We suggest that oral care may be useful in preventing pneumonia in older patients in nursing homes.

Boron deficiency hampers the productivity of 132 crops in more than 80 countries. Boron is essential in higher plants primarily for maintaining the integrity of cell walls and is also beneficial and might be essential in animals and in yeast. Understanding the molecular mechanism(s) of boron transport is crucial for alleviating boron deficiency. Here we describe the molecular identification of boron transporters in biological systems. The Arabidopsis thaliana mutant bor1-1 is sensitive to boron deficiency. Uptake studies indicated that xylem loading is the key step for boron accumulation in shoots with a low external boron supply and that the bor1-1 mutant is defective in this process. Positional cloning identified BOR1 as a membrane protein with homology to bicarbonate transporters in animals. Moreover, a fusion protein of BOR1 and green fluorescent protein (GFP) localized to the plasma membrane in transformed cells. The promoter of BOR1 drove GFP expression in root pericycle cells. When expressed in yeast, BOR1 decreased boron concentrations in cells. We show here that BOR1 is an efflux-type boron transporter for xylem loading and is essential for protecting shoots from boron deficiency.

SummaryTo investigate how plants acquire and assimilate sulfur from their environment, we isolated and characterized two mutants of Arabidopsis thaliana de®cient in sulfate transport. The mutants are resistant to selenate, a toxic analogue of sulfate. They are allelic to each other and to the previously isolated sel1 (selenate-resistant) mutants, and have been designated sel1-8 and sel1-9. Root elongation in these mutants is less sensitive to selenate than in wild-type plants. Sulfate uptake into the roots is impaired in the mutants under both sulfur-suf®cient and sulfur-de®cient conditions, but transport of sulfate to the shoot is not affected. The sel1 mutants contain lesions in the sulfate transporter gene Sultr1;2 located on the lower arm of chromosome 1. The sel1-1, sel1-3 and sel1-8 mutants contain point mutations in the coding sequences of Sultr1;2, while the sel1-9 mutant has a T-DNA insertion in the Sultr1;2 promoter. The Sultr1;2 cDNA derived from wild-type plants is able to complement Saccharomyces cerevisiae mutants defective in sulfate transport, but the Sultr1;2 cDNA from sel1-8 is not. The Sultr1;2 gene is expressed mainly in roots, and accumulation of transcripts increases during sulfate deprivation. Examination of transgenic plants containing the Sultr1;2 promoter fused to the GUS-reporter gene indicates that Sultr1;2 is expressed mainly in the root cortex, the root tip and lateral roots. Weaker expression of the reporter gene was observed in hydathodes, guard cells and auxiliary buds of leaves, and in anthers and the basal parts of¯owers. The results indicate that Sultr1;2 is primarily involved in importing sulfate from the environment into the root.

The present investigation was carried out to study some aspects of the recolonization of a subgingival microbiota following subgingival instrumentation in sites with deep pockets. 16 patients were recruited for the study. From each patient 4 inflamed gingival sites with deep pockets were selected. These sites were examined for plaque, overt gingivitis, bleeding on probing and probing depth. Samples of the subgingival microbiota were obtained and examined in the darkfield microscope and in a Neubauer chamber. Following the Baseline examination the teeth of all 4 jaw quadrants were carefully scaled and planed. Subgingival instrumentation was carried out under local anesthesia and required between 2-4 appointments. The patients were subsequently divided into 2 groups (Groups A and B) consisting of 9 and 7 subjects, respectively. During the first 16 weeks of maintenance the patients of Group A were not supervised regarding their self-performed plaque control measures and they accumulated supragingival plaque. The patients of Group B, however, were during these 16 weeks recalled once every 2 weeks for professional tooth cleaning. In addition they rinsed twice daily with a 0.2% solution of chlorhexidine digluconate. Reexaminations including assessments of the same parameters as those studied at Baseline were performed after 2, 4, 8, 12 and 16 weeks. After the 16-week examination the patients of Group A received a new sequence of subgingival scaling and root planing. During the subsequent 16 weeks the patients of Group A were also recalled for professional tooth cleaning. They were reexamined 18, 20, 24, 28 and 32 weeks after the Baseline examination. Subgingival scaling followed by carefully supervised oral hygiene measures resulted in a marked improvement of periodontal conditions. This improvement was accompanied by a pronounced and sustained reduction in the motile segments of the subgingival microbiota. In the presence of supragingival plaque (Group A), however, a subgingival microbiota containing large numbers of spirochetes and motile rods was soon (4-8 weeks) reestablished. A small number of sites with deep pockets (greater than or equal to 8 mm) was not substantially reduced in depth following subgingival instrumentation. In these sites which were kept free from supragingival deposits a subgingival microbiota with a large proportion of motile bacteria soon recurred.

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