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The results of coal sink and float tests are plotted as washability curves. Analysis of these curves indicates the most effective method by which the coal can be cleaned. Sink and float experiments are sampling-dependent, destructive, and use toxic chemicals. The present research introduces an alternative method based on a 3D imaging system called RhoVol, in which the density of individual particles is determined from mass and volume measurements. A quantitative error analysis was conducted on coal sample density measurements obtained by RhoVol, and the main factors influencing the errors identified and investigated. The results show that the drawback of this technique is related to its not being able to detect hidden concavities in the particle, resulting in an overestimation of particle volume. Furthermore, it is difficult to capture the impact of porosity and cracks on the volume of coal particles obtained from 3D silhouette images. This mismatch between the RhoVol data and sink and float test results has led to attempts to apply neural network (NN) and linear regression techniques to produce a fully reliable model for correction and estimation of coal density. The NN approach offers superior predictive capability over linear regression, and the estimated density distribution is in line with the sink and float analysis. The root mean square error in estimation of density using the NN model was less than 0.05 g/cm3.

Lombard, Natasha, Le Roux, M. Marianne (2023): Thesium hispidifructum (Santalaceae), a New Hispidulous Species from Limpopo, South Africa and Notes on Enigmatic T. celatum. Taxonomy (Clifton, N.J.) 3 (1): 95-108, DOI: 10.3390/taxonomy3010009, URL: http://dx.doi.org/10.3390/taxonomy3010009

Thesium hispidifructum N.Lombard & M.M.le Roux, sp. nov. (Figure 5) Type: SOUTH AFRICA. Limpopo Province: Lebowa, Blouberg, Farm Beauly 260 LR, 12 February 1991, L. Smook 7447 (holotype PRE 0775984). Diagnosis: Thesium hispidifructum is morphologically similar to T. disparile in its hairy indumentum, ascending to spreading leaves (4–15 mm long in T. hispidifructum; 7–11 mm long in T. disparile), flowers placed in determinate racemose cymes and flower lobes (0.8–1.2 mm long in T. hispidifructum; ± 0.7–1.2 mm long in T. disparile) bearded at the inner apex. Thesium hispidifructum is easily distinguished from T. disparile by its tall robust stature (woody stems up to 1 m tall), intricate branching pattern and compact inflorescences with flowers solitary in the bract axils. Comparatively, T. disparile has a short slender stature (herbaceous stems up to 0.15(0.5?) m tall), virgate branching pattern and lax inflorescences with single flowers usually replaced by compound monochasial or dichasial cymes. Description: Shrub or subshrub, up to 1 m tall, rootstock not known; stems erect, up to 4 mm in diameter, intricately branched above, hispidulous to hispid. Leaves spreading to ascending, sparse below and densely arranged above, often imbricate, linear, 4–15 × 0.3–1.0 mm, hispidulous to hispid. Flowers solitary in bract axils, arranged in 5–10-flowered determinate raceme-like inflorescences; pedicels 0–1.3 mm long. Bracts and bracteoles usually three, leaf-like but smaller, 2–7 mm long, not forming an involucre, bracts fused to at least half of pedicel. Perianth ±campanulate, 2.6–2.7 mm long, elongate receptacle often present, “glands” often visible on outside, exterior hispidulous to hispid; hypanthium 0.3–0.6 mm long; corolla lobes triangular, 0.8–1.2 mm long, apex very slightly cucullate, with dense apical beard of long hairs. Stamens inserted at base of corolla lobes; anthers ± 0.3 mm long. Style 0.2–0.4 mm long, stigma below or reaching the bottom of anthers. Placental column straight; ovules 3. Fruit ± globose, 3.6–4.1 × 1.8–2.3 mm including stipe and persistent perianth, stipe ± 0.4 mm long, persistent perianth 0.9–1.3 mm long, longitudinally and reticulately veined when dry, hispid. Distribution and habitat: Thesium hispidifructum is endemic to the Limpopo Province in South Africa, where it is known from only four gatherings between Blouberg and Mount Letsjume in the westernmost reaches of the Soutpansberg (Figure 6). Little is known about its habitat. It has been collected among grass in rocky areas as well as in wet wooded areas, on both south facing and northeast facing slopes at elevations between 1675 and 1980 m a.s.l. It is likely restricted to the Soutpansberg Mountain Bushveld [21] and Soutpansberg Summit Sourveld [21], but field studies are needed to confirm this. Phenology: Thesium hispidifructum has been collected in flower and fruit in January, February, June, and July. Etymology: The specific epithet hispidifructum refers to the hispidulous fruit of the species. Conservation status: Thesium hispidifructum has an extent of occurrence (EOO) of 44 km 2 and an area of occurrence (AOO) of 12 km 2. It is known from only four gatherings at two to three locations in mountainous areas (Blouberg and Mount Letsjume), surrounded by much-transformed low-lying areas (Vivo and surrounds). As the most recent collection/observation of this species was in 1991, the state of these subpopulations is unknown, and needs to be verified during field studies. It is likely that the extensive human settlements and crop development in low-lying areas surroundings these mountains have already resulted in the loss of suitable habitat. Furthermore, expanding anthropogenic influences may easily push this very restricted species to extinction. It therefore qualifies for a threat status of Vulnerable (VU) under Criterion D2 [20]. Additional specimens examined: SOUTH AFRICA. Limpopo: Blauwberg, 10 May 1933, A. C. Leeman 110 (PRE 0374089); Blauwberg, near trig. beacon, 12 January 1955, L. E. Codd and R. A. Dyer 9063 (PRE 0374090); Zoutpansberg, Mt Letsjume, at foot, on S slope, 25 July 1981, F. Venter (PRE 0620517) ., Published as part of Lombard, Natasha & Le Roux, M. Marianne, 2023, Thesium hispidifructum (Santalaceae), a New Hispidulous Species from Limpopo, South Africa and Notes on Enigmatic T. celatum, pp. 95-108 in Taxonomy (Clifton, N. J.) (Clifton, N. J.) 3 (1) on pages 103-105, DOI: 10.3390/taxonomy3010009, http://zenodo.org/record/7981347, {"references":["21. Mucina, L.; Rutherford, M. The Vegetation of South Africa, Lesotho and Swaziland; Strelitzia 19; South African National Biodiversity Institute: Pretoria, South Africa, 2006","20. IUCN Standards and Petitions Subcommittee. Guidelines for Using the IUCN Red List Categories and Criteria. Version 13; IUCN: Gland, Switzerland, 2017."]}

La Broncho-Pneumopathie Chronique Obstructive (BPCO) est une cause majeure de mortalité et de morbidité. Selon l'OMS, la BPCO est la troisième cause de décès dans le monde. Caractérisée par une limitation progressive et irréversible du débit d'air, le principalfacteur de risque de développer une BPCO est le tabagisme. L'exposition chronique à lafumée de cigarette (Cigarette Smoke (CS)) déclenche des processus inflammatoires qui finissent par altérer la fonction respiratoire et les mécanismes de défense immunitaire de cette muqueuse, entraînant une susceptibilité accrue aux infections respiratoires. Ces exacerbations de la BPCO peuvent aussi bien être déclenchées par des champignons, des bactéries ou encore des virus.[1].L’IL-22 joue un rôle important dans les mécanismes de défense contre les pathogènes, notamment en intervenant comme un élément protecteur de l'épithélium [2–4]. Alors que l'IL-22 agit via un récepteur spécifique dépendant de la sous-unité IL-10Rb, l’IL-19, l’IL-20 et l’IL-24 se lient au récepteur IL-20 de type I (IL-20R), un récepteur hétérodimérique composé de l'IL-20Ra et de l’IL-20Rb. L'IL-20 et l'IL-24 se lient également au récepteur de type II composé de la sous-unité α1 du récepteur IL-22 et de l'IL-20Rb [5]. Ces différents récepteurs sont fortement exprimés au niveau pulmonaire, notamment sur les cellules épithéliales des voies aériennes (AEC) [6]. Le blocage de la sous-unité IL-20Rb peutneutraliser efficacement la réponse aux cytokines IL-20 (IL-19, IL-20 et IL-24) [6] et limiter les infections bactériennes cutanées et pulmonaires [6,7].Étant donné que l’expression des cytokines IL-20 est associée au développement de la BPCO [8] et de l'infection virale [9,10], notre objectif était d’évaluer leur rôle physiopathologique lors de l'exacerbation virale de la BPCO et des surinfections bactériennes. Pour cela, nous avons utilisé le modèle murin mimant la BPCO après l’exposition chronique à la fumée de cigarette et le rôle des cytokines IL-20 a été évalué lors de l’infection par des virus respiratoires grâce à l’utilisation de souris IL-20Rb KO et le traitement par un anticorps bloquant l’IL-20Rb. Pour se rapprocher de la clinique, un modèle de surinfection post-grippale par Streptococcus pneumoniae a aussi été utilisé.Ainsi, nos données révèlent que l’exposition à la fumée de cigarette et l’infection virale ont un effet additif sur l’expression des cytokines IL-20. La déficience en IL-20Rb, au cours de l’exacerbation viro-induite de souris BPCO, facilite la préservation de l’intégrité de la barrière épithéliale pulmonaire notamment via le maintien de l’expression de la protéine de jonction E-cadhérine. Dans le contexte de la surinfection bactérienne, les cytokines IL-20ne semblent pas avoir un effet majeur sur le contrôle de l’infection virale ou bactérienne mais elles participent également dans le développement des lésions épithéliales. L’ensemble des données, acquises au cours de cette thèse, a permis de mettre au jour le rôle délétère des cytokines IL-20 au cours de la physiopathologie de l’exacerbation virale de la BPCO ;désignant ainsi le récepteur aux cytokines IL-20 (IL-20Rb) comme cible thérapeutique potentielle dans le traitement des exacerbations virales de la BPCO. Chronic Obstructive Pulmonary Disease (COPD) is a major cause of mortality andmorbidity worldwide. According to the WHO, COPD is the third leading cause of death in theworld. Characterized by a progressive and irreversible limitation of air flow, the main riskfactor for developing COPD is smoking. Chronic exposure to cigarette smoke (CigaretteSmoke (CS)) triggers inflammatory processes that eventually alter the functions of thepulmonary epithelial barrier and reduce immune defense mechanisms, resulting in increasedsusceptibility to respiratory infections. These exacerbations of COPD can also be triggered byfungi, bacteria or viruses [1].IL-22 plays an important role in antimicrobial mechanisms, in particular by itprotective role on epithelium [2]-[4]. IL-22 along with IL-19, IL-20 and IL-24 belong to the IL-20 cytokine subfamily. While IL-22 acts through a specific receptor dependent on the IL-10Rbsubunit, IL-19, IL-20 and IL-24 bind to the type I receptor (IL-20R), a heterodimeric receptorcomposed by IL-20Ra and IL-20Rb. IL-20 and IL-24 also bind to the type II receptor composedby the α1 subunit of the IL-22 receptor and IL-20Rb [5]. Interestingly, these receptors arehighly expressed in airway epithelial cells (AECs) [6]. Blockade of the IL-20Rb subunit caneffectively neutralize the response to IL-20 cytokines (IL-19, IL-20 and IL-24) [6] and limitbacterial infections of the skin and lungs [6], [7].Since the expression of IL-20 cytokines is associated with the development of COPD[8] and viral infection [9], [10], the objective of my thesis work was to evaluate thepathophysiologic role of IL-20 cytokines during viral exacerbations of COPD. For this, micewere chronically exposed to cigarette smoke in order to mimic COPD and then infected withrespiratory viruses. The role of IL-20 cytokines was evaluated using IL-20Rb KO mice ortreatment with a blocking anti-IL-20Rb antibody during viral infection or a post-flu bacterialinfection.Thus, our data demonstrate that cigarette smoke exposure and viral infection havean additive effect on IL-20 cytokine expression. Interestingly, the IL-20Rb deficiency duringvirus-induced exacerbation of COPD mice, facilitates the preservation of the integrity of thepulmonary epithelial barrier, especially via the maintenance of the expression of the E-cadherin junction protein. During post-flu bacterial superinfection, these cytokines are notessential for the control of viral or bacterial replication although they are involved in thedevelopment of epithelial lesions in this context.All of the data acquired during this thesis helped to shed light on the deleterious roleof IL-20 cytokines in the pathophysiology of viral exacerbation of COPD; thus, designating thecytokine receptor IL-20 (IL-20Rb) as a potential therapeutic target during viral infections andtheir bacterial surinfections in the context of COPD.