Atmospheric modeling and source reconstruction of radioactive ruthenium from an undeclared major release in 2017.

In October 2017 unusual 106Ru detections across most of Europe prompted the Institut de Radioprotection et de Sûreté Nucléaire (IRSN) to analyze the event in order to locate the origin and identify the magnitude of the release. This paper presents the inverse modeling techniques used during the event to achieve this goal. The method is based on a variational approach and consists of using air concentration measurements with the ldX long-range dispersion model included in the IRSN's C3X operational platform. The method made it possible to quickly identify the southern Urals as the most likely geographical origin of the release. Despite uncertainties regarding the starting date of the release, calculations show that it potentially began on 23 September, while most of the release was emitted on 26 September. Among the nuclear plants identified in the southern Urals, the Mayak complex is that from which the dispersion of the 106Ru plume is most consistent with observations. The reconstructed 106Ru source term from Mayak is ∼250 TBq. In total, it was found that for 72% of the measurements simulated and observed air concentration agreed within a factor of 5. In addition, the simulated deposition of 106Ru agrees with the observed deposition. Outside the southern Urals, the simulations indicate that areas with highest deposition values are located in southern Scandinavia and southeastern Bulgaria and are explained by rainfall events occurring while the plume was passing over.

Effect of spontaneous fermentation location on the fingerprint of volatile compound precursors of cocoa and the sensory perceptions of the end-chocolate.

Cocoa pod-opening delay and bean fermentation promote the organoleptic quality of chocolate. The present research investigated the changes in the volatile fingerprint of cocoa harvested at a traditional plantation. Cocoa beans extracted from 2-days pod-opening delay were simultaneously fermented for 5 days using container and then sun-dried to 7-8% moisture content at five different locations: Akoupé, San Pedro, Soubré, Djekanou and Daloa. The aromatic analysis were done on cocoa using the HS-SPME-GC/MS technique. Professional panelists evaluated the sensory perceptions of the chocolate. The results shows that cocoa fermented in both Daloa and Soubré regions were differentiated by 2,3-butanediol while those processed in other regions presented highest acetoin content. However, fermented cocoa from Soubré region exhibited most amount of 2,3-butanediol, diacetate A whereas 2,3,5,6-tetramethylpyrazine differentiated those from Daloa region. Sensory properties of chocolate were not linked to the aromatic compound precursors profile of beans. The fermentation performed in San Pédro region promote both the generation of more desirable aromatic compounds of cocoa and sensory attributes of the finished chocolate. The fermentation location generates a greater differentiation of the volatile fingerprint of cocoa and the sensory perceptions of the finished chocolate.

Rasch analysis of the Forgotten Joint Score in patients undergoing knee arthroplasty.

PURPOSE: The purpose of this study was to test the hypothesis that the "Forgotten Joint Score" (FJS-12) is a unidimensional interval-level scale. Unidimensionality refers to measuring a single attribute, i.e., the single ability to forget the arthroplasty. If this property is not verified, the interpretation of the score can be confusing. Unidimensionality is an essential prerequisite of construct validity and required if FJS-12 response data are to be validly summated into a single score. Interval-level dimension is an essential prerequisite of the parametric statistics. Rasch analysis was used to test our study hypothesis. METHODS: The FJS-12 questionnaire was validated in 248 unilateral knee arthroplasty patients. Successive analyses were used to select items with good psychometric qualities to constitute the new "FJS". The external validity was assessed with the KUJALA questionnaire. RESULTS: Quantity of relevant items was greater than 50%. Of the 12 original items, nine showed disturbed thresholds, indicating that patients were unable to discriminate among the five levels for these items. The data set was reanalyzed using a four-level scale. The new analysis indicated that the internal consistency was good (r = 0.84). Three items did not fit with the model and they were removed. The nine items of the final scale defined a unidimensional and linear measure of the forgotten joint, and showed a continuous progression in their difficulty. The perception of difficulty was group-independent. The correlation coefficient was moderate between FJS and KUJALA score (r = 0.4). CONCLUSIONS: This new and items reduced FJS can be used in clinical practice with good psychometric qualities. It provides a reliable tool to follow up patient's evolution and document changes related to knee arthroplasty. This valid FJS is needed in evaluating patients' assessment, one indicator of quality of care. LEVEL OF EVIDENCE: III-Therapeutic.

Control of allergen-induced inflammation and hyperresponsiveness by the metalloproteinase ADAMTS-12.

A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) constitute a family of endopeptidases related to matrix metalloproteinases. These proteinases have been largely implicated in tissue remodeling associated with pathological processes. Among them, ADAMTS12 was identified as an asthma-associated gene in a human genome screening program. However, its functional implication in asthma is not yet documented. The present study aims at investigating potential ADAMTS-12 functions in experimental models of allergic airways disease. Two different in vivo protocols of allergen-induced airways disease were applied to the recently generated Adamts12-deficient mice and corresponding wild-type mice. In this study, we provide evidence for a protective effect of ADAMTS-12 against bronchial inflammation and hyperresponsiveness. In the absence of Adamts12, challenge with different allergens (OVA and house dust mite) led to exacerbated eosinophilic inflammation in the bronchoalveolar lavage fluid and in lung tissue, along with airway dysfunction assessed by increased airway responsiveness following methacholine exposure. Furthermore, mast cell counts and ST2 receptor and IL-33 levels were higher in the lungs of allergen-challenged Adamts12-deficient mice. The present study provides, to our knowledge, the first experimental evidence for a contribution of ADAMTS-12 as a key mediator in airways disease, interfering with immunological processes leading to inflammation and airway hyperresponsiveness.

New eastern Pacific Ocean records of Hydrolagus melanophasma, with annotations of a juvenile female.

Two new records of Hydrolagus melanophasma, one juvenile female from off the central Mexican coast and one adult male from off the coast of Ecuador, confirm the presence of this species throughout its known range in the eastern Pacific Ocean, from southern California, U.S.A., to Valdivia, Chile. This report gives a description and comparison of proportional measurements, head shape and colouration for juvenile and adult H. melanophasma. A taxonomic key to distinguish the eastern Pacific Ocean species of Hydrolagus is included.

First identification of the SARS-COV-2/XBB.1.5 sublineage among indigenous COVID-19 cases through the influenza sentinel surveillance system in Niger.

The emergence of the Omicron variant in November 2021, has caused panic worldwide due to the rapid evolution and the ability of the virus to escape the immune system. Since, several Omicron sublineages (BA.1 to BA.5) and their descendent recombinant lineages have been circulating worldwide. Furthermore, in December 2022, a new Omicron subvariant XBB.1.5 characterized by an unusual mutation in the spike protein evolved in the United States and rapidly spread to the other continents. Our study reports on the first cases of XBB.1.5 sublineage among indigenous Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-COV-2) positive cases detected through the influenza sentinel surveillance system in Niger. All influenza suspected cases were tested for both influenza and SARS-COV-2 using the Centre for Disease Control and prevention (CDC) Influenza SARS-COV-2 Multiplex quantitative Reverse-Transcription Polymerase Chain Reaction (qRT-PCR) Assay. SARS-COV-2 positive samples with cycle threshold ≤28 were selected for whole genome sequencing subsequently using the Oxford Nanopore Midnight protocol with rapid barcoding on a MinIon MK1B device. A total of 51 SARS-COV-2 positive samples were confirmed between December 2022 and March 2023. We successfully obtained 19 sequences with a predominance of the XBB.1/XBB.1.5 sublineages (73.7 %). In addition, a recombinant XBD sequence was also first-ever identified in early March 2023. Our findings support the need to strengthen the influenza sentinel surveillance for routine Coronavirus Disease 2019 (COVID-19) surveillance and SARS-COV-2 variants monitoring in Niger.

Nebulized anti-IL-13 monoclonal antibody Fab' fragment reduces allergen-induced asthma.

IL-13 is a prototypic T helper type 2 cytokine and a central mediator of the complex cascade of events leading to asthmatic phenotype. Indeed, IL-13 plays key roles in IgE synthesis, bronchial hyperresponsiveness, mucus hypersecretion, subepithelial fibrosis, and eosinophil infiltration. We assessed the potential efficacy of inhaled anti-IL-13 monoclonal antibody Fab' fragment on allergen-induced airway inflammation, hyperresponsiveness, and remodeling in an experimental model of allergic asthma. Anti-IL-13 Fab' was administered to mice as a liquid aerosol generated by inExpose inhalation system in a tower allowing a nose-only exposure. BALB/c mice were treated by PBS, anti-IL-13 Fab', or A33 Fab' fragment and subjected to ovalbumin exposure for 1 and 5 weeks (short-term and long-term protocols). Our data demonstrate a significant antiasthma effect after nebulization of anti-IL-13 Fab' in a model of asthma driven by allergen exposure as compared with saline and nonimmune Fab fragments. In short- and long-term protocols, administration of the anti-IL-13 Fab' by inhalation significantly decreased bronchial responsiveness to methacholine, bronchoalveolar lavage fluid eosinophilia, inflammatory cell infiltration in lung tissue, and many features of airway remodeling. Levels of proinflammatory mediators and matrix metalloprotease were significantly lower in lung parenchyma of mice treated with anti-IL-13 Fab'. These data demonstrate that an inhaled anti-IL-13 Fab' significantly reduces airway inflammation, hyperresponsiveness, and remodeling. Specific neutralization of IL-13 in the lungs using an inhaled anti-IL-13 Fab' could represent a novel and effective therapy for the treatment of asthma.

ADAM-8, a metalloproteinase, drives acute allergen-induced airway inflammation.

Asthma is a complex disease linked to various pathophysiological events including the activity of proteinases. The multifunctional A disintegrin and metalloproteinases (ADAMs) displaying the ability to cleave membrane-bound mediators or cytokines appear to be key mediators in various inflammatory processes. In the present study, we investigated ADAM-8 expression and production in a mouse model of allergen-induced airway inflammation. In allergen-exposed animals, increased expression of ADAM-8 was found in the lung parenchyma and in DC purified from the lungs. The potential role of ADAM-8 in the development of allergen-induced airway inflammation was further investigated by the use of an anti-ADAM-8 antibody and ADAM-8 knockout animals. We observed a decrease in allergen-induced acute inflammation both in BALF and the peribronchial area in anti-ADAM-8 antibody-treated mice and in ADAM-8-deficient mice (ADAM-8(-/-) ) after allergen exposure. ADAM-8 depletion led to a significant decrease of the CD11c(+) lung DC. We also report lower levels of CCL11 and CCL22 production in antibody-treated mice and ADAM-8- deficient mice that might be explained by decreased eosinophilic inflammation and lower numbers of DC, respectively. In conclusion, ADAM-8 appears to favour allergen-induced acute airway inflammation by promoting DC recruitment and CCL11 and CCL22 production.

Tracking of airborne radionuclides from the damaged Fukushima Dai-ichi nuclear reactors by European networks.

Radioactive emissions into the atmosphere from the damaged reactors of the Fukushima Dai-ichi nuclear power plant (NPP) started on March 12th, 2011. Among the various radionuclides released, iodine-131 ((131)I) and cesium isotopes ((137)Cs and (134)Cs) were transported across the Pacific toward the North American continent and reached Europe despite dispersion and washout along the route of the contaminated air masses. In Europe, the first signs of the releases were detected 7 days later while the first peak of activity level was observed between March 28th and March 30th. Time variations over a 20-day period and spatial variations across more than 150 sampling locations in Europe made it possible to characterize the contaminated air masses. After the Chernobyl accident, only a few measurements of the gaseous (131)I fraction were conducted compared to the number of measurements for the particulate fraction. Several studies had already pointed out the importance of the gaseous (131)I and the large underestimation of the total (131)I airborne activity level, and subsequent calculations of inhalation dose, if neglected. The measurements made across Europe following the releases from the Fukushima NPP reactors have provided a significant amount of new data on the ratio of the gaseous (131)I fraction to total (131)I, both on a spatial scale and its temporal variation. It can be pointed out that during the Fukushima event, the (134)Cs to (137)Cs ratio proved to be different from that observed after the Chernobyl accident. The data set provided in this paper is the most comprehensive survey of the main relevant airborne radionuclides from the Fukushima reactors, measured across Europe. A rough estimate of the total (131)I inventory that has passed over Europe during this period was <1% of the released amount. According to the measurements, airborne activity levels remain of no concern for public health in Europe.

Matrix metalloproteinase-19 deficiency promotes tenascin-C accumulation and allergen-induced airway inflammation.

Matrix metalloproteinases (MMPs) recently appeared as key regulators of inflammation, allowing the recruitment and clearance of inflammatory cells and modifying the biological activity of many peptide mediators by cleavage. MMP-19 is newly described, and it preferentially cleaves matrix proteins such as collagens and tenascin-C. The role of MMP-19 in asthma has not been described to date. The present study sought to assess the expression of MMP-19 in a murine asthma model, and to address the biological effects of MMP-19 deficiency in mice. Allergen-exposed, wild-type mice displayed increased expression of MMP-19 mRNA and an increased number of MMP-19-positive cells in the lungs, as detected by immunohistochemistry. After an allergen challenge of MMP-19 knockout (MMP-19(-/-)) mice, exacerbated eosinophilic inflammation was detected in bronchoalveolar lavage fluid and bronchial tissue, along with increased airway responsiveness to methacholine. A shift toward increased T helper-2 lymphocyte (Th2)-driven inflammation in MMP-19(-/-) mice was demonstrated by (1) increased numbers of cells expressing the IL-33 receptor T(1)/ST(2) in lung parenchyma, (2) increased IgG(1) levels in serum, and (3) higher levels of IL-13 and eotaxin-1 in lung extracts. Tenascin-C was found to accumulate in peribronchial areas of MMP-19(-/-) after allergen challenges, as assessed by Western blot and immunohistochemistry analyses. We conclude that MMP-19 is a new mediator in asthma, preventing tenascin-C accumulation and directly or indirectly controlling Th2-driven airway eosinophilia and airway hyperreactivity. Our data suggest that MMP-19 may act on Th2 inflammation homeostasis by preventing the accumulation of tenascin protein.

A unique sequence of the NZW I-E beta chain and its possible contribution to autoimmunity in the (NZB x NZW)F1 mouse.

The (NZB x NZW)F1 mouse strain develops a syndrome of accelerated autoimmunity including severe renal disease and early death. Evidence suggests that class II molecules play a central role in this process. Previous studies have suggested that the NZW strain contributes at least one gene to the development of accelerated autoimmunity that is linked to the H-2 complex, and antibodies to murine class II molecules have been used to ameliorate disease in (NZB x NZW)F1 mice. We therefore wished to sequence the class II molecules from NZW mice to identify any unique sequences that may contribute to disease development. We constructed oligonucleotide primers corresponding to the 5' and 3' regions of the second exon of class II genes from a variety of haplotypes, and used these primers in a polymerase chain reaction to sequence the second exon of the NZW I-A alpha, I-A beta, and I-E beta genes. We report that the second exons of NZW I-A alpha, I-A beta, and I-E alpha are identical to their counterparts of the previously sequenced u haplotype, and that the second exon of NZW I-E beta is identical to its counterpart from u except for a single base change that results in a substitution of arginine for threonine at amino acid 72. This base and amino acid are identical to those found at the same positions in the s haplotype.

The role of imaging and molecular imaging in the early detection of metabolic and cardiovascular dysfunctions.

Despite intense effort, obesity is still rising throughout the world. Links between obesity and cardiovascular diseases are now well established. Most of the cardiovascular changes related to obesity can be followed by magnetic resonance imaging (MRI) or by magnetic resonance spectroscopy (MRS). In particular, we will see in this review that MRI/MRS is extremely well suited to depict (1) changes in cardiac mass and function, (2) changes in stroke volume, (3) accumulation of fat inside the mediastinum or even inside the cardiomyocytes, (4) cell viability and (5) molecular changes during early cardiovascular diseases.

Mouse models to unravel the role of inhaled pollutants on allergic sensitization and airway inflammation.

Air pollutant exposure has been linked to a rise in wheezing illnesses. Clinical data highlight that exposure to mainstream tobacco smoke (MS) and environmental tobacco smoke (ETS) as well as exposure to diesel exhaust particles (DEP) could promote allergic sensitization or aggravate symptoms of asthma, suggesting a role for these inhaled pollutants in the pathogenesis of asthma. Mouse models are a valuable tool to study the potential effects of these pollutants in the pathogenesis of asthma, with the opportunity to investigate their impact during processes leading to sensitization, acute inflammation and chronic disease. Mice allow us to perform mechanistic studies and to evaluate the importance of specific cell types in asthma pathogenesis. In this review, the major clinical effects of tobacco smoke and diesel exhaust exposure regarding to asthma development and progression are described. Clinical data are compared with findings from murine models of asthma and inhalable pollutant exposure. Moreover, the potential mechanisms by which both pollutants could aggravate asthma are discussed.

Respiratory distress after surgery of RVOT pathologies: a word of caution on pseudoaneurysm development.

Pseudoaneurysm of the right ventricle outflow tract (RVOT) is a rare complication in pediatric cardiac surgery. We report a patient who developed a right ventricular pseudoaneurysm 8 months after RVOT enlargement using a pericardial patch for infundibular pulmonary stenosis. Our patient was born with severe pulmonary valvular stenosis and treated with percutaneous balloon valvotomy in the neonatal period. Six months later, she developed infundibular pulmonary stenosis, which required surgical resection of right ventricle infundibular trabeculations and bovine pericardial patch enlargement. The postoperative period was normal. She was readmitted to hospital 5 months later complaining of wheezing, coughing and shortness of breath. Echocardiography showed a huge aneurysmal dilatation of the outflow patch in connection with the right ventricular cavity. The patient underwent resection of the pseudoaneurysm and former patch, followed by interposition of a bovine jugular vein conduit between the RVOT and pulmonary bifurcation. The early postoperative period was uncomplicated. On echocardiography, no significant residual gradient was measured through the conduit and there was no insufficiency of the valve. RVOT reconstruction with patch enlargement, homograft or conduit implantation can be the origin of pseudoaneurysms. Although their incidence is rare, they are often asymptomatic before becoming quite large and causing compression symptoms as in our patient with respiratory complaints due to airway compression. It is important to follow up these patients closely, especially in the first year after surgery since most aneurysms develop within 6 months of surgery.

Disability and functioning in primary and secondary hip osteoarthritis in Benin.

BACKGROUND: In Africa, primary hip osteoarthritis seems to be less frequent than in Europe. Sickle cell disease is responsible for aseptic osteonecrosis of the femoral head associated with secondary hip osteoarthritis. Very little evidence is available on the influence of aetiology (primary and secondary) and radiographic status on pain and disability in a Beninese population with hip osteoarthritis. OBJECTIVES: The aim of this study was to compare the impacts of aetiology and radiographic status on pain, disability and quality of life in a Beninese population with hip osteoarthritis. METHOD: This was a descriptive cross-sectional study, including participants recruited in the Clinic of Physical Medicine and Rehabilitation at the National Teaching Hospital in Cotonou.Assessment was based on the International Classification of Functioning, Disability and Health model. The main outcomes were severity of osteoarthritis, pain, range of motion, muscle strength, gait speed and quality of life. Statistical comparisons between the aetiologies were performed using a t-test or rank sum test. One-way analysis of variance was used to test the effect of radiographic status. RESULTS: Forty-nine participants (26 women and 23 men; mean age [standard deviation] 40.5 [17.9] years) were recruited. According to the aetiology (59.2% and 40.8% of primary and secondary osteoarthritis, respectively), there were no significant differences for any of the outcomes. Grades I, II, III and IV osteoarthritis were observed in 22.4%, 14.3%, 26.5% and 36.7% of the participants, respectively. Participants with grade IV osteoarthritis were more affected than those with grades I, II and III based on the Kellgren and Lawrence classification. CONCLUSION: Aetiology did not influence pain, gait speed or quality of life. Participants with grade IV osteoarthritis had more pain, were more limited in walking and had a more impaired quality of life.

Role of ADAM and ADAMTS metalloproteinases in airway diseases.

Lungs are exposed to the outside environment and therefore to toxic and infectious agents or allergens. This may lead to permanent activation of innate immune response elements. A Disintegrin And Metalloproteinases (ADAMs) and ADAMs with Thrombospondin motifs (ADAMTS) are proteinases closely related to Matrix Metalloproteinases (MMPs). These multifaceted molecules bear metalloproteinase and disintegrin domains endowing them with features of both proteinases and adhesion molecules. Proteinases of the ADAM family are associated to various physiological and pathological processes and display a wide spectrum of biological effects encompassing cell fusion, cell adhesion, "shedding process", cleavage of various substrates from the extracellular matrix, growth factors or cytokines... This review will focus on the putative roles of ADAM/ADAMTS proteinases in airway diseases such as asthma and COPD.

Comparison of acute inflammatory and chronic structural asthma-like responses between C57BL/6 and BALB/c mice.

BACKGROUND: The interactions between airway responsiveness, structural remodelling and inflammation in allergic asthma remain poorly understood. Prolonged challenge with inhaled allergen is necessary to replicate many of the features of airway wall remodelling in mice. In both mice and humans, genetic differences can have a profound influence on allergy, inflammation, airway responsiveness and structural changes. METHODS: The aim of this study was to provide a comparative analysis of allergen-induced airway changes in sensitized BALB/c and C57BL/6 mice that were exposed to inhaled allergen for 2 ('acute'), 6 or 9 weeks ('chronic'). Inflammation, remodelling and responsiveness were analyzed. RESULTS: Both strains developed a Th-2-driven airway inflammation with allergen-specific IgE, airway eosinophilia and goblet cell hyperplasia upon 2 weeks of allergen inhalation. This was accompanied by a significant increase in airway smooth muscle mass and hyperresponsiveness in BALB/c but not in C57BL/6 mice. However, airway eosinophilia was more pronounced in the C57BL/6 strain. Chronic allergen exposure (6 or 9 weeks) resulted in an increase in airway smooth muscle mass as well as subepithelial collagen and fibronectin deposition in both strains. The emergence of these structural changes paralleled the disappearance of inflammation in both C57BL/6 and BALB/c mice and loss of hyperresponsiveness in the BALB/c strain. TGF-beta(1 )was accordingly elevated in both strains. CONCLUSION: Airway inflammation, remodelling and hyperresponsiveness are closely intertwined processes. Genetic background influences several aspects of the acute allergic phenotype. Chronic allergen exposure induces a marked airway remodelling that parallels a decreased inflammation, which was largely comparable between the two strains.

Mouse models of asthma: a comparison between C57BL/6 and BALB/c strains regarding bronchial responsiveness, inflammation, and cytokine production.

OBJECTIVE: Animal models of asthma mimic major features of human disease. Since the genetic background of experimental animals might affect hyperresponsiveness and inflammation, we studied its potential influence and the mechanisms leading to differences in strains. METHODS: We applied a mouse model of allergic asthma to BALB/c and C57BL/6 mice. RESULTS: BALB/c mice displayed greater levels of airway reactivity to methacholine than C57BL/6 mice. Moreover, BALB/c mice exhibited higher numbers of mast cells in lung tissue when compared to C57BL/6. On the contrary, eosinophil and neutrophil counts in bronchoalveolar lavage fluid (BALF) as well as peribronchial eosinophilia were greater in C57BL/6. IL (Interleukin)-4, IL-5, IL-13, and CCL11 levels measured in whole-lung extracts were higher in BALB/c, while, in sharp contrast, CCL11 and CCL5 levels were higher in BALF of C57BL/6 mice. CONCLUSIONS: We observed phenotypic differences between C57BL/6 and BALB/c mice in an asthma model with different distributions of pro-inflammatory cytokines and inflammatory cells.

Characterization of a local renin-angiotensin system in rat gingival tissue.

BACKGROUND: The systemic renin-angiotensin system (RAS) promotes the plasmatic production of angiotensin (Ang) II, which acts through interaction with specific receptors. There is growing evidence that local systems in various tissues and organs are capable of generating angiotensins independently of circulating RAS. The aims of this study were to investigate the expression and localization of RAS components in rat gingival tissue and evaluate the in vitro production of Ang II and other peptides catalyzed by rat gingival tissue homogenates incubated with different Ang II precursors. METHODS: Reverse transcription-polymerase chain reaction assessed mRNA expression. Immunohistochemical analysis aimed to detect and localize renin. A standardized fluorimetric method with tripeptide hippuryl-histidyl-leucine was used to measure tissue angiotensin-converting enzyme (ACE) activity, whereas high performance liquid chromatography showed products formed after the incubation of tissue homogenates with Ang I or tetradecapeptide renin substrate (TDP). RESULTS: mRNA for renin, angiotensinogen, ACE, and Ang II receptors (AT(1a), AT(1b), and AT(2)) was detected in gingival tissue; cultured gingival fibroblasts expressed renin, angiotensinogen, and AT(1a) receptor. Renin was present in the vascular endothelium and was intensely expressed in the epithelial basal layer of periodontally affected gingival tissue. ACE activity was detected (4.95 +/- 0.89 nmol histidyl-leucine/g/minute). When Ang I was used as substrate, Ang 1-9 (0.576 +/- 0.128 nmol/mg/minute), Ang II (0.066 +/- 0.008 nmol/mg/minute), and Ang 1-7 (0.111 +/- 0.017 nmol/mg/minute) were formed, whereas these same peptides (0.139 +/- 0.031, 0.206 +/- 0.046, and 0.039 +/- 0.007 nmol/mg/minute, respectively) and Ang I (0.973 +/- 0.139 nmol/mg/minute) were formed when TDP was the substrate. CONCLUSION: Local RAS exists in rat gingival tissue and is capable of generating Ang II and other vasoactive peptides in vitro.