The preservation of shoulder function after radical neck dissection

The most disabling side effect of radical neck dissection is the 'shoulder syndrome', caused by denervation of the trapezius muscle. This is due to division of the spinal accessory nerve, the motor nerve to the trapezius. Using cadaver dissections the anatomy of the cervical spinal nerve supply to the trapezius has been studied. At radical neck dissection stimulation of these cervical spinal nerves produced contraction of the trapezius muscle. Thus a modified technique of radical dissection has been developed preserving the cervical spinal nerves to the trapezius. Comparison of patients undergoing this modified radical neck dissection with patients undergoing a classical radical neck dissection shows them to have better shoulder function.     

Metabolism of cryptolepine and 2-fluorocryptolepine by aldehyde oxidase

Objectives To investigate the metabolism of cryptolepine and some cryptolepine analogues by aldehyde oxidase, and to assess the implications of the results on the potential of cryptolepine analogues as antimalarial agents. Methods The products resulting from the oxidation of cryptolepine and 2‐fluorocryptolepine by a rabbit liver preparation of aldehyde oxidase were isolated and identified using chromatographic and spectroscopic techniques. The antiplasmodial activity of cryptolepine‐11‐one was assessed against Plasmodium falciparum using the parasite lactate dehydrogenase assay. Key findings Cryptolepine was oxidized by aldehyde oxidase give cryptolepine‐11‐one. Although 2‐fluorocryptolepine was found to have less affinity for the enzyme than cryptolepine, it was a better substrate for aldehyde oxidase than the parent compound. In contrast, quindoline, the 11‐chloro‐ , 2,7‐dibromo‐ and 2‐methoxy analogues of cryptolepine were not readily oxidized. Cryptolepine‐11‐one was found to be inactive against P. falciparum in vitro raising the possibility that the effectiveness of cryptolepine as an antimalarial, may be compromised by metabolism to an inactive metabolite by liver aldehyde oxidase. Conclusions Cryptolepine and 2‐fluorocryptolepine are substrates for aldehyde oxidase. This may have implications for the design and development of cryptolepine analogues as antimalarial agents.     

Noninvasive ventilator triggering in chronic obstructive pulmonary disease. A test lung comparison.

To be most effective, noninvasive ventilation (NIV) ventilators should synchronize well with patients' breathing. However, the speed with which different ventilators can respond to the transitions between inspiration and expiration may vary, and abnormal respiratory mechanics and mask leaks may exacerbate this problem. This study explored synchronization using a new test lung model designed to simulate acute exacerbations of chronic obstructive pulmonary disease (COPD). Thirteen ventilators were tested against different combinations of tidal volume (VT), airways resistance (Raw), FRC, and mask leak. These combinations ranged from those of a severe exacerbation of COPD, to a mild condition reflecting the optimal triggering conditions a ventilator is likely to encounter. The triggering delays from the beginning and end of "inspiration" of the test lung, to the appropriate responses from the ventilators were measured. Three of the ventilators had trigger delays less than approximately 120 ms at both the beginning and end of expiration under all conditions. Trigger delays of other ventilators were mainly in the range of 120 to 300 ms, although exceptionally as long as 500 ms. Varying the conditions had a variable but generally small effect on triggering times, suggesting that there is a largely unavoidable element to the triggering delays intrinsic to the design of the ventilators.