scholarly journals Visualizing Cell Death in Experimental Focal Cerebral Ischemia: Promises, Problems, and Perspectives

2011 ◽  
Vol 32 (2) ◽  
pp. 213-231 ◽  
Author(s):  
Marietta Zille ◽  
Tracy D Farr ◽  
Ingo Przesdzing ◽  
Jochen Müller ◽  
Clemens Sommer ◽  
...  
Keyword(s):  
Cell Death ◽  
Complex Disease ◽  
Focal Cerebral Ischemia ◽  
Cell Damage ◽  
Brain Cells ◽  
Pathological Features ◽  
Advantages And Disadvantages ◽  
Different Types ◽  
Immunohistochemical Techniques ◽  
Eventual Death

One of the hallmarks of stroke pathophysiology is the widespread death of many different types of brain cells. As our understanding of the complex disease that is stroke has grown, it is now generally accepted that various different mechanisms can result in cell damage and eventual death. A plethora of techniques is available to identify various pathological features of cell death in stroke; each has its own drawbacks and pitfalls, and most are unable to distinguish between different types of cell death, which partially explains the widespread misuse of many terms. The purpose of this review is to summarize the standard histopathological and immunohistochemical techniques used to identify various pathological features of stroke. We then discuss how these methods should be properly interpreted on the basis of what they are showing, as well as advantages and disadvantages that require consideration. As there is much interest in the visualization of stroke using noninvasive imaging strategies, we also specifically discuss how these techniques can be interpreted within the context of cell death.

Cell response analysis to synchrotron radiation X-ray microbeam cytoplasm limited irradiation

Impact ◽  
2020 ◽  
Vol 2020 (7) ◽  
pp. 37-39
Author(s):  
Masao Suzuki
Keyword(s):  
Cell Death ◽  
Synchrotron Radiation ◽  
Cancer Cells ◽  
The Body ◽  
Response Analysis ◽  
X Ray ◽  
Advantages And Disadvantages ◽  
Different Types ◽  
Principal Researcher ◽  
Combine Surgery

The cells responsible for cancer start their journey much like any other in the body. However, they grow uncontrollably through the body as a result of the accumulation of certain mutations. If left unchecked, cancer will impact on a number of the human body's key processes, leading, ultimately, to death. There are many challenges associated with treating this disease, but they generally stem from the difficulty in differentiating the disease from the host and the ability of even a few cells to survive, recover and return. The most common treatments generally combine surgery with some type of chemotherapy or radiotherapy. Chemotherapy utilises chemicals that kill fast-growing cells and thereby disproportionally affect the rapidly multiplying cancer cells. Radiotherapy targets the tumour with radiation to cause damage and cell death. Both have their advantages and disadvantages, and both are often not 100 per cent effective. To improve these treatments, it is necessary to understand more about their precise effects on cells and, particularly, what defences cells have against their effects. Senior Principal Researcher Dr Masao Suzuki of the National Institutes for Quantum and Radiological Science and Technology (QST) is utilising the considerable radiological resources of QST to investigate the effects of different types of radiation on cells under different conditions.

Cell response analysis to synchrotron radiation X-ray microbeam cytoplasm limited irradiation

Impact ◽  
2021 ◽  
Vol 2021 (6) ◽  
pp. 21-23
Author(s):  
Masao Suzuki
Keyword(s):  
Cell Death ◽  
Synchrotron Radiation ◽  
Cancer Cells ◽  
The Body ◽  
Response Analysis ◽  
X Ray ◽  
Advantages And Disadvantages ◽  
Different Types ◽  
Principal Researcher ◽  
Combine Surgery

The cells responsible for cancer start their journey much like any other in the body. However, they grow uncontrollably through the body as a result of the accumulation of certain mutations. If left unchecked, cancer will impact on a number of the human body's key processes, leading, ultimately, to death. There are many challenges associated with treating this disease, but they generally stem from the difficulty in differentiating the disease from the host and the ability of even a few cells to survive, recover and return. The most common treatments generally combine surgery with some type of chemotherapy or radiotherapy. Chemotherapy utilises chemicals that kill fast-growing cells and thereby disproportionally affect the rapidly multiplying cancer cells. Radiotherapy targets the tumour with radiation to cause damage and cell death. Both have their advantages and disadvantages, and both are often not 100 per cent effective. To improve these treatments, it is necessary to understand more about their precise effects on cells and, particularly, what defences cells have against their effects. Senior Principal Researcher Dr Masao Suzuki of the National Institutes for Quantum and Radiological Science and Technology (QST) is utilising the considerable radiological resources of QST to investigate the effects of different types of radiation on cells under different conditions.

Alpha-Tocopherol Protects Cultured Human Cells from the Acute Lethal Cytotoxicity of Dioxin

2002 ◽  
Vol 72 (3) ◽  
pp. 147-153 ◽  
Author(s):  
Kei-Ichi Hirai ◽  
Jie-Hong Pan ◽  
Ying-Bo Shui ◽  
Eriko Simamura ◽  
Hiroki Shimada ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Damage ◽  
Smooth Endoplasmic Reticulum ◽  
Dehydroascorbic Acid ◽  
Human Cells ◽  
Alpha Tocopherol ◽  
Cervical Cancer Cells ◽  
Cultured Human Cells ◽  
Nuclear Damage ◽  
Conjunctival Epithelial Cells

The possible protection of cultured human cells from acute dioxin injury by antioxidants was investigated. The most potent dioxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), caused vacuolization of the smooth endoplasmic reticulum and Golgi apparatus in cultured human conjunctival epithelial cells and cervical cancer cells. Subsequent nuclear damage included a deep irregular indentation resulting in cell death. A dosage of 30–40 ng/mL TCDD induced maximal intracellular production of H2O2 at 30 minutes and led to severe cell death (0–31% survival) at two hours. A dose of 1.7 mM alpha-tocopherol or 1 mM L-dehydroascorbic acid significantly protected human cells against acute TCDD injuries (78–97% survivals), but vitamin C did not provide this protection. These results indicate that accidental exposure to fatal doses of TCDD causes cytoplasmic free radical production within the smooth endoplasmic reticular systems, resulting in severe cytotoxicity, and that vitamin E and dehydroascorbic acid can protect against TCDD-induced cell damage.

Studies on Chemical Methods to Expose Gate/Tunnel Oxide and Identification of Gate/Tunnel Oxide Defects in Wafer Fabrication

2002 ◽  
Author(s):  
Y. N. Hua ◽  
G. B. Ang ◽  
S. Redkar ◽  
Yogaspari ◽  
Wilma Richter
Keyword(s):  
Acetic Acid ◽  
Silicon Oxide ◽  
Wafer Fabrication ◽  
Chemical Methods ◽  
Advantages And Disadvantages ◽  
Different Types ◽  
Capacitor Structure ◽  
Oxide Defects ◽  
Buffer Oxide Etchant ◽  
Etch Time

Abstract In failure analysis of wafer fabrication, currently, three different types of chemical methods including 6:6:1 (Acetic Acid/HNO3/HF), NaOH and Choline are used in removing polysilicon (poly) layer and exposing the gate/tunnel oxide underneath. However, usage is limited due to their disadvantages. For example, 6:6:1 is a relatively fast etchant, but it is difficult to control the etch time and keep the oxide layer intact. Also, while using NaOH to remove poly and expose the silicon oxide, the solution needs to be heated. It is also difficult to etch a poly layer with a WSix or a CoSix silicide using NaOH. In this paper, we will discuss these 3 etchants in terms of their advantages and disadvantages. We will then introduce a new poly etchant, called HB91. HB91 is useful for removing poly to expose the gate/tunnel oxide for identification of related defects. HB91 is actually a mixture of two chemicals namely nitric acid (HNO3) and buffer oxide etchant (BOE) in a 9:1 ratio. The experimental results show that it is highly selective in poly removal with respect to the gate/tunnel oxide and is a suitable poly etchant especially for removing polysilicon with/without WSix and CoSix in the large capacitor structure. Application results of this poly etchant (HB91) will be presented.

Inhibition of Autophagy Potentiated Hippocampal Cell Death Induced by Endoplasmic Reticulum Stress and its Activation by Trehalose Failed to be Neuroprotective

2019 ◽  
Vol 16 (1) ◽  
pp. 3-11
Author(s):  
Luisa Halbe ◽  
Abdelhaq Rami
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Er Stress ◽  
Cell Damage ◽  
Protective Mechanism ◽  
Unfolded Proteins ◽  
Neuronal Viability ◽  
Hippocampal Cell ◽  
Trigger Cell Death ◽  
Autophagy Inhibition

Introduction: Endoplasmic reticulum (ER) stress induced the mobilization of two protein breakdown routes, the proteasomal- and autophagy-associated degradation. During ERassociated degradation, unfolded ER proteins are translocated to the cytosol where they are cleaved by the proteasome. When the accumulation of misfolded or unfolded proteins excels the ER capacity, autophagy can be activated in order to undertake the degradative machinery and to attenuate the ER stress. Autophagy is a mechanism by which macromolecules and defective organelles are included in autophagosomes and delivered to lysosomes for degradation and recycling of bioenergetics substrate. Materials and Methods: Autophagy upon ER stress serves initially as a protective mechanism, however when the stress is more pronounced the autophagic response will trigger cell death. Because autophagy could function as a double edged sword in cell viability, we examined the effects autophagy modulation on ER stress-induced cell death in HT22 murine hippocampal neuronal cells. We investigated the effects of both autophagy-inhibition by 3-methyladenine (3-MA) and autophagy-activation by trehalose on ER-stress induced damage in hippocampal HT22 neurons. We evaluated the expression of ER stress- and autophagy-sensors as well as the neuronal viability. Results and Conclusion: Based on our findings, we conclude that under ER-stress conditions, inhibition of autophagy exacerbates cell damage and induction of autophagy by trehalose failed to be neuroprotective.

scholarly journals Apoptosis and inflammation

1995 ◽  
Vol 4 (1) ◽  
pp. 5-15 ◽  
Author(s):  
C. Haanen ◽  
I. Vermes
Keyword(s):  
Cell Death ◽  
Inflammatory Reaction ◽  
Inflammatory Diseases ◽  
Apoptotic Cell ◽  
Cell Damage ◽  
Target Cells ◽  
Apoptotic Bodies ◽  
Accidental Injury ◽  
Inflammatory Reactions ◽  
Inflammatory Processes

During the last few decades it has been recognized that cell death is not the consequence of accidental injury, but is the expression of a cell suicide programme. Kerr et al. (1972) introduced the term apoptosis. This form of cell death is under the influence of hormones, growth factors and cytokines, which depending upon the receptors present on the target cells, may activate a genetically controlled cell elimination process. During apoptosis the cell membrane remains intact and the cell breaks into apoptotic bodies, which are phagocytosed. Apoptosis, in contrast to necrosis, is not harmful to the host and does not induce any inflammatory reaction. The principal event that leads to inflammatory disease is cell damage, induced by chemical/physical injury, anoxia or starvation. Cell damage means leakage of cell contents into the adjacent tissues, resulting in the capillary transmigration of granulocytes to the injured tissue. The accumulation of neutrophils and release of enzymes and oxygen radicals enhances the inflammatory reaction. Until now there has been little research into the factors controlling the accumulation and the tissue load of granulocytes and their histotoxic products in inflammatory processes. Neutrophil apoptosis may represent an important event in the control of intlamtnation. It has been assumed that granulocytes disintegrate to apoptotic bodies before their fragments are removed by local macrophages. Removal of neutrophils from the inflammatory site without release of granule contents is of paramount importance for cessation of inflammation. In conclusion, apoptotic cell death plays an important role in inflammatory processes and in the resolution of inflammatory reactions. The facts known at present should stimulate further research into the role of neutrophil, eosinophil and macrophage apoptosis in inflammatory diseases.

scholarly journals The Crosstalk Between Long Non-Coding RNAs and Various Types of Death in Cancer Cells

2021 ◽  
Vol 20 ◽  
pp. 153303382110330
Author(s):  
Wenwen Tang ◽  
Shaomi Zhu ◽  
Xin Liang ◽  
Chi Liu ◽  
Linjiang Song
Keyword(s):  
Cell Death ◽  
Cancer Cell ◽  
Causes Of Death ◽  
Vital Role ◽  
Cancer Cell Proliferation ◽  
Biological Targets ◽  
Cancer Cell Death ◽  
Different Types ◽  
Non Coding Rnas ◽  
Tumor Death

With the increasing aging population, cancer has become one of the leading causes of death worldwide, and the number of cancer cases and deaths is only anticipated to grow further. Long non-coding RNAs (lncRNAs), which are closely associated with the expression level of downstream genes and various types of bioactivity, are regarded as one of the key regulators of cancer cell proliferation and death. Cell death, including apoptosis, necrosis, autophagy, pyroptosis, and ferroptosis, plays a vital role in the progression of cancer. A better understanding of the regulatory relationships between lncRNAs and these various types of cancer cell death is therefore urgently required. The occurrence and development of tumors can be controlled by increasing or decreasing the expression of lncRNAs, a method which confers broad prospects for cancer treatment. Therefore, it is urgent for us to understand the influence of lncRNAs on the development of different modes of tumor death, and to evaluate whether lncRNAs have the potential to be used as biological targets for inducing cell death and predicting prognosis and recurrence of chemotherapy. The purpose of this review is to provide an overview of the various forms of cancer cell death, including apoptosis, necrosis, autophagy, pyroptosis, and ferroptosis, and to describe the mechanisms of different types of cancer cell death that are regulated by lncRNAs in order to explore potential targets for cancer therapy.

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