Optimising the use of carotid duplex sonography.

Aim: We analysed factors influencing diagnostic yield and treatment and their potential for optimising the use of carotid duplex sonography (CDS).

Method: Patients referred for CDS were divided into three groups: 1: high likelihood of carotid symptoms, 2: suspected presence of asymptomatic carotid lesions, 3: other indications. Clinical data, the grading of stenosis and the therapeutic consequences were analysed.

[Headache, general malaise and left-side ptosis].

A 82-year-old female was admitted to hospital because of deteriorated general condition, severe diffuse headache and complete left-sided ptosis. A computed tomography scan of the head revealed no subarachnoid haemorrhage. Based on the hypothesis that the symptoms resulted from an infarction in the brain stem, the previous medication with Aspirin was continued.

Ultraviolet radiation triggers the ribotoxic stress response in mammalian cells.

The ribotoxic stress response, which is conserved between prokaryotes and eukaryotes, is a cellular reaction to cytotoxic interference with the function of the 3'-end of the large (23 S/28 S) ribosomal RNA. The 3'-end of the large rRNA is directly involved in the three sequential steps of translational elongation: the aminoacyl-tRNA binding, the peptidyl transfer, and the ribosomal translocation. In mammalian cells, the ribotoxic stress response involves activation of the stress-activated protein kinase/c-Jun NH2-terminal kinase and the p38 mitogen-activated protein kinase and transcriptional induction of immediate early genes such as c-fos and c-jun.

Ribotoxic stress response: activation of the stress-activated protein kinase JNK1 by inhibitors of the peptidyl transferase reaction and by sequence-specific RNA damage to the alpha-sarcin/ricin loop in the 28S rRNA.

Inhibition of protein synthesis per se does not potentiate the stress-activated protein kinases (SAPKs; also known as cJun NH2-terminal kinases [JNKs]). The protein synthesis inhibitor anisomycin, however, is a potent activator of SAPKs/JNKs. The mechanism of this activation is unknown.

[Acute and subacute leg and foot paralysis of radicular origin: clinical aspects, examination technique and differential diagnosis of root syndromes].

We describe symptoms and physical findings consistent with acute or subacute radicular lesions in the lower limb: radicular pain syndromes in the leg and the motor as well as sensory deficits of lumbar and sacral roots L2 to S1. We emphasize the importance of anterior thigh pain which is not sufficiently known, and we point out our neurological findings which do not correspond to descriptions in standard textbooks. Aids to the examination of these radicular syndromes are given, stressing the technique of examining motor signs.