Repair and recovery mechanisms following critical illness

2016 ◽  
Author(s):  
Geoffrey Bellingan ◽  
Brijesh V. Patel
Keyword(s):  
Critical Illness ◽  
Inflammatory Response ◽  
Inflammatory Responses ◽  
Tissue Injury ◽  
Structure And Function ◽  
Tissue Structure ◽  
Inflammatory Activation ◽  
Recovery Mechanisms ◽  
And Function

Inflammation is the beneficial host response to foreign challenge or tissue injury that ultimately leads to the restoration of tissue structure and function. Critical illness is associated with an overwhelming and prolonged inflammatory activation. Resolution of the inflammatory response is an active process that requires removal of the inciting stimuli, cessation of the pro-inflammatory response, a timely coordinated removal of tissue leukocyte infiltration, a conversion from ‘toxic’ to reparative tissue environment, and restoration of normal tissue structure and function. Mortality may result from deficits in these resolution mechanisms. Improved delivery of critical care through prevention of harm and removal of stimuli has already delivered significant mortality benefits. Most critically-ill patients present with uncontrolled inflammation, hence anti-inflammatory strategies ameliorating this response are likely to be too late and thus futile. Rather, strategies augmenting endogenous pathways involved in the control and appropriate curtailment of such inflammatory responses may promote resolution, repair, and catabasis. Recent evidence showing that inflammation does not simply ‘fizzle out’, but its resolution involves an active and coordinated series of events. Dysfunction of these resolution checkpoints alters the normal inflammatory pathway, and is implicated in the induction and maintenance of states such as ARDS and sepsis. Improved understanding of resolution biology should provide translational pathways to not only improve survival, but also to prevent long-term morbidity resulting from tissue damage.

scholarly journals Flavonoids in Skin Senescence Prevention and Treatment

2021 ◽  
Vol 22 (13) ◽  
pp. 6814
Author(s):  
Anna Domaszewska-Szostek ◽  
Monika Puzianowska-Kuźnicka ◽  
Alina Kuryłowicz
Keyword(s):  
Therapeutic Strategy ◽  
Cancer Susceptibility ◽  
Skin Aging ◽  
Structure And Function ◽  
Tissue Structure ◽  
Delayed Wound Healing ◽  
Secretory Phenotype ◽  
Cellular Pathways ◽  
And Function ◽  
Increased Susceptibility

Skin aging is associated with the accumulation of senescent cells and is related to many pathological changes, including decreased protection against pathogens, increased susceptibility to irritation, delayed wound healing, and increased cancer susceptibility. Senescent cells secrete a specific set of pro-inflammatory mediators, referred to as a senescence-associated secretory phenotype (SASP), which can cause profound changes in tissue structure and function. Thus, drugs that selectively eliminate senescent cells (senolytics) or neutralize SASP (senostatics) represent an attractive therapeutic strategy for age-associated skin deterioration. There is growing evidence that plant-derived compounds (flavonoids) can slow down or even prevent aging-associated deterioration of skin appearance and function by targeting cellular pathways crucial for regulating cellular senescence and SASP. This review summarizes the senostatic and senolytic potential of flavonoids in the context of preventing skin aging.

Lung Structure And Function Relation In Elastase-Treated Rats: A Long-Term Follow Up Study

2012 ◽  
Author(s):  
Margit V. Szabari ◽  
Jozsef Tolnai ◽  
Balazs Maar ◽  
Harikrishnan Parameswaran ◽  
Elizabeth Bartolak-Suki ◽  
...  
Keyword(s):  
Structure And Function ◽  
Follow Up Study ◽  
Lung Structure ◽  
Long Term Follow Up ◽  
And Function ◽  
Function Relation

Abstract P138: Long-term Effects Of Severe Caloric Restriction To The Heart Function

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Aline M De Souza ◽  
Jonathas Almeida ◽  
Nataliia Shults ◽  
Hong Ji ◽  
Kathryn Sandberg
Keyword(s):  
Cardiovascular Disease ◽  
Caloric Restriction ◽  
Heart Function ◽  
Left Ventricular ◽  
Structure And Function ◽  
Long Term Effects ◽  
Isolated Hearts ◽  
Ad Libitum ◽  
And Function

Severe caloric restriction (sCR) increases the risk for acute cardiovascular disease. Less understood are the long-term effects on cardiovascular disease risk after the sCR period has ended. We investigated the effects of sCR on heart structure and function months after refeeding (sCR-Refed). Female Fischer rats (3-months-old) were maintained on (CT) ad libitum or a 60% caloric restricted diet for 2 weeks. Thereafter, all rats received ad libitum chow for 3 months and they were analyzed by precision ultrasound to assess their heart function. After imaging, the animals were sacrificed and the hearts were subjected to ischemia-reperfusion (I/R) using a Langendorff preparation. After 2 weeks of sCR, rats lost 15% of their initial body weight (BW) [% (100*(Final-Initial/Initial)): CT, 1.5±0.8 vs sCR, -15.4±1.1; p<0.001;n=8]. After 3 months of refeeding, there was no detectable difference in BW between CT and sFR-Refed groups. Isolated hearts from the sCR-Refed rats exhibited worse myocardial pathology after I/R compared to CT rats. The parallel orientation of myofibers and striations normally present in cardiomyocytes was lost in sCR-Refed rats. Further analysis revealed uneven blood-filling of the microcirculatory vessels and prominent interstitial edema of the myocardium. Hearts from sCR-Refed rats had more atrophied cardiomyocytes than CT [Atrophied/Total (%): CT, 0.2±0.1 vs sCR-Refed, 50.6±1.1; p<0.001; n=5]. The number of arrhythmic events during a 30 min ischemic interval in isolated hearts doubled after 2 weeks on the sCR diet ( data not shown ) and remained doubled 3 months later [Arrhythmias (% of time): CT, 34±8 vs sCR-Refed, 68±9; p=0.02; n=8]. Ultrasound imaging showed no difference in stroke volume, coronary perfusion pressure and left ventricular mass. However, the thickness of the left ventricular posterior wall was significantly reduced in sCR-Refed rats [(mm): CT, 2.55 ±0.03 vs sCR-Refed, 2.10±0.04; p=0.002; n=4]. These findings indicate heart structure and function remained damaged months after the sCR period ended and BW was restored. These studies have adverse cardiovascular risk implications for who are subjected either voluntarily (crash diets) or involuntarily (very low food security) to periods of inadequate caloric intake.

Long-term changes in structure and function of a tropical headwater stream following a disease-driven amphibian decline

2014 ◽  
Vol 60 (3) ◽  
pp. 575-589 ◽  
Author(s):  
Heidi M. Rantala ◽  
Amanda M. Nelson ◽  
Jessica N. Fulgoni ◽  
Matt R. Whiles ◽  
Robert O. Hall ◽  
...  
Keyword(s):  
Amphibian Decline ◽  
Structure And Function ◽  
Headwater Stream ◽  
Long Term Changes ◽  
And Function

scholarly journals Alterations of the thyroid structure and function in experimental hypopinealism

2011 ◽  
Vol 57 (2) ◽  
pp. 32-35
Author(s):  
L A Bondarenko ◽  
L Iu Sergienko ◽  
N N Sotnik ◽  
A N Cherevko
Keyword(s):  
Thyroid Gland ◽  
Structural Changes ◽  
Structure And Function ◽  
Initial Increase ◽  
Histological Structure ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis ◽  
And Function ◽  
Sexually Mature

The pituitary-thyroid axis of young sexually mature rabbits kept under a 24-hour daylight photoperiod was shown to undergo phase-modulated variations of hormonal activity with its initial increase (during the first month) and subsequent progressive decrease (within 2-5 months after the onset of exposure to light). These changes correlated with the time-dependent fall in the blood T3, T4, and TSH levels. Simultaneously, the animals developed pathological changes in the histological structure of the thyroid gland similar to those in patients with secondary or tertiary hypothyroidism. It is concluded that hormonal and structural changes in the thyroid gland during long-term hypopinealism should be regarded as an experimental model of hypothyroidism of neuroendocrine origin.

Abstract 2468: Is the LV Reverse Remodeling Imparted by Aortic Valve Replacement for Severe Aortic Stenosis Durable? A Cardiovascular MRI Study sponsored by the American Heart Association

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Robert W Biederman ◽  
James A Magovern ◽  
Saundra Grant ◽  
Ronald Williams ◽  
June Yamrozik ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Aortic Stenosis ◽  
Aortic Valve Replacement ◽  
Severe Aortic Stenosis ◽  
Structure And Function ◽  
Reverse Remodeling ◽  
Beneficial Effects ◽  
And Function ◽  
Surgically Induced

Background In patients with severe aortic stenosis (AS), long-term data tracking surgically induced beneficial effects of afterload reduction on reverse LV remodeling are not available. Echocardiographic data is available short term, but in limited fashion beyond one year. Cardiac MRI (CMR) offers the ability to track changes in LV metrics with small numbers due to its inherent high spatial resolution and low variability. Hypothesis We hypothesize that progressive changes following aortic valve replacement (AVR) are detectable by CMR and changes in LV structure and function, triggered by AVR, continue for an extended period following AVR. Methods Ten patients (67±12 yrs, 6 female) with severe, but compensated AS, underwent CMR pre-AVR and post AVR at 6±2mo, 1yr±2mo, 4yrs±5mo. LV mass index (LVMI), LV geometry, volumetrics and EF were measured (GE, EXCITE 1.5T, Milwaukee, WI). A Kruskall-Wallis one-way ANOVA was performed. Results All 10 pts survived AVR and underwent CMR at the 4-year time point (40 total time points). LVMI markedly decreased at 6 months (157±42 to 134±32g/m 2 , p<0.005) and continued to trend down at 4 yrs (127±32g/m 2 ). Similarly, EF increased pre to post AVR (55±22 to 65±11%, (p<0.05)) and continued trending upward, remaining stable at years 1–4 (66±11 vs. 65±9%). LVEDV index, initially high pre AVR, normalized post AVR (83±30 to 68±11ml/m 2 , p<0.05) trending even lower by yr 4 (66±10 ml/m 2 ). LV stroke volume increased rapidly from pre to post AVR (40±11 to 44±7ml) continuing to increase at 4 yrs (49±14ml, p=0.3). Most importantly, LVMI/volume, a 3D measure of LV geometry, remained unchanged initially but over 4 yrs markedly improved (1.07±0.2 to 0.94±0.24, p<0.05) all paralleling improvements in NYHA (3.2±1.0 to 1.5±1.1, p<0.05). Conclusion After the initial beneficial effects imparted by AVR in severe AS patients, there are, as expected, marked improvements in LV reverse remodeling. We have shown, via CMR, that surgically induced benefits to LV structure and function, including favorable alterations in LV geometry, are durable and, unexpectedly, show continued improvement past 4 years concordant with sustained improved clinical status. This supports down regulation of both mRNA and MMP activity acutely and robust suppression long term.

Diarrheal Episodes and Diarrheal Disease: Acute Disease with Chronic Implications

1984 ◽  
Vol 47 (4) ◽  
pp. 321-327 ◽  
Author(s):  
DOUGLAS L. ARCHER
Keyword(s):  
Defense Mechanisms ◽  
Diarrheal Disease ◽  
Systemic Circulation ◽  
Structure And Function ◽  
Opportunistic Pathogens ◽  
Essential Nutrient ◽  
And Function ◽  
Limited Duration ◽  
Normal Defense

Diarrheal episodes and diarrheal disease are often considered to be acute events of limited duration; a review of current literature indicates that this is not true. Diarrheal episodes caused by many bacteria, viruses, protozoans and other parasites cause alteration of intestinal structure and function. Consequences of such diarrhea-associated gut alterations include loss of normal defense mechanisms against secondary opportunistic pathogens and the ability to exclude macromolecules from systemic circulation. Additionally, loss of endogenous nutrients and malabsorption of essential nutrients result from diarrheal episodes; the consequences of such losses, even of a single essential nutrient, is compromised immune function, which predisposes to further infection. The net result of such events in some persons is long-term debilitating disease(s) such as allergy, autoimmune disorders and neoplasia.

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