scholarly journals Вплив реній-платинової системи у вигляді наноліпосом на проліферативну активність ракових клітин

2011 ◽  
Vol 2 (1) ◽  
pp. 59-67
Author(s):  
G. S. Kononova ◽  
S. V. Antonuk ◽  
N. I. Shtemenko
Keyword(s):  
Cell Death ◽  
Proliferative Activity ◽  
Apoptotic Cell ◽  
Organic Ligand ◽  
Tumour Tissue ◽  
Control Group ◽  
Effective Agent ◽  
Guerin’S Carcinoma ◽  
Morphological Indices ◽  
Tumour System

Decrease of proliferative activity of the cells of Guerin’s carcinoma T8 in the different conditions of administration of the Rhenium-Platinum anti-tumour system as nanolyposomes is shown. The Rhenium-Platinum anti-tumour system influenced on the morphological indices of tumour tissue. The cluster rhenium compounds reduced the indices of pathological mitoses 3.0–3.6 times in comparison with a control group. The amount of PCNA-positive cells under the Rhenium-Platinum system treatment went down by 82.5–84.5 %. The anti-tumour system led to the predominance of apoptotic cell death over the necrotic one. The most effective agent was the compound with cis-adamantan organic ligand cis-Re2(C10H15COO)2Cl4·2DMSO introducted on the 9th day.

Vascular Endothelium Is Severely Perturbed and Undergoes Apoptosis in Experimental Heatstroke in Primates.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3972-3972
Author(s):  
George T. Roberts ◽  
Muhammad A. Chishti ◽  
Fallah H. Al-Mohanna ◽  
Raafat M. El-Sayed ◽  
Abderezak Bouchama
Keyword(s):  
Cell Death ◽  
Endothelial Cell ◽  
Vascular Endothelium ◽  
Apoptotic Cell ◽  
Chromatin Condensation ◽  
Apoptotic Cell Death ◽  
Control Group ◽  
Tissue Sections ◽  
Endothelial Cell Death

Abstract Introduction: Ultrastructural evidence of endothelial cell (EC) injury has been associated with diffuse microvascular thrombosis in human heatstroke (HS). In vitro studies have also shown that heat stress accelerates apoptotic cell death. Using a recently described baboon model of heatstroke, we sought to examine pathological changes in the vascular endothelium and whether apoptosis is a mechanism of endothelial cell death. Hypothesis: Major structural vascular endothelium alterations occur in HS and apoptosis is a mechanism of endothelial cell death in HS. Methods: Anesthetized baboons (Papio hamadyras) were heat-stressed in a neonatal incubator maintained at 44 1.5 °C, until rectal temperature attained 42.5°C (moderate heatstroke; n =4) or systolic blood pressure fell to < 90 mm Hg (severe heatstroke n =4). Animals were resuscitated with normal saline and allowed to cool at room temperature. Four sham-heated animals served as control group. Spleen, liver, heart, kidney, gut, lung and adrenal tissue were obtained either by immediate autopsy in non-survivors or after euthanasia at 72-h for survivors. Vascular endothelium ultrastructure was evaluated by transmission electron microscopy (TEM) of ultra-thin tissue sections. Biological activity of EC was determined by light microscopy (LM) using a polyclonal antibody targeting von Willebrand Factor (vWF). Apoptosis was assessed, also in tissue sections, by deoxyuridine triphosphate nick end-labeling (TUNEL) procedure. Results: In heatstroke animals, there were marked EC changes in lungs, spleen, jejunum, kidneys and liver, demonstrated by TEM, as increased cytoplasmic membrane convolutions that included formation of villi projecting into the vessel lumina, and increase in the width of the gaps between ECs. Migration of neutrophils, platelets and erythrocytes through these widened gaps was noted. Weibel-Palade bodies were increased both in size and number in EC of jejunum, lungs and kidneys. This increase correlated with increased endothelial expression of immunologically detectable vWF. TEM also showed that there was increased apoptosis manifested by nuclear chromatin condensation and karyorrhexis and formation of cytoplasmic myelin whorls. Increased EC apoptosis was also observed by TUNEL in the jejunum, lungs, liver and spleen. All these changes were greater in animals with severe HS than in animals with moderate HS, whereas sham heated control animals showed no significant changes. Conclusion: Widespread EC injury with apoptotic cell death is consistent with the hypothesis that the endothelium may play a pathogenic role in heatstroke.

Selective iNOS-inhibition does not influence apoptosis in ruptured canine cranial cruciate ligaments

2009 ◽  
Vol 22 (03) ◽  
pp. 198-203 ◽  
Author(s):  
D. Hofer ◽  
S. Forterre ◽  
A. Schweighauser ◽  
M. Krayer ◽  
M. Doherr ◽  
...  
Keyword(s):  
Cell Death ◽  
Articular Cartilage ◽  
Apoptotic Cell ◽  
Cruciate Ligament ◽  
Control Group ◽  
No Production ◽  
Cranial Cruciate Ligament ◽  
Stifle Joint ◽  
Nos Inhibitor ◽  
Inos Inhibition

SummaryAbnormal patterns of cell death, including increased apoptosis, can influence homeostasis of ligaments and could be involved in the pathogenesis of cranial cruciate ligament (CCL) rupture. Increased nitric oxide (NO) production has been implicated as a stimulus to increased apoptosis in articular cartilage. This study investigated apoptotic cell death in ruptured canine CCL (CCL group, n = 15), in ruptured CCL of dogs treated with oral L-N6-(1-iminoethyl)-lysine (L-NIL), a selective NO-synthetase(NOS)-inhibitor, (L-NIL group, n = 15) and compared the results with normal canine CCL (control group, n = 10).Orally administered L-NIL at a dosage of 25 mg/m2 of body surface area was effective in inhibiting NO production in the articular cartilage of dogs in the L-NIL group, but it did not significantly influence the increased quantity of apoptotic cells found in ruptured CCL specimens. The results of this study suggest that apoptosis of ligamentocytes in the canine CCL is not primarily influenced by increased NO production within the stifle joint.

scholarly journals Rare norisodinosterol derivatives from Xenia umbellata: Isolation and anti-proliferative activity

2021 ◽  
Vol 19 (1) ◽  
pp. 400-407
Author(s):  
Nahed Obaid Bawakid ◽  
Walied Mohamed Alarif ◽  
Ahmed Abdel-Lateff
Keyword(s):  
Mass Spectrometry ◽  
Nuclear Magnetic Resonance ◽  
Cell Death ◽  
Magnetic Resonance ◽  
Cancer Cells ◽  
Proliferative Activity ◽  
Biosynthetic Pathway ◽  
Apoptotic Cell ◽  
Ht 29 ◽  
Treated Tumour

Abstract Two new rare 30-norisodinosterol derivatives, 23,24-dimethylcholest-16-ene-3β,5α,6β,11α,20(R)-pentol 3-monoacetate (1) and 23,24-dimethylcholest-16-ene-3β,5α,6β,20(R)-tertrol 3-monoacetate (2), along with a known steroid, 3β,5α,6β,11α,20β-pentahydroxygorgosterol (3), were identified from Xenia umbellata. The structures of the isolated compounds were determined by analyses of the measured spectra (1D and 2D nuclear magnetic resonance, mass spectrometry, and infrared). The biosynthetic pathway of the new norisodinosterols was proposed. Compound 1 exhibited potent cytotoxicity against HepG2, PC-3, and HT-29 with IC50 values of 4.70 ± 0.2, 5.60 ± 0.6, and 4.00 ± 0.4 μg/mL, respectively. On the contrary, compound 3 showed less potent cytotoxicity against HepG2 with IC50 value of 22.20 ± 1.0 μg/mL. Two DNA-binding dyes have been used for the morphological detection of viable, apoptotic, and necrotic cells. The early apoptotic cell death was observed in all types of treated tumour cells. The late apoptotic cells are highly present in HepG2 cells with compound 3 compared with other cancer cells except for compound 1. The anti-proliferative activity of compounds 1 and 3 warranted further investigation.

scholarly journals Annexin V Levels as an Indicator of Myocardial Cell Death after Myocardial Infarction

2020 ◽  
Vol 19 (2) ◽  
pp. 78-84
Author(s):  
Mohammed Karem Ahmed ◽  
◽  
Adil Hassan Mohammed ◽  
Amed Medb Athab
Keyword(s):  
Myocardial Infarction ◽  
Cell Death ◽  
Apoptotic Cell ◽  
Plasma Concentrations ◽  
Annexin V ◽  
Myocardial Cell ◽  
Early Morning ◽  
Control Group ◽  
P Value ◽  
The Mean

Background:Myocardial ischemia is associated with apoptosis of cardiomyocyte and because of apoptotic cell death is characterized by externalization of Phosphatidylserine on the cell membrane, so it is amenable to targeting by Annexin V. Objective: To compare plasma concentrations of Annexin V in patients who had an early infarct with patients without infarction. And to analyze the plasma concentration of Annexin V in relationship to cardiovascular risk factors. Patients and Methods: A Case-control study of 100 patients (case) who are diagnosed with Myocardial Infarction (MI) and admitted to the coronary care unit of Baqubah Teaching Hospital and another 100 patients homogenous in terms of age and gender and who attended the hospital for other cause than myocardial infarction is selected as the control group during a period between the first of April and the first of July 2019. A special questionnaire used to collect the required information, an early morning blood sample is taken to measure the level of Annexin V by ELISA, Student’s t-test, ANOVA test and Chi_square test to find an association and differences between variables. Results: The results showed that The mean Annexin V level is significantly higher in cases (10.48155ng/ml) than control (1.28803ng/ml) with p-value =0.001 and a sample taken within 24 hours after MI is significantly higher in the mean level of Annexin V then the sample taken after 24 hours of MI. Conclusion: Generally, the measurement of Annexin V level has provided a good diagnostic test to evaluate myocardial infarction. Keywords: Myocardial infarction, Annexin V, Phosphatidylserine, Apoptosis

115 APOPTOSIS EVENT OF PREIMPLANTATION DEVELOPMENT STAGES IN PORCINE IN VITRO-FERTILIZED EMBRYOS

2009 ◽  
Vol 21 (1) ◽  
pp. 157
Author(s):  
S. M. Hong ◽  
S. H. Jeong ◽  
S. H. Hyun
Keyword(s):  
Cell Death ◽  
Actinomycin D ◽  
Apoptotic Cell ◽  
Formation Rate ◽  
Preimplantation Development ◽  
Preimplantation Embryos ◽  
Control Group ◽  
Cell Stage ◽  
Development Stages

Little is known about apoptosis events in porcine preimplantation embryos. In this study, we aimed to determine whether the evaluated markers of cell death could be found at particular developmental stages of normal porcine in vitro-fertilized (IVF) embryos. We investigated the characteristics of spontaneous and induced apoptosis during preimplantation development stages of porcine IVF embryos. In experiment 1, to induce apoptosis of porcine IVF embryos, porcine IVF embryos at 22 h postinsemination were treated at different concentrations of actinomycin D (0, 5, 50 and 500 ng mL–1 in NCSU medium). Four groups were incubated at 37°C in 5% CO2, 5%O2 for 8 h, and then washed to NCSU medium and incubated until blastocyst (BL) stage. We examined cleavage rate at 2 days and BL development rate at 7 days after in vitro culture (IVC). A significantly less rate of cleavage was found in the 500 ng mL–1 group compared with others (500 ng mL–1 v. 0, 5, 50 ng mL–1; 15.4% v. 48.6%, 40%, 32%). In the results of BL formation rate, there was a significantly less BL formation rate in 500 ng mL–1 compared with others (500 ng mL–1 v. 0, 5, 50 ng mL–1; 0% v. 10%, 8.8%, 9%). In experiment 2, to evaluate apoptotic cells at different stage (2-cell, 4-cell, 8-cell and BL stage) of all groups, we conducted TUNEL assay based on morphological assessment of nuclei and on detection of specific DNA degradation under fluorescence microscope. This result showed that apoptosis is a normal event during preimplantation development in control group (0 ng mL–1 actinomycin D). A high number of the BL derived control group contained at least one apoptotic cell. Actinomycin D treated BL responded to the presence of apoptotic inductor by a significant decrease in the average number of blastomeres and a significant increase in the incidence of apoptotic cell death. In the 500 ng mL–1 group, the incidence of apoptosis increased at the 4-cell stage and later. This result suggested that apoptosis is a process of normal embryonic development and actinomycin D is a useful tool for the apoptosis study of porcine preimplantation embryos. This work was supported by a grant (#20070301034040) from BioGreen 21 program, Rural Development Administration, Republic of Korea.

Effect of ONC201 and bortezomib on apoptosis in non-Hodgkin'™s lymphoma (NHL) xenografts.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e19016-e19016 ◽  
Author(s):  
Mala Kiran Talekar ◽  
Junior Hall ◽  
Gerald B Wertheim ◽  
Daniel Martinez ◽  
Joshua E. Allen ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Necrosis ◽  
Apoptotic Cell ◽  
Xenograft Model ◽  
Combination Group ◽  
Control Group ◽  
Minimal Cell ◽  
Tumor Cell Death ◽  
Mouse Xenograft Model

e19016 Background: Our group has previously shown preclinical in vitro efficacy of novel small molecule, ONC201 across several pediatric NHL cell lines (Talekar et al, 2015) as a monoagent as well as in combination with chemotherapy agents, significantly cytarabine and bortezomib. We investigated the preclinical efficacy of ONC201 and bortezomib combination in vivo in a NHL mouse xenograft model. Methods: Burkitt’s lymphoma cell line (Ramos) transduced with lentiviral GFP was utilized to establish subcutaneous flank xenografts in 5-7 week(wk) old immunodeficient SCID mice [NOD.Cg- Prkdcscid Il2rgtm1Wjl/SzJ]. All tumors were established by Day 10, detected by bioluminescent imaging and were serially imaged x1/wk. Mice were studied in 4 treatment arms (7 mice per arm) as tabulated in the table. Results: Mice in Arms 1, 2 & 3 had continued tumor growth and were humanely euthanized during Wk 3- 4 of treatment when the tumor volume reached the maximum allowable size per the approved institutional IACUC protocol. Mice in Arm 4 showed gross tumor necrosis and had to be euthanized in Wk 4. Upon treatment initiation, 2 mice in each arm were sacrificed at 48 and 72 hours respectively and tumor samples harvested for histology and IHC analysis (TRAIL and CHOP/GADD). Histological analysis revealed that the control group had predominantly viable tumor cells at both 48 & 72 H. The monoagent groups showed minimal cell death with bortezomib alone and modest cell death with ONC201 as monoagent in clustered regions. In contrast, the combination group showed: i) extensive global tumor necrosis with nuclear debris on H&E, ii) prominent TRAIL induction by IHC analysis, and, iii) significant apoptotic cell death accompanied by CHOP /GADD overexpression indicating potential ER stress. Induction of these pharmacodynamic markers in Arm 4 were evident at 48H and more prominent at the 72H. Conclusions: ONC201 effectively synergizes with bortezomib to cause apoptotic tumor cell death in pediatric NHL murine xenograft and merits further investigation. [Table: see text]

scholarly journals Endosomal dysfunction in iPSC-derived neural cells from Parkinson’s disease patients with VPS35 D620N

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Keiko Bono ◽  
Chikako Hara-Miyauchi ◽  
Shunsuke Sumi ◽  
Hisayoshi Oka ◽  
Yasuyuki Iguchi ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Death ◽  
Apoptotic Cell ◽  
Induced Pluripotent Stem Cell ◽  
Control Group ◽  
Neural Cells ◽  
Endosomal Trafficking ◽  
Induced Pluripotent ◽  
Vacuolar Protein

Abstract Mutations in the Vacuolar protein sorting 35 (VPS35) gene have been linked to familial Parkinson’s disease (PD), PARK17. VPS35 is a key component of the retromer complex, which plays a central role in endosomal trafficking. However, whether and how VPS35 deficiency or mutation contributes to PD pathogenesis remain unclear. Here, we analyzed human induced pluripotent stem cell (iPSC)-derived neurons from PD patients with the VPS35 D620N mutation and addressed relevant disease mechanisms. In the disease group, dopaminergic (DA) neurons underwent extensive apoptotic cell death. The movement of Rab5a- or Rab7a-positive endosomes was slower, and the endosome fission and fusion frequencies were lower in the PD group than in the healthy control group. Interestingly, vesicles positive for cation-independent mannose 6-phosphate receptor transported by retromers were abnormally localized in glial cells derived from patient iPSCs. Furthermore, we found α-synuclein accumulation in TH positive DA neurons. Our results demonstrate the induction of cell death, endosomal dysfunction and α -synuclein accumulation in neural cells of the PD group. PARK17 patient-derived iPSCs provide an excellent experimental tool for understanding the pathophysiology underlying PD.

scholarly journals Endosomal Dysfunction in iPSC-Derived Neural Cells from Parkinson’s Disease Patients with VPS35 D620N

2020 ◽  
Author(s):  
Keiko Bono ◽  
Chikako Miyauchi-Hara ◽  
Shunsuke Sumi ◽  
Hisayoshi Oka ◽  
Yasuyuki Iguchi ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Death ◽  
Apoptotic Cell ◽  
Induced Pluripotent Stem Cell ◽  
Control Group ◽  
Neural Cells ◽  
Endosomal Trafficking ◽  
Induced Pluripotent ◽  
Vacuolar Protein

Abstract Mutations in the Vacuolar protein sorting 35 (VPS35) gene have been linked to familial Parkinson’s disease (PD), PARK17. VPS35 is a key component of the retromer complex, which plays a central role in endosomal trafficking. However, whether and how VPS35 deficiency or mutation contributes to PD pathogenesis remain unclear. Here, we analyzed human induced pluripotent stem cell (iPSC)-derived neurons from PD patients with the VPS35 D620N mutation and addressed relevant disease mechanisms. In the disease group, dopaminergic (DA) neurons underwent extensive apoptotic cell death. The movement of Rab5a- or Rab7a-positive endosomes was slower, and the endosome fission and fusion frequencies were lower in the PD group than in the healthy control group. Interestingly, vesicles positive for cation-independent mannose 6-phosphate receptor transported by retromers were abnormally localized in glial cells derived from patient iPSCs. Furthermore, we found a-synuclein accumulation in TH positive DA neurons. Our results demonstrate the induction of cell death, endosomal dysfunction and a-synuclein accumulation in neural cells of the PD group. PARK17 patient-derived iPSCs provide an excellent experimental tool for understanding the pathophysiology underlying PD.

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