Beyond Digestion: Can Animals Shape the Landscape According to Their Species–Specific Salivary Secretions?

Several functions are acknowledged for saliva secretion in different animal species following prehension and mastication of feed. Most of such are linked to the specific role of lubrication and softening of the bolus to allow taste perception and easy swallowing. Moreover, enzymatic components are produced in the saliva, some of which are destined to contribute to the digestion of different nutrients (to various extents according to animal species) and to exert antimicrobial activity (lysozyme). In addition, the buffering power and the virtuous recycle of water, electrolytes, and other metabolites are of particular importance for proper digestion and for nutrition–related aspects. Moreover, salivation appears to be involved in a number of other functions. Recent studies on salivary production and roles point to salivary glands as target organs of neuroendocrine regulation in response to many external stimuli coming from the outer world, for which feed still represents the chief external stimulus. Various animal species establish an adaptive strategy when coming into contact with different feeding stuffs and/or dietary substances by modifying both the composition and amount of saliva produced. In the light of recent updates, this review provides a focus on the functional roles of saliva secretions, showing the broad involvement of salivary response in several mechanisms beyond the digestive function and influencing feed selection.

Skeletal Muscle Histidine Containing Dipeptide Contents are Increased in Freshwater Turtles (Chrysemys picta bellii) with Cold-Acclimation

Freshwater turtles found in higher latitudes can experience extreme challenges to acid-base homeostasis while overwintering, due to a combination of cold temperatures along with the potential for environmental hypoxia. Histidine containing dipeptides (HCDs; carnosine, anserine and balenine) may facilitate pH regulation in response to these challenges, through their role as pH buffers. We measured the HCDs content of three tissues (liver, cardiac muscle and skeletal muscle) from the anoxia-tolerant painted turtle (Chrysemys picta bellii) acclimated to either 3 or 20 C. HCDs were detected in all tissues, with the highest content shown in the skeletal muscle. Turtles acclimated to 3 C had more HCD in their skeletal muscle than those acclimated to 20 C (carnosine = 20.8 +/- 4.5 vs 12.5 +/- 5.9 mmol/kg DM; ES = 1.59 (95%CI: 0.16 - 3.00), P = 0.013). The higher HCD content observed in the skeletal muscle of the cold-acclimated turtles suggests a role in acid-base regulation in response to physiological challenges associated with living in the cold, with the increase possibly related to the temperature sensitivity of carnosine's dissociation constant and buffering power of the skeletal muscle during anoxic submergence.

Buffering Power of Spirituality against Death Anxiety

Spirituality, being a virtuous approach against dark materialistic world has an ability to transcend any phase of life. As a matter of fact during old age the fear of death generally overpowers elderly. They overcome this anxiety successfully by moving and focusing towards spirituality, which is considered a path leading to piousness and inner peace. Experience of spirituality helps them to think beyond this materialistic world, where old age is not considered as an end to life, but a preparation for the welcome of a new life. Thus with these ideas in mind, the present study was an attempt to explore the relation between spirituality and death anxiety among geriatrics. A purposive sample of 200 elderly both male and female with the age range of 60-80 years was drawn from Rohtak city, Haryana. The descriptive statistics indicated the high level of spirituality and average level of death anxiety among elderly. Further, correlational analysis showed that there existed a negative correlation between spirituality and death anxiety which indicates the healing power of spirituality among elderly.

Fluid transport by the cornea endothelium is dependent on buffering lactic acid efflux

Maintenance of corneal hydration is dependent on the active transport properties of the corneal endothelium. We tested the hypothesis that lactic acid efflux, facilitated by buffering, is a component of the endothelial fluid pump. Rabbit corneas were perfused with bicarbonate-rich (BR) or bicarbonate-free (BF) Ringer of varying buffering power, while corneal thickness was measured. Perfusate was collected and analyzed for lactate efflux. In BF with no added HEPES, the maximal corneal swelling rate was 30.0 ± 4.1 μm/h compared with 5.2 ± 0.9 μm/h in BR. Corneal swelling decreased directly with [HEPES], such that with 60 mM HEPES corneas swelled at 7.5 ± 1.6 μm/h. Perfusate [lactate] increased directly with [HEPES]. Similarly, reducing the [HCO3−] increased corneal swelling and decreased lactate efflux. Corneal swelling was inversely related to Ringer buffering power (β), whereas lactate efflux was directly related to β. Ouabain (100 μM) produced maximal swelling and reduction in lactate efflux, whereas carbonic anhydrase inhibition and an monocarboxylic acid transporter 1 inhibitor produced intermediate swelling and decreases in lactate efflux. Conversely, 10 μM adenosine reduced the swelling rate to 4.2 ± 0.8 μm/h and increased lactate efflux by 25%. We found a strong inverse relation between corneal swelling and lactate efflux ( r = 0.98, P < 0.0001). Introducing lactate in the Ringer transiently increased corneal thickness, reaching a steady state (0 ± 0.6 μm/h) within 90 min. We conclude that corneal endothelial function does not have an absolute requirement for bicarbonate; rather it requires a perfusing solution with high buffering power. This facilitates lactic acid efflux, which is directly linked to water efflux, indicating that lactate flux is a component of the corneal endothelial pump.

Leaky ryanodine receptors delay the activation of store overload-induced Ca2+ release, a mechanism underlying malignant hyperthermia-like events in dystrophic muscle

The mouse model of Duchenne muscular dystrophy, the mdx mouse, displays changes in Ca2+ homeostasis that may lead to the pathology of the muscle. Here we examine the activation of store overload-induced Ca2+ release (SOICR) in mdx muscle. The activation of SOICR is associated with the depolymerization of the sarcoplasmic reticulum (SR) Ca2+ buffer calsequestrin and the reduction of SR Ca2+ buffering power (BSR). The role of SOICR in healthy and dystrophic muscle is unclear. Using skinned fibers we show that lowering the Mg2+ concentration can activate discrete Ca2+ release events that did not necessarily lead to activation of SOICR. However, SOICR waves could propagate into these fiber segments. The average delay to activation of SOICR in mdx fibers was longer than in wild-type (WT) fibers. In the lowered Ca2+-buffered environment following large SOICR events, brief waves in mdx fibers displayed a low amplitude and propagation rate, in contrast to WT fibers that showed a range of amplitudes correlated with wave propagation rate. The distinct properties of SOICR in mdx fibers were consistent with a ryanodine receptor (RyR) that was leakier to Ca2+ than in WT. The consequence of delayed SOICR and leaky RyRs is prolonged high BSR and a reduction in free Ca2+ concentration inside the SR as total SR calcium drops. We present a hypothesis that SOICR activation is required in healthy muscle and that this mechanism works suboptimally in mdx fibers to fail to limit the activation of store-operated Ca2+ entry.

Recharging Red Blood Cell Surface by Hemodialysis

Background: Similar as in vascular endothelium the negatively charged glycocalyx of erythrocytes selectively buffers sodium. Loss of glycocalyx (i.e. loss of negative charges) leads to increased erythrocyte sodium sensitivity (ESS) quantified by a recently developed salt-blood-test (SBT). The hypothesis was tested whether a regular 4-hour hemodialysis (4h-HD) alters ESS. Methods: In 38 patients with end stage renal disease (ESRD) ESS was measured before and after 4h-HD, together with standard laboratory and clinical parameters (electrolytes, acid-base status, urea, creatinine, hemoglobin, c-reactive protein and blood pressure). Results: Before 4h-HD, 20 patients (out of 38) were classified as “salt sensitive” by SBT. After 4h-HD, this number decreased to 11. Erythrocyte sodium buffering power remained virtually constant in patients with already low ESS before dialysis, whereas in patients with high ESS, 4h-HD improved the initially poor sodium buffering power by about 20%. No significant correlations could be detected between standard blood parameters and the respective ESS values except for plasma sodium concentration which was found increased by 3.1 mM in patients with high salt sensitivity. Conclusions: 4h-HD apparently recharges “run-down” erythrocytes and thus restores erythrocyte sodium buffering capacity. Besides the advantage of efficient sodium buffering in blood, erythrocytes with sufficient amounts of free negative charges at the erythrocyte surface will cause less (mechanical) injury to the negatively charged endothelial surface due to efficient repulsive forces between blood and vessel wall. Hemodialysis improves erythrocyte surface properties and thus may prevent early vascular damage in patients suffering from ESRD.

Contrasting phagosome pH regulation and maturation in human M1 and M2 macrophages

Macrophages respond to changes in environmental stimuli by assuming distinct functional phenotypes, a phenomenon referred to as macrophage polarization. We generated classically (M1) and alternatively (M2) polarized macrophages—two extremes of the polarization spectrum—to compare the properties of their phagosomes. Specifically, we analyzed the regulation of the luminal pH after particle engulfment. The phagosomes of M1 macrophages had a similar buffering power and proton (equivalent) leakage permeability but significantly reduced proton-pumping activity compared with M2 phagosomes. As a result, only the latter underwent a rapid and profound acidification. By contrast, M1 phagosomes displayed alkaline pH oscillations, which were caused by proton consumption upon dismutation of superoxide, followed by activation of a voltage- and Zn2+-sensitive permeation pathway, likely HV1 channels. The paucity of V-ATPases in M1 phagosomes was associated with, and likely caused by, delayed fusion with late endosomes and lysosomes. The delayed kinetics of maturation was, in turn, promoted by the failure of M1 phagosomes to acidify. Thus, in M1 cells, elimination of pathogens through deployment of the microbicidal NADPH oxidase is given priority at the expense of delayed acidification. By contrast, M2 phagosomes proceed to acidify immediately in order to clear apoptotic bodies rapidly and effectively.