Cerebrospinal fluid lactate: measurement of an adult reference interval.

Background: Differentiating bacterial meningitis from viral meningitis is a diagnostic challenge. Cerebrospinal fluid lactate has been proposed as a valuable test to differentiate disease states; however, its use in adults is limited by a lack of robust reference interval data.

Methods: Cerebrospinal fluid samples with no cells or organisms detected, no culture growth after 48 h, and no increase in cerebrospinal fluid bilirubin were used to derive reference interval data for cerebrospinal fluid lactate in adults (n = 120).

Abdominal pain and hyperamylasaemia--not always pancreatitis.

A raised serum amylase concentration, at least four times the upper limit of normal (ULN), is used to support the diagnosis of acute pancreatitis in a patient presenting with abdominal pain. The authors report a case of toxic shock syndrome complicated by a raised serum amylase concentration that peaked at 50 times the ULN in a patient with recurrent abdominal pain. The commonest cause of hyperamylasaemia is pancreatic; however, further investigation of serum lipase and amylase isoenzyme studies found this to be of salivary origin and attributable to soft tissue inflammation of the salivary gland.

Delayed appearance of markers of intravascular haemolysis in a case of paroxysmal cold haemoglobinuria.

The aetiology of haemolytic disease is diverse and the diagnosis often relies on laboratory testing. We describe a case of intravascular haemolysis, which illustrates that significant intravascular haemolysis can occur in the absence of any abnormal haematological findings. Despite gross haemoglobinuria at presentation, the haemoglobin and reticulocyte counts were both within reference limits and a normal blood film was observed.

Response to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) differs in mouse strains and reveals a divergence in JNK signaling and COX-2 induction prior to loss of neurons in the substantia nigra pars compacta.

Parkinson's disease (PD) is a neurodegenerative disease whose hallmark pathological features include a selective loss of dopaminergic neurons in the midbrain. Recent studies have described the activation of a stress-induced signal cascade, c-Jun N-terminal kinase (JNK)-mediated activation of c-Jun, and an increase in the expression of a downstream effector, cyclooxygenase 2 (COX-2), in postmortem PD brains. The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), which induces selective neuronal loss in the midbrain similar to that seen in PD, also induces JNK-mediated activation of c-Jun and generates a COX-2 response in C57BL/6J mice.