Identification of antibacterial principles against Streptococcus mutans and inhibitory principles against glucosyltransferase from the seed of Areca catechu L

During the course of our studies on dental caries prevention by traditional medicines, fatty acids (myristic and oleic acids etc.) and procyanidins from betel nuts (the seed of Areca catechu L.) were respectively revealed to be the major antibacterial principles against a primary cariogenic bacterium, Streptococcus mutans, and the major inhibitory principles against glucosyltransferase from S. mutans.     

A reusable, custom-made warming blanket prevents core hypothermia during major neonatal surgery

PURPOSE: To introduce a reusable model of neonatal forced air warming blanket for intraoperative use during major noncardiac neonatal surgery and to determine clinical efficacy of this reusable blanket compared with the commonly used disposable blankets. METHODS: Delivered air temperature and calorie uptake of standard thermal bodies within the reusable blankets, Bair Hugger(R) blanket model 530 and model 555 were studied. Also, an efficacy study was conducted in 90 neonatal patients scheduled for major noncardiac surgery comparing the reusable blanket, the Bair Hugger(R) blanket model 530 and passive heat conservation as a control. The covered reusable blanket was used as a rescue procedure if the core temperature was < 35.5 degrees C. RESULTS: Delivered air temperature and heat transfer from the covered reusable blanket did not differ significantly from those of the Bair Hugger(R) blanket model 530 and model 555 (despite 0.75 degrees C-1.2 degrees C of heat trapped under the sheet and 1.3 Kcal less energy transfer). Temperatures measured underneath patients (correlated to poorly perfused areas) were highest using the Bair Hugger(R) blanket model 555. The reusable blanket was efficacious in preventing intraoperative core hypothermia and not different from the Bair Hugger(R) blanket model 530. About 1/3 of the patients in the control group had presented a core temperature < 35.5 degrees C but were successfully rescued using the reusable blanket. No adverse events were associated with any of these warming methods. CONCLUSION: This study shows the clinical efficacy of our reusable blanket for the prevention of core hypothermia during major neonatal surgery, which is not different from commonly used disposable blankets.     

Activation of macrophages in an experimental rat model of arthritis induced by Erysipelothrix rhusiopathiae infection.

Infection of Lewis rats with Erysipelothrix rhusiopathiae represents an experimental model system of acute and chronic arthritis. We studied here the acute inflammatory phase with respect to stimulation of macrophages and lymphocytes. Intragluteal injection of viable E. rhusiopathiae (10(2) to 10(4) bacteria) rapidly induced generalized inflammation, loss of body weight, hind leg arthritis, and systemic macrophage activation within 2 to 3 days. The same symptoms could also be evoked by injection of dead E. rhusiopathiae. Ex vivo, peritoneal macrophages released large amounts of tumor necrosis factor alpha on day 2 and interleukin-1 on day 3, whereas production of prostaglandin E2 was delayed to days 5 to 7 and appeared to counteract tumor necrosis factor alpha synthesis. The inflammatory response and development of arthritis were strongly dependent on T lymphocytes, as evidenced by the following findings: (i) lymphocytes released lymphokines that activated macrophages to enhanced mediator release; (ii) treatment of rats with cyclosporin A reduced infection-induced macrophage activation; (iii) mitogen-stimulated thymocyte proliferation was enhanced, indicating an infection-induced maturation-differentiation process in the thymus; and (iv) in T-cell-deficient nude rats, a higher dose of bacteria was required for infection, the inflammatory response was less severe, and only mild, but not chronic, arthritis developed. Thus, an E. rhusiopathiae-induced inflammation in rats provides a useful tool to characterize activated macrophages and T lymphocytes during the development of acute arthritis and its transition into the chronic form.     

Interleukin 1 as a tumor cytostatic mediator released from tumor ascites-treated macrophages

Peritoneal macrophages from DBA/2 mice, elicited by injection of Corynebacterium parvum (C.p.), were in vitro activated to Eb tumor cytostasis by incubation with tumor-induced ascites that was harvested 7 days after intraperitoneal Eb injection. The active cytostasis-mediating compound was found to be interleukin 1 (IL 1). When tumor ascites was fractionated according to molecular weight size, the most active IL 1-inducing fraction was found to comprise molecules of greater than 100,000 daltons. The data show that tumor-bearing hosts are capable of producing compounds that induce a high IL 1 secretion which may enable macrophages to mount an antiproliferative effect against tumor cells.     

Is This Phantom Pain?

Right upper quadrant abdominal pain may be due to many causes, and at times may give rise to diagnostic dilemma. We present here a young lady with biliary type of pain who was eventually found to have gall bladder agenesis with aerobilia, in the absence of prior biliary intervention.     

Lipopolysaccharide suppresses cytokine release from coxsackie virus-infected human monocytes.

Infections by coxsackie virus B3 (CVB3) have been reported to be associated with an enhanced influx of mononuclear leukocytes into afflicted tissue. Current evidence indicates that monocytes/macrophages are specifically involved in CVB3-induced myocarditis by maintaining a chronic inflammatory response. To examine susceptibility and reactivity to CVB3, freshly isolated human monocytes were exposed to various virus doses (0.1-10 MOI) in the presence or absence of macrophage-activating lipopolysaccharide (LPS). CVB3 infection alone induced an activation of monocytes as evidenced by enhanced adherence, release of cytokines and secretion of prostaglandin E2 (PGE2). Simultaneous addition of LPS almost entirely suppressed LPS-specific production of tumour necrosis factor alpha (TNF alpha) and PGE2, partially inhibited release of interleukin 1 beta (IL 1 beta) and did not affect interleukin 6 (IL6) synthesis of CVB3-infected monocytes. These data show that CVB3 activates monocytes to cytokine production but renders them unreactive to further activating stimuli. Further studies should determine the extent to which continuous cytokine release from persistently CVB3-infected monocytes, and their apparent unresponsiveness to other stimuli, contribute to chronic myocarditis.