Skin folds in the gekkonid lizard genus Rhacodactylus: a natural test of the damage limitation hypothesis of mite pocket function

Aaron M. Bauer; Anthony P. Russell; Norman R. Dollahon

doi:10.1139/z90-178

Skin folds in the gekkonid lizard genus Rhacodactylus: a natural test of the damage limitation hypothesis of mite pocket function

Canadian Journal of Zoology ◽

10.1139/z90-178 ◽

1990 ◽

Vol 68 (6) ◽

pp. 1196-1201 ◽

Cited By ~ 13

Author(s):

Aaron M. Bauer ◽

Anthony P. Russell ◽

Norman R. Dollahon

Keyword(s):

Tissue Damage ◽

Host Response ◽

Terrestrial Species ◽

Damage Limitation ◽

Selective Forces ◽

Natural Test

The hypothesis that lizard mite pockets have evolved as a host response to limit damage by ectoparasites is tested. Evidence from the New Caledonian geckos of the genus Rhacodactylus does not support the hypothesis. Putative pockets in popliteal position are present in all taxa examined, but are infested by trombiculid chiggers only in Rhacodactylus auriculatus, a partially terrestrial species. Tissue damage results from the formation of a stylostome within the host pocket. No mechanisms for host amelioration of parasite effect are evident. At least in Rhacodactylus, chiggers appear to facultatively exploit skin folds or pockets, which may have evolved and been maintained as a result of selective forces unrelated to ectoparasite damage limitation.

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PENGGUNAAN DOKSISIKLIN HYCLATE SEBAGAI INHIBITOR MATRIKS METALLOPROTEINASE PADA TERAPI TAMBAHAN PERIODONTITIS

SAINSTIS ◽

10.18860/sains.v0i0.2302 ◽

2013 ◽

Author(s):

Risma Aprinda Kristanti

Keyword(s):

Tissue Damage ◽

Host Response ◽

Alveolar Bone ◽

Periodontal Tissue ◽

Junctional Epithelium ◽

Inhibit Activity ◽

Collagenase Activity ◽

Periodontal Tissues ◽

Mmp Inhibitor ◽

Extracellular Matrix Molecules

Terbit.com Daily has reported that the prevalence of periodontitis increases related with age person. Found that 35,7% of patients with periodontitis in the group 30-39 years old to 66,5% in the group 50-59 years old, increase 89,2% in the group 80-90 years old. Periodontitis that commonly found is a chronic periodontitis which is occurs in individuals older than 45 years, but can also be found in children. The main characteristic of periodontitis is the damage of the periodontal connective tissue, alveolar bone, and the movement of the junctional epithelium to the apical. Bacterial components may directly or indirectly cause tissue damage. Inflammatory mediators product such as proteinases, cytokines, and prostaglandins are part of the host response that can also cause tissue damage. Matrix metalloproteinase (MMP) is a proteinase that can cause periodontal tissue damage by disrupting the extracellular matrix molecules in periodontal tissues. Since is known that MMP has a role in various pathological processes, therapy to inhibit activity MMP in pathological processes has developed. MMP inhibitors will be a useful adjunct therapy for the treatment of periodontal disease. Many products have been introduced as an MMP inhibitor, for example: tetracycline and various derivatives, such as doxycycline and minocycline which are capable of inhibiting the activity of several classes of MMPs. Doxycycline has the ability to inhibit the increase in collagenase activity that is pathological in subgingival and prevent periodontitis to become more severe.

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Aspergillus fumigatus drives tissue damage via iterative assaults upon mucosal integrity and immune homeostasis

10.1101/2021.11.09.468003 ◽

2021 ◽

Author(s):

Uju Joy Okaa ◽

Margherita Bertuzzi ◽

Rachael Fortune-Grant ◽

Darren D Thomson ◽

David L Moyes ◽

...

Keyword(s):

Aspergillus Fumigatus ◽

Tissue Damage ◽

Host Response ◽

Nuclear Translocation ◽

Hyphal Growth ◽

Host Responses ◽

Significant Feature ◽

Pulmonary Tissue ◽

Mechanistic Basis

The human lung is constantly exposed to Aspergillus fumigatus spores, the most prevalent worldwide cause of fungal respiratory disease. Pulmonary tissue damage is a unifying feature of Aspergillus-related diseases; however, the mechanistic basis of damage is not understood. In the lungs of susceptible hosts A. fumigatus undergoes an obligatory morphological switch involving spore germination and hyphal growth. We modelled A. fumigatus infection in cultured A549 human pneumocytes, capturing phosphoactivation status of five host signalling pathways, nuclear translocation & DNA binding of eight host transcription factors, and expression of nine host response proteins over six time points encompassing exposures to live fungus and the secretome thereof. The resulting dataset, comprised of more than 1000 data points, reveals that pneumocytes mount differential responses to A. fumigatus spores, hyphae and soluble secreted products via the NF-kB, JNK, and JNK + p38 pathways respectively. Importantly, via selective degradation of host pro-inflammatory (IL-6 and IL-8) cytokines and growth factors (FGF-2), fungal secreted products reorchestrate the host response to fungal challenge as well as driving multiparametric epithelial damage, culminating in cytolysis. Dysregulation of NF-kB signalling, involving iterative stimulation of canonical and non-canonical signalling, was identified as a significant feature of host damage both in vitro and in a mouse model of invasive aspergillosis. Our data demonstrate that composite tissue damage results from iterative exposures to different fungal morphotypes and secreted products and suggest that modulation of host responses to fungal challenge might represent a unified strategy for therapeutic control of pathologically distinct types of Aspergillus-related disease.

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Mast cell-independent impairment of host defense and muscle contraction inT. spiralis-infected W/WVmice

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.2001.280.4.g640 ◽

2001 ◽

Vol 280 (4) ◽

pp. G640-G648 ◽

Cited By ~ 13

Author(s):

Bruce A. Vallance ◽

Patricia A. Blennerhassett ◽

Jan D. Huizinga ◽

Stephen M. Collins

Keyword(s):

Mast Cells ◽

Tissue Damage ◽

Host Response ◽

Contractile Response ◽

Trichinella Spiralis ◽

Tissue Injury ◽

Contractile Activity ◽

Wild Type ◽

Worm Expulsion

In response to nematode infection, the host presumably attempts to create an unfavorable environment to prevent larval penetration of the host and to expedite parasite expulsion from the gut. In this study, we have used W/WVmice with or without mast cells after bone marrow reconstitution (BMR-W/WV) to examine the role of mast cells in the host response. W/WV, BMR-W/WV, and wild-type (+/+) mice were infected with Trichinella spiralis. Infected W/WVmice exhibited less tissue damage and experienced a delay in worm expulsion and a greater degree of larval penetration of the gut leading to encystment in skeletal muscle. Tissue injury was greater and worm expulsion was normalized in BMR-W/WVmice, but larval penetration remained unchanged. Spontaneous contractile activity of jejunal muscle was disrupted in W/WVmice, as was the contractile response to carbachol. These abnormalities were also present in BMR-W/WVmice. These results indicate that mast cells mediate tissue damage and contribute to the timely expulsion of nematodes from the gut during primary infection.

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The Host Response to Invasion by Streptococcus pneumoniae: Protection and the Pathogenesis of Tissue Damage

Clinical Infectious Diseases ◽

10.1093/clinids/3.2.282 ◽

1981 ◽

Vol 3 (2) ◽

pp. 282-288 ◽

Cited By ~ 21

Author(s):

R. B. Johnston

Keyword(s):

Streptococcus Pneumoniae ◽

Tissue Damage ◽

Host Response

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Artifacts caused by dehydration and epoxy embedding in TEM

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s042482010008599x ◽

1991 ◽

Vol 49 ◽

pp. 338-339

Author(s):

Hilton H. Mollenhauer

Keyword(s):

Electron Microscopy ◽

Electron Beam ◽

Volume Change ◽

Tissue Damage ◽

Beam Specimen ◽

Chemical Fixation ◽

Resin Impregnation ◽

Storage Vesicles ◽

A Cell ◽

Tissue Shrinkage

Various means have been devised to preserve biological specimens for electron microscopy, the most common being chemical fixation followed by dehydration and resin impregnation. It is intuitive, and has been amply demonstrated, that these manipulations lead to aberrations of many tissue elements. This report deals with three parts of this problem: specimen dehydration, epoxy embedding resins, and electron beam-specimen interactions. However, because of limited space, only a few points can be summarized.Dehydration: Tissue damage, or at least some molecular transitions within the tissue, must occur during passage of a cell or tissue to a nonaqueous state. Most obvious, perhaps, is a loss of lipid, both that which is in the form of storage vesicles and that associated with tissue elements, particularly membranes. Loss of water during dehydration may also lead to tissue shrinkage of 5-70% (volume change) depending on the tissue and dehydrating agent.

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Ultrastructure and analytical microprobe analysis of simian lung mite pigments

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100143249 ◽

1986 ◽

Vol 44 ◽

pp. 324-325

Author(s):

R. W. Cole ◽

J. C. Kim

Keyword(s):

Biomedical Research ◽

Tissue Damage ◽

Microprobe Analysis ◽

Old World Monkeys ◽

Old World ◽

Experimental Animals ◽

The Past ◽

Lung Mite ◽

Mite Infestations ◽

Cardiopulmonary System

In recent years, non-human primates have become indispensable as experimental animals in many fields of biomedical research. Pharmaceutical and related industries alone use about 2000,000 primates a year. Respiratory mite infestations in lungs of old world monkeys are of particular concern because the resulting tissue damage can directly effect experimental results, especially in those studies involving the cardiopulmonary system. There has been increasing documentation of primate parasitology in the past twenty years.

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