The issue of bone volume loss is playing an increasing role in bone tissue engineering. Research has focused on studying the preparation and use of different types of human or xenogenic materials and their osteogenic properties. An alternative source for this purpose could be autologous extracted teeth. The simple preparation protocol, minimal immune response, and rapid organizing of the newly formed bone with optimal mechanical properties predispose autologous hard teeth tissues (HTTs) as a promising material suitable in the indication of augmentation of maxillary and mandible defects, comparable to other high-end augmentation materials. The aim of this study was to experimentally evaluate the osteogenic potential of ground native autologous HTTs prepared by different demineralization procedures, aimed at potentiating the osteoinductive and osteoconductive properties of their organic components. The results indicate that the most effective preparation process for HTT stimulation is the application of Cleanser for 10 min followed by exposure to 0.6 N HCl for 5 min with a wash in phosphate-buffered saline solution.
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Hepatocellular carcinoma (HCC) is the second-largest cause of death among all cancer types. Many drugs have been used to treat the disease for a long time but have been mostly discontinued because of their side effects or the development of resistance in the patients with HCC. The administration of DZ orally is a great focus to address the clinical crisis. Daidzein (DZ) is a prominent isoflavone polyphenolic chemical found in soybeans and other leguminous plants. It has various pharmacological effects, including anti-inflammatory, antihemolytic, and antioxidant. This present study investigates the protective effect of DZ on chemically induced HCC in rat models. The DZ was administered orally four weeks before HCC induction and continued during treatment. Our study included four treatment groups: control (group 1, without any treatment), HCC-induced rats (group II), an HCC group treated with DZ at 20 mg/kg (group III), and an HCC group treated with DZ at 40 mg/kg (group IV). HCC rats showed elevation in all the HCC markers (AFP, GPC3, and VEGF), liver function markers (ALP, ALT, and AST), inflammatory markers (IL-6, TNF-α, and CRP), and lipid markers concomitant with a decrease in antioxidant enzymes and protein. However, groups III and IV demonstrated dose-dependent alleviation in the previous parameters resulting from HCC. In addition, the high dose of DZ reduces many hepatological changes in HCC rats. All study parameters improved with DZ administration. Due to its antioxidant and anti-inflammatory characteristics, DZ is a promising HCC treatment option for clinical use.
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Engagement of PRRs in recognition of PAMPs or DAMPs is one of the processes that initiates cellular stress. These sensors are involved in signaling pathways leading to induction of innate immune processes. Signaling initiated by PRRs is associated with the activation of MyD88-dependent signaling pathways and myddosome formation. MyD88 downstream signaling depends upon the context of signaling initiation, the cell (sub)type and the microenvironment of signal initiation. Recognition of PAMPs or DAMPs through PRRs activates the cellular autonomous defence mechanism, which orchestrates the cell responses to resolve specific insults at the single cell level. In general, stressed endoplasmic reticulum is directly linked with the induction of autophagy and initiation of mitochondrial stress. These processes are regulated by the release of Ca2+ from ER stores accepted by mitochondria, which respond through membrane depolarization and the production of reactive oxygen species generating signals leading to inflammasome activation. In parallel, signaling from PRRs initiates the accumulation of misfolded or inappropriately post-translationally modified proteins in the ER and triggers a group of conserved emergency rescue pathways known as unfolded protein response. The cell-autonomous effector mechanisms have evolutionarily ancient roots and were gradually specialized for the defence of specific cell (sub)types. All of these processes are common to the innate immune recognition of microbial pathogens and tumorigenesis as well. PRRs are active in both cases. Downstream are activated signaling pathways initiated by myddosomes, translated by the cellular autonomous defence mechanism, and finalized by inflammasomes.
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Morphine plays a critical regulatory role in both simple and complex plant species. Dopamine is a critical chemical intermediate in the morphine biosynthetic pathway and may have served as a primordial agonist in developing catecholamine signaling pathways. While dopamine remains the preeminent catecholamine in invertebrate neural systems, epinephrine is the major product of catecholamine synthetic pathways in vertebrate species. Given that the enzymatic steps leading to the generation of morphine are similar to those constraining the evolutionary adaptation of the biosynthesis of catecholamines, we hypothesize that the emergence of these more advanced signaling pathways was based on conservation and selective "retrofitting" of pre-existing enzyme activities. This is consistent with observations that support the recruitment of enzymatically synthesized tetrahydrobiopterin (BH4), which is a cofactor for tyrosine hydroxylase, the enzyme responsible for dopamine production. BH4 is also an electron donor involved in the production of nitric oxide (NO). The links that coordinate BH4-mediated NO and catecholaminergic-mediated processes provide these systems with the capacity to regulate numerous downstream signaling pathways. We hypothesize that the evolution of catecholamine signaling pathways in animal species depends on the acquisition of a mobile lifestyle and motivationally driven feeding, sexual, and self-protective responses.
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- přehledy MeSH
The purpose of this study was to investigate the relationship between adolescents' biological maturation level and their muscle power, as well as their overall muscle strength. Overall, 691 adolescents (414 boys and 277 girls) aged 12.01-11.96 (measured for body mass, body height as well as vertical jump, muscle power, and muscle strength). There was a statistically significant difference in terms of average right and left grip strength, vertical jump, and power in the late maturation group. For the body height and vertical jump averages in male adolescents, it was observed that the body height and vertical jump averages in the late group were significantly lower than in the early and on-time maturation groups. For female adolescents' chronological age, sitting height, body mass, BMI, left and right grip strength, and power averages were found to be significantly higher compared with the on-time group (p < 0.05). It was established that biological maturation has a substantial link with vertical jump height and power, as well as grip strength on the right and left hands.
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It was recently shown that coffee polyphenolic extract exerts preventive effects on central neuropathic pain development, but it is unknown whether its beneficial effects are associated with only one of its major polyphenolic compounds or if the whole extract is needed to exert such effects. The main objective of this study was to determine whether the separate administration of major polyphenols from coffee extract exerts preventive effects on the development of central neuropathic pain in mice compared with the effects of the whole coffee extract. Thus, spinal-cord-injured female ICR-CD1 mice were daily treated with either coffee extract or its major polyphenolic compounds during the first week, and reflexive and nonreflexive pain responses were evaluated within the acute phase of spinal cord injury. In addition, the injury-induced gliosis and dorsal horn sprouting were evaluated with immunohistochemistry. The results showed that the coffee extract prevented spinal cord injury-induced neuropathic pain, whereas its major polyphenolic compounds resulted in reflexive pain response attenuation. Both preventive and attenuation effects were associated with gliosis and afferent fiber sprouting modulation. Overall, the results suggested that coffee extract effects may be associated with potential synergistic mechanisms exerted by its major polyphenolic compounds and not by the sole effect of only one of them.
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The aim of this study was to determine the effect of low and moderate doses of caffeine ingestion via caffeinated coffee on repeated sprint test (RST) and plasma catecholamine concentration in trained female team-sport athletes. In a randomized, double-blind, crossover design, 13 female team-sport athletes (VO2max: 48.7 ± 4 mL·kg·min-1) completed three RST trials, separated by 4-day, 60 min post-ingestion of either 3 mg·kg-1 (LCOF) or 6 mg·kg-1 (MCOF) or placebo (PLA). The RST consisted of 12 × 4 s sprints on a cycle ergometer interspersed with 20 s of active recovery. Blood lactate (BLa) and glucose (GLU) and epinephrine and norepinephrine concentrations were collected before and 60 min after coffee ingestion, and after RST. Heart rate (HR) and ratings of perceived exertion (RPE) were measured at the beginning of RST, and after the 6th and 12th sprints. Average peak power score during RST was significantly improved after LCOF (p = 0.016) and MCOF (p = 0.041) compared to PLA, but peak and mean power output of the individual sprints, and fatigue index were not different between trials (all p > 0.05). Epinephrine and norepinephrine concentrations were significantly higher before and after RST in LCOF and MCOF compared to PLA (all p < 0.05). BLa was also higher after RST in both LCOF and MCOF compared to PLA (p = 0.005). HR, RPE, and GLU were not different between conditions (p > 0.05). In conclusion, low and moderate dose of caffeine ingestion can enhance the average peak power score during repeated sprints. These findings partly support low and moderate doses of caffeine supplementation via coffee as a nutritional ergogenic aid for trained female team-sport players during repeated sprint exercise.
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Although preliminary studies suggested sex-related differences in physiological responses to hypoxia, the effects of sex on sprint interval training (SIT) performance in different degrees of hypoxia are largely lacking. The aim of this study was to examine the acute effect of different doses of normobaric hypoxia on SIT performance as well as heart rate variability (HRV) and cognitive performance (CP) in amateur-trained team sport players by comparing potential sex differences. In a randomized, double-blind, crossover design, 26 (13 females) amateur team-sport (football, basketball, handball, rugby) players completed acute SIT (6 × 15 s all-out sprints, separated with 2 min active recovery, against a load equivalent to 9% of body weight) on a cycle ergometer, in one of four conditions: (I) normoxia without a mask (FiO2: 20.9%) (CON); (II) normoxia with a mask (FiO2: 20.9%) (NOR); (III) moderate hypoxia (FiO2: 15.4%) with mask (MHYP); and (IV) high hypoxia (FiO2: 13.4%) with mask (HHYP). Peak (PPO) and mean power output (MPO), HRV, heart rate (HR), CP, capillary lactate (BLa), and ratings of perceived exertion (RPE) pre- and post-SIT were compared between CON, NOR, MHYP and HHYP. There were no significant differences found between trials for PPO (p = 0.55), MPO (p = 0.44), RPE (p = 0.39), HR (p = 0.49), HRV (p > 0.05) and CP (response accuracy: p = 0.92; reaction time: p = 0.24). The changes in MP, PP, RPE, HR, CP and HRV were similar between men and women (all p > 0.05). While BLa was similar (p = 0.10) between MHYP and HHYP trials, it was greater compared to CON (p = 0.01) and NOR (p = 0.01), without a sex-effect. In conclusion, compared to normoxia, hypoxia, and wearing a mask, have no effect on SIT acute responses (other than lactate), including PP, MP, RPE, CP, HR, and cardiac autonomic modulation either in men or women.
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Note: The authors apologize for the rather extensive text corrections [...].
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We investigated the effects of PPARα activators fenofibrate and WY-14643 as well as the PPARα inhibitor GW6471 on the PI3K/Akt/PTEN pathway of intestinal cell differentiation. Our previous study showed that all these compounds increased the expression of villin, a specific marker of intestinal cell differentiation in HT-29 and Caco2 cells. Our current results confirmed the central role of lipid messenger phosphatidylinositol-4,5-bisphosphate (PIP2), a known player in brush border formation, in mediating the effects of tested PPARα ligands. Although all tested compounds increased its levels, surprisingly, each of them affected different PIP2-metabolizing enzymes, especially the levels of PIP5K1C and PTEN. Moreover, we found a positive relationship between the expression of PPARα itself and PIP2 as well as PIP5K1C. By contrast, PPARα was negatively correlated with PTEN. However, the expression of antigens of interest was independent of PPARα subcellular localization, suggesting that it is not directly involved in their regulation. In colorectal carcinoma tissues we found a decrease in PTEN expression, which was accompanied by a change in its subcellular localization. This change was also observed for the regulatory subunit of PI3K. Taken together, our data revealed that fenofibrate, WY-14643, and GW6471 affected different members of the PI3K/Akt/PTEN pathway. However, these effects were PPARα-independent.
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