Differential evaluation of bronchoalveolar lavage cells and leukotrienes in unilateral acture lung injury and ARDS patients

Patients with unilateral acute lung injury (UALI; n=6) and ARDS (n=4) were evaluated by bronchoalveolar lavage, as controls we used 5 patients suffering from cerebral hemorrhage and without pulmonary, cardiac or infectious disease who were mechanically ventilated. For each group of patients two independent bronchoalveolar lavages (BAL) were performed. The BAL fluid recovered from the two lungs was immediately analyzed for leukotrienes (LTS) by means of RP-HPLC and stained for cell counts. The BAL from the control group did not show any LTS and the percentage of neutrophils was within the normal range: 1±0.2% right lung and 1.2±0.4% left lung. The BAL fluid from UALI patients showed two different patterns, the injured lung showed high levels of LTS (39.1±8 ng ml^-1 LTB₄; 25±6 ng ml^-1 LTD₄ and 27.8±8.2 ng ml^-111-trans LTC₄) and an increased percentage of neutrophils (74.2±7%) compared to controls. Only 2 out of the 6 patients from the UALI group showed small amounts of LTB₄ (4 ng ml^-1) and LTD₄ (3.2 ng ml^-1). The BAL obtained from the healthy lung in both cases showed values of LTS almost eight fold lower than those present in the injured lung. The percentage of neutrophils from the unaffected lungs (4.3±7%) was not significantly different from controls. Lavage fluid from ARDS patients showed a similar picture to that of the affected lung from UALI patients. Evaluation of ARDS lavage fluid demonstrated the presence of the same LTS (LTB₄, LTD₄ and 11-trans LTC₄) with concentrations similar to those found in the injured lung of UALI subjects. The amount of LTB₄ (a very potent chemotatic factor) correlated directly with the percentage of neutrophils both in ARDS and the diseased lung of UALI patients. These findings suggest that LTS and neutrophils participate in the pathophysiology of UALI and ARDS, and that UALI is a localized pathologic entity similar to ARDS.The data from this study have been partially presented, as communication, during the 4th European Congress on Intensive Care Medicine in Baveno, June 14–18, 1988.This work is partially supported by MPI 601 CAP 02112.01.04 1984/1989.     

Increased release of interleukin-6 by oesophageal mucosa in children with reflux oesophagitis.

OBJECTIVE: To evaluate the release of interleukin-6 (IL-6) by oesophageal mucosa and to establish the serum levels of IL-6 and C-reactive protein (CRP), and plasma fibrinogen in children with reflux oesophagitis. DESIGN: In a prospective study, IL-6 release by tissue fragments obtained from oesophageal biopsies was determined and serum IL-6 and CRP as well as plasma fibrinogen were analysed. METHODS: The study population comprised ten children with reflux oesophagitis, diagnosed on the basis of 24 h oesophageal pH monitoring and endoscopy with biopsies. Ten children with recurrent abdominal pain were studied for comparative purposes. Biopsy tissue fragments were processed to obtain a cell suspension and the release of IL-6 was determined in culture medium. Serum IL-6 levels were measured by ELISA, serum CRP by turbidimetry, and plasma fibrinogen by spectrophotometry. RESULTS: Oesophageal cells obtained from reflux oesophagitis patients synthesize and release in vitro a significantly higher amount of IL-6 than controls (71.26+/-19.5 versus 31.67+/-8.02 pg/10(6) cells; P<0.01). Serum IL-6, serum CRP and plasma fibrinogen levels were not statistically different between patients with reflux oesophagitis and controls. CONCLUSIONS: These results suggest a short-term action of IL-6 since its effects could be exerted only in the microenvironment of the oesophageal mucosa.     

High levels of serum prostaglandin E2 in children with osteogenesis imperfecta are reduced by neridronate treatment

Prostaglandin E2 (PGE2) is an activator of bone remodeling, and increase levels of PGE2 are found in several disorders characterized by chronic inflammation. Bisphosphonates are used in the treatment of osteogenesis imperfecta (OI), an inherited disorder characterized by bone fragility and low bone mass. We evaluated the serum PGE2 (ng/mL) level in 16 children affected by OI (11 with mild and 5 with severe forms) at basal time and during treatment with neridronate. The levels of PGE2 in mild and severe forms were increased at basal time compared with controls (13.14 +/- 4.2 versus 0.72 +/- 0.05, p < 0.01; 15.1 +/- 1.5 versus 0.72 +/- 0.05, p < 0.01, respectively) and showed a significant decrease after the second (T1) cycle of treatment (mild: 4.97 +/- 5.0 versus 13.14 +/- 4.2, p < 0.01; severe: 5.32 +/- 4.5 versus 15.1 +/- 1.5, p < 0.01) with a further significant decrease after the fourth (T2) cycle. The high basal PGE2 levels in OI, a noninflammatory disorder, could be explained by stress-induced release mediated by inducible cyclooxygenase-2-catalyzed pathway. The reduction obtained by treatment with bisphosphonates could be attributed to a direct pharmacological effect since these drugs has been reported to modulate the release of proinflammatory mediators.     

Leukotrienes in human umbilical plasma at birth

The aim of this study was to see whether leukotrienes are present in human umbilical plasma at birth either before or after labour. Plasma concentrations of LTB4 (6.02 ng/ml) and LTD4 (6.11 ng/ml) were significantly higher (P less than 0.01) after spontaneous vaginal delivery than during elective caesarean section before labour (LTB4 = 1.96 ng/ml, LTD4 = 0.18 ng/ml). A possible involvement of leukotrienes in the biochemical and metabolic events of human labour is suggested.     

Bonding effectiveness and sealing ability of fiber-post bonding

OBJECTIVES: To evaluate the push-out bond strength and the sealing ability of five adhesive cements routinely used for fiber-post bonding. METHODS: Fifty extracted single-rooted teeth were randomly divided in five groups and restored using Parapost FiberLux and the following luting agents: Panavia 21 (PAN), Clearfil Esthetic Cement (CLF), Variolink II (VAR), RelyX Unicem (UNI) and experimental GC self-adhesive cement (EGC). After 1 week of water storage at 37 degrees C, three sections (coronal, middle and apical) of 2mm thickness were prepared from each specimen. Sealing ability was quantified with a fluid-filtration system (Flodec) during 10 min, after which the push-out bond strength was immediately measured. Data were analyzed with ANOVA (push-out) and Kruskal-Wallis (sealing ability). RESULTS: The push-out bond strength and sealing ability were not significantly different among the coronal, middle and apical sections for each luting agent. The highest push-out bond strength was measured for CLF (14.60+/-3.63 MPa), which was not significantly different from PAN (12.57+/-2.45 MPa), but significantly higher than VAR (11.09+/-4.09 MPa), UNI (11.29+/-4.31 MPa) and EGC (7.65+/-4.79 MPa). When evaluating the sealing ability, significant differences were not found among PAN, CLF and VAR, and between UNI and EGC. The latter luting agents scored significantly lower than the former ones. The push-out bond strength was correlated to the sealing ability (p<0.001). SIGNIFICANCE: The self-etching MDP-based cements presented the highest push-out bond strength. Although the bonding effectiveness of self-adhesive cements appears promising, their interaction with root dentin might be too weak to minimize microleakage at the post-cement-dentin interface.     

An overview on immune system and migraine

The pathogenesis of migraine is still unclear, but much evidence led us hypothesize that it can be associated with immune system modification, so that a role for cytokines has been suggested. Cytokines are important mediators of the immune and inflammatory pathways and their receptors are widely express in central nervous system (CNS) by all cell types, including neurons, indicating that they can act on neuronal receptors. Cytokines are now considered to be the pain mediators in neurovascular inflammation. Furthermore cytokines may be a cause of the migraine pain: in fact an high levels of chemokines could stimulate the activation of trigeminal nerves, the release of vasoactive peptides or other biochemical mediators, such as nitric oxide, and then to cause inflammation. In this scenario, many studies on humans have focused the attention on peripheral and central levels of cytokines, but data obtained are highly controversial. Since at the moment there is not a conclusive evidence of the role played by cytokines in migraine, the authors present and comment the latest reports regarding cytokine modification and the role of the immune system in migraine.     

Linked activation of nitric oxide synthase and cyclooxygenase in peripheral monocytes of asymptomatic migraine without aura patients

Many reports indicate that nitric oxide (NO) could be involved in migraine without aura (MWA), an extremely diffuse clinical event. Since monocyte may be a relevant source of NO, we analysed monocyte activation in MWA patients, in a period in which they were free of symptoms. NO basal production by MWA peripheral monocytes was significantly higher than in healthy subjects (91.25+/-8.6 microM/10(6) cells vs. 22.6+/-3.2 microM/106 cells). Interestingly, even the release of prostaglandin E2 (PGE2), was higher in MWA patients than in healthy subjects (3137+/-320 pg/10(6) cells vs. 1531+/-220 pg/10(6) cells). The incubation of monocytes from healthy subjects and MWA patients with N-nitro-L-arginine methyl ester caused a marked decrease of both NO and PGE2 release. We hypothesise that NOS and cyclooxygenase pathways in monocytes are linked and are, in MWA patients, up-regulated, even in a symptoms-free period. NO and PGE2 hyperproduction could therefore be involved in the neurovascular modifications leading to migraine attacks.