Nasal Myiasis in Leprosy Leading to Unusual Tissue Destruction

1995 ◽  
Vol 22 (5) ◽  
pp. 348-350 ◽  
Author(s):  
Gurvinder Pal Thami ◽  
Manik Chandra Baruah ◽  
Subhash Chondee Sharmce ◽  
Niranjan Kumar Behera
Keyword(s):  
Tissue Destruction ◽  
Nasal Myiasis

The Intravascular Generation of Fibrinogen Derivatives and the Blood Vessel Wall in Venous Thrombosis and Disseminated Intravascular Coagulation

1977 ◽  
Vol 38 (04) ◽  
pp. 0831-0849 ◽  
Author(s):  
Gwendolyn J. Stewart
Keyword(s):  
Blood Vessel ◽  
Venous Thrombosis ◽  
Vessel Wall ◽  
Fluid Phase ◽  
Primary Site ◽  
Blood Vessel Wall ◽  
Fibrin Deposition ◽  
Tissue Destruction ◽  
Fibrin Formation ◽  
Rich Material

SummaryBoth deep venous thrombosis and DIC are intermediate mechanisms of disease – both are a consequence of the deposition of fibrin-rich material in blood vessels some distance from the primary site of tissue destruction. The great difference in the sites of fibrin deposition may depend on the extent and site of activation of the clotting mechanism. DIC likely occurs in the fluid phase of the blood as a consequence of massive fibrin formation while thrombosis results from limited fibrin formation at the interface between blood and vessel wall. Leukocytes may be essential for attaching thrombi to the vessel wall in many places.

Lung resections with the CO2 laser: Uses beyond tissue destruction

1984 ◽  
Author(s):  
J. LoCicero ◽  
J. W. Frederiksen ◽  
R. S. Hartz ◽  
M. W. Kaufman ◽  
L. L. Michaelis
Keyword(s):  
Co2 Laser ◽  
Tissue Destruction ◽  
Lung Resections

Salivary Diagnosis - Clinical Uses in Assessing Oral Inflammation

2017 ◽  
Vol 68 (6) ◽  
pp. 1201-1204 ◽  
Author(s):  
Iulia Ioana Stanescu ◽  
Alexandra Totan ◽  
Florentina Rus ◽  
Daniela Miricescu ◽  
Brandusa Mocanu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Periodontal Disease ◽  
Gingival Crevicular Fluid ◽  
Oxidative Stress Marker ◽  
Clinical Settings ◽  
Tissue Destruction ◽  
Whole Saliva ◽  
Oral Inflammation ◽  
Positive Correlations ◽  
Crevicular Fluid

The past decades demonstrated that saliva and its components represent a remarkable diagnosis fluid with valuable clinical uses for both oral and systemic diseases. At the same time it is well established that oxidative stress is involved in a wide number of pathologies, including periodontitis. The specific aim of the present study which included 50 subjects is to determine if saliva can be used in clinical settings to correlate oxidative stress and tissue destruction markers with the severity of periodontal disease. An important oxidative stress marker - 8-hydroxydesoxyguanosine (8-OHdG) and a collagen degradation marker - beta-crosslaps (b-CTX) were quantified in both saliva and gingival crevicular fluid (GCF) using ELISA kits and were found to be significantly increased in the chronic periodontitis group when compared to respective controls (p[0.05). At the same time positive correlations were observed between whole saliva and gingival crevicular fluid (p[0.05). Significant correlations were also determined between GCF and salivary markers and clinical parameters of periodontal disease. Present results demonstrate that saliva and its components can successfully be used in clinical settings and represents a reliable tool for assessing periodontal disease severity.

Curcumin-containing Silver Nanoparticles prevent carbon tetrachlorideinduced hepatotoxicity in mice

2020 ◽  
Vol 23 ◽  
Author(s):  
Hossam Ebaid ◽  
Mohamed Habila ◽  
Iftekhar Hassan ◽  
Jameel Al-Tamimi ◽  
Mohamed S. Omar ◽  
...  
Keyword(s):  
Dna Damage ◽  
Silver Nanoparticles ◽  
Nuclear Dna ◽  
Liquid Paraffin ◽  
Tail Length ◽  
Hepatic Tissue ◽  
Tissue Destruction ◽  
Group 2 ◽  
The Impact

Background: Hepatotoxicity remains an important clinical challenge. Hepatotoxicity observed in response to toxins and hazardous chemicals may be alleviated by delivery of the curcumin in silver nanoparticles (AgNPs-curcumin). In this study, we examined the impact of AgNPs-curcumin in a mouse model of carbon tetrachloride (CCl4)-induced hepatic injury. Methods: Male C57BL/6 mice were divided into three groups (n=8 per group). Mice in group 1 were treated with vehicle control alone, while mice in Group 2 received a single intraperitoneal injection of 1 ml/kg CCl4 in liquid paraffin (1:1 v/v). Mice in group 3 were treated with 2.5 mg/kg AgNPs-curcumin twice per week for three weeks after the CCl4 challenge. Results: Administration of CCL4 resulted in oxidative dysregulation, including significant reductions in reduced glutathione and concomitant elevations in the level of malondialdehyde (MDA). CCL4 challenge also resulted in elevated levels of serum aspartate transaminase (AST) and alanine transaminase (ALT); these findings were associated with the destruction of hepatic tissues. Treatment with AgNPs-curcumin prevented oxidative imbalance, hepatic dysfunction, and tissue destruction. A comet assay revealed that CCl4 challenge resulted in significant DNA damage as documented by a 70% increase in nuclear DNA tail-length; treatment with AgNPs-curcumin inhibited the CCL4-mediated increase in nuclear DNA tail-length by 34%. Conclusion: Administration of AgNPs-curcumin resulted in significant antioxidant activity in vivo. This agent has the potential to prevent the hepatic tissue destruction and DNA damage that results from direct exposure to CCL4.

Caveolin-1 Regulates CCL5 and PPARγ Expression in Nthy-ori 3-1 Cells: Possible Involvement of Caveolin-1 and CCL5 in the Pathogenesis of Hashimoto’s Thyroiditis

2020 ◽  
Vol 20 (4) ◽  
pp. 609-618
Author(s):  
Baocui Liu ◽  
Tingting Zheng ◽  
Liyang Dong ◽  
Chaoming Mao ◽  
Chengcheng Xu ◽  
...  
Keyword(s):  
Hashimoto’S Thyroiditis ◽  
Mononuclear Cells ◽  
Nodular Goiter ◽  
Human Thyroid ◽  
Hashimoto's Thyroiditis ◽  
Tissue Destruction ◽  
Migration Ability ◽  
Caveolin 1 ◽  
Pparγ Agonist ◽  
Pparγ Expression

Background: Hashimoto’s thyroiditis (HT) is characterized by lymphocytic infiltration of the thyroid parenchyma, which ultimately leads to tissue destruction and loss of function. Caveolin-1 (Cav-1) is an essential structural constituent of lipid rafts in the plasma membrane of cells and is reported to be significantly reduced in thyrocytes from HT patients. However, the mechanism of Cav-1 involvement in HT pathogenesis is still largely unclear. Methods: Cav-1 expression in thyroid tissues from HT patients and euthyroid nodular goiter tissues was detected by immunohistochemistry staining. Cav-1 knockdown and overexpression were constructed by lentiviral transfection in the human thyroid follicular epithelial cell (TFC) line of Nthy-ori 3-1. The mRNA expression levels of chemokines in TFCs were determined by quantitative real-time PCR (qPCR). Cav-1 and peroxisome proliferator-activated receptor gamma (PPARγ) levels were analysed by qPCR and Western blot analysis. The migration ability of peripheral blood mononuclear cells (PBMCs) was detected by the Transwell assay. Results: In this study, Cav-1 and PPARγ expression was reduced in the thyroid tissues from HT patients. In vitro experiments showed that the expressions of chemokine (C-C motif) ligand 5 (CCL5) and migration of PBMCs were markedly increased, while the level of PPARγ was significantly decreased after the lentivirus-mediated knockdown of Cav-1 in Nthy-ori 3-1 cells. Interestingly, pioglitazone, a PPARγ agonist, not only upregulated PPARγ and Cav-1 proteins significantly, but also effectively reversed the Cav-1-knockdown-induced upregulation of CCL5 in Nthy-ori 3-1 cells and reduced the infiltration of lymphocytes. Conclusion: The inhibition of Cav-1 upregulated the CCL5 expression and downregulated the PPARγ expression in TFC while pioglitazone, a PPARγ agonist, reversed the detrimental consequence. This outcome might be a potential target for the treatment of lymphocyte infiltration into the thyroid gland and HT development.

scholarly journals Digestive Enzyme Activity and Protein Degradation in Plasma of Heart Failure Patients

2021 ◽  
Author(s):  
Vasiliki Courelli ◽  
Alla Ahmad ◽  
Majid Ghassemian ◽  
Chris Pruitt ◽  
Paul J. Mills ◽  
...  
Keyword(s):  
Heart Failure ◽  
Digestive Enzymes ◽  
Digestive Enzyme ◽  
Myocardial Cell ◽  
Systemic Circulation ◽  
Tissue Destruction ◽  
Cell Functions ◽  
Tnf Α ◽  
Elevated Activity ◽  
Trigger Mechanisms

Abstract Introduction Heart failure is associated with degradation of cell functions and extracellular matrix proteins, but the trigger mechanisms are uncertain. Our recent evidence shows that active digestive enzymes can leak out of the small intestine into the systemic circulation and cause cell dysfunctions and organ failure. Methods Accordingly, we investigated in morning fasting plasma of heart failure (HF) patients the presence of pancreatic trypsin, a major enzyme responsible for digestion. Results Western analysis shows that trypsin in plasma is significantly elevated in HF compared to matched controls and their concentrations correlate with the cardiac dysfunction biomarker BNP and inflammatory biomarkers CRP and TNF-α. The plasma trypsin levels in HF are accompanied by elevated pancreatic lipase concentrations. The trypsin has a significantly elevated activity as determined by substrate cleavage. Mass spectrometry shows that the number of plasma proteins in the HF patients is similar to controls while the number of peptides was increased about 20% in HF patients. The peptides are derived from extracellular and intracellular protein sources and exhibit cleavage sites by trypsin as well as other degrading proteases (data are available via ProteomeXchange with identifier PXD026332). Connclusions These results provide the first evidence that active digestive enzymes leak into the systemic circulation and may participate in myocardial cell dysfunctions and tissue destruction in HF patients. Conclusions These results provide the first evidence that active digestive enzymes leak into the systemic circulation and may participate in myocardial cell dysfunctions and tissue destruction in HF patients.

scholarly journals Nexus between COVID-19 and periodontal disease

2021 ◽  
Vol 49 (3) ◽  
pp. 030006052110026
Author(s):  
Kanchana Sukumar ◽  
Anupama Tadepalli
Keyword(s):  
Periodontal Disease ◽  
Host Cells ◽  
Multifactorial Disease ◽  
Tissue Destruction ◽  
The Past ◽  
Appropriate Care ◽  
Bacterial Stimulation ◽  
Plaque Control ◽  
Disease Understanding ◽  
Pro Inflammatory Cytokines

Over the past several decades, studies have demonstrated the existence of bi-directional relationships between periodontal disease and systemic conditions. Periodontitis is a polymicrobial and multifactorial disease involving both host and environmental factors. Tissue destruction is primarily associated with hyperresponsiveness of the host resulting in release of inflammatory mediators. Pro-inflammatory cytokines play a major role in bacterial stimulation and tissue destruction. In addition, these cytokines are thought to underlie the associations between periodontitis and systemic conditions. Current research suggests that increased release of cytokines from host cells, referred to as the cytokine storm, is associated with disease progression in patients with coronavirus disease 2019 (COVID-19). An intersection between periodontitis and pulmonary disease is biologically plausible. Hence, we reviewed the evidence linking COVID-19, cytokines, and periodontal disease. Plaque control is essential to prevent exchange of bacteria between the mouth and the lungs, reducing the risk of lung disease. Understanding these associations may help identify individuals at high risk and deliver appropriate care at early stages.

scholarly journals Inhibition of the CXCL9-CXCR3 axis suppresses the progression of experimental apical periodontitis by blocking macrophage migration and activation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tatsuya Hasegawa ◽  
V. Venkata Suresh ◽  
Yoshio Yahata ◽  
Masato Nakano ◽  
Shigeto Suzuki ◽  
...  
Keyword(s):  
Peritoneal Macrophages ◽  
Lesion Size ◽  
Chronic Inflammatory Disease ◽  
Apical Periodontitis ◽  
Host Immune System ◽  
Tissue Destruction ◽  
Complex Interactions ◽  
Infected Root ◽  
Principal Factors ◽  
Infected Root Canal

AbstractApical periodontitis (AP) is an acute or chronic inflammatory disease caused by complex interactions between infected root canal and host immune system. It results in the induction of inflammatory mediators such as chemokines and cytokines leading to periapical tissue destruction. To understand the molecular pathogenesis of AP, we have investigated inflammatory-related genes that regulate AP development. We found here that macrophage-derived CXCL9, which acts through CXCR3, is recruited by progressed AP. The inhibition of CXCL9 by a CXCR3 antagonist reduced the lesion size in a mouse AP model with decreasing IL-1β, IL-6 and TNFα expression. The treatment of peritoneal macrophages with CXCL9 and LPS induced the transmigration and upregulation of osteoclastogenic cytokines such as IL-1β, IL-6 and matrix metalloprotease 2, a marker of activated macrophages. This suggests that the CXCL9-CXCR3 axis plays a crucial role in the development of AP, mediated by the migration and activation of macrophages for periapical tissue destruction. Our data thus show that CXCL9 regulates the functions of macrophages which contribute to AP pathogenesis, and that blocking CXCL9 suppresses AP progression. Knowledge of the principal factors involved in the progression of AP, and the identification of related inflammatory markers, may help to establish new therapeutic strategies.

scholarly journals Molecular Mechanisms of Periodontal Disease

2021 ◽  
Vol 22 (2) ◽  
pp. 930
Author(s):  
Mikihito Kajiya ◽  
Hidemi Kurihara
Keyword(s):  
Infectious Diseases ◽  
Periodontal Disease ◽  
Molecular Mechanisms ◽  
Alveolar Bone ◽  
Tissue Destruction ◽  
Connective Tissues ◽  
Inflammatory Tissue

Periodontal disease, one of the most prevalent human infectious diseases, is characterized by chronic inflammatory tissue destruction of the alveolar bone and the connective tissues supporting the tooth [...]

scholarly journals Orchestration of Neutrophil Extracellular Traps (Nets), a Unique Innate Immune Function during Chronic Obstructive Pulmonary Disease (COPD) Development

Biomedicines ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 53
Author(s):  
Anjali Trivedi ◽  
Meraj A. Khan ◽  
Geetanjali Bade ◽  
Anjana Talwar
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Neutrophil Extracellular Traps ◽  
Innate Immune ◽  
Chronic Obstructive ◽  
Tissue Destruction ◽  
Mucus Production ◽  
Obstructive Pulmonary Disease ◽  
Extracellular Traps ◽  
Endothelial Cell Death

Morbidity, mortality and economic burden caused by chronic obstructive pulmonary disease (COPD) is a significant global concern. Surprisingly, COPD is already the third leading cause of death worldwide, something that WHO had not predicted to occur until 2030. It is characterized by persistent respiratory symptoms and airway limitation due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles of gases. Neutrophil is one of the key infiltrated innate immune cells in the lung during the pathogenesis of COPD. Neutrophils during pathogenic attack or injury decide to undergo for a suicidal death by releasing decondensed chromatin entangled with antimicrobial peptides to trap and ensnare pathogens. Casting neutrophil extracellular traps (NETs) has been widely demonstrated to be an effective mechanism against invading microorganisms thus controlling overwhelming infections. However, aberrant and massive NETs formation has been reported in several pulmonary diseases, including chronic obstructive pulmonary disease. Moreover, NETs can directly induce epithelial and endothelial cell death resulting in impairing pulmonary function and accelerating the progression of the disease. Therefore, understanding the regulatory mechanism of NET formation is the need of the hour in order to use NETs for beneficial purpose and controlling their involvement in disease exacerbation. For example, DNA neutralization of NET proteins using protease inhibitors and disintegration with recombinant human DNase would be helpful in controlling excess NETs. Targeting CXC chemokine receptor 2 (CXCR2) would also reduce neutrophilic inflammation, mucus production and neutrophil-proteinase mediated tissue destruction in lung. In this review, we discuss the interplay of NETs in the development and pathophysiology of COPD and how these NETs associated therapies could be leveraged to disrupt NETopathic inflammation as observed in COPD, for better management of the disease.

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