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PubMed1994

Actinobacillus actinomycetemcomitans in adult periodontitis. II. Characterization of isolated strains and effect of mechanical periodontal treatment.

Ten systemically healthy subjects (ages 28 to 60 years) with untreated moderate to severe periodontal disease and evidence of presence of A. actinomycetemcomitans underwent standard mechanical periodontal treatment consisting of oral hygiene instruction and systematic deep scaling and root planing. Before, and 4 to 5 weeks after treatment, clinical measurements and separate subgingival microbiological samples were taken from the mesial and distal aspect of every tooth, with the exception of the third molars. A. actinomycetemcomitans could still be detected in all patients after treatment. In 9 of the 10 patients, all tested isolates from both examinations were of a single type. Two patients carried serotype a; 2 serotype b; 2 serotype c; and 1 serotype e. Two individuals showed only non-typeable isolates lacking serotype a, b, c, d, or e specific antigens. Another subject was colonized by serotype c and, in addition, yielded a non-typeable isolate. Persistence of A. actinomycetemcomitans after treatment was significantly correlated with the frequency of A. actinomycetemcomitans before treatment (P < 0.001) and the mean probing depth before treatment (P < 0.05). No serotype-specific patterns of treatment outcome could be recognized. The analysis of the site specific effect of treatment showed a significant relationship between post treatment levels of A. actinomycetemcomitans and both probing depth reduction as well as attachment gain. Individuals showing evidence of A. actinomycetemcomitans in a multitude of sites appeared to be more difficult to treat than patients with few positive sites only. Within such individuals, the deeper pockets showed the greater resistance to eradication of A. actinomycetemcomitans.

Adult↗
PubMed2000

Autosomal recessive lissencephaly with cerebellar hypoplasia is associated with human RELN mutations.

Normal development of the cerebral cortex requires long-range migration of cortical neurons from proliferative regions deep in the brain. Lissencephaly ("smooth brain," from "lissos," meaning smooth, and "encephalos," meaning brain) is a severe developmental disorder in which neuronal migration is impaired, leading to a thickened cerebral cortex whose normally folded contour is simplified and smooth. Two identified lissencephaly genes do not account for all known cases, and additional lissencephaly syndromes have been described. An autosomal recessive form of lissencephaly (LCH) associated with severe abnormalities of the cerebellum, hippocampus and brainstem maps to chromosome 7q22, and is associated with two independent mutations in the human gene encoding reelin (RELN). The mutations disrupt splicing of RELN cDNA, resulting in low or undetectable amounts of reelin protein. LCH parallels the reeler mouse mutant (Reln(rl)), in which Reln mutations cause cerebellar hypoplasia, abnormal cerebral cortical neuronal migration and abnormal axonal connectivity. RELN encodes a large (388 kD) secreted protein that acts on migrating cortical neurons by binding to the very low density lipoprotein receptor (VLDLR), the apolipoprotein E receptor 2 (ApoER2; refs 9-11 ), alpha3beta1 integrin and protocadherins. Although reelin was previously thought to function exclusively in brain, some humans with RELN mutations show abnormal neuromuscular connectivity and congenital lymphoedema, suggesting previously unsuspected functions for reelin in and outside of the brain.

Animals↗
PubMed1992

Abnormal cerebellar output in rats with an inherited movement disorder.

Biochemical and metabolic mapping techniques have consistently identified the deep cerebellar nuclei (DCN) of the genetically dystonic rat as a site of abnormality. Extracellular single-unit recording techniques were used to assess the functional significance of these findings in affected rats and normal littermates between 16 and 25 days of age. Cells in the medial nucleus of the mutant rats had significantly increased spontaneous firing rates in comparison with cells from normal rats. In both the medial and the interpositus nuclei, cells from the mutants fired more rhythmically than those from the normal rats. When harmaline was administered systemically to activate the olivo-cerebellar system, in normal rats, increased firing rate and bursting patterns of activity were seen. There was no reliable change in the average firing rate or rhythmicity of cells in the medial nucleus of the dystonic rats, although previous studies have shown that harmaline activates neurons in the inferior olive in the mutants. It is likely that naturally stimulated olivary activity also fails to modulate cerebellar output in this model of inherited movement disorder. Anatomical studies did not reveal any consistent changes in the number of Purkinje cells, the volume of the DCN, or the soma size of DCN neurons. Since the electrophysiological findings cannot be ascribed to a loss of the Purkinje cells that normally provide an inhibitory input to the cerebellar nuclei, the results of this study indicate the presence of a functional defect in the control of cerebellar output in the dystonic rat that accounts for the failure of these animals to display harmaline tremor and which may be critical to the motor syndrome.

Animals↗
PubMed2005

Marinilactibacillus piezotolerans sp. nov., a novel marine lactic acid bacterium isolated from deep sub-seafloor sediment of the Nankai Trough.

A piezotolerant, mesophilic, marine lactic acid bacterium (strain LT20T) was isolated from a deep sub-seafloor sediment core collected at Nankai Trough, off the coast of Japan. Cells were Gram-positive, rod-shaped, non-sporulating and non-motile. The NaCl concentration range for growth was 0-120 g l(-1), with the optimum at 10-20 g l(-1). The temperature range for growth at pH 7.0 was 4-50 degrees C, with the optimum at 37-40 degrees C. The optimum pH for growth was 7.0-8.0. The optimum pressure for growth was 0.1 MPa with tolerance up to 30 MPa. The main cellular phospholipids were phosphatidylglycerols (25 %), diphosphatidylglycerols (34 %) and a group of compounds tentatively identified as ammonium-containing phosphatidylserines (32 %); phosphatidylethanolamines (9 %) were minor components. The fatty acid composition was dominated by side chains of 16 : 0, 14 : 0 and 16 : 1. The G+C content of the genomic DNA was 42 mol%. On the basis of 16S rRNA gene sequence analysis and the secondary structure of the V6 region, this organism was found to belong to the genus Marinilactibacillus and was closely related to Marinilactibacillus psychrotolerans M13-2(T) (99 %), Marinilactibacillus sp. strain MJYP.25.24 (99 %) and Alkalibacterium olivapovliticus strain ww2-SN4C (97 %). Despite the high similarity between their 16S rRNA gene sequences (99 %), the DNA-DNA hybridization levels were less than 20 %. On the basis of physiological and genetic characteristics, it is proposed that this organism be classified as a novel species, Marinilactibacillus piezotolerans sp. nov. The type strain is LT20T (=DSM 16108T=JCM 12337T).

Bacterial Typing Techniques↗
PubMed1984

Cellular origins and target cells of immunoregulatory factors in mice with disseminated histoplasmosis.

Disseminated infection with Histoplasma capsulatum stimulates the production of a suppressor factor (SF-H) by spleen cells from C3H/HeJ mice and a helper factor (HF-H) by spleen cells from C57BL/6 mice. In the present study these disparate immunoregulatory factors were analyzed in detail with regard to: a) the surface phenotype of the cells that produce SF-H and HF-H; b) the role of accessory cells in the production of these factors; and c) the surface phenotype of the target cells activated by SF-H and HF-H. Treatment of spleen cells from Histoplasma-infected C3H/HeJ mice with anti-Thy-1.2 plus complement (C) or with anti-Ly-2 plus C or with anti-I-Jk antiserum plus C abolished production of SF-H. Conversely, generation of HF-H by spleen cells from C57BL/6 mice was abrogated by treatment with either anti-Thy-1.2 plus C or with anti-Ly-1 plus C. Thus, a Thy-1.2+, Ly-2+, I-J+ T cell releases SF-H, and a Thy-1.2+, Ly-1+ T cell secretes HF-H. Production of SF-H and HF-H by splenic T cells was reduced markedly by depletion of macrophages (M phi); readdition of 1% syngeneic, plastic-adherent splenocytes from normal or infected mice to M phi-depleted, splenic T cell cultures of either strain restored the capacity to generate immunoregulatory factors. Furthermore, adherent splenocytes from normal or infected mice liberated a factor or factors that enhanced production of both SF-H and HF-H. Kinetic studies demonstrated that activation of normal spleen cells required at least 48 hr of exposure to SF-H or HF-H. Both factors failed to activate splenocytes pretreated with anti-Thy-1.2 plus C. Spleen cells from C3H/HeJ mice depleted of Ly-1+, Ly-2+, or I-J+ cells and exposed to SF-H did not demonstrate suppressor activity, whereas Ly-1-depleted splenocytes from C57BL/6 mice exposed to HF-H failed to exert helper activity. Therefore, the target of SF-H is a Thy-1.2+, Ly-1+2+, I-J+ T cell, and the target of HF-H is a Thy-1.2+, Ly-1+ T cell.

Animals↗
PubMed2006

Norepinephrine modulates the inflammatory and proliferative phases of wound healing.

BACKGROUND: Injury results in the massive release of norepinephrine (NE) into the peripheral circulation. Recent investigations have demonstrated functional adrenoreceptors on the cellular mediators of cutaneous wound healing and NE-induced phenotypic alterations in immune cells have been demonstrated in vitro. Despite this, there is little description of how NE might alter the phases of wound healing in vivo. The purpose of this study was to compare cutaneous wound healing in norepinephrine-intact and norepinephrine-depleted mice. METHODS: Norepinephrine-depleted (NED) mice were generated by chemical axotomy with 6-hydroxydopamine and compared with norepinephrine-intact (NEI) animals (n = 6-12 per group, per time point). Using an excisional wound model, neutrophil recruitment was measured by myeloperoxidase assay. Macrophage recruitment and angiogenesis were measured by immunohistochemistry and re-epithelialization was determined histologically. The development of incisional wound disruption strength was determined over time. Finally, macrophage scavenger function was assessed by an in vitro latex bead phagocytosis assay. RESULTS: Wounds from NEI mice demonstrated greater neutrophil infiltration than NED wounds (24, 72 hours; p < 0.05). Wound macrophage recruitment was initially higher in NEI animals (24 hours, p < 0.05), but was eventually surpassed by that of NED animals (120 hours, p < 0.05). Angiogenesis was decreased while re-epithelialization was accelerated in NEI animals (p < 0.05). Wound disruption strength and macrophage scavenger function were unaltered between NED and NEI mice. CONCLUSIONS: Norepinephrine modulates the inflammatory and proliferative phases of wound healing in a temporally defined, cell-specific manner. By increasing recruitment of innate immune cells and expediting wound closure, norepinephrine appears to play a protective role in defense against infection.

Animals↗
PubMed2002

Radiosurgery for residual or recurrent nonfunctioning pituitary adenoma.

OBJECT: Nonfunctioning pituitary adenomas comprise approximately 30% of all pituitary tumors. The purpose of this retrospective study is to evaluate the efficacy and role of gamma knife radiosurgery (GKS) in the management of residual or recurrent nonfunctioning pituitary adenomas. METHODS: A review was conducted of the data obtained in 42 patients who underwent adjuvant GKS at the University of Pittsburgh between 1987 and 2001. Prior treatments included transsphenoidal resection, craniotomy and resection, or conventional radiotherapy. Endocrinological, ophthalmological, and radiological responses were evaluated. The duration of follow-up review varied from 6 to 102 months (mean 31.2 months). Fifteen patients were observed for more than 40 months. The mean radiation dose to the tumor margin was 16 Gy. Conformal radiosurgery planning was used to restrict the dose to the optic nerve and chiasm. Tumor control after GKS was achieved in 100% of patients with microadenomas and 97% of patients with macroadenomas. Gamma knife radiosurgery was equally effective in controlling adenomas with cavernous sinus invasion and suprasellar extension. No patient developed a new endocrinological deficiency following GKS. One patient's tumor enlarged with an associated decline in visual function. Another patient experienced a deterioration of visual fields despite a decrease in tumor size. CONCLUSIONS: Gamma knife radiosurgery can achieve tumor control in virtually all residual or recurrent nonfunctioning pituitary adenomas. Dose sparing facilitates tumor management even when the adenoma is close to the optic apparatus or invades the cavernous sinus.

Adenoma↗