scholarly journals Conventional frequency ultrasound detection of tumor response in vivo to cancer treatment administration

2021 ◽  
Author(s):  
Naum Papanicolau
Keyword(s):  
Cell Death ◽  
Cancer Therapy ◽  
Structural Changes ◽  
Apoptotic Cell ◽  
High Frequency Ultrasound ◽  
Patient Response ◽  
Tumor Morphology ◽  
Frequency Ultrasound

Current methods employed to evaluate patient response to cancer therapy are typically invasive requiring examination of excised tissue. The development of a non-invasive method of monitoring patient response to cancer therapy administration would potentiate clinical decisions permitting clinicians to adjust therapy regimens early in a treatment course based upon individual patient responses. It has been previously demonstrated that high frequency ultrasound is capable of reliably quantifying structural changes in tumor morphology in response to cancer therapies. Preliminary work has also indicated that ultrasound employed at clinically relevant frequencies (1-15 MHz) can detect apoptotic cell death using in vitro models. This thesis examines changes in tumor morphology in response to cancer therapy administration employing ultrasound at a clinically applicable frequency in a preclinical in vivo mouse model. The power spectrum of the radiofrequency data obtained from tumors was analyzed via linear regression spectroscopic analysis, as well as evaluating a statistical analysis of the amplitude distribution of the signal envelope. It is demonstrated here for the first time that 7 MHz ultrasound can detect apoptotic and other forms of cell death in vivo. A potential for a parametric imaging technique to visually represent analysis results is also demonstrated.

scholarly journals Conventional frequency ultrasound detection of tumor response in vivo to cancer treatment administration

2021 ◽  
Author(s):  
Naum Papanicolau
Keyword(s):  
Cell Death ◽  
Cancer Therapy ◽  
Structural Changes ◽  
Apoptotic Cell ◽  
High Frequency Ultrasound ◽  
Patient Response ◽  
Tumor Morphology ◽  
Frequency Ultrasound

Current methods employed to evaluate patient response to cancer therapy are typically invasive requiring examination of excised tissue. The development of a non-invasive method of monitoring patient response to cancer therapy administration would potentiate clinical decisions permitting clinicians to adjust therapy regimens early in a treatment course based upon individual patient responses. It has been previously demonstrated that high frequency ultrasound is capable of reliably quantifying structural changes in tumor morphology in response to cancer therapies. Preliminary work has also indicated that ultrasound employed at clinically relevant frequencies (1-15 MHz) can detect apoptotic cell death using in vitro models. This thesis examines changes in tumor morphology in response to cancer therapy administration employing ultrasound at a clinically applicable frequency in a preclinical in vivo mouse model. The power spectrum of the radiofrequency data obtained from tumors was analyzed via linear regression spectroscopic analysis, as well as evaluating a statistical analysis of the amplitude distribution of the signal envelope. It is demonstrated here for the first time that 7 MHz ultrasound can detect apoptotic and other forms of cell death in vivo. A potential for a parametric imaging technique to visually represent analysis results is also demonstrated.

27. Low Frequency Ultrasound Imaging of Apoptosis in Tumor Response: Non-Invasive Monitoring of Chemotherapy Effects

2018 ◽  
Author(s):  
Stephanie Zhou
Keyword(s):  
Cell Death ◽  
Ultrasound Imaging ◽  
Structural Changes ◽  
Imaging Techniques ◽  
Low Frequency ◽  
Acoustic Properties ◽  
High Frequency Ultrasound ◽  
Noninvasive Methods ◽  
Frequency Ultrasound

Due to the growing costs of chemotherapy, previous imaging techniques such as MRI or CT scans have become too time-consuming in the assessment of chemotherapy’s effects. With results generated about 2 weeks later, the patient is exposed to the negative side effects of these medications with the possibility that chemotherapy may not be improving their prognosis. Thus, ultrasound has become increasingly popular as a method to determine chemotherapy’s effect on tumors within 24 hours. Both low and high-frequency ultrasound are novel, noninvasive methods for detecting cell death based on changes in cell morphology. Condensation, fragmentation and alterations in the cell nucleus during apoptosis are linked to changes in the cell’s acoustic properties, as indicated by experimental evidence. In this study, quantitative ultrasound was used to follow responses of tumor models to chemotherapy in vivo. As studies have shown that structural changes can occur as early as 24 hours after treatment, ultrasound imaging was administered before and 24 hours after treatment. Changes in ultrasound parameters such as spectral slope, Y-intercept, and midband fit were analyzed relative to pretreatment control data and when compared to changes in the tumors seen through cell staining, changes consistent with cell death were observed.

scholarly journals KUS121 attenuates the progression of monosodium iodoacetate-induced osteoarthritis in rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Sachiko Iwai ◽  
Hanako O. Ikeda ◽  
Hisashi Mera ◽  
Kohei Nishitani ◽  
Motoo Saito ◽  
...  
Keyword(s):  
Cell Death ◽  
Er Stress ◽  
Apoptotic Cell ◽  
Intraperitoneal Administration ◽  
Atp Depletion ◽  
Knee Joints ◽  
Cellular Protection ◽  
Monosodium Iodoacetate

AbstractCurrently there is no effective treatment available for osteoarthritis (OA). We have recently developed Kyoto University Substances (KUSs), ATPase inhibitors specific for valosin-containing protein (VCP), as a novel class of medicine for cellular protection. KUSs suppressed intracellular ATP depletion, endoplasmic reticulum (ER) stress, and cell death. In this study, we investigated the effects of KUS121 on chondrocyte cell death. In cultured chondrocytes differentiated from ATDC5 cells, KUS121 suppressed the decline in ATP levels and apoptotic cell death under stress conditions induced by TNFα. KUS121 ameliorated TNFα-induced reduction of gene expression in chondrocytes, such as Sox9 and Col2α. KUS121 also suppressed ER stress and cell death in chondrocytes under tunicamycin load. Furthermore, intraperitoneal administration of KUS121 in vivo suppressed chondrocyte loss and proteoglycan reduction in knee joints of a monosodium iodoacetate-induced OA rat model. Moreover, intra-articular administration of KUS121 more prominently reduced the apoptosis of the affected chondrocytes. These results demonstrate that KUS121 protects chondrocytes from stress-induced cell death in vitro and in vivo, and indicate that KUS121 is a promising novel therapeutic agent to prevent the progression of OA.

scholarly journals The Role of Herbal Bioactive Components in Mitochondria Function and Cancer Therapy

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Fangfang Tao ◽  
Yanrong Zhang ◽  
Zhiqian Zhang
Keyword(s):  
Cancer Therapy ◽  
Cancer Cell ◽  
Apoptotic Cell ◽  
Redox Status ◽  
Cancer Therapies ◽  
Bioactive Components ◽  
Atp Production

Mitochondria are highly dynamic double-membrane organelles which play a well-recognized role in ATP production, calcium homeostasis, oxidation-reduction (redox) status, apoptotic cell death, and inflammation. Dysfunction of mitochondria has long been observed in a number of human diseases, including cancer. Targeting mitochondria metabolism in tumors as a cancer therapeutic strategy has attracted much attention for researchers in recent years due to the essential role of mitochondria in cancer cell growth, apoptosis, and progression. On the other hand, a series of studies have indicated that traditional medicinal herbs, including traditional Chinese medicines (TCM), exert their potential anticancer effects as an effective adjunct treatment for alleviating the systemic side effects of conventional cancer therapies, for reducing the risk of recurrence and cancer mortality and for improving the quality of patients’ life. An amazing feature of these structurally diverse bioactive components is that majority of them target mitochondria to provoke cancer cell-specific death program. The aim of this review is to summarize the in vitro and in vivo studies about the role of these herbs, especially their bioactive compounds in the modulation of the disturbed mitochondrial function for cancer therapy.

scholarly journals Targeting Sphingolipids for Cancer Therapy

2021 ◽  
Vol 11 ◽  
Author(s):  
Osmel Companioni ◽  
Cristina Mir ◽  
Yoelsis Garcia-Mayea ◽  
Matilde E. LLeonart
Keyword(s):  
Clinical Trials ◽  
Cell Death ◽  
Cancer Therapy ◽  
Preclinical Studies ◽  
Hepatic Toxicity ◽  
Multiple Cancers ◽  
Extensive Class ◽  
Effective Drugs

Sphingolipids are an extensive class of lipids with different functions in the cell, ranging from proliferation to cell death. Sphingolipids are modified in multiple cancers and are responsible for tumor proliferation, progression, and metastasis. Several inhibitors or activators of sphingolipid signaling, such as fenretinide, safingol, ABC294640, ceramide nanoliposomes (CNLs), SKI-II, α-galactosylceramide, fingolimod, and sonepcizumab, have been described. The objective of this review was to analyze the results from preclinical and clinical trials of these drugs for the treatment of cancer. Sphingolipid-targeting drugs have been tested alone or in combination with chemotherapy, exhibiting antitumor activity alone and in synergism with chemotherapy in vitro and in vivo. As a consequence of treatments, the most frequent mechanism of cell death is apoptosis, followed by autophagy. Aslthough all these drugs have produced good results in preclinical studies of multiple cancers, the outcomes of clinical trials have not been similar. The most effective drugs are fenretinide and α-galactosylceramide (α-GalCer). In contrast, minor adverse effects restricted to a few subjects and hepatic toxicity have been observed in clinical trials of ABC294640 and safingol, respectively. In the case of CNLs, SKI-II, fingolimod and sonepcizumab there are some limitations and absence of enough clinical studies to demonstrate a benefit. The effectiveness or lack of a major therapeutic effect of sphingolipid modulation by some drugs as a cancer therapy and other aspects related to their mechanism of action are discussed in this review.

In vitro and in vivo high‐frequency ultrasound response of microbubbles

2006 ◽  
Vol 119 (5) ◽  
pp. 3438-3438
Author(s):  
Orlando Aristizábal ◽  
Daniel H. Turnbull ◽  
Jeffrey A. Ketterling
Keyword(s):  
High Frequency ◽  
High Frequency Ultrasound ◽  
Frequency Ultrasound

scholarly journals Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage

2019 ◽  
Vol 4 (2) ◽  
pp. 93-95 ◽  
Author(s):  
Jieru Wan ◽  
Honglei Ren ◽  
Jian Wang
Keyword(s):  
Lipid Peroxidation ◽  
Cell Death ◽  
Intracerebral Haemorrhage ◽  
Neuronal Death ◽  
Molecular Mechanisms ◽  
Apoptotic Cell ◽  
Iron Toxicity ◽  
Secondary Brain Injury

Intracerebral haemorrhage (ICH) is a devastating type of stroke with high mortality and morbidity. However, we have few options for ICH therapy and limited knowledge about post-ICH neuronal death and related mechanisms. In the aftermath of ICH, iron overload within the perihaematomal region can induce lethal reactive oxygen species (ROS) production and lipid peroxidation, which contribute to secondary brain injury. Indeed, iron chelation therapy has shown efficacy in preclinical ICH studies. Recently, an iron-dependent form of non-apoptotic cell death known as ferroptosis was identified. It is characterised by an accumulation of iron-induced lipid ROS, which leads to intracellular oxidative stress. The ROS cause damage to nucleic acids, proteins and lipid membranes, and eventually cell death. Recently, we and others discovered that ferroptosis does occur after haemorrhagic stroke in vitro and in vivo and contributes to neuronal death. Inhibition of ferroptosis is beneficial in several in vivo and in vitro ICH conditions. This minireview summarises current research on iron toxicity, lipid peroxidation and ferroptosis in the pathomechanisms of ICH, the underlying molecular mechanisms of ferroptosis and the potential for combined therapeutic strategies. Understanding the role of ferroptosis after ICH will provide a vital foundation for cell death-based ICH treatment and prevention.

scholarly journals Soluble Asialoglycoprotein Receptors Reflect the Apoptosis of Hepatocytes

2002 ◽  
Vol 11 (5) ◽  
pp. 407-415 ◽  
Author(s):  
Tetsuji Kakegawa ◽  
Hirohiko Ise ◽  
Nobuhiro Sugihara ◽  
Toshio Nikaido ◽  
Naoki Negishi ◽  
...  
Keyword(s):  
Cell Death ◽  
Liver Tissue ◽  
Liver Diseases ◽  
Culture Medium ◽  
Apoptotic Cell ◽  
Rabbit Serum ◽  
Mouse Serum ◽  
Apoptosis And Necrosis

Cell death is thought to take place through at least two distinct processes: apoptosis and necrosis. There is increasing evidence that dysregulation of the apoptotic program is involved in liver diseases. However, there is no method to simply evaluate apoptosis in the liver tissue at present. It has been reported that the expression of asialoglycoprotein receptors (AGPRs) increases with apoptosis, but there is no report until now that investigates the influence of soluble AGPRs on apoptosis of hepatocytes. Soluble AGPRs have been reported to be present in human serum under physiological conditions. In the present study, in order to investigate the correlation between apoptosis of hepatocytes and soluble AGPR, mouse soluble AGPRs were detected using SDS-PAGE and Western blot analysis was conducted using anti-extracellular mouse hepatic lectin-1 (Ex-MHL-1) antiserum (polyclonal rabbit serum). The mouse soluble AGPRs were present in culture medium and mouse serum when hepatocytes were damaged. The soluble AGPRs increased proportionately, as the number of dead hepatocytes increased. In addition, soluble AGPRs existed more when apoptotic cell death was observed in in vitro and in vivo than when necrotic cell death was observed. The extracellular moiety of MHL-1 exists in the culture medium and mouse serum as a soluble AGPR, but the detailed mechanism of releasing soluble AGPR from hepatocytes has not been revealed yet. We described the first evidence for the relation between quantity of soluble AGPRs with two kinds of cell death: necrosis and apoptosis. Based on the results of our study, soluble AGPRs might become a new marker of apoptosis in the liver tissue and be useful for clinical diagnosis and treatment for liver diseases.

scholarly journals Sindbis Virus-Induced Neuronal Death Is both Necrotic and Apoptotic and Is Ameliorated byN-Methyl-d-Aspartate Receptor Antagonists

2001 ◽  
Vol 75 (15) ◽  
pp. 7114-7121 ◽  
Author(s):  
Jennifer L. Nargi-Aizenman ◽  
Diane E. Griffin
Keyword(s):  
Cell Death ◽  
Cortical Neurons ◽  
Sindbis Virus ◽  
Apoptotic Cell ◽  
Time Lapse ◽  
Apoptotic Cell Death ◽  
Time Lapse Imaging ◽  
Alphavirus Infection

ABSTRACT Virus infection of neurons leads to different outcomes ranging from latent and noncytolytic infection to cell death. Viruses kill neurons directly by inducing either apoptosis or necrosis or indirectly as a result of the host immune response. Sindbis virus (SV) is an alphavirus that induces apoptotic cell death both in vitro and in vivo. However, apoptotic changes are not always evident in neurons induced to die by alphavirus infection. Time lapse imaging revealed that SV-infected primary cortical neurons exhibited both apoptotic and necrotic morphological features and that uninfected neurons in the cultures also died. Antagonists of the N-methyl-d-aspartate (NMDA) subtype of glutamate receptors protected neurons from SV-induced death without affecting virus replication or SV-induced apoptotic cell death. These results provide evidence that SV infection activates neurotoxic pathways that result in aberrant NMDA receptor stimulation and damage to infected and uninfected neurons.

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