scholarly journals Effects of Acute Ammonia Stress on Antioxidant Responses, Histopathology and Ammonia Detoxification Metabolism in Triangle Sail Mussels (Hyriopsis cumingii)

Water ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 425
Author(s):  
Qianqian Zhao ◽  
Ke Feng ◽  
Lianbo Zhang ◽  
Yunpeng Bai ◽  
Weizhi Yao
Keyword(s):  
Tissue Injury ◽  
Exposure Period ◽  
Antioxidant Response ◽  
The Body ◽  
Antioxidant Responses ◽  
Hyriopsis Cumingii ◽  
Ammonia Detoxification ◽  
Eutrophic Water ◽  
Glutathione S Transferases ◽  
Oxidation Effect

Ammonia is one of the major pollutants in the aquatic ecosystem. Hyriopsis cumingii has great potential for the restoration of eutrophic water. However, there is no study investigating the effect of ammonia exposure in H. cumingii. The median lethal concentration (96 h LC50) of unionized ammonium was 12.86 mg/L in H. cumingii. In the study, H. cumingii were exposed to 6.43 mg L−1 unionized ammonium (1/2 96 h LC50) for 0, 6, 12, 24, 48, 72, and 96 h. High environment ammonia induced antioxidant response to protect the body from oxidative damage. After exposure to ammonia, there was a same trend of induction followed by inhibition of the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione-S-transferases (GST) in the hepatopancreas and gills of H. cumingii. However, the antioxidant response could not completely counteract the oxidation effect during the exposure period, resulting in lipid peroxidation (LPO) and tissue injury in the hepatopancreas and gills of H. cumingii eventually. Moreover, this study indicated that glutamine synthetase (GS), glutamate dehydrogenase (GDH), alanine aminotransaminase (ALT), and aspartate aminotransaminase (AST) in the hepatopancreas and gills may play an important role in ammonia detoxification of H. cumingii. Our results will be helpful to understand the mechanism of aquatic toxicology induced by ammonia in shellfish.

scholarly journals Inflammation-Related Carcinogenesis: Lessons from Animal Models to Clinical Aspects

Cancers ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 921
Author(s):  
Futoshi Okada ◽  
Runa Izutsu ◽  
Keisuke Goto ◽  
Mitsuhiko Osaki
Keyword(s):  
Animal Models ◽  
Tissue Injury ◽  
Economic Status ◽  
Gene Mutations ◽  
Inflammatory Cells ◽  
The Body ◽  
Clinical Aspects ◽  
Promote Cell Proliferation ◽  
Organ Specific ◽  
Altered Gene

Inflammation-related carcinogenesis has long been known as one of the carcinogenesis patterns in humans. Common carcinogenic factors are inflammation caused by infection with pathogens or the uptake of foreign substances from the environment into the body. Inflammation-related carcinogenesis as a cause for cancer-related death worldwide accounts for approximately 20%, and the incidence varies widely by continent, country, and even region of the country and can be affected by economic status or development. Many novel approaches are currently available concerning the development of animal models to elucidate inflammation-related carcinogenesis. By learning from the oldest to the latest animal models for each organ, we sought to uncover the essential common causes of inflammation-related carcinogenesis. This review confirmed that a common etiology of organ-specific animal models that mimic human inflammation-related carcinogenesis is prolonged exudation of inflammatory cells. Genotoxicity or epigenetic modifications by inflammatory cells resulted in gene mutations or altered gene expression, respectively. Inflammatory cytokines/growth factors released from inflammatory cells promote cell proliferation and repair tissue injury, and inflammation serves as a “carcinogenic niche”, because these fundamental biological events are common to all types of carcinogenesis, not just inflammation-related carcinogenesis. Since clinical strategies are needed to prevent carcinogenesis, we propose the therapeutic apheresis of inflammatory cells as a means of eliminating fundamental cause of inflammation-related carcinogenesis.

scholarly journals Proton block of proton-activated TRPV1 current

2015 ◽  
Vol 146 (2) ◽  
pp. 147-159 ◽  
Author(s):  
Bo Hyun Lee ◽  
Jie Zheng
Keyword(s):  
Tissue Injury ◽  
Ion Selectivity ◽  
Extracellular Ph ◽  
The Body ◽  
Ion Permeation ◽  
Nociceptive Neurons ◽  
Trpv1 Channels ◽  
Highly Sensitive ◽  
Body Core ◽  
Polymodal Nociceptor

The TRPV1 cation channel is a polymodal nociceptor that is activated by heat and ligands such as capsaicin and is highly sensitive to changes in extracellular pH. In the body core, where temperature is usually stable and capsaicin is normally absent, H+ released in response to ischemia, tissue injury, or inflammation is the best-known endogenous TRPV1 agonist, activating the channel to mediate pain and vasodilation. Paradoxically, removal of H+ elicits a transient increase in TRPV1 current that is much larger than the initial H+-activated current. We found that this prominent OFF response is caused by rapid recovery from H+ inhibition of the excitatory current carried by H+-activated TRPV1 channels. H+ inhibited current by interfering with ion permeation. The degree of inhibition is voltage and permeant ion dependent, and it can be affected but not eliminated by mutations to acidic residues within or near the ion selectivity filter. The opposing H+-mediated gating and permeation effects produce complex current responses under different cellular conditions that are expected to greatly affect the response of nociceptive neurons and other TRPV1-expressing cells.

scholarly journals Sustained elevation of MG53 in the bloodstream increases tissue regenerative capacity without compromising metabolic function

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Zehua Bian ◽  
Qiang Wang ◽  
Xinyu Zhou ◽  
Tao Tan ◽  
Ki Ho Park ◽  
...  
Keyword(s):  
Blood Circulation ◽  
Tissue Injury ◽  
Eccentric Contraction ◽  
The Body ◽  
Muscle Performance ◽  
Membrane Repair ◽  
Injury Repair ◽  
Family Protein ◽  
Normal Glucose ◽  
Dermal Wound

Abstract MG53 is a muscle-specific TRIM-family protein that presides over the cell membrane repair response. Here, we show that MG53 present in blood circulation acts as a myokine to facilitate tissue injury-repair and regeneration. Transgenic mice with sustained elevation of MG53 in the bloodstream (tPA-MG53) have a healthier and longer life-span when compared with littermate wild type mice. The tPA-MG53 mice show normal glucose handling and insulin signaling in skeletal muscle, and sustained elevation of MG53 in the bloodstream does not have a deleterious impact on db/db mice. More importantly, the tPA-MG53 mice display remarkable dermal wound healing capacity, enhanced muscle performance, and improved injury-repair and regeneration. Recombinant human MG53 protein protects against eccentric contraction-induced acute and chronic muscle injury in mice. Our findings highlight the myokine function of MG53 in tissue protection and present MG53 as an attractive biological reagent for regenerative medicine without interference with glucose handling in the body.

Evaluation of the PEAK PlasmaBlade for ENT Surgery

2008 ◽  
Vol 139 (2_suppl) ◽  
pp. P104-P105
Author(s):  
Kay W Chang ◽  
Grace A Carlson ◽  
Huang Eric
Keyword(s):  
Thermal Imaging ◽  
Tissue Injury ◽  
The Body ◽  
Histological Evaluation ◽  
Radiofrequency Energy ◽  
Tissue Samples ◽  
Left Behind ◽  
Post Operative Pain ◽  
New Instrument ◽  
Residual Tissue

Problem Traditional electrosurgical instruments are known to have an associated zone of thermal injury to the residual tissue. The compromised tissue left behind in the body may compromise wound healing and also may cause post operative pain. The PEAK PlasmaBlade is a new tissue dissection tool that uses pulsed radiofrequency energy to generate a highly focused plasma field at the tip of the device. This creates an effective cutting edge with simultaneous hemostasis while the blade remains near body temperature. A comparative study of tissue cutting and hemostasis was conducted to evaluate the characteristics of this technology. Methods Porcine mucosal and lymphoid tissue was subjected to a series of surgical incisions using the PlasmaBlade, a scalpel, a traditional electrosurgery (bovie) blade style tip, and a Coblation EVac 70 wand. Both low and high settings were evaluated for PlasmaBlade, bovie, and Coblation. Blood loss following the cut was evaluated. Histology samples were harvested immediately after and evaluated for collateral tissue damage at the incision site. Thermal imaging of all the devices in an active cutting mode was also conducted. Results Histological evaluation of the tissue samples showed that the PlasmaBlade cuts produced minimal collateral damage compared to cuts made with the other electrosurgical instruments, which demonstrated greater thermal damage. Bleeding control (hemostasis) was equivalent for the Plasma-Blade versus bovie and Coblation. Thermal imaging showed the PlasmaBlade operating in a range of 40 to 100 C which was similar to the Coblation operating temperatures. Traditional electrosurgery produced temperatures well in excess of 200 C. Conclusion The PEAK PlasmaBlade is a promising new instrument which provides atraumatic, scalpel–like, cutting and bovie-like hemostasis, resulting in minimal bleeding and tissue injury. Significance There is great potential for this becoming an important tool for common ENT procedures such as tonsillectomy and adenoidectomy, specifically in reducing the pain and morbidity of recovery.

Studies on Heme Oxygenase 1 During Erythroid Differentiation

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 4254-4254
Author(s):  
Daniel Garcia Santos ◽  
Jesse Eisenberg ◽  
Matthias Schranzhofer ◽  
Prem Ponka
Keyword(s):  
Aminolevulinic Acid ◽  
Conflicts Of Interest ◽  
Tissue Injury ◽  
Erythroid Differentiation ◽  
The Body ◽  
Cellular Damage ◽  
Erythroid Cell ◽  
Heme Oxygenase 1 ◽  
Erythroid Cells ◽  
Murine Erythroleukemia

Abstract Abstract 4254 Heme is indispensable for the function of all aerobic cells as a prosthetic group of innumerable proteins. However, “free heme” (uncommitted) can initiate the formation of free radicals and cause lipid peroxidation, which can lead to cellular damage and tissue injury. Therefore, the rate of heme biosynthesis and catabolism must be well balanced by tight control mechanisms. The highest amounts of organismal heme (75-80%) are present in circulating red blood cells (RBC), whose precursors synthesize heme with rates that are at least one order of magnitude higher (on the per cell basis) than those in the liver – the second most active heme producer in the body. The degradation of heme is exclusively carried out by heme oxygenases 1 and 2 (HO1 and HO2), which catalyze the rate-limiting step in the oxidative degradation of heme. Although the heme-inducible HO isoform, HO1, has been extensively studied in hepatocytes and many other non-erythroid cells, virtually nothing is known about the expression of HO1 in developing RBC. Similarly, it is unknown whether HO1 plays any role in erythroid cell development under physiological or pathophysiological conditions. Using both a murine erythroleukemia cell line (MEL) and primary erythroid cells isolated from mouse fetal livers, we have demonstrated that during erythroid differentiation HO1 is up-regulated at both mRNA and protein levels. This increase in HO1 can be prevented by succinylacetone (SA), an inhibitor of heme synthesis that blocks 5-aminolevulinic acid dehydratase. These data suggest that in developing RBC, in addition to the continuous assembly of heme with globin chains, there is an increase in levels of uncommitted heme, which upregulates HO1 expression. Additionally, we have shown that down-regulation of HO1 via siRNA increased hemoglobinization in differentiating MEL cells. In contrast, induction of HO1 expression by NaAsO2 reduced the hemoglobinization of MEL cells. This effect could be reversed to control levels by the addition of HO1 inhibitor tin-protophorphyrin (SnPP). These results show that in differentiating erythroid cells the balance between levels of heme and HO1 have to be tightly regulated to maintain hemoglobinization at appropriate levels. Our results lead us to propose that disturbances in HO1 expression could play a role in some pathophysiological conditions such as thalassemias. Disclosures: No relevant conflicts of interest to declare.

A Case Study of Severe Hypercalcemia Secondary to Subcutaneous Fat Necrosis: A Diagnosis of Exclusion

2019 ◽  
Vol 38 (4) ◽  
pp. 236-241 ◽  
Author(s):  
Mary Whalen
Keyword(s):  
Tissue Injury ◽  
Rare Complication ◽  
Subcutaneous Fat ◽  
Ischemic Injury ◽  
The Body ◽  
Whole Body ◽  
Fat Necrosis ◽  
Subcutaneous Fat Necrosis ◽  
Severe Hypercalcemia

Subcutaneous fat necrosis (SCFN) is a rare complication, usually occurring in otherwise healthy full-term infants who have experienced some level of trauma that causes ischemic injury to adipose tissue. Tissue injury usually occurs in areas of the body that are exposed to excessive pressure as during delivery. Tissue injury has also been described secondary to therapeutic cooling. This case study presents an infant who received whole body cooling for hypoxic ischemic injury and later developed severe hypercalcemia at one month of age without the skin lesions consistent with SCFN. The differential diagnosis for hypercalcemia and how it relates to SCFN is presented, as well as clinical presentation, treatment, and prognosis.

scholarly journals Pengaruh pemberian vitamin E terhadap kadar neutrofil setelah latihan fisik

2016 ◽  
Vol 4 (2) ◽  
Author(s):  
Kristo Warong ◽  
Damajanty H.C. Pangemanan ◽  
Joice N.A. Engka
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Physical Exercise ◽  
Tissue Injury ◽  
The Body ◽  
Control Group ◽  
Control Group Design ◽  
Group Design ◽  
Post Test ◽  
Test Control

Absract: Physical exercise can improve and maintain physical fitness. However, physical exercise can lead to oxidative stress that can reduce the activity of antioxidants. Vitamin E is a fat-soluble antioxidant that could free radicals in the body. Neutrophils play an active role in the process of phagocytosis of bacteria and other microorganisms the damaged tissue caused by tissue injury. This study was aimed to obtain the effect of vitamin E on neutrophil count after physical exercise. This was a field experimental study with a pre post test control group design. Data were analyzed with the Mann Whitney U (α = 0.05). The physical exercise was playing futsal for 60 minutes. Respondents were 30 male respondents divided into 2 groups: treatment and control groups. The levels of neutrophils were examined after physical exercise and after the administration of vitamin E 400 IU for seven days. Data analysis of the effect of vitamin E on neutrophil level after physical exercise showed a p value of 0.031. Conclusion: Vitamin E influenced the levels of neutrophils after physical exercise.Keywords: physical exercise, oxidative stress, vitamin E, neutrophil Abstrak: Latihan fisik merupakan aktivitas yang dilakukan seseorang untuk meningkatkan atau memelihara kebugaran tubuh. Latihan fisik dapat menimbulkan stres oksidatif sehingga dapat menurunkan aktivitas antioksidan. Vitamin E merupakan antioksidan yang larut dalam lemak dan berfungsi untuk mengurangi radikal bebas yang terdapat dalam tubuh. Neutrofil berperan aktif dalam proses fagositosis bakteri, mikroorganisme, dan membersihkan sisa jaringan rusak yang disebabkan oleh cedera jaringan. Penelitian ini bertujuan untuk mengetahui pengaruh vitamin E terhadap kadar neutrofil setelah latihan fisik. Jenis penelitian ialah eksperimental lapangan dengan pre post test control group design. Untuk menguji signifikansi penelitian digunakan uji Mann Whitney U (α = 0,05). Latihan fisik berupa olahraga futsal selama 60 menit dilakukan oleh 30 responden laki-laki yang dibagi dalam 2 kelompok yaitu perlakuan dan kontrol. Kadar neutrofil diukur setelah latihan fisik dan setelah pemberian vitamin E 400 IU selama 7 hari. Hasil statistik menunjukkan terdapat pengaruh bermakna dari vitamin E pada kelompok perlakuan (p=0,031). Simpulan: Terdapat pengaruh vitamin E terhadap kadar neutrofil setelah latihan fisik. Kata kunci: latihan fisik, stres oksidatif, vitamin E, neutrofil

scholarly journals Chronic Distal Radioulnar Instability- Diagnosis and Treatment: A Review

2020 ◽  
pp. 65-72
Author(s):  
Sanad Younes ◽  
Ahmad Saad ◽  
Zeyad Buahlaika
Keyword(s):  
Joint Instability ◽  
Tissue Injury ◽  
Soft Tissue Injury ◽  
Distal Radioulnar Joint ◽  
The Body ◽  
Restricted Movement ◽  
Radioulnar Joint ◽  
Proper Form ◽  
Bony Injury ◽  
Type Of Injury

The distal radioulnar joint is one of the inherently unstable joint in the body, its injury is commonly missed and the patient may present later with pain and restricted movement because of joint instability.  The distal radioulnar joint instability could be dorsal , volar , or bidirectional, and it could be caused by soft tissue injury or bony injury and malunion. It is fundamentall to recognize the type of injury and the cause of instability to be able to provide the proper form of treatment to get the best results.

scholarly journals Epigenetic Regulation of Cell-Fate Changes That Determine Adult Liver Regeneration After Injury

2021 ◽  
Vol 9 ◽  
Author(s):  
Luigi Aloia
Keyword(s):  
Liver Disease ◽  
Cell Fate ◽  
Tissue Injury ◽  
The Body ◽  
Epigenetic Mechanisms ◽  
Adult Liver ◽  
Cell Fate Decisions ◽  
Epithelial Regeneration ◽  
Cellular Turnover ◽  
Chromatin Modifiers

The adult liver has excellent regenerative potential following injury. In contrast to other organs of the body that have high cellular turnover during homeostasis (e.g., intestine, stomach, and skin), the adult liver is a slowly self-renewing organ and does not contain a defined stem-cell compartment that maintains homeostasis. However, tissue damage induces significant proliferation across the liver and can trigger cell-fate changes, such as trans-differentiation and de-differentiation into liver progenitors, which contribute to efficient tissue regeneration and restoration of liver functions. Epigenetic mechanisms have been shown to regulate cell-fate decisions in both embryonic and adult tissues in response to environmental cues. Underlying their relevance in liver biology, expression levels and epigenetic activity of chromatin modifiers are often altered in chronic liver disease and liver cancer. In this review, I examine the role of several chromatin modifiers in the regulation of cell-fate changes that determine efficient adult liver epithelial regeneration in response to tissue injury in mouse models. Specifically, I focus on epigenetic mechanisms such as chromatin remodelling, DNA methylation and hydroxymethylation, and histone methylation and deacetylation. Finally, I address how altered epigenetic mechanisms and the interplay between epigenetics and metabolism may contribute to the initiation and progression of liver disease and cancer.

The Effects of Pressure and Shear on Capillary Closure in the Microstructure of Skeletal Muscles: Computational Studies

2007 ◽  
Author(s):  
Eran Linder-Ganz ◽  
Amit Gefen
Keyword(s):  
Muscle Tissue ◽  
Skeletal Muscles ◽  
Tissue Injury ◽  
The Body ◽  
Acute Ischemia ◽  
Fe Model ◽  
Mechanical Forces ◽  
Deep Tissue ◽  
Deep Tissue Injury ◽  
Complete Closure

Deep tissue injury (DTI) is a serious and potentially deadly type of pressure ulcers, which initiate in deep muscle tissue under bony prominences of immobilized patients, and progress outwards towards the skin with no clear visual indications of the injury at the surface of the body. It had been suggested that DTI appear in muscle tissue first, due to the dense capillary vasculature in skeletal muscles which is susceptible to obstruction and occlusion by mechanical forces [1–3]. Though mechanical forces may cause capillaries to collapse and thus induce ischemic conditions in adjacent muscle cells [2], some investigators stipulated that ischemia alone cannot explain the etiology of DTI, and so, other mechanisms, particularly excessive cellular deformations must be involved [1]. We hypothesize that physiological levels of stresses and strains in muscle tissue under bony prominences — even when muscles are highly loaded as during sitting — do not cause complete closure of muscle capillaries, and therefore, do not cause an acute ischemia in muscles. If this is indeed the case, then ischemia cannot be the only factor contributing to DTI onset. In order to test our hypothesis, we developed a finite element (FE) model of the microstructure of skeletal muscle, at the level of muscle fascicles, and employed the model to determine the stress and strain levels required for causing partial and complete closure of capillaries.

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