Biomechanics of the tympanic membrane

The tympanic membrane is a key component of the human auditory apparatus which is a complex biomechanical system, devoted to sound reception and perception. Over the past 30 years, various bioengineering approaches have been applied to the ear modeling and particularly to the middle part. The tympanic membrane, included in the middle ear, transfers sound waves into mechanical vibration from the ear canal into the middle ear. Changes in structure and mechanical properties of the tympanic membrane due to middle ear diseases or damages can deteriorate sound transmission. An accurate model of the tympanic membrane, which simulates the acoustic-mechanical transmission, could improve clinical surgical intervention. In this paper a detailed survey of the biomechanics and the modeling of the tympanic membrane focusing on the finite element method is conduced. Eight selected models are evaluated and compared deducing the main features and most design parameters from published models, mainly focusing on geometric, constraint and material aspects. Non-specified parameters are replaced with the most commonly employed values. Our simulation results (in terms of modal frequencies and umbo displacement), compared with published numerical and experimental results, show a good agreement even if some scattering appears to indicate the need of further investigation and experimental validation.     

Channel Formation by Yeast F-ATP Synthase and the Role of Dimerization in the Mitochondrial Permeability Transition

Purified F-ATP synthase dimers of yeast mitochondria display Ca²⁺-dependent channel activity with properties resembling those of the permeability transition pore (PTP) of mammals. After treatment with the Ca²⁺ ionophore ETH129, which allows electrophoretic Ca²⁺ uptake, isolated yeast mitochondria undergo inner membrane permeabilization due to PTP opening. Yeast mutant strains ΔTIM11 and ΔATP20 (lacking the e and g F-ATP synthase subunits, respectively, which are necessary for dimer formation) display a striking resistance to PTP opening. These results show that the yeast PTP originates from F-ATP synthase and indicate that dimerization is required for pore formation in situ.     

Adaptation of middle aged rats to long-term restriction of dietary vitamin D and calcium

Previous studies have shown that middle aged rats do not increase renal 1,25-dihydroxyvitamin D3(1,25(OH)2D3) production in response to short-term (4 weeks) dietary vitamin D and calcium restriction. The purpose of the experiments reported here was to determine if middle aged rats demonstrate adaptation to long-term restriction of dietary calcium and vitamin D and to compare that adaptation to the adaptation seen in young rats. Middle aged (14-16 months) Fischer 344 rats were fed either a 0.02% calcium, vitamin D-deficient (restricted) or a 1.2% calcium, vitamin D-replete (control) diet. Rats from each group were sacrificed after 1.5, 3.0, 4.5, and 6.0 months on the diets. Renal conversion of 25(OH)D3 to 1,25(OH)2D3 and 24,25(OH)2D3 was measured in vitro using isolated renal cortical slices. Renal 1,25(OH)2D3 production in the restricted group was not significantly increased until 3 months and reached a maximum of 85% higher than the control at 4.5 months. Renal 24,25(OH)2D3 production was significantly decreased after only 1.5 months of restriction and was decreased maximally by 70% at 3.0 months. Serum calcium remained in the range 11-12 mg/100 ml in both diet groups, and serum immunoreactive PTH (iPTH) was modestly increased one- to twofold in the restricted group compared to the control group. In contrast, young rats (3 months old) fed the deficient diet for 1 month had a fourfold increase in renal 1,25(OH)2D3 production and a 71% decrease in 24,25(OH)2D3 production. Feeding the deficient diet also produced a 43% reduction in serum calcium and a 13-fold increase in serum iPTH. These findings demonstrate that middle aged rats do alter their 25(OH)D metabolism in response to long-term vitamin D and calcium restriction. However, both the rapidity and the magnitude of the response is decreased compared to that seen in the young rat. This blunted vitamin D response in the middle aged rat reflects the lack of a decrease in serum calcium and the marginal increase in serum iPTH in response to vitamin D and calcium restriction.     

The membrane-recruitment-and-recycling hypothesis of gastric HCl secretion

In the unstimulated oxyntic (or parietal) cell, the primary pump for gastric HCl secretion, the H+/K+-ATPase, is retained within the cytoplasm in a membranous compartment of tubulovesicles. Neural or hormonal stimulation of acid secretion induces extensive membrane transformations consistent with a fusion and recruitment of tubulovesicles to the apical plasma membrane. The consequent placement of H+/K+-ATPase in parallel with K(+) and Cl(-) channels provides the necessary ionic flow and ATP-driven exchange for net HCl secretion. Current evidence is consistent with a recruitment and recycling of membrane transporters, such as H+/K+-ATPase, through docking/fusion machinery analogous to that in many other systems.     

Focus: Microbiome: Gut Microbiome and Infant Health: Brain-Gut-Microbiota Axis and Host Genetic Factors

The development of the neonatal gut microbiome is influenced by multiple factors, such as delivery mode, feeding, medication use, hospital environment, early life stress, and genetics. The dysbiosis of gut microbiota persists during infancy, especially in high-risk preterm infants who experience lengthy stays in the Neonatal intensive care unit (NICU). Infant microbiome evolutionary trajectory is essentially parallel with the host (infant) neurodevelopmental process and growth. The role of the gut microbiome, the brain-gut signaling system, and its interaction with the host genetics have been shown to be related to both short and long term infant health and bio-behavioral development. The investigation of potential dysbiosis patterns in early childhood is still lacking and few studies have addressed this host-microbiome co-developmental process. Further research spanning a variety of fields of study is needed to focus on the mechanisms of brain-gut-microbiota signaling system and the dynamic host-microbial interaction in the regulation of health, stress and development in human newborns.     

Radiocarbon-Based Assessment of Heterotrophic Soil Respiration in Two Mediterranean Forests

The amount of soil organic carbon (SOC) released into the atmosphere as carbon dioxide (CO₂), which is referred to as heterotrophic respiration (Rh), is technically difficult to measure despite its necessity to the understanding of how to protect and increase soil carbon stocks. Within this context, the aim of this study is to determine Rh in two Mediterranean forests dominated by pine and oak using radiocarbon measurements of the bulk SOC from different soil layers. The annual Rh was 3.22 Mg C ha^?1 y^?1 under pine and 3.13 Mg C ha^?1 y^?1 under oak, corresponding to 38 and 31% of the annual soil respiration, respectively. The accuracy of the Rh values was evaluated by determining the net primary production (NPP), as the sum of the Rh and the net ecosystem production measured by eddy covariance, then comparing it with the NPP obtained through independent biometric measurements. No significant differences were observed, which suggested the suitability of our methodology to infer Rh. Assuming the C inputs to soil to consist exclusively of the aboveground and belowground litter and the C output exclusively of the Rh, both soils were C sinks, which is consistent with a previous modeling study that was performed in the same stands. In conclusion, radiocarbon analysis of bulk SOC provided a reliable estimate of the average annual amount of soil carbon released to the atmosphere; hence, its application is convenient for calculating Rh because it utilizes only a single soil sampling and no time-consuming monitoring activities.     

The major human rhinovirus receptor is ICAM-1

The major human rhinovirus receptor has been identified with monoclonal antibodies that inhibit rhinovirus infection. These monoclonal antibodies recognize a 95 kd cell surface glycoprotein on human cells and on mouse transfectants expressing a rhinovirus binding phenotype. Purified 95 kd protein binds to rhinovirus in vitro. Protein sequence from the 95 kd protein showed an identity with that of intercellular adhesion molecule-1 (ICAM-1); a cDNA clone obtained from mouse transfectants expressing the rhinovirus receptor had essentially the same sequence as ICAM-1. Thus, the major human rhinovirus receptor is ICAM-1. The gene for this receptor maps to human chromosome 19, which also contains the genes for a number of other picornavirus receptors.