scholarly journals Histiocyte X positivity for nonspecific esterase.

1980 ◽  
Vol 28 (1) ◽  
pp. 45-46 ◽  
Author(s):  
F Jaubert ◽  
S Barbey ◽  
C Nogues ◽  
J P Monnet ◽  
M Grun ◽  
...  
Keyword(s):  
Enzyme Activity ◽  
Cell Membrane ◽  
Alveolar Macrophages ◽  
Eosinophilic Granuloma ◽  
Nonspecific Esterase ◽  
A Cell

The cell membrane and X bodies of histiocytes X from two cases of eosinophilic granuloma were stained by nonspecific esterase. The results show that histiocytes X possess a cell membrane exoenzyme similar to that of other histiocytes, such as alveolar macrophages, but the role of the X body as related to enzyme activity remains an unknown.

Computational investigation for endocytosis of CoVID-19 virus SARS-CoV-2 in cell membrane

2021 ◽  
pp. 095440622110299
Author(s):  
Soumya Mukherjee ◽  
Paritosh Mahata
Keyword(s):  
Cell Membrane ◽  
Virus Particle ◽  
Coupling Model ◽  
Lipid Exchange ◽  
Peripheral Proteins ◽  
A Cell ◽  
Anisotropic Elastic ◽  
Anisotropic Elastic Material ◽  
Infinite Reservoir

CoVID-19 virus SARS-CoV-2 follows the endocytosis process to enter inside a cell to infect it. It is important to study the endocytosis of SARS-CoV-2 in cell membrane to prevent the pandemic of CoVID-19. In this paper we develop a finite element based computational model for endocytosis of SARS-CoV-2 in cell membrane and determine curvature generation on it during the process. The virus SARS-CoV-2 is modeled as a rigid spherical particle and cell membrane as an anisotropic elastic material, while its fluidic nature due to lipid exchange with infinite reservoir is preserved using suitable conditions. With the help of a contact pair created between the virus particle and cell membrane, endocytosis process is computationally studied and the curvature of membrane is evaluated as the time progresses during the endocytosis process. At the tip of the virus particle and half-radius distance from it, the membrane follows the curvature of virus very quickly. However, it takes more time for the membrane point located at a distance equal to the radius of the virus particle. This is compensated by the cytoplasmic peripheral proteins binding onto the inside surface of the cell membrane. The role of cytoplasmic peripheral BAR proteins is investigated by using a linear curvature-coupling model with protein concentrations. It is observed that F-BAR protein is more sensitive to the curvature of virus particle in comparison to the other BAR proteins. The sensitiveness deteriorates as the curvature is increased.

Calcium influx is required for tannin-mediated arachidonic acid release from alveolar macrophages

1995 ◽  
Vol 268 (1) ◽  
pp. L33-L40
Author(s):  
P. J. Bates ◽  
N. V. Ralston ◽  
Z. Vuk-Pavlovic ◽  
M. S. Rohrbach
Keyword(s):  
Arachidonic Acid ◽  
Alveolar Macrophages ◽  
Calcium Influx ◽  
Tetraacetic Acid ◽  
Textile Mill ◽  
Physiological Concentration ◽  
A Cell ◽  
Acid Release ◽  
Dose Dependent

The role of Ca2+ was investigated in the response of alveolar macrophages to cotton tannin, an agent implicated in the lung disease byssinosis in textile mill workers. A physiological concentration of extracellular Ca2+ was found to be required for tannin-mediated release of radiolabeled arachidonic acid (AA). Flow cytometry using indo 1 indicated that tannin caused a rapid and dose-dependent Ca2+ increase in macrophages that also required extracellular Ca2+. Ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid virtually abolished the Ca2+ influx mediated by tannin but had little effect on intracellular Ca2+ release induced by thapsigargin, N-formylmethionyl-leucylphenylalanine, or thimerosal. A mechanism for extracellular Ca2+ influx was demonstrated by rapid Mn2+ quenching of indo 1 by tannin. Verapamil inhibited tannin-mediated Ca2+ influx and AA release, but the effective concentration was 100 microM. 1,2-Bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid chelated all Ca2+ in the cells and effectively abolished the tannin response. Exposure to tannin was not associated with cytotoxicity, as judged by 51Cr release. The data suggest that tannin induces Ca2+ influx in alveolar macrophages, which represents an important prerequisite for a cell-signaling pathway resulting in the accumulation of free AA.

scholarly journals Detoxification of 7-Dehydrocholesterol Fatal to Helicobacter pylori Is a Novel Role of Cholesterol Glucosylation

2012 ◽  
Vol 195 (2) ◽  
pp. 359-367 ◽  
Author(s):  
Hirofumi Shimomura ◽  
Kouichi Hosoda ◽  
David J. McGee ◽  
Shunji Hayashi ◽  
Kenji Yokota ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Cell Membrane ◽  
Membrane Lipid ◽  
Host Immune System ◽  
Content Type ◽  
Mucosal Tissues ◽  
Gene Mutant ◽  
A Cell ◽  
H Pylori

ABSTRACTThe glucosylation of free cholesterol (FC) byHelicobacter pyloricells has various biological significances for the survival of this bacterium.H. pyloricells with glucosylated FC are capable of evading host immune systems, such as phagocytosis by macrophages and activation of antigen-specific T cells, and surviving in the gastric mucosal tissues for long periods. An additional role of cholesterol glucosylation in the survival ofH. pyloriwhich is distinct from the role of escaping the host immune system, however, has yet to be identified. This study demonstrated that 7-dehydrocholesterol (7dFC), an FC precursor, is a toxic compound fatal toH. pyloricells, but the cell membrane ofH. pyloriis capable of absorbing this toxic sterol via glucosylation. In contrast to the case with 7dFC, no toxicity toH. pyloricells was detected from the glucosylated 7dFC. In addition,cgtgene mutantH. pyloricells that cannot glucosylate cholesterols had higher susceptibility to the toxic action of 7dFC than wild-typeH. pyloricells. These results indicate that thecgtgene product ofH. pyloriserves to detoxify the sterol fatal to this bacterium and to permit this toxic sterol as a cell membrane lipid component. In summary, this study defined a novel role of cholesterol glucosylation inH. pylori.

scholarly journals Letter to editor: Evaluation of the relationship between TREM- 1/TREM- 2 ratio and clinical course in COVID- 19 pneumonia

2021 ◽  
Author(s):  
zhihong wang
Keyword(s):  
Cell Membrane ◽  
Clinical Course ◽  
Myeloid Cells ◽  
Cytoplasmic Tail ◽  
Soluble Form ◽  
A Cell ◽  
Membrane Bound ◽  
Kidney Functions ◽  
The Relationship

Dear editor, we read with great interest the well written article by Dr Kerget et al with the main objective of investigating the role of TREM-1/TREM-2 ratio on patients with COVID-19 pneumonia. The article pointed that TREM-1 and TREM-2 have important role in inflammation and TREM-1/TREM-2 ratio was higher in severe COVID-19 patients compared with moderate COVID-19 patients. We have certain comments to understand the conclusions of this article. Firstly, triggering receptor expressed on myeloid cells-1 (TREM-1) is mainly express on neutrophils and monocytes in a cell membrane-bound form. A soluble form of TREM-1(sTREM-1), which lacks the cytoplasmic tail and transmembrane part, were detected in the blood in recent studies. Since you have mentioned “serum TREM-1”, we were confused whether you detected TREM-1 or sTREM-1. Secondly, we wanted to know more about the treatment and the kidney functions of the patients. Thirdly, We are curious to see if high TREM-1/TREM-2 ratio could predict the distribution of ILD. We would be glad to hear the opinion of the author on the points, to get a more convincing conclusion.

scholarly journals A Cell Membrane-Level Approach to Cicatricial Alopecia Management: Is Caveolin-1 a Viable Therapeutic Target in Frontal Fibrosing Alopecia?

Biomedicines ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 572
Author(s):  
Ivan Jozic ◽  
Jérémy Chéret ◽  
Beatriz Abdo Abujamra ◽  
Mariya Miteva ◽  
Jennifer Gherardini ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Epithelial Mesenchymal Transition ◽  
Scaffolding Protein ◽  
Membrane Microdomains ◽  
Mesenchymal Transition ◽  
Caveolin 1 ◽  
Important Player ◽  
A Cell ◽  
Multiple Signaling

Irreversible destruction of the hair follicle (HF) in primary cicatricial alopecia and its most common variant, frontal fibrosing alopecia (FFA), results from apoptosis and pathological epithelial-mesenchymal transition (EMT) of epithelial HF stem cells (eHFSCs), in conjunction with the collapse of bulge immune privilege (IP) and interferon-gamma-mediated chronic inflammation. The scaffolding protein caveolin-1 (Cav1) is a key component of specialized cell membrane microdomains (caveolae) that regulates multiple signaling events, and even though Cav1 is most prominently expressed in the bulge area of human scalp HFs, it has not been investigated in any cicatricial alopecia context. Interestingly, in mice, Cav1 is involved in the regulation of (1) key HF IP guardians (TGF-β and α-MSH signaling), (2) IP collapse inducers/markers (IFNγ, substance P and MICA), and (3) EMT. Therefore, we hypothesize that Cav1 may be an unrecognized, important player in the pathobiology of cicatricial alopecias, and particularly, in FFA, which is currently considered as the most common type of primary lymphocytic scarring alopecia in the world. We envision that localized therapeutic inhibition of Cav1 in management of FFA (by cholesterol depleting agents, i.e., cyclodextrins/statins), could inhibit and potentially reverse bulge IP collapse and pathological EMT. Moreover, manipulation of HF Cav1 expression/localization would not only be relevant for management of cicatricial alopecia, but FFA could also serve as a model disease for elucidating the role of Cav1 in other stem cell- and/or IP collapse-related pathologies.

The role of (bio)surfactant sorption in promoting the bioavailability of nutrients localized at the solid-water interface

1999 ◽  
Vol 39 (7) ◽  
pp. 91-98 ◽  
Author(s):  
Ryan N. Jordan ◽  
Eric P. Nichols ◽  
Alfred B. Cunningham
Keyword(s):  
Mass Transfer ◽  
Cell Membrane ◽  
Substrate Concentration ◽  
Water Interface ◽  
Industrial Systems ◽  
Solid Liquid Interface ◽  
Solid Liquid ◽  
Surfactant Sorption

Bioavailability is herein defined as the accessibility of a substrate by a microorganism. Further, bioavailability is governed by (1) the substrate concentration that the cell membrane “sees,” (i.e., the “directly bioavailable” pool) as well as (2) the rate of mass transfer from potentially bioavailable (e.g., nonaqueous) phases to the directly bioavailable (e.g., aqueous) phase. Mechanisms by which sorbed (bio)surfactants influence these two processes are discussed. We propose the hypothesis that the sorption of (bio)surfactants at the solid-liquid interface is partially responsible for the increased bioavailability of surface-bound nutrients, and offer this as a basis for suggesting the development of engineered in-situ bioremediation technologies that take advantage of low (bio)surfactant concentrations. In addition, other industrial systems where bioavailability phenomena should be considered are addressed.

CD38 as an immunomodulator in cancer

2020 ◽  
Vol 16 (34) ◽  
pp. 2853-2861
Author(s):  
Yanli Li ◽  
Rui Yang ◽  
Limo Chen ◽  
Sufang Wu
Keyword(s):  
Multiple Myeloma ◽  
Cell Activation ◽  
Human Tissues ◽  
Transmembrane Glycoprotein ◽  
Cell Activation Marker ◽  
Research Findings ◽  
A Cell ◽  
And Function ◽  
Human Molecule

CD38 is a transmembrane glycoprotein that is widely expressed in a variety of human tissues and cells, especially those in the immune system. CD38 protein was previously considered as a cell activation marker, and today monoclonal antibodies targeting CD38 have witnessed great achievements in multiple myeloma and promoted researchers to conduct research on other tumors. In this review, we provide a wide-ranging review of the biology and function of the human molecule outside the field of myeloma. We focus mainly on current research findings to summarize and update the findings gathered from diverse areas of study. Based on these findings, we attempt to extend the role of CD38 in the context of therapy of solid tumors and expand the role of the molecule from a simple marker to an immunomodulator.

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