A mathematical model of anaerobic digestion with syntrophic relationship, substrate inhibition and distinct removal rates

In this work, we consider a mathematical model of syntrophic relationship between two microbial species of the anaerobic digestion process including mortality (or decay) terms. We focus on the acetogenesis and hydrogenotrophic methanogenesis phases. Our study gives a quite comprehensive analysis of a syntrophic model by analyzing the joined effects of syntrophy relationship, mortality, substrate inhibition and input concentrations that were neglected in previous studies. Using a general class of growth rates, the necessary and sufficient conditions of existence and local stability of all steady states of the four-dimensional system are determined according to the operating parameters. This general model exhibits a rich behavior with the coexistence of two microbial species, the bi-stability, the multiplicity of coexistence steady states, and the existence of two steady states of extinction of the first species. The operating diagram shows how the model behaves by varying the control parameters and illustrates the effect of the inhibition and the new input substrate concentration (hydrogen) on the reduction of the coexistence region and the emergence of a bi-stability region. Similarly to the classical chemostat model, including the substrate inhibition can destabilize a two-tiered microbial 'food chain' where the stability depends on the initial condition

Modèles mathématiques de digestion anaérobie: effet de l’hydrolyse sur la production du biogaz

International audienceWe investigate, in this work, the effects of hydrolysis on the behavior of the anaero- bic digestion process and the production of biogas (namely, the methane and the hydrogen). Two modelisations of the hydrolysis process are involved. We consider, first, that the microbial enzymatic activity is constant, then we take into consideration an explicit hydrolytic microbial compartiment for the substrate biodegradation. The considered models include the inhibition of acetoclastic and hy- drogenotrophic methanogens. To examine the effects of these inhibitions in presence of a hydrolysis step, we first study an inhibition-free model. We determine the steady states and give sufficient and necessary conditions for their stability. The existence and stability of the steady states are illustrated by operating diagrams. We prove that modelling the hydrolysis phase by a constant enzymatic activity affects the production of methane and hydrogen. Furthermore, introducing the hydrolytic microbial compartment makes appear new steady states and affects the stability regions. We prove that the biogas production occurs at only one of the steady states according to the operating parameters and state variables and we determine the maximal rate of biogas produced, in each case.Nous analysons, dans ce travail, l’effet de l’hydrolyse sur le comportement du processus de la digestion anaérobie et sur la production du biogas (méthane et hydrogène). Nous considé- rons deux modélisations possibles de l’hydrolyse. Nous supposons, dans un premier temps, que l’hydrolyse se fait d’une manière purement enzymatique puis nous faisons intervenir un compar- timent microbien hydrolytique dans le modèle. Les modèles considérés font intervenir l’inhibition de la croissance des bactéries acétogènes (respectivement méthanogènes hydrogénétrophes) par l’hydrogène (respectivement, par l’acétate). Pour analyser l’effet de ces inhibitions, en présence de l’étape d’hydrolyse, nous faisons, dans un premier temps, l’étude d’un modèle sans inhibition. Nous déterminons les équilibres des modèles étudiés et nous donnons des conditions nécessaires et suffi- santes pour leur stabilité. Les régions d’existence et de stabilité des équilibres sont illustrées par des diagrammes opératoires. Nous montrons que la modélisation de la phase d’hydrolyse par une activité enzymatique constante affecte la production du méthane et de l’hydrogène. En outre, l’introduction du compartiment microbien hydrolytique fait apparaître de nouveaux équilibres et affecte les régions de stabilité. Nous prouvons que la production de biogaz se produit en un seul équilibre, selon les paramètres opératoires et les variables d’état et nous déterminons le taux maximal de biogaz produit

Splenogonadal Fusion Discovered by Testicular Torsion

Splenogonadal fusion, which is adherence of splenic tissue to gonads, is an uncommon congenital anomaly which mainly affects males. Herein, we report a case of splenogonadal fusion in a 20-month-old boy presenting with acute scrotal pain and inflammation. With the suspicion of left testicular torsion, an emergent left scrotal exploration was carried out. It revealed a necrotic left testicle along with a 360° rotation of the spermatic cord and three accessory structures in the lower pole of the testicle. Histology showed the presence of a splenic tissue. Splenogonadal fusion can present as an acute condition mimicking a testicular torsion. But, one should always bear in mind the possibility of this association. Splenogonadal fusion should be included in differential diagnosis of testicular mass to avoid unnecessary orchidectomy

Duchenne Muscular Dystrophy (DMD) Diagnosis: Past and Present Perspectives

Duchenne muscular dystrophy (DMD) is a fatal X-linked disorder, characterized by progressive skeletal muscle wasting. The disease is caused by various types of mutations in the dystrophin gene (DMD). The disease occurs at a frequency of about 1 in 5000 male births, making it the most common severe neuro-muscular disease. In addition to clinical examinations of muscle strength and function, diagnosis of DMD usually involves a combination of immunological assays using muscle biopsies, typically immunohistochemistry and western blotting, and molecular techniques such as DMD gene sequencing or Multiplex Ligation Dependent Probe Amplification (MLPA) using blood samples. In fact, precise molecular diagnosis is a prerequisite for determining the appropriate personalized therapeutic approach such as exon-skipping, gene therapy or stem cell-based therapies in conjunction with gene editing techniques like CRISPR-Cas9. However, the quest for reliable biomarkers with high sensitivity and specificity for DMD from liquid biopsy is still a hotspot of research, as such non-invasive biomarker(s) would not only facilitate disease diagnosis but would also help in carrier detection, which will eventually result in better disease management. In this chapter, we will illustrate the detailed current and prospect strategies for disease

Small bowel perforation secondary to accidental magnetic objects ingestion: (Two pediatric cases report)

Foreign bodies ingestion is considered as a common pediatric problem, it is mostly encountred in infants between 6months and 2 years. Ingestion of magnets was documented in only few reports. We report two uncommon cases of bowel perforations owing to magnets ingestion. Patients were respectively aged of 10 months and 20 months .they were successfully managed. Once ingested, magnetic objects would attach each other through intestinal wall leading subsequently to intestinal necrosis. Thus their surgical removal is unavoidable.

Case presentation: villous tumor of rectum in a child

Introduction: The rectum villous tumour is an uncommon pathology in paediatrics, it represents 1% of all the children’s malignant tumours.Case Presentation: An eleven-year-old girl presented a rectal adenocarcinoma arising from a villous tumour. The aim of this study is to overview of the literature, asses the frequency of rectum villous tumours, specify the value of the clinical examination, of the radiologic findings in the assessment of the loco-regional extension of villous tumours and rectum adenocarcinoma and finally to discuss the treatment modalities.Conclusion: The rectum villous tumour symptomatology in children is not very specific. Therefore, a good knowledge of its clinical presentation and the predisposing pathological situations can improve the prognosis of this rare disease

Duchenne Muscular Dystrophy (DMD) Treatment: Past and Present Perspectives

Duchenne muscular dystrophy (DMD) is one of the fatal X-linked disorders that are characterized by progressive muscle weakness and occur due to mutation in the largest human gene known as the DMD gene which encodes dystrophin protein that is mandatory for keeping the muscles structurally and functionally intact. The disease always affects boys (1 from every ~5000), and in some cases the female carriers are symptomatic. The disease usually leads to impairment in cardiac and pulmonary functions leading to the death of the patients in very young ages. Understanding DMD through precise molecular diagnosis will aid in determining the suitable therapeutic approach for the cases like designing exon-skipping antisense oligonucleotides (AOs) or stem cell-based therapies in conjunction with gene editing techniques (CRISPR/Cas9). Such therapies can correct the genetic defect in the DMD gene and ameliorate the symptoms. In this chapter, we will illustrate the past and current strategies for DMD disease treatment

Multi-ancestry genome-wide association analyses improve resolution of genes and pathways influencing lung function and chronic obstructive pulmonary disease risk

Lung-function impairment underlies chronic obstructive pulmonary disease (COPD) and predicts mortality. In the largest multi-ancestry genome-wide association meta-analysis of lung function to date, comprising 580,869 participants, we identified 1,020 independent association signals implicating 559 genes supported by ≥2 criteria from a systematic variant-to-gene mapping framework. These genes were enriched in 29 pathways. Individual variants showed heterogeneity across ancestries, age and smoking groups, and collectively as a genetic risk score showed strong association with COPD across ancestry groups. We undertook phenome-wide association studies for selected associated variants as well as trait and pathway-specific genetic risk scores to infer possible consequences of intervening in pathways underlying lung function. We highlight new putative causal variants, genes, proteins and pathways, including those targeted by existing drugs. These findings bring us closer to understanding the mechanisms underlying lung function and COPD, and should inform functional genomics experiments and potentially future COPD therapies