1,533,350 research outputs found
Metabolic Responses on Transport Stress and the Effect on Meat Characteristics (a Review)
Transportasi memainkan peran penting dalam USAha peternakan dan hasil-hasil ternak dengan mendistribusikannya fari produsen ke konsumen. Akan tetapi, transportasi dari peternakan ke tempat pemotongan hewan merupakan titik riskan yang berpengaruh terhadap sifat-sifat daging yang disebabkan oleh stres transportasi. Glikogen dan glukosa pada ternak stres lebih dipacu oleh epineprin dan norepineprin. Proses glikogenolisis dan glikolisis dapat terjadi secara aerobik atau anaerobik. Jika proses anaerobik lebih dominan maka produksi asam laktat sangat tinggi dan menghasilkan daging PSE. Jika ternak mampu mempertahakan status fisiologi dalam kesetimbangan dengan menghabiskan glikogen otot dan ini menyebabkan daging DFD. Baik PSE maupun DFD merupakan daging yang berkualitas rendah, konskuensinya, produk olahan yang berasal dari keduanya juga memiliki sifat dan daya terima yang rendah. Untuk menghindari kasus-kasus tersebut maka perlu penanganan sebelum penyembelihan, yaitu dengan cara pengistirahatan yang cukup, pemberian elektrolit dan larutan gula dan lain-lain
Prolonged elevations in haemostatic and rheological responses following psychological stress in low socioeconomic status men and women
Low socioeconomic status (SES) and psychological stress are associated with increased risk of coronary heart disease, and both may influence haemostatic responses. Von Willebrand factor (vWF), Factor VIII, plasma viscosity, haematocrit, blood viscosity, tissue plasminogen activator (t-PA) and fibrin D- dimer were measured at rest and following stressful tasks in 238 middle-aged British civil servants. SES was defined by grade of employment. Lower SES was associated with higher resting vWF, Factor VIII and plasma viscosity. Psychological stress stimulated increases in haemostatic and rheological factors. Initial stress responses did not vary with SES, but Factor VIII, plasma viscosity and blood viscosity remained more elevated 45 minutes post-stress in lower SES participants. High blood pressure stress reactivity was also associated with greater haemostatic responses. We conclude that lower SES is characterised by more prolonged elevations in procoagulant responses following psychological stress, and that these processes might contribute to increased cardiac risk
Reciprocal associations between youth's responses to interpersonal stress and depression: the moderating role of sex
This study examined reciprocal associations between responses to interpersonal stress and depression in youth. Specifically, it tested the hypothesis that depression predicts fewer effortful, planful responses to peer stress and more involuntary, dysregulated responses over time, and that these types of responses then predict future depression. In addition, sex differences in these reciprocal associations were explored. Youth (M age = 12.41; SD = 1.19; 86 girls, 81 boys) and their maternal caregivers completed semi-structured interviews and questionnaires at three annual waves. Path analyses were conducted to examine associations between responses to stress and depression. Multi-group comparison analyses revealed sex differences in these associations; in girls, maladaptive interpersonal stress responses predicted depression, whereas in boys, depression predicted maladaptive interpersonal stress responses. These findings indicate that engaging in adaptive responses to stressful interpersonal situations may be more important for girls??? than boys??? psychological well-being, and that boys??? stress responses may be more susceptible than girls??? to their mood states. Findings are discussed with regard to interventions designed to prevent the onset and persistence of depression
Environmental stress responses in Lactococcus lactis
Bacteria can encounter a variety of physical conditions during their life. Bacterial cells are able to survive these (often adverse) conditions by the induction of specific or general protection mechanisms. The lactic acid bacterium Lactococcus lactis is widely used for the production of cheese. Before and during this process as well as in its natural habitats, it is subjected to several stressful conditions. Such conditions include oxidation, heating and cooling, acid, high osmolarity/dehydration and starvation. In many environments combinations of these parameters occur. Understanding the stress response behaviour of L. lactis is important to optimize its application in industrial fermentations and is of fundamental interest as L. lactis is a non-differentiating Gram-positive bacterium. The stress response mechanisms of L. lactis have drawn increasing attention in recent years. The presence in L. lactis of a number of the conserved systems (e.g. the heat shock proteins) has been confirmed. Some of the regulatory mechanisms responding to an environmental stress condition are related to those found in other Gram-positive bacteria. Other stress response systems are conserved at the protein level but are under control of mechanisms unique for L. lactis. In a number of cases exposure to a single type of stress provides resistance to other adverse conditions. The unravelling of the underlying regulatory systems gives insight into the development of such cross resistance. Taken together, L. lactis has a unique set of stress response mechanisms, most of which have been identified on the basis of homology with proteins known from other bacteria. A number of the regulatory elements may provide attractive tools for the development of food grade inducible gene expression systems. Here an overview of the growth limits of L. lactis and the molecular characterization of its stress resistance mechanisms is presented.
Bacillus cereus responses to acid stress
Coping with acid environments is one of the prerequisites for the soil saprophytic and human pathogenic lifestyle of Bacillus cereus. This minireview highlights novel insights in the responses displayed by vegetative cells and germinating spores of B. cereus upon exposure to low pH as well as organic acids, including acetic acid, lactic acid and sorbic acid. Insights regarding the possible acid-inflicted damage, physiological responses and protective mechanisms have been compiled based on single cell fluorescence microscopy, flow cytometry and transcriptome analyses
Contribution of time of day and the circadian clock to the heat stress responsive transcriptome in Arabidopsis.
In Arabidopsis, a large subset of heat responsive genes exhibits diurnal or circadian oscillations. However, to what extent the dimension of time and/or the circadian clock contribute to heat stress responses remains largely unknown. To determine the direct contribution of time of day and/or the clock to differential heat stress responses, we probed wild-type and mutants of the circadian clock genes CCA1, LHY, PRR7, and PRR9 following exposure to heat (37 °C) and moderate cold (10 °C) in the early morning (ZT1) and afternoon (ZT6). Thousands of genes were differentially expressed in response to temperature, time of day, and/or the clock mutation. Approximately 30% more genes were differentially expressed in the afternoon compared to the morning, and heat stress significantly perturbed the transcriptome. Of the DEGs (~3000) specifically responsive to heat stress, ~70% showed time of day (ZT1 or ZT6) occurrence of the transcriptional response. For the DEGs (~1400) that are shared between ZT1 and ZT6, we observed changes to the magnitude of the transcriptional response. In addition, ~2% of all DEGs showed differential responses to temperature stress in the clock mutants. The findings in this study highlight a significant role for time of day in the heat stress responsive transcriptome, and the clock through CCA1 and LHY, appears to have a more profound role than PRR7 and PRR9 in modulating heat stress responses during the day. Our results emphasize the importance of considering the dimension of time in studies on abiotic stress responses in Arabidopsis
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Delivery as a traumatic event: prevalence, risk factors, screening & treatment
This review looks at the evidence for postnatal posttraumatic stress disorder (PTSD). Postnatal traumatic stress responses are divided into: appraisal of birth as traumatic, traumatic stress responses (severe symptoms of intrusions and avoidance that do not fulfil criteria for PTSD), and PTSD. Evidence is examined for the prevalence of these types of responses after birth, and for prenatal, perinatal, and postnatal vulnerability and risk factors. Screening tools that could be used are outlined and possible intervention and treatment approaches considered. Various conceptual and methodological issues are also raised.
It is concluded that up to 10% of women have severe traumatic stress responses to birth although only 1-2% of women actually develop chronic postnatal PTSD. The limited research available suggests that a history of psychiatric problems, mode of delivery, and low support during labour put women at increased risk of postnatal PTSD, although there is unlikely to be a simple relationship between mode of delivery and traumatic stress responses. A model of the possible pathways between vulnerability/risk factors and postnatal PTSD is proposed. Current evidence suggests that brief cognitive-behavioural therapy (CBT) interventions should be used with women who have a severe traumatic stress response, and longer CBT interventions with women with postnatal PTSD. More research is needed to further explore and confirm prenatal, birth, and postnatal risk factors
Some Like It Hot, Some Like It Warm: Phenotyping To Explore Thermotolerance Diversity
Plants have evolved overlapping but distinct cellular responses to different aspects of high temperature stress. These responses include basal thermotolerance, short- and long-term acquired thermotolerance, and thermotolerance to moderately high temperatures. This ‘thermotolerance diversity’ means that multiple phenotypic assays are essential for fully describing the functions of genes involved in heat stress responses. A large number of genes with potential roles in heat stress responses have been identified using genetic screens and genome wide expression studies. We examine the range of phenotypic assays that have been used to characterize thermotolerance phenotypes in both Arabidopsis and crop plants. Three major variables differentiate thermotolerance assays: (1) the heat stress regime used, (2) the developmental stage of the plants being studied, and (3) the actual phenotype which is scored. Consideration of these variables will be essential for deepening our understanding of the molecular genetics of plant thermotolerance
How innate immunity proteins kill bacteria and why they are not prone to resistance
Recent advances on antibacterial activity of peptidoglycan recognition proteins (PGRPs) offer some insight into how innate immunity has retained its antimicrobial effectiveness for millions of years with no frequent emergence of resistant strains. First, PGRP can bind to multiple components of bacterial envelope (peptidoglycan, lipoteichoic acid, and lipopolysaccharide). Second, PGRP simultaneously induces oxidative, thiol, and metal stress responses in bacteria, which individually are bacteriostatic, but in combination are bactericidal. Third, PGRP induces oxidative, thiol, and metal stress responses in bacteria through three independent pathways. Fourth, antibacterial effects of PGRP are enhanced by other innate immune responses. Thus, emergence of PGRP resistance is prevented by bacteriostatic effect and independence of each PGRP-induced stress response, as PGRP resistance would require simultaneous acquisition of three separate mechanisms disabling the induction of all three stress responses. By contrast, each antibiotic has one primary target and one primary antibacterial mechanism, and for this reason resistance to antibiotics can be generated by inhibition of this primary mechanism. Manipulating bacterial metabolic responses can enhance bacterial killing by antibiotics and elimination of antibiotic-tolerant bacteria, but such manipulations do not overcome genetically encoded antibiotic resistance. Pathogens cause infections by evading, inhibiting, or subverting host immune responses
Market responses to economic stress
Presentation to the Little Rock Downtown Rotary Club, Little Rock - Nov. 20, 2001Economic conditions - United States ; Financial markets ; Terrorism
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