The inability of Streptococcus mutans and Lactobacillus acidophilus to form a biofilm in vitro on dentine pretreated with ozone

Background: The use of ozone therapy in the treatment of dental caries is equivocal. The aim of this study was to use an in vitro model to determine the effects of prior ozone application to dentine on biofilm formation and to measure any associated reduction in bacteria viability. Methods: Twenty dentine discs were bonded to the bases of 5 mL polycarbonate screw top vials. Ten dentine discs were infused with ozone for 40 seconds, 10 samples remained untreated as a control. The vials were filled with nutrient medium, sterilized and placed into the outflow from a continuous chemostat culture of Streptococcus mutans and Lactobacillus acidophilus for four weeks. At the conclusion of the experiment bacterial growth was monitored by taking optical density readings of the growth medium in each vial and the outer surface of the dentine specimens were examined by scanning electron microscopy as shown by SEM analysis. Results: Ozone infusion prevented biofilm formation on all the treated samples while there was substantial biofilm present on the control specimens. While the average optical density of the control specimens was almost twice that of the ozone infused dentine (0.710 for the control with a SD of 0.288 and 0.446 for the ozonated samples with a SD of 0.371), the results were not significant (p > 0.05). Conclusions: This preliminary study has shown that the infusion of ozone into non‐carious dentine prevented biofilm formation in vitro from S. mutans and L. acidophilus over a four‐week period. The possibility exists that ozone treatment may alter the surface wettability of dentine through reaction with organic constituents.     

Hemiazygous Coil Placement for High‐Defibrillation Thresholds in a Patient with a Right‐Sided Implantable Cardioverter Defibrillator

A 41‐year‐old man underwent implantation of a right‐sided implantable cardioverter defibrillator after removal of an infected left‐sided system. Defibrillation threshold (DFT) testing on the right‐sided system failed to convert ventricular fibrillation at maximum device output (35 J) compared with a DFT of less than 15 J on the previous left‐sided system. A single‐coil lead was selectively placed into the hemiazygous vein, which courses leftward of the spine in a posterior‐anterior projection, resulting in an improved shocking vector and reduction in DFTs to less than 25 J. (PACE 2012; 35:e10–e12)     

Streptococcus sanguinis‐induced cytokine release from platelets

Summary. Background: There is increasing evidence that both chronic and acute infections play a role in the development and progression of atherothrombotic disorders. One potential mechanism is the direct activation of platelets by bacteria. A wide range of bacterial species activate platelets through heterogeneous mechanisms. The oral micro‐organism S. sanguinis stimulates platelet aggregation in vitro in a strain‐dependent manner, although there are no reports of associated cytokine production. Objective: The aim of the present study was to determine whether platelet activation by S. sanguinis involved the release of pro‐inflammatory and immune modulating factors, and whether activation was enhanced by epinephrine. Methods and results: Four strains of S. sanguinis and one of S. gordonii stimulated the release of RANTES, PF4, sCD40L and PDGF‐AB, whereas only one S. sanguinis strain caused the release of sCD62p. Epinephrine enhanced S. sanguinis‐induced platelet aggregation and phosphorylation of phospholipase Cγ2 and Erk, but inhibited RANTES, PF4, sCD40L and PDGF‐AB release. Wortmannin inhibited S. sanguinis‐induced aggregation and release; however, only aggregation was partially reversed by epinephrine. Conclusions: The present study demonstrates that platelets respond to S. sanguinis with both prothrombotic and pro‐inflammatory/immune‐modulating responses. Epinephrine, potentially released in response to infection and/or stress, can significantly enhance the prothrombotic response, thereby providing a putative link between bacteraemia and acute coronary events during stress. In contrast, epinephrine inhibited the pro‐inflammatory/immune‐modulating response by an undetermined mechanism.     

THE RELATIONSHIP BETWEEN THE COMPLEX OF IMMUNOGLOBULIN A AND ALPHA-1-ANTITRYPSIN, ITS CONSTITUENT COMPONENTS AND THE ACUTE-PHASE RESPONSE AS MEASURED BY C-REACTIVE PROTEIN IN RHEUMATOID ARTHRITIS TREATED WITH GOLD OR D-PENICILLAMINE

Serum levels of immunoglobulin A (IgA), ₁ (AT), their complex(IgA-₁AT) and C-reactive protein (CRP) were measured prior totreatment and at 6 months, in 45 rheumatoid arthritis (RA) patients.Twenty-five patients were treated with D-penicillamine (DPA)and 20 patients with gold (sodium aurothiomalate). The levelof circulating complex was reduced by both treatments (p<0.001).There was a significant correlation between the circulatinglevels of IgA-₁AT complex and serum IgA (p<0.05). No relationshipwas observed between the level of circulating complex and CRP. These findings suggest that formation of IgA-₁AT complex inRA is dependent on the level of IgA. The complex is reducedby gold and DPA but it does not reflect an acute phase responseas measured by CRP. KEY WORDS: C-reactive protein, Immunoglobulin A, Alpha-1-antitrypsin, Rheumatoid arthritis, Immune complex     

THE EFFECT OF OXYTOCIN INFUSION ON ADENOHYPOPHYSEAL FUNCTION IN MAN

The responses of the adenohypophyseal hormones adrenocorticotrophin (ACTH), growth hormone (GH), thyroid stimulating hormone (TSH), prolactin, luteinizing hormone (LH) and follicle stimulating hormone (FSH) to sub-maximal doses of hypothalamic releasing factors were studied in six lean male volunteers (age 23-35 years) with and without infusions of oxytocin (OXT). OXT infusion (mean plasma concentration 133.6 +/- 2.6 pmol/l) completely inhibited the plasma ACTH responses to corticotrophin releasing hormone (CRH) (saline, peak increment ACTH 1.61 +/- 0.75 pmol/l; OXT, peak increment ACTH - 0.04 +/- 0.28 pmol/l; P less than 0.05). OXT infusion had no significant effect on the GH response to growth hormone releasing hormone (GHRH), the TSH and prolactin responses to thyrotrophin releasing hormone (thyroliberin, TRH) or the LH and FSH responses to gonadotrophin releasing hormone (luteoliberin, GnRH). The data support a role for OXT in the modulation of ACTH secretion in man.     

Shwachman syndrome: Exocrine pancreatic dysfunction and variable phenotypic expression

BACKGROUND & AIMS: Shwachman syndrome is an inherited condition with multisystemic abnormalities, including exocrine pancreatic dysfunction. The aim of this study was to evaluate the occurrence and progression of features in a large cohort of patients. METHODS: Clinical records of 25 patients with Shwachman syndrome were reviewed. RESULTS: Mean birth weight (2.92 +/- 0.51 kg) was at the 25th percentile. However, by 6 months of age, mean heights and weights were less than the 5th percentile. After 6 months of age, growth velocity was normal. Severe fat maldigestion due to pancreatic insufficiency was present in early life (fecal fat, 26% +/- 17% of fat intake; age, < 2 years). Serial assessment of exocrine pancreatic function showed persistent deficits of enzyme secretion, but 45% of patients showed moderate age-related improvements leading to pancreatic sufficiency. Neutropenia was the most common hematologic abnormality (88%), but leukopenia, thrombocytopenia, and anemia were also frequently encountered. Patients with hypoplasia of all three bone marrow cellular lines (n = 11) had the worst prognosis; 5 patients died, 2 of sepsis and 3 of acute myelogenous leukemia. Other findings included hepatomegaly and/or abnormal liver function test results and skeletal abnormalities. CONCLUSIONS: A wide and varied spectrum of phenotypic abnormalities among patients with Shwachman syndrome is described. Pancreatic acinar dysfunction is an invariable abnormality. Patients with severe bone marrow involvement may have a guarded prognosis. (Gastroenterology 1996 Dec;111(6):1593-602)     

Interleukin-6 enhances growth factor-dependent proliferation of the blast cells of acute myeloblastic leukemia

The effects of recombinant interleukin-6 (IL-6) on the proliferation of blast precursors present in the peripheral blood of patients with acute myeloblastic leukemia (AML) was investigated. IL-6 had little effect by itself; however, it synergized with granulocyte macrophage colony- stimulating factor (GM-CSF) and interleukin-3 (IL-3) in the stimulation of AML blast colony formation. Responsiveness of blast progenitors to IL-6 was heterogeneous. On normal bone marrow cells the same synergy was observed on granulocyte and monocyte precursors (GM-CFC), while there was no significant effect on erythroid and multipotential precursors.     

Blastomycosis in a young African man presenting with a pleural effusion

Blastomyces dermatitidis is a dimorphic fungus endemic to northwestern Ontario, Manitoba and some parts of the United States. The fungus is also endemic to parts of Africa. Pulmonary and extrapulmonary findings of a 24-year-old African man who presented with weight loss, dry cough and chronic pneumonia not resolving with antibiotic treatment are presented. The unusual occurrence of pulmonary blastomycosis associated with skin lesions and a moderate pleural effusion is reported.