Search

Inclusion body myositis is a rare, late-onset myopathy. Both inflammatory and myodegenerative features play an important role in their pathogenesis. Overlapping clinicopathological entities are the familial inclusion body myopathies with or without dementia. These myopathies share several clinical and pathological features with the sporadic inflammatory disease. Therefore, better understanding of the genetic basis and pathomechanism of these rare familial cases may advance our knowledge and enable more effective treatment options in sporadic IBM, which is currently considered a relentlessly progressive incurable disease.

Meningiomas are one of the most frequent intracranial tumours, with 13 histological types and three grades according to the 2007 WHO Classification of Tumours of the Central Nervous System. p53, as one of the most potent tumour suppressor proteins, plays a role in nearly 50% of human tumours. Poly(ADP-ribose) polymerase (PARP) is a DNA repair enzyme with high ATP demand. It plays a role in apoptosis by activating an apoptosis inducing factor, and in necrosis by consuming NAD+ and ATP. Only PARP1 has been investigated in detail in tumours out of the 17 members of the PARP superfamily; however, its role has not been studied in meningiomas yet. The aim of this study was to determine the role ofp53 and PARP1 in meningiomas of different grade and to establish whether there is any correlation between the p53 and PARP1 expression. Both PARP1 and p53 have been expressed in all examined meningiomas. PARP1 labelled grade II tumours with a higher intensity as compared to grade I and III neoplasms, respectively. An increased p53 expression was noted in grade III meningiomas. There was no statistical correlation between p53 and PARP1 expression. Our data indicate that both PARP1 and p53 activation is a feature in meningiomas of higher grade, PARP1 overexpression being an early, whereas p53 overexpression, a late event in tumour progression. [ABSTRACT FROM AUTHOR]

Herpes simplex virus encephalitis (HSVE) is a rare and life-threatening infection. The clinical signs are diverse and often misleading regarding the aetiology. However, focal seizure with fever and typical CT/MRI finding should always raise the possibility of HSVE as early diagnosis and antiviral therapy is crucial. Before the advent of molecular techniques and high-tech imaging histological examination from multiple brain biopsies were often necessary. Although nowadays PCR and other molecular methods may provide an aetiological diagnosis some cases need neuropathological verification. Due to the high IgG seropositivity rate in the population the plasma IgG titer is not diagnostic and elevation of its plasma level requires several weeks. We report the case of a 25-years old male patient who initially presented with epileptic seizures. There was no final diagnosis and no causal treatment in the district general hospital. The patient was admitted to our institution in comatose state on day 9; the initiated diagnostic tests and therapy could not save the patient who died next day. The autopsy and subsequent neuropathological examination revealed HSVE. We present a flowchart on diagnostic work-up and special techniques to aid diagnosis in suspected viral encephalitis.