Protective mechanisms of the body

Adolescent refugees face many challenges but also have the potential to become resilient. The purpose of this study was to identify and characterize the protective agents, resources, and mechanisms that promote their psychosocial well-being. Participants included a purposively sampled group of 73 Burundian and Liberian refugee adolescents and their families who had recently resettled in Boston and Chicago. The adolescents, families, and their service providers participated in a two-year longitudinal study using ethnographic methods and grounded theory analysis with Atlas/ti software. A grounded theory model was developed which describes those persons or entities who act to protect adolescents (Protective Agents), their capacities for doing so (Protective Resources), and how they do it (Protective Mechanisms). Protective agents are the individuals, groups, organizations, and systems that can contribute either directly or indirectly to promoting adolescent refugees' psychosocial well-being. Protective resources are the family and community capacities that can promote psychosocial well-being in adolescent refugees. Protective mechanisms are the processes fostering adolescent refugees' competencies and behaviors that can promote their psychosocial well-being. Eight family and community capacities were identified that appeared to promote psychosocial well-being in the adolescent refugees. These included 1) finances for necessities; 2) English proficiency; 3) social support networks; 4) engaged parenting; 5) family cohesion; 6) cultural adherence and guidance; 7) educational support; and 8) faith and religious involvement. Nine protective mechanisms identified were identified and grouped into three categories: 1) Relational (supporting, connecting, belonging); 2) Informational (informing, preparing), and; 3) Developmental (defending, promoting, adapting). To further promote the psychosocial well-being of adolescent refugees, targeted prevention focused policies and programs are needed to enhance the identified protective agents, resources, and mechanisms. Because resilience works through protective mechanisms, greater attention should be paid to understanding how to enhance them through new programs and practices, especially informational and developmental protective mechanisms.

Sulfate reducers have developed a multifaceted adaptative strategy to survive against oxidative stresses. Along with this oxidative stress response, we recently characterized an elegant reversible disulfide bond-dependent protective mechanism in the pyruvate:ferredoxin oxidoreductase (PFOR) of various Desulfovibrio species. Here, we searched for thiol redox systems involved in this mechanism. Using thiol fluorescent labeling, we show that glutathione is not the major thiol/disulfide balance-controlling compound in four different Desulfovibrio species and that no other plentiful low molecular weight thiol can be detected. Enzymatic analyses of two thioredoxins (Trxs) and three thioredoxin reductases allow us to propose the existence of two independent Trx systems in Desulfovibrio vulgaris Hildenborough (DvH). The TR1/Trx1 system corresponds to the typical bacterial Trx system. We measured a TR1 apparent K(m) value for Trx1 of 8.9 μM. Moreover, our results showed that activity of TR1 was NADPH-dependent. The second system named TR3/Trx3 corresponds to an unconventional Trx system as TR3 used preferentially NADH (K(m) for NADPH, 743 μM; K(m) for NADH, 5.6 μM), and Trx3 was unable to reduce insulin. The K(m) value of TR3 for Trx3 was 1.12 μM. In vitro experiments demonstrated that the TR1/Trx1 system was the only one able to reactivate the oxygen-protected form of Desulfovibrio africanus PFOR. Moreover, ex vivo pulldown assays using the mutant Trx1(C33S) as bait allowed us to capture PFOR from the DvH extract. Altogether, these data demonstrate that PFOR is a new target for Trx1, which is probably involved in the protective switch mechanism of the enzyme.

Clostridium difficile infection (CDI) represents the most prevalent cause of antibiotic-associated gastrointestinal infections in health care facilities in the developed world. Disease symptoms are caused by the two homologous exotoxins, TcdA and TcdB. Standard therapy for CDI involves administration of antibiotics that are associated with a high rate of disease recurrence, highlighting the need for novel treatment paradigms that target the toxins rather than the organism itself. A combination of human monoclonal antibodies, actoxumab and bezlotoxumab, directed against TcdA and TcdB, respectively, has been shown to decrease the rate of recurrence in patients treated with standard-of-care antibiotics. However, the exact mechanism of antibody-mediated protection is poorly understood. In this study, we show that the antitoxin antibodies are protective in multiple murine models of CDI, including systemic and local (gut) toxin challenge models, as well as primary and recurrent models of infection in mice. Systemically administered actoxumab-bezlotoxumab prevents both the damage to the gut wall and the inflammatory response, which are associated with C. difficile in these models, including in mice challenged with a strain of the hypervirulent ribotype 027. Furthermore, mutant antibodies (N297Q) that do not bind to Fcγ receptors provide a level of protection similar to that of wild-type antibodies, demonstrating that the mechanism of protection is through direct neutralization of the toxins and does not involve host effector functions. These data provide a mechanistic basis for the prevention of recurrent disease observed in CDI patients in clinical trials.

Sister chromatid cohesion, mediated by a complex called cohesin, is crucial--particularly at centromeres--for proper chromosome segregation in mitosis and meiosis. In animal mitotic cells, phosphorylation of cohesin promotes its dissociation from chromosomes, but centromeric cohesin is protected by shugoshin until kinetochores are properly captured by the spindle microtubules. However, the mechanism of shugoshin-dependent protection of cohesin is unknown. Here we find a specific subtype of serine/threonine protein phosphatase 2A (PP2A) associating with human shugoshin. PP2A colocalizes with shugoshin at centromeres and is required for centromeric protection. Purified shugoshin complex has an ability to reverse the phosphorylation of cohesin in vitro, suggesting that dephosphorylation of cohesin is the mechanism of protection at centromeres. Meiotic shugoshin of fission yeast also associates with PP2A, with both proteins collaboratively protecting Rec8-containing cohesin at centromeres. Thus, we have revealed a conserved mechanism of centromeric protection of eukaryotic chromosomes in mitosis and meiosis.

Mechanism of Protection by Diethyldithiocarbamate against Cisplatin Ototoxicity: Antioxidant System

Protective defense mechanisms are well documented across the animal kingdom, but there are still examples of antipredator defenses that do not fit easily into the current conceptualization. They either fall within the intersection of multiple mechanisms or fail to fall neatly into pre‐existing categories. Here, using Endler's predatory sequence as a framework, we identify problematic examples of antipredator defenses, separating them into protective mechanisms that are difficult to classify and those which act sequentially depending on context. We then discuss three ways of improving underlying terminological and definitional problems: (1) issues with English and polysemy, (2) overlapping aspects of similar mechanisms, and (3) unclear definitions. By scrutinizing the literature, we disentangle several opaque areas in the study of protective defense mechanisms and highlight questions that require further research. An unclear conceptual framework for protective defense mechanisms can lead to misconceptions in understanding the costs and benefits of defenses displayed by animals, while interchangeable terminologies and ambiguous definitions can hinder communication in antipredator studies.

With the fast growth of Internet and a new widespread interest in optical networks, the unparalleled potential of MultiProtocol Label Switching (MPLS) is leading to further research and development efforts. One of those areas of research is Path Protection Mechanism. It is widely accepted that layer three protection and recovery mechanisms are too slow for today's reliability requirements. Failure recovery latencies ranging from several seconds to minutes, for layer three routing protocols, have been widely reported. For this reason, a recovery mechanism at the MPLS layer capable of recovering from failed paths in 10's of milliseconds has been sought. In light of this, several MPLS based protection mechanisms have been proposed, such as end-to-end path protection and local repair mechanism. Those mechanisms are designed for intra-domain recoveries and little or no attention has been given to the case of non-homogenous independent inter-domains. This paper presents a novel solution for the setup and maintenance of independent protection mechanisms within individual domains and merged at the domain boundaries. This innovative solution offers significant advantages including fast recovery across multiple non-homogeneous domains and high scalability. Detailed setup and operation procedures are described. Finally, simulation results using OPNET are presented showing recovery times of a few milliseconds.

Oligochitosan glycosylation of casein by TGase: Protective effect and mechanism on alcohol-induced intestinal injury in C57BL/6 mice

The protective effects and mechanisms of modified Lvdou Gancao decoction on acute alcohol intoxication in mice

Background:Ambient aerosol fine particulate matter (PM2.5) is associated with male reproductive toxicity in experiments and may have adverse effects in the female. However, studies evaluating the protective effects and precise mechanisms of aspirin, Vitamin C, Vitamin E, or ozone against toxic effects of PM2.5 are sparse. This study was conducted to investigate the possible protective effects and mechanisms of aspirin, Vitamin C, Vitamin E, or ozone on fertility in female mice treated with PM2.5.Methods:Eighty-four ICR mice were divided into six groups: control group, PM2.5 group, PM2.5 + aspirin group, PM2.5 + Vitamin C group, PM2.5 + Vitamin E group, and PM2.5 + ozone group. PM2.5 was given by intratracheal instillation every 2 days for 3 weeks. Aspirin, Vitamin C, and Vitamin E were given once a day by oral gavage for 3 weeks, and ozone was administered by intraperitoneal injection once a day for 3 weeks. The levels of anti-Müllerian hormone (AMH), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and 8-hydroxy-2’-deoxyguanosine (8-OHdG) were measured using enzyme-linked immunosorbent assay. Western blotting analysis was used to analyze the expressions of Bcl-2, Bax, and caspase-3 in ovaries. Changes in histological structure were examined by light microscope and electron microscopy was used to detect ultramicrostructure.Results:The results demonstrated that PM2.5 decreased AMH levels (P < 0.001); however, aspirin (P < 0.001), Vitamin C (P < 0.001), Vitamin E (P = 0.001), and ozone (P = 0.002) alleviated the decrease. Changes of IL-6, TNF-α, 8-OHdG, Bax/Bcl-2, and caspase-3 in PM2.5 group were increased compared to control group (P < 0.001), while in PM2.5 + aspirin, PM2.5 + Vitamin C, PM2.5 + Vitamin E, and PM2.5 + ozone groups, they were statistically decreased compared to PM2.5 group (P < 0.001 or P < 0.05).Conclusions:PM2.5 cause the damage of ovaries, and aspirin, Vitamin C, Vitamin E, and ozone antagonizes the damage. The protective mechanism is probably due to its ability to blunt the inflammatory and oxidative stress caused by PM2.5, which subsequently suppressing the expression of apoptotic regulatory protein and reducing the incidence of ovary apoptosis.

The Role of Steroid Metabolism in Protective and Specificity Conferring Mechanisms of Mineralocorticoid Action

A novel coronavirus has resulted in a pandemic with over 176 million confirmed cases and over 3.8 million recorded deaths. In the USA, SARS-CoV-2 infection has a significant burden on minority communities, especially Hispanic and Black communities, which are overrepresented in cases compared to their percentage in the population. SARS-CoV-2 infection can manifest differently in children and adults, with children tending to have less severe disease. A review of current literature was performed to identify the hypothesized protective immune mechanisms in children, and to describe the rare complication of multisystem inflammatory syndrome in children (MIS-C) that has been documented in children post-SARS-CoV-2 infection. Epidemiologic data and case studies have indicated that children are less susceptible to more severe clinical features of SARS-CoV-2 infection, a finding that may be due to differences in the cytokine response generated by the innate immune system, high amounts of ACE-2 which maintain homeostatic functions by preventing inflammation, and trained immunity acquired from regular vaccinations. Despite these protective mechanisms, children are still susceptible to severe complications, such as MIS-C. The racial disparities seen in MIS-C are extremely apparent, and certain populations are more affected. Most specifically, 33% of MIS-C patients are Hispanic/Latino, and 30% Black. Current studies published on MIS-C do not detail whether certain symptoms are more present in certain racial/ethnic groups. Knowledge of these disparities could assist health care professionals with devising appropriate strategies for post-acute SARS-CoV-2 infection follow-up in children as well as vaccine distribution in specific communities to help slow the spread of SARS-CoV-2 infection, and ultimately reduce the potential for complications such as MIS-C.

Investor protection is one of the most important objectives of the securities regulation. Functional approach demonstrates that investors play different roles in the market place, and that they face different market failures with respect to each role. Therefore, sufficient protective mechanisms need to be developed to address these market failures. This paper analyzes the theoretical dimensions of investor protection and protective mechanisms, and compares investor protection mechanisms provided by United Kingdom and Turkish legislations.

Aim . To identify the relationship between various human rights protection mechanisms and their features in terms of their functioning and further development. Methodology . Great attention is paid to the peculiarities of the mechanism of human rights protection of various types, the dynamics of their development and improvement, the influence of information and telecommunication technologies on them. Results . The types of human rights protection mechanisms and their features are clearly formulated. Considering the action of human rights protection mechanisms, the authors show the tasks solved in the process of implementing such mechanisms, and indicate the priority of developing preventive human rights protection mechanisms based on information and telecommunication technologies. Research implications . The results obtained are intended to contribute to the study of human rights protection mechanisms and their types. The features of the traditional type of human rights protection mechanism and the preventive human rights protection mechanism are considered. The effectiveness of the specified human rights protection mechanisms is assessed. The need for priority development of preventive human rights protection mechanisms is substantiated, primarily due to the fact that the traditional type of human rights protection mechanism has already reached its peak and the widespread introduction of information and telecommunication technologies into state and legal practice.

Many flavonoids have cardioprotection against myocardial ischemia/reperfusion (I/R) injury. Total flavones from Rhododendron simsii Planch flower (TFR) can protect myocardial ischemic injuries. However, its protective mechanism is still unknown. The present study was designed to investigate the mechanism of TFR on myocardial I/R and anoxia/reoxygenation (A/R) injuries. Rat model of myocardial I/R injury was made, and myocardial infarction was determined. A/R injury was induced in cultured rat cardiomyocytes; cellular damage was evaluated by measuring cell viability, LDH and cTnT releases, and MDA content. Expressions of ROCK1 and ROCK2 protein were examined by Western blot analysis, and K+ currents were recorded by using whole-cell patch clamp technique. TFR 20~80 mg/kg markedly reduced I/R-induced myocardial infarction. TFR 3.7~300 mg/L significantly inhibited A/R-induced reduction of cell viability, LDH and cTnT releases, and MDA production. Exposure to A/R significantly increased ROCK1 and ROCK2 expressions in rat cardiomyocytes, but TFR 33.3~300 mg/L obviously inhibited this increase. 300 mg/L TFR significantly augmented inward rectifier K+ current and other K+ currents in rat cardiomyocytes. These results indicate that TFR has a protective effect on rat cardiomyocytes A/R damage, and the protective mechanism may be engaged with the inhibition of ROCK1 and ROCK2 and activation of K+ channels.