout mice. Adamts1−/−/PyMT mice displayed significantly reduced mammary tumor and lung metastatic tumor burden and increased survival, compared with their wild-type and heterozygous littermates. Histological examination revealed an increased proportion of tumors with ductal carcinoma in situ and a lower proportion of high-grade invasive tumors in Adamts1−/−/PyMT mice, compared with Adamts1+/+/PyMT mice. Increased apoptosis with unaltered proliferation and vascular density in the Adamts1−/−/PyMT tumors suggested that reduced cell survival accounts for the lower tumor burden in ADAMTS1-deficient mice. Furthermore, Adamts1−/− tumor stroma had significantly lesser amounts of proteolytically cleaved versican and increased numbers of CD45+ leukocytes. Characterization of immune cell gene expression indicated that cytotoxic cell activation was increased in Adamts1−/− tumors, compared with Adamts1+/+ tumors. This finding is supported by significantly elevated IL-12+ cell numbers in Adamts1−/− tumors. Thus, in vivo ADAMTS1 may promote mammary tumor growth and progression to metastasis in the PyMT model and is a potential therapeutic target to prevent metastatic breast cancer.

Primary meningeal glioma

SummaryA 59 yr old man presented with headaches and was shown to have a posterior fossa tumor arising from the inferior surface of the tentorium cerebelli. At operation the tumor was discrete from the cerebellum and was thought to be a meningioma. Pathological examination showed the tumor had features similar to those of a meningioma. It consisted of interlacing bundles of spindle cells with a considerable amount of connective tissue. Some mitoses were present. The tumor cells, however, showed abundant staining for glial fibrillary acidic protein indicating their astrocytic nature. The tumor was diagnosed as astrocytoma Grade 2. The tumor ’recurred’ 4 mths later and a second surgical removal was attempted. Pathological examination showed features similar to those in the first operative specimen but this time invasion of the cerebellum was present. Deep x-ray treatment (D.X.R.T.) did not alter the tumor growth which proved fatal 7 mths after presentation. The differential diagnosis of an apparently meningeal-based tumor includes the rare entity of primary meningeal glioma. The case is presented as an example of this rare entity which both clinically and pathologically may be mistaken for a meningioma. The prognosis of intracranial solitary primary leptomeningeal gliomas is variable with recurrence and survival being months to years.

Pathologic studyCircle of Willis anatomy as a predictor of posterior cerebral artery territory infarction in the presence of tentorial herniation

AbstractTwenty-two brains in which tentorial herniation was present were examined to see whether the circle of Willis anatomy was a predictor of posterior cerebral artery territory infarction. This factor was considered in the context of the patients' known survival interval. Three brains in which tentorial herniation was not present were included as negative controls. Of the 22 brains in which tentorial herniation was present, 12 showed posterior communicating arteries smaller than the P1 segments of the posterior cerebral arteries; posterior cerebral artery territory infarction occurred in 8 of these. In these cases the survival interval was greater than 24 h (40 h to 2 months). In the 4 cases in which no infarction was seen the survival interval was less than 14 h. In 10 of the 22 cases the posterior communicating arteries were larger than, or equal in size to, the P1 segments of the posterior cerebral arteries and no infarction was seen in the posterior cerebral artery territories. No infarction was seen in the three control brains. These were trauma cases with no tentorial herniation. Statistical analysis indicated there was a true relationship between the sizes of the arteries and the occurrence of infarction. It cannot be excluded that other factors may have relevance in terms of whether infarction occurs. However, from the results of this study it appears that one can predict whether infarction in the posterior cerebral artery territory will occur as a complication of tentorial herniation by consideration of the anatomy of the circle of Willis in relation to the survival interval. The reasons for the presence or absence of posterior cerebral artery territory infarction have not previously been satisfactorily explained.

Case reportSuspected MPTP-induced parkinsonism

AbstractThe case of an intravenous heroin user who developed parkinsonian symptoms from the age of 28 years is presented. Neuropathologic examination revealed a marked loss of neurons and gliosis with the presence of Lewy bodies in the substantia nigra and locus ceruleus; they stained variably with antibody to ubiquitin and negatively with antibodies to tau and neurofibrillary tangles. Pseudo-Lewy bodies were also seen. Electron microscopy showed features in keeping with other electron microscopic studies of Lewy bodies in idiopathic Parkinson's disease and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced inclusion bodies in monkeys. Given that the deceased was a known heroin user, the rarity of the early age of onset, that MPTP is a recognized cause of parkinsonism in the drug abusing population, the absence of history of exposure to neuroleptics and the neuropathologic features, the parkinsonism was considered to be due to MPTP contamination of heroin. However, given the onset of parkinsonism 11 years prior to death it was not possible to obtain samples of the heroin injected to test for the presence of MPTP. Therefore it could not be absolutely excluded that this was a case of idiopathic Parkinson's disease occurring at a very young age in a heroin abuser. The immunohistochemical and electron microscopic features of Lewy bodies in such a case have not been previously described. The similarity of the neuropathological features to those of idiopathic Parkinson's disease and MPTP-induced parkinsonism further strengthens the hypothesis of MPTP or an MPTP-like agent being a cause of idiopathic Parkinson's disease.

Clinical studyFalse positive diagnosis of subarachnoid haemorrhage on computed tomography scan

AbstractFive cases are presented in which subarachnoid haemorrhage (SAH) was diagnosed by clinicians and/or radiologists on computed tomography (CT) scan. No macroscopic SAH was present on neuropathologic examination. In retrospect it was considered that the neurologic signs and the neuropathologic features close to the time of CT scan were in keeping with the patients being brain dead, i.e. had no cerebral blood flow at the time of the scans. On review of the CT scans it was considered the hyperdense material seen in the subarachnoid space must have been blood in congested subarachnoid blood vessels. The cases demonstrate that if a patient presents comatose and CT scan shows cerebral oedema then the presence of high attenuation material in the subarachnoid space should not necessarily be considered to represent SAH. The value of seeking radiological opinion is highlighted but even then diagnosis may be difficult.

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