Effects of sitting posture and bolus volume on activation of swallowing-related muscles.

BACKGROUND: The pharyngeal phase is a particularly important clinical factor related to swallowing dysfunctions. Head and neck posture, as well as bolus volume, are important factors affecting the pharyngeal stages of normal swallowing. OBJECTIVE: The aim of our study was to identify the effects of sitting posture and bolus volume on the activation of swallowing-related muscles. MATERIALS AND METHODS: Twenty-four subjects participated in the study. The subjects were positioned in three sitting postures-slump sitting (SS), lumbo-pelvic upright sitting (LUS), and thoracic upright sitting (TUS). While sitting in the chair, the subject was instructed to swallow 10 and 20 mL of water. Surface electromyography (EMG) was used to measure the muscle activity of the supra-hyoid (SH) and infra-hyoid (IH) muscles. Also, sitting posture alignment (head, cervical and shoulder angle) was also performed. Data were analysed with a repeated measures analysis of variance (RMANOVA) using a generalised linear model. RESULTS: There was no significant difference in terms of the head angle (P = .395). However, significant differences were found in relation to the cervical angle (P < .001) and shoulder angle (P < .001). The TUS produced the lowest SH EMG activity (P = .001), in comparison to SS and LUS. The bolus volume for 20 mL showed greater SH and IH EMG activity (P < .001) than did the bolus volume for 10 mL. CONCLUSIONS: Correcting sitting posture from SS to TUS may better assist swallowing-related muscles with less effort, irrespective of the bolus volume.

Alternative production of avermectin components in Streptomyces avermitilis by gene replacement.

The avermectins are composed of eight compounds, which exhibit structural differences at three positions. A family of four closely-related major components, A1a, A2a, B1a and B2a, has been identified. Of these components, B1a exhibits the most potent antihelminthic activity. The coexistence of the "1" components and "2" components has been accounted for by the defective dehydratase of aveAI module 2, which appears to be responsible for C22-23 dehydration. Therefore, we have attempted to replace the dehydratase of aveAI module 2 with the functional dehydratase from the erythromycin eryAII module 4, via homologous recombination. Erythromycin polyketide synthetase should contain the sole dehydratase domain, thus generating a saturated chain at the C6-7 of erythromycin. We constructed replacement plasmids with PCR products, by using primers which had been derived from the sequences of avermectin aveAI and the erythromycin eryAII biosynthetic gene cluster. If the original dehydratase of Streptomyces avermitilis were exchanged with the corresponding erythromycin gene located on the replacement plasmid, it would be expected to result in the formation of precursors which contain alkene at C22-23, formed by the dehydratase of erythromycin module 4, and further processed by avermectin polyketide synthase. Consequently, the resulting recombinant strain JW3105, which harbors the dehydratase gene derived from erythromycin, was shown to produce only C22,23-unsaturated avermectin compounds. Our research indicates that the desired compound may be produced via polyketide gene replacement.

Widespread activation of antibiotic biosynthesis by S-adenosylmethionine in streptomycetes.

The effect of S-adenosylmethionine (SAM) on the production of various antibiotics was investigated to determine whether SAM-dependent methylation is required in biosynthetic pathways of antibiotics. Pristinamycin II(B) and granaticin do not require SAM-dependent methylation in their biosynthesis pathways, and production of these two antibiotics was increased about 2-fold when a low concentration (50 and 10 microM, respectively) of SAM was treated; in contrast, oleandomycin and avermectin B1a require SAM as a methyl donor in their biosynthesis, and production of these two antibiotics was increased 5-fold and 6-fold, depending on the SAM concentration within a certain range. We also found that the transcription of a pathway-specific regulator, gra-ORF9, was activated by exogenous SAM treatment. Production of oleandomycin and avermectin B1a was decreased by using a methyltransferase inhibitor, sinefungin, but the production levels of these antibiotics were restored to the control level by simultaneously adding SAM and sinefungin. Interestingly, we have found a similar stimulatory effect of S-adenosylhomocysteine (SAH), the methylation product of SAM, on antibiotic production in the four strains. Our results clearly demonstrate the widespread activation of antibiotic production using SAM in streptomycetes.