Journal articles: 'TUNEL'

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Komór, Kinga, Magda Kołaczyńska, and Dominika Kosylak. "Drążenie tuneli technologią TBM." BUILDER 262, no. 5 (May 1, 2019): 100–102. http://dx.doi.org/10.5604/01.3001.0013.3569.

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W artykule została scharakteryzowana metoda wykonania tunelu z wykorzystaniem technologii TBM. Na przykładzie linii metra warszawskiego zaprezentowany został schemat wykonywania prac ta metoda oraz monitoring bezpieczenstwa przylegajacej infrastruktury. Metoda ta jest równie z powodzeniem wykorzystywana do draenia tuneli drogowych, wodociagowych, kanalizacyjnych, hydroenergetycznych czy wielozadaniowych. Za pomoca technologii TBM utworzono ju 369 projektów tuneli metra o długosci ponad 880 km, 440 km tuneli kolejowych i 171 km drogowych. Łacznie ta technologia wydraono ponad 1900 km tuneli na całym swiecie [7]. Przewanie jest ona bardziej ekonomiczna i efektywna w stosunku do metod tradycyjnych (odkrywkowych). Nie powoduje nadmiernych utrudnien w komunikacji transportu ulicznego, a w ciagu doby może powstac nawet trzykrotnie dłuższy tunel, aniżeli ten wykonany w tradycyjny sposób. Ponadto, co istotne z punktu widzenia ekonomicznego, całkowity koszt wydrażenia metra technologia TBM jest niższy [7].

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Gergeta Sotončić, Kristina. "Rezultati arheoloških radova uz poligonalnu kulu u Carrarinoj ulici u Puli 2021. godine." Histria, no. 11 (December 30, 2021): 11–28. http://dx.doi.org/10.32728/h2021.01.

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U veljači 2021. arheološki je istražen prostor u polovici širine poligonalne kule uz ulaz u tunel Zerostrasse i ulazni dio tunela u Carrarinoj ulici u Puli. Povod tomu bila je zamjena kabelskoga voda za dizalo koje će povezivati mrežu podzemnih tunela i utvrdu Kaštel. Istraživanjem je utvrđena fazna izgrađenost kule: kasnoantička kula poligonalnoga oblika, čija je struktura vidljiva u današnjoj hodnoj razini, nalegla je na antičku kulu kružnoga oblika, koja je temeljena na četvrtastoj kuli iz najranije faze formiranja pulskoga gradskog obrambenog sustava. Na samom ulazu u tunel otkriveni su ostaci kasnoantičkoga bedema. Istraživanjem je utvrđen način spoja kasnoantičkoga bedema na poligonalnu kulu: preslojavanjem četvrtaste kule i sloja popločenja te oslanjanjem na okruglu kulu koja je pridodana potezu najranijega gradskog bedema.

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Gergeta Sotončić, Kristina. "Rezultati arheoloških radova uz poligonalnu kulu u Carrarinoj ulici u Puli 2021. godine." Histria, no. 11 (December 30, 2021): 11–28. http://dx.doi.org/10.32728/h2021.01.

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U veljači 2021. arheološki je istražen prostor u polovici širine poligonalne kule uz ulaz u tunel Zerostrasse i ulazni dio tunela u Carrarinoj ulici u Puli. Povod tomu bila je zamjena kabelskoga voda za dizalo koje će povezivati mrežu podzemnih tunela i utvrdu Kaštel. Istraživanjem je utvrđena fazna izgrađenost kule: kasnoantička kula poligonalnoga oblika, čija je struktura vidljiva u današnjoj hodnoj razini, nalegla je na antičku kulu kružnoga oblika, koja je temeljena na četvrtastoj kuli iz najranije faze formiranja pulskoga gradskog obrambenog sustava. Na samom ulazu u tunel otkriveni su ostaci kasnoantičkoga bedema. Istraživanjem je utvrđen način spoja kasnoantičkoga bedema na poligonalnu kulu: preslojavanjem četvrtaste kule i sloja popločenja te oslanjanjem na okruglu kulu koja je pridodana potezu najranijega gradskog bedema.

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Gergeta Sotončić, Kristina. "Rezultati arheoloških radova uz poligonalnu kulu u Carrarinoj ulici u Puli 2021. godine." Histria, no. 11 (December 30, 2021): 11–28. http://dx.doi.org/10.32728/h2021.01.

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U veljači 2021. arheološki je istražen prostor u polovici širine poligonalne kule uz ulaz u tunel Zerostrasse i ulazni dio tunela u Carrarinoj ulici u Puli. Povod tomu bila je zamjena kabelskoga voda za dizalo koje će povezivati mrežu podzemnih tunela i utvrdu Kaštel. Istraživanjem je utvrđena fazna izgrađenost kule: kasnoantička kula poligonalnoga oblika, čija je struktura vidljiva u današnjoj hodnoj razini, nalegla je na antičku kulu kružnoga oblika, koja je temeljena na četvrtastoj kuli iz najranije faze formiranja pulskoga gradskog obrambenog sustava. Na samom ulazu u tunel otkriveni su ostaci kasnoantičkoga bedema. Istraživanjem je utvrđen način spoja kasnoantičkoga bedema na poligonalnu kulu: preslojavanjem četvrtaste kule i sloja popločenja te oslanjanjem na okruglu kulu koja je pridodana potezu najranijega gradskog bedema.

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., Supriya, Sneha G. Kalthur, and Guruprasad Kalthur. "Cellular Changes and Effect on DNA Integrity of the Epididymal Cells of Swiss Albino Mice Post Exposure to High Dose of Cyclophosphamide: A Histological and TUNEL Assay Study." International Journal of Science and Healthcare Research 7, no. 1 (January 21, 2022): 54–64. http://dx.doi.org/10.52403/ijshr.20220111.

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Background: Many studies done in past literature focuses on gonadal toxicity of Cyclophosphamide, but very less studies are done on the epididymis post exposure to this drug. Hence a sincere attempt is made in present study to look into the cellular changes in the epididymis through histology and TUNEL Assay. Subjects & Methods: Healthy male Swiss albino adult mice, were obtained from Central Animal Research Facility, Manipal were used for the study. The adult as well as prepubertal male mice were divided into control and test groups. In test group, the mice were injected with Cyclophosphamide at variable doses. From each group certain no. of mice was sacrificed on different days. A control group was kept for each intervals. The epididymal tissue was then extracted and used in histological and Tunnel Assay study. Results: Even though there was no significant change in the number of basal cells, the apical cells decreased marginally at higher doses of CP. A TUNEL assay was performed in the epididymal sections to understand its effect on the DNA integrity. Up to 100 mg/kg, CP did not induce any significant increase in the TUNEL positive tubules. However, at 200 mg/kg dose and above, there was an increase in the number of tubules with TUNEL positive cells indicating its DNA damaging effect. However, this increase was statistically not significant Conclusion: The present study highlights the need for looking into the cellular damage of the cells after exposure to one of the commonly used anticancer drug- cyclophosphamide. Keywords: Epididymal Histology, Tunnel Assay, Cyclophosphamide, Swiss Albino mice.

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Negoescu, A., P. Lorimier, F. Labat-Moleur, C. Drouet, C. Robert, C. Guillermet, C. Brambilla, and E. Brambilla. "In situ apoptotic cell labeling by the TUNEL method: improvement and evaluation on cell preparations." Journal of Histochemistry & Cytochemistry 44, no. 9 (September 1996): 959–68. http://dx.doi.org/10.1177/44.9.8773561.

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TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling) is a method of choice for rapid identification and quantification of the apoptotic cell fraction in cultured cell preparations. However, TUNEL application has been restricted to a narrow spectrum of sample conditions, and only detergents have been proposed as labeling enhancers. This study was aimed at extending TUNEL to variously fixed cells and improving TUNEL sensitivity by optimized pretreatments, the specificity being assessed by reference to the apoptotic morphology. Comparative TUNEL was performed with three protocols on CEM-C7 cells, a model of glucocorticoid-induced apoptosis. Samples were submitted to six modalities of fixation and TUNEL was performed after each of the following conditions: no pretreatment; detergent permeabilization; proteolytic digestion; microwave irradiation; and a recently published combination of the latter two. The proportion of TUNEL-stained elements within the cell fraction, with and without apoptotic morphology, was quantified. Our results showed that: (a) with an adequate pretreatment, reliable TUNEL can be obtained after each fixative tested; (b) detergent was inefficient in improving sensitivity; (c) whatever the fixation, microwave pretreatment provided the best TUNEL sensitivity without notable loss of specificity; (d) under adaptive technical conditions, TUNEL can be associated with detection of various proteins by double labeling; and (e) the existence of a limited population of intensely TUNEL-positive cells that lacked apoptotic morphology contributes to the current debate about a preapoptotic state.

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Moore, Christopher L., Alena V. Savenka, and Alexei G. Basnakian. "TUNEL Assay: A Powerful Tool for Kidney Injury Evaluation." International Journal of Molecular Sciences 22, no. 1 (January 2, 2021): 412. http://dx.doi.org/10.3390/ijms22010412.

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Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay is a long-established assay used to detect cell death-associated DNA fragmentation (3’-OH DNA termini) by endonucleases. Because these enzymes are particularly active in the kidney, TUNEL is widely used to identify and quantify DNA fragmentation and cell death in cultured kidney cells and animal and human kidneys resulting from toxic or hypoxic injury. The early characterization of TUNEL as an apoptotic assay has led to numerous misinterpretations of the mechanisms of kidney cell injury. Nevertheless, TUNEL is becoming increasingly popular for kidney injury assessment because it can be used universally in cultured and tissue cells and for all mechanisms of cell death. Furthermore, it is sensitive, accurate, quantitative, easily linked to particular cells or tissue compartments, and can be combined with immunohistochemistry to allow reliable identification of cell types or likely mechanisms of cell death. Traditionally, TUNEL analysis has been limited to the presence or absence of a TUNEL signal. However, additional information on the mechanism of cell death can be obtained from the analysis of TUNEL patterns.

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Masiakowska-Osses, Dorota. "Nie do przebycia? O granicach i ich przekraczaniu w powieści "Tunel" Magdaleny Parys." Acta Neophilologica 2, no. XXIII (September 25, 2021): 229–40. http://dx.doi.org/10.31648/an.6668.

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This article is an analysis of Tunel (The Tunnel), the novel by Magdalena Parys, a Polish author living in Germany. The action of the book focuses on the fictional construction of an escape tunnel built under the border wall between the western and eastern part of Berlin in the early 1980s. This, somehow, predestines Parys’s work to be read in the context of transgression, and crossing limitations. Starting with the writer’s non-literary inspirations, the article shows the multiplicity of literal and metaphorical meanings of the term “border” and examines how the motif functions in the presented world.

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Wu, Yi-Chun, Gillian M. Stanfield, and H. Robert Horvitz. "NUC-1, a Caenorhabditis elegans DNase II homolog, functions in an intermediate step of DNA degradation during apoptosis." Genes & Development 14, no. 5 (March 1, 2000): 536–48. http://dx.doi.org/10.1101/gad.14.5.536.

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One hallmark of apoptosis is the degradation of chromosomal DNA. We cloned the Caenorhabditis elegans gene nuc-1, which is involved in the degradation of the DNA of apoptotic cells, and found that nuc-1 encodes a homolog of mammalian DNase II. We used the TUNEL technique to assay DNA degradation in nuc-1 and other mutants defective in programmed cell death and discovered that TUNEL labels apoptotic cells only during a transient intermediate stage. Mutations in nuc-1 allowed the generation of TUNEL-reactive DNA but blocked the conversion of TUNEL-reactive DNA to a subsequent TUNEL-unreactive state. Completion of DNA degradation did not occur in the absence of cell-corpse engulfment. Our data suggest that the process of degradation of the DNA of a cell corpse occurs in at least three distinct steps and requires activities provided by both the dying and the engulfing cell.

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Masetto, Tathiana Elisa, and José Marcio Rocha Faria. "In situ DNA fragmentation during the re-establishment of desiccation tolerance in germinated seeds of Cedrela fissilis Vell." Journal of Seed Science 41, no. 2 (April 2019): 244–49. http://dx.doi.org/10.1590/2317-1545v42n2207417.

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Abstract: Dehydration is a necessary procedure prior to exposing seeds to long term storage, but this is associated with metabolism-linked injury mediated by cell injury. In order to assess cellular alterations during re-establishment of desiccation tolerance (DT) in C. fissilis germinated seeds and their relation to DNA damage, we verified the occurrence of DNA fragmentation through the TUNEL test and its evidence through the cytological analyses. To re-establish DT, germinated seeds were incubated for 72 h in polyethylene glycol (PEG, -2.04 MPa) before dehydration in silica gel (at 10% moisture content) followed by rehydration. The moisture content changes during the reestablishment of the desiccation tolerance was accomplished. (DT)TdT-dUPT terminal nick-end labeling (TUNEL) was used to assess rates of cell death. TUNEL staining was performed using Click-iT-TUNEL Alexa Flour imaging assay. The TUNEL test showed a consistent DNA fragmentation in the 2 and 5 mm long radicles. Moreover, nuclear and chromosomal alterations were observed in the 5 mm meristematic root cell cycle, contributing to the identification of diagnostic markers of cell death.

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Mirzayans, Razmik, and David Murray. "Do TUNEL and Other Apoptosis Assays Detect Cell Death in Preclinical Studies?" International Journal of Molecular Sciences 21, no. 23 (November 29, 2020): 9090. http://dx.doi.org/10.3390/ijms21239090.

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The terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay detects DNA breakage by labeling the free 3ʹ-hydroxyl termini. Given that genomic DNA breaks arise during early and late stages of apoptosis, TUNEL staining continues to be widely used as a measure of apoptotic cell death. The advantages of the assay include its relative ease of performance and the broad availability of TUNEL assay kits for various applications, such as single-cell analysis of apoptosis in cell cultures and tissue samples. However, as briefly discussed herein, aside from some concerns relating to the specificity of the TUNEL assay itself, it was demonstrated some twenty years ago that the early stages of apoptosis, detected by TUNEL, can be reversed. More recently, compelling evidence from different biological systems has revealed that cells can recover from even late stage apoptosis through a process called anastasis. Specifically, such recovery has been observed in cells exhibiting caspase activation, genomic DNA breakage, phosphatidylserine externalization, and formation of apoptotic bodies. Furthermore, there is solid evidence demonstrating that apoptotic cells can promote neighboring tumor cell repopulation (e.g., through caspase-3-mediated secretion of prostaglandin E2) and confer resistance to anticancer therapy. Accordingly, caution should be exercised in the interpretation of results obtained by the TUNEL and other apoptosis assays (e.g., caspase activation) in terms of apoptotic cell demise.

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Chambers, Steven A., Mathew Newman, Melissa M. Frangie, Alena V. Savenka, Alexei G. Basnakian, and Mohammad A. Alam. "Antimelanoma activities of chimeric thiazole–androstenone derivatives." Royal Society Open Science 8, no. 8 (August 2021): 210395. http://dx.doi.org/10.1098/rsos.210395.

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The discovery of chimeric anti-melanoma agents is reported. These molecules are potent growth suppressors of melanoma cells in vitro with growth inhibition of 50% (GI 50 ) values as low as 1.32 µM. Compounds were more toxic to melanoma cells in vitro than commonly used anti-melanoma agent dacarbazine as measured by TUNEL assay. They induced both caspase-independent apoptosis evident by colocalization of TUNEL with endonuclease G (EndoG) and caspase-mediated apoptosis measured by colocalization of TUNEL with caspase-activated DNase (CAD). In addition, compounds 3 and 5 strongly induced oxidative injury to melanoma cells as measured by TUNEL colocalization with heme oxygenase-1 (HO1). Dacarbazine induced only caspase-independent apoptosis, which may explain why it is less cytotoxic to melanoma cells than compounds 3 , 4 and 5 .

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Kelly, K. J., Ruben M. Sandoval, Kenneth W. Dunn, Bruce A. Molitoris, and Pierre C. Dagher. "A novel method to determine specificity and sensitivity of the TUNEL reaction in the quantitation of apoptosis." American Journal of Physiology-Cell Physiology 284, no. 5 (May 1, 2003): C1309—C1318. http://dx.doi.org/10.1152/ajpcell.00353.2002.

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Apoptosis is an important mode of cell death under both physiological and pathophysiological conditions. Numerous techniques are available for the study and quantitation of apoptosis in cell culture, but only few are useful when applied to complex tissues. Among these, the terminal transferase-mediated dUTP nick end-labeling (TUNEL) assay remains the most widely used technique. However, its specificity and sensitivity for the detection of apoptosis remain controversial. We developed a technique consisting of staining live cells and tissues with Hoechst 33342 and the vital dye propidium iodide (PI), followed by fixation and the TUNEL reaction. We demonstrate excellent retention of PI in necrotic cells after fixation. We also examined the distribution of TUNEL staining among necrotic and apoptotic cells in various models of cell injury in vitro and in vivo. We show that the sensitivity of the TUNEL varied between 61 and 90% in the models examined. The specificity exceeded 87% in all models but fell to 70% when a predominantly necrotic injury was induced. This novel and simple method will permit the determination of indices of sensitivity and specificity for the TUNEL assay in other tissues and experimental conditions.

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Isailović, Slobodan. "MIKROMREŽA TUNELA "STRAŽEVICA" U RESNIKU (BEOGRAD)." Zbornik radova Fakulteta tehničkih nauka u Novom Sadu 35, no. 02 (January 29, 2020): 360–63. http://dx.doi.org/10.24867/06kg02isailovic.

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Tunel je najčešće saobraćajni ili hidrotehnički objekat koji se nalazi u zemljištu, na jednom ili oba kraja izlazi na površinu, ili uopšte ne izlazi na površinu. U radu je opisan projekat i realizacija projekta mikromreže za tunel "Straževica" u Beogradu.

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Umemura, S., M. Yasuda, R. Y. Osamura, Y. Kawarada, T. Sugiyama, and Y. Tsutsumi. "Enhancement of TdT-mediated dUTP-biotin nick end-labeling (TUNEL) method using mung bean nuclease, a single-stranded DNA digestion enzyme." Journal of Histochemistry & Cytochemistry 44, no. 2 (February 1996): 125–32. http://dx.doi.org/10.1177/44.2.8609368.

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The TdT-mediated dUTP-biotin nick end-labeling (TUNEL) method has been employed widely to demonstrate apoptotic cells in routinely prepared paraffin sections. Because the apoptotic cells were reactive with the antibody to single-stranded DNA, we attempted to enhance the TUNEL positivity by pretreatment with single-stranded DNA digestion enzymes, S1 nuclease, and mung bean nuclease. When mung bean nuclease (5 U/50 microliter/section) was incubated at 37 degrees C for 30 min, the TUNEL reaction was most effectively enhanced. Pretreatment with S1 nuclease (0.25 U/50 microliter/section) at 37 degrees C for 45 min was less reliable. Compared with the conventional TUNEL sequence, the enhancement technique using mung bean nuclease enabled us to detect more apoptotic cells in human small intestine, colon, tonsil, thymus, endometrium, ovary, liver, kidney, and pancreas. The positivity was not affected by autolytic change. The mechanism of enhancement is discussed.

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Sloop, Gregory D., Juan C. Roa, Alberto G. Delgado, John T. Balart, Merrill O. Hines, and James M. Hill. "Histologic Sectioning Produces TUNEL Reactivity." Archives of Pathology & Laboratory Medicine 123, no. 6 (June 1, 1999): 529–32. http://dx.doi.org/10.5858/1999-123-0529-hsptr.

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Abstract Objective.—To determine if the DNA strand breaks caused by tissue sectioning result in terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick end-labeling (TUNEL) reactivity. Methods.—The incidence and location of TUNEL-positive nuclei were determined in 5- and 15-μm sections of human stomach. Five- and 15-μm sections of tonsil were stained as a positive control. Results.—In 5-μm gastric sections, 69% of nuclei were labeled; in 15-μm sections, only 30% were labeled. In the latter sections, almost all labeled nuclei were located at the cut surface of sections. Labeled nuclei did not have apoptotic morphology. Apototic bodies and tingible body macrophages were labeled throughout 15-μm sections of tonsil. Conclusions.—Tissue sectioning creates TUNEL reactivity. The morphologic findings on routine stains should be considered the gold standard for the detection of apoptosis on tissue sections.

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Machado, D. A., and W. P. Martins. "Síndrome do tunel do carpo." Experts in Ultrasound: Reviews and Perspectives 1, no. 3 (July 1, 2009): 136–40. http://dx.doi.org/10.4281/eurp.2009.03.02.

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Obradović, Nadežda, and Vanja Bulić. "Tunel: Lepa sela lepo gore." World Literature Today 72, no. 1 (1998): 168. http://dx.doi.org/10.2307/40153659.

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Short, Ben. "TUNEL vision spots apoptotic cells." Journal of Cell Biology 208, no. 1 (January 5, 2015): 7. http://dx.doi.org/10.1083/jcb.2081fta.

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Walker, J. A., and P. Quirke. "Viewing apoptosis through a ?TUNEL?" Journal of Pathology 195, no. 3 (2001): 275–76. http://dx.doi.org/10.1002/path.979.

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SATOH, Kasumi, Tetsuo NAGATANI, and Hiroshi NAKAJIMA. "Examination of BCC by TUNEL method. Examination of apotosis in BCC by TUNEL method." Skin Cancer 13, no. 2 (1998): 154–57. http://dx.doi.org/10.5227/skincancer.13.154.

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Dagistanli, F., H. Ozkaya, B. Kucukyoruk, H. Biceroglu, D. Metin, N. Gazioglu, B. Oz, P. Kadioglu, and M. Ozturk. "Preoperative Somatostatin Analogue Treatment Might Trigger Apoptosis and Autophagy in Tumor Tissues of Patients with Acromegaly: A Pilot Study." Experimental and Clinical Endocrinology & Diabetes 126, no. 03 (June 20, 2016): 168–75. http://dx.doi.org/10.1055/s-0042-107243.

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Abstract Objective: To evaluate the effect of preoperative somatostatin analog (SRL) treatment on proteins associated with apoptosis and autophagy in patients with acromegaly and to determine factors correlating with these parameters. Methods: Ex-vivo tumor samples of 11 SRL-treated and 9 SRL-untreated patients were retrospectively included in the study. Apoptotic and autophagic proteins were determined via immunohistochemical staining and apoptosis was evaluated via in situ DNA end labeling (TUNEL). Results: TUNEL, caspase-3, and ATG-5 immunopositivity was significantly increased (p<0.01, p=0.01, p=0.01, respectively), survivin and beclin-1 immunopositivity was significantly decreased (p=0.03, p=0.02, respectively) in SRL-treated patients as compared with SRL-untreated controls. Ki-67 index was decreased significantly in the SRL-treated group (p=0.01). Significant positive correlations were detected between TUNEL and caspase-3 immunopositivity (r=0.577, p<0.01), and between survivin and beclin-1 immunopositivity (r=0.503, p=0.03). Age at diagnosis, preoperative GH, IGF-1 levels, tumor size, and invasion status were not found to affect TUNEL positivity nor did they correlate with caspase-3, survivin, beclin-1, ATG-5 immunopositivity (p>0.05 for all). Preoperative SRL treatment was the only factor that had a significant effect on TUNEL positivity (adjusted R2=0.39, p=0.02). Preoperative treatment duration was positively correlated with TUNEL and caspase-3 immunopositivity (r=0.526, p=0.02; r=0.475, p=0.04, respectively) and negatively correlated with survivin immunopositivity (r=−0.533, p=0.01). Conclusions: Somatostatin analog treatment might induce apoptosis, increase autophagy, and decrease cell proliferation in GH-secreting adenomas. Also, proteins related to cross-talk between autophagy and apoptosis are upregulated after SRL treatment.

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Britton, Mark, Jose Rafols, Sarah Alousi, and Joseph C. Dunbar. "The Effects of Middle Cerebral Artery Occlusion on Central Nervous System Apoptotic Events in Normal and Diabetic Rats." Experimental Diabesity Research 4, no. 1 (2003): 13–20. http://dx.doi.org/10.1080/15438600303727.

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Apoptosis and neural degeneration are characteristics of cerebral ischemia and brain damage. Diabetes is associated with worsening of brain damage following ischemic events. In this study, the authors characterize the influence of focal cerebral ischemia, induced by middle cerebral artery occlusion, on 2 indexes of apoptosis,TUNEL(terminal deoxynucleotidyl transferase–mediated deoxyuridine 5-triphosphate nick end-labeling) staining and caspase- 3 immunohistochemistry. Diabetes was induced in normal rats using streptozotocin and maintained for 5 to 6 weeks. The middle cerebral artery of both normal and diabetic rats was occluded and maintained from 24 or 48 hours. Sham-operated normal and diabetic animals served as controls. Following 24 to 48 hours of occlusion, the animals were sacrificed and the brains were removed, sectioned, and processed for TUNEL staining or caspase-3 immunohistochemistry. Middle cerebral artery occlusion in normal rats was associated with an increase in the number of both TUNEL-positive and caspase-3– positive cells in selected brain regions (hypothalamic preoptic area, piriform cortex, and parietal cortex) when compared to nonoccluded controls. Diabetic rats without occlusion showed significant increases in both TUNEL-positive and caspase-3–positive cells compared to normal controls. Middle cerebral artery occlusion in diabetic rats resulted in increases in TUNEL-positive as well as caspase-3–positive cells in selected regions, above those seen in nonoccluded diabetic rats. Both TUNEL staining and caspase-3 immunohistochemistry revealed that the number of apoptotic cells in diabetic animals tended to be greatest in the preoptic area and parietal cortex. The authors conclude that focal cerebral ischemia is associated with a significant increase in apoptosis in nondiabetic rats, and that diabetes alone or diabetes plus focal ischemia are associated with significant increases in apoptotic cells.

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Meiyanto, Edy. "PENINGKATAN EKSPRESI p53 OLEH EKSTRAK ETANOLIK RUMPUT MUTIARA (Hedyotis corymbosa) PADA SEL HEPAR TIKUS SPRAGUE DAWLEY TERINDUKSI 7,12-DIMETILBENZ[a]ANTRASENA." Pharmacon: Jurnal Farmasi Indonesia 11, no. 1 (January 31, 2015): 1–6. http://dx.doi.org/10.23917/pharmacon.v11i1.62.

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Asam ursolat dan asam oleanolat yang terdapat dalam Rumput Mutiara (Hedyotis corymbosa) diduga dapat menghambat kanker dengan berbagai mekanisme. Penelitian ini dirancang untuk mengetahui kemampuan ekstrak etanolik rumput mutiara sebagai agen pemacu apoptosis melalui uji in vivo menggunakan tikus galur Sprague Dawley terinduksi 7,12-dimetilbenz[a]antrasena (DMBA). Kelompok hewan uji yang digunakan terdiri dari kontrol ekstrak 1500mg/kgBB, kontrol pelarut CMC-Na, kontrol DMBA, perlakuan DMBA+ekstrak dosis 750mg/kgBB dan perlakuan DMBA+ekstrak 1500mg/kgBB. Hasil percobaan selanjutnya dianalisis menggunakan metode TUNEL (TUNEL assay) dan Imunohistokimia terhadap ekspresi protein p53 untuk mengetahui tingkat pemacuan apoptosis dari sel kanker hepar hewan uji. Hasil analisa menggunakan metode TUNEL menunjukkan hasil bahwa hepar tikus mengalami apoptosis relatif tinggi pada kelompok perlakuan DMBA+ekstrak. Hasil pengamatan menggunakan metode Imunohistokimia diketahui bahwa sel kanker hepar mengalami pemacuan ekspresi protein p53 yang menunjukkan terjadinya apoptosis pada sel hepar tersebut. Hal ini menunjukkan bahwa ekstrak rumput mutiara dapat memacu apoptosis dan dapat digunakan sebagai salah satu alternatif pengobatan penyakit kanker. Kata Kunci: H.corymbosa, DMBA, apoptosis, p53, TUNEL

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Pini, Taylor, Rachel Makloski, Karen Maruniak, William B. Schoolcraft, and Mandy G. Katz-Jaffe. "Mitigating the Effects of Oxidative Sperm DNA Damage." Antioxidants 9, no. 7 (July 6, 2020): 589. http://dx.doi.org/10.3390/antiox9070589.

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Sperm DNA damage is correlated with reduced embryo development and increased miscarriage risk, reducing successful conception. Given its links with oxidative stress, antioxidants have been investigated as a potential treatment, yet results are conflicting. Importantly, individual antioxidants are not identical in composition, and some compounds may be more effective than others. We investigated the use of the polyphenol-rich, high-antioxidant-capacity fruit acai as a treatment for elevated sperm DNA fragmentation (>16%), measured by terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL). Following ≥ 74 days of treatment, we observed a significant decrease in sperm DNA fragmentation (−17.0% ± 2.5%) to 11.9 ± 1.7% (0–37%), with a 68.6% success rate (defined as post-treatment TUNEL < 16%). Post-treatment decreases in DNA fragmentation and success rates were not significantly impacted by low motility and/or concentration, or exceptionally high (> 25%) TUNEL. Treatment significantly reduced concentration in men with normal semen parameters, but 88% remained normal. Overall, successful treatment was not associated with age, semen parameters or TUNEL result at baseline. However, body mass index was significantly higher in nonresponders at baseline. This study provides evidence of a low-cost, effective treatment for elevated sperm DNA damage using acai.

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Shabisgh, Ahmad, Nozomu Tanji, Vivette D’Agati, Martin Burchardt, Mark Rubin, Erik T. Goluboff, Daniel Heitjan, Alex Kiss, and Ralph Buttyan. "Early Effects of Castration on the Vascular System of the Rat Ventral Prostate Gland*." Endocrinology 140, no. 4 (April 1, 1999): 1920–26. http://dx.doi.org/10.1210/endo.140.4.6644.

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Abstract Recent studies have found that blood flow to the rat ventral prostate gland is drastically reduced at an early time after castration. These observations caused us to reevaluate the effects of castration on the various cell populations of the ventral prostate, especially those in the prostatic vascular system. Sections of ventral prostate glands obtained at different times after castration were analyzed using the TUNEL (terminal deoxynucleotide transferase-mediated dUTP nick END labeling) staining method to quantify apoptosis in different cell types. The results of this analysis showed a significant increase in TUNEL staining of prostate endothelial and (nonendothelial) stromal cells as early as 12 h postcastration that continued to 24 h after castration. In contrast, TUNEL labeling of prostate epithelial cells was not significantly increased compared with control values until 72 h after castration. The use of dual immunohistochemical staining procedures (anti-CD31 for endothelial cells or antismooth muscle actin for smooth muscle cells combined with TUNEL labeling) allowed us to confirm that the TUNEL-positive vascular cells at these early times after castration were endothelial in nature, whereas smooth muscle cells surrounding the prostate glands or portions of the afferent vascular endothelium were rarely TUNEL labeled. Electron microscopic evaluation of ventral prostate tissues at 48 h after castration provided further morphological evidence for the occurrence of apoptosis in prostate endothelial cells. Finally, the Lendrum-Fraser histochemical procedure used to identify fibrin leakage in tissues with vascular damage was applied to sections of the ventral prostate gland. This stain revealed diffuse fibrin accumulation in periglandular areas outside the capillaries and blood vessels in prostates from 24-h castrated rats, but not in prostates of sham-operated rats. Our results confirm an early effect of castration on the vascular system of the rat ventral prostate identified by increased apoptosis of endothelial cells and vascular leakiness. As these changes temporally precede the loss of epithelial cells, we propose that they may be causal rather than incidental to regression of the rat ventral prostate after castration.

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McCall, Cordero L., James Stinson, Ryan W. Dobbs, Neil Mistry, Adrian Rosenberg, Oluwarotimi Nettey, Pooja Sharma, et al. "Abstract A079: Genetic ancestry and vitamin D may predict degree of prostatic apoptosis in prostate tumor and benign epithelium among men undergoing radical prostatectomy." Cancer Epidemiology, Biomarkers & Prevention 32, no. 1_Supplement (January 1, 2023): A079. http://dx.doi.org/10.1158/1538-7755.disp22-a079.

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Abstract There is evidence that vitamin D metabolites such as 25 hydroxyvitamin D [25(OH)D], may be protective against prostate cancer (PCa). Vitamin D and its analogs are hypothesized to have pro-apoptotic effects in multiple cell lines. Blacks have higher rates of vitamin D deficiency, higher tumor progression rates 1,2, and higher apoptosis rates3 compared to Whites. West African ancestry (WAA) may confound this relationship if it is associated with both vitamin D status and apoptosis rates. Our objective is to assess for independent associations between in vivo vitamin D status, genetic ancestry, and degree of apoptosis using prostatic epithelial Terminal deoxynucleotide transferase dUTP Nick End Labeling (TUNEL) staining. Radical prostatectomy specimens of men with clinically localized PCa were stained for TUNEL. Prostatic and serum levels of 25(OH)D and serum levels of 1,25 hydroxyvitamin D were assessed at the time of surgery. Ancestry informative markers were used to estimate the percentage of genetic West African, Native American, and European ancestry. Continuous variables were compared using medians tests across three groups of vitamin D status. Categorical variables were compared using the Chi-Squared test. Correlations between the degree of TUNEL staining and vitamin D metabolites were assessed using Spearman correlations. Linear regressions were used to access the bivariant associations between tumor and benign epithelial TUNEL staining with quartiles of ancestry, and serum and prostatic vitamin D metabolite levels. Multivariate linear regressions for the percentage of benign and tumor TUNEL staining were used to test the independent associations of vitamin D metabolites and genetic ancestry. Overall, 121 men, age 40-79, who underwent radical prostatectomy were enrolled between 2013-2018. Serum 25(OH)D correlated positively with both tumor (ρ = 0.17, p = 0.03), and benign (ρ = 0.16, p = 0.04) prostatic epithelial TUNEL staining. Similarly, prostatic 25(OH)D correlated positively with both tumor (ρ = 0.31, p < 0.001) and benign (ρ = 0.20, p = 0.03) prostatic tissue TUNEL staining. Relative to West African ancestry, Native American ancestry was more strongly positively correlated with tumor (ρ = 0.22, p = 0.05) and benign (ρ = 0.27, p= 0.02) TUNEL staining. In multivariate regression models, increasing quartiles of prostatic 25(OH)D (β = 0.25, p = 0.04) and Native American ancestry (β = 0.327, p = 0.004) were significant predictors of tumor TUNEL staining. Physiologic levels of serum and prostatic 25(OH)D and percentage of Native American ancestry are positively associated with the degree of apoptosis in tumor and benign prostatic epithelium from men with clinically localized PCa. Vitamin D may have secondary chemoprevention benefits in preventing PCa progression in localized disease. Citation Format: Cordero L. McCall, James Stinson, Ryan W. Dobbs, Neil Mistry, Adrian Rosenberg, Oluwarotimi Nettey, Pooja Sharma, Michael Dixon, Jamila Sweis, Virgilia Macias, Roohollah Sharifi, Rick A. Kittles, Andre Kajdacsy Balla, Adam B. Murphy. Genetic ancestry and vitamin D may predict degree of prostatic apoptosis in prostate tumor and benign epithelium among men undergoing radical prostatectomy [abstract]. In: Proceedings of the 15th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2022 Sep 16-19; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2022;31(1 Suppl):Abstract nr A079.

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WINSTON, BRION, MICHAEL NALESNIK, and RAVEEN BAZAZ. "TUNEL Assay for Identifying Ablated Myocardium." Pacing and Clinical Electrophysiology 33, no. 12 (September 1, 2010): 1548–49. http://dx.doi.org/10.1111/j.1540-8159.2010.02883.x.

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Baima, Bozena, and Michael Sticherling. "How Specific Is the TUNEL Reaction?" American Journal of Dermatopathology 24, no. 2 (April 2002): 130–34. http://dx.doi.org/10.1097/00000372-200204000-00004.

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Porras-Estrada, L. F., J. A. Rodríguez-Sánchez, L. García-Yagüe, and C. García-Flores. "¿Síndrome del tunel carpiano? Case report." Neurocirugía 14, no. 4 (2003): 338–40. http://dx.doi.org/10.1016/s1130-1473(03)70536-3.

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Groves-Kirkby, Nick. "TUNEL evaluation of sperm DNA damage." Nature Reviews Urology 7, no. 8 (August 2010): 421. http://dx.doi.org/10.1038/nrurol.2010.109.

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Yoneda, Kozo, Atsushi Kon, Toshio Demitsu, Nobuya Inagaki, Chieko Sadahira, and Yasuo Kubota. "Tunel positive keratinocytes in keratin disease." Journal of Dermatological Science 40, no. 1 (October 2005): 65–67. http://dx.doi.org/10.1016/j.jdermsci.2005.07.005.

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SATO, TOSHINOBU, MIENEKE G. A. VAN DIXHOORN, FRANS A. PRINS, ANDREW MOONEY, NICOLE VERHAGEN, YVONNE MUIZERT, JOHN SAVILL, LEENDERT A. VAN ES, and MOHAMED R. DAHA. "The Terminal Sequence of Complement Plays an Essential Role in Antibody-Mediated Renal Cell Apoptosis." Journal of the American Society of Nephrology 10, no. 6 (June 1999): 1242–52. http://dx.doi.org/10.1681/asn.v1061242.

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Abstract. Mesangial cell (MC) injury is a characteristic feature in the early phase of Thy.1 nephritis. The present study investigates the contribution of complement to MC apoptosis in this experimental model of kidney disease in rats. Thy.1 nephritis was induced by injection of mouse anti-Thy.1 monoclonal antibody (ER4G). To assess the contribution of the terminal sequence of complement on apoptosis, the studies were performed in complement-sufficient PVG/c (PVG/c+) rats and in rats deficient in complement C6 (PVG/c-). Apoptosis was monitored by assessment of the number of condensed nuclei in kidney sections stained with periodic acid-Schiff (PAS) and by the terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) method and expressed as number of apoptotic cells per 50 glomerular cross sections. In the PAS method, 1 h after intravenous injection of ER4G, PVG/c+ rats exhibited 160.9 ± 49.5 apoptotic cells, whereas PVG/c- rats had only 3.2 ± 1.4 apoptotic cells. Control rats exhibited 0.9 ± 0.6 apoptotic cells. These findings were confirmed with the TUNEL method. In PVG/c- rats, a maximum number of 8.8 ± 3.1 TUNEL-positive (TUNEL+) cells was found at 6 h followed by a decline thereafter. In PVG/c+ rats, apoptosis was associated with deposition of C6 and C5b-9. Restoration of the complement system of PVG/c- rats with purified human C6 resulted in an increase of apoptosis at 1 h after injection of ER4G from minimal numbers to 239.9 ± 52.4 TUNEL+ cells. These studies appear to indicate for the first time that the terminal sequence of complement is involved in induction of apoptosis.

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Prunell, Giselle F., Niels-Aage Svendgaard, Kanar Alkass, and Tiit Mathiesen. "Delayed cell death related to acute cerebral blood flow changes following subarachnoid hemorrhage in the rat brain." Journal of Neurosurgery 102, no. 6 (June 2005): 1046–54. http://dx.doi.org/10.3171/jns.2005.102.6.1046.

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Object. The authors tested the hypotheses that subarachnoid hemorrhage (SAH) leads to delayed cell death with the participation of apoptotic-like mechanisms and is influenced by the degree of acute decrease in the cerebral blood flow (CBF) following hemorrhage. Methods. Subarachnoid hemorrhage was induced in rats by endovascular perforation of the internal carotid artery or injection of blood into the prechiasmatic cistern. Cerebral blood flow was measured using laser Doppler flowmetry for 60 minutes. Brain sections stained with terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) showed DNA fragmentation at 2 and 7 days after both methods of inducing SAH in one third to two thirds of the surviving animals in the different experimental groups. More than 80% of the TUNEL-positive cells were neuron-specific nuclear protein—positive (neurons), but immunoreactivity to glial fibrillary acidic protein (astrocytes) and transferrin (oligodendrocytes) were markedly decreased in TUNEL-positive areas. Most of the TUNEL-positive cells displayed chromatin condensation and/or blebs and immunostained for increased Bax; approximately 50% of them were immunoreactive to cleaved caspase-3 and a few to Bcl-2. The duration of the acute CBF decrease below 30% of the baseline level was related to the degree of TUNEL staining. Conclusions. Subarachnoid hemorrhage resulted in delayed cell death in a large proportion, but not all, of the surviving animals. The acute CBF decrease was related to the degree of subsequent cell death. These findings indicated the relevance of apoptotic-like pathways. There appears to be a temporal therapeutic window during which adequate treatment might reduce the final damage following SAH.

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Júnior, Luiz Carlos de Souza Cabral, Renan Estaquioti Rizo, Lucas Freitas Miranda, Lucas de Araújo Correia, Vinícius Moraes Moreira, Ian Spala Ataíde Aguiar, Sabrina Costalonga Dadalto, and João Frigini Junior. "Sindrome do tunel do carpo: revisão de literatura / Sindrome do tunel do carpo: revisão de literatura." Brazilian Journal of Development 7, no. 12 (December 29, 2021): 111361–66. http://dx.doi.org/10.34117/bjdv7n12-086.

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Sun, Yun, Changman Zhou, Paula Polk, Anil Nanda, and John H. Zhang. "Mechanisms of Erythropoietin-induced Brain Protection in Neonatal Hypoxia-Ischemia Rat Model." Journal of Cerebral Blood Flow & Metabolism 24, no. 2 (February 2004): 259–70. http://dx.doi.org/10.1097/01.wcb.0000110049.43905.ac.

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Erythropoietin, a hemotopoietic growth factor, has brain protective actions. This study investigated the mechanisms of Recombinant Human EPO (rhEPO)-induced brain protection in neonates. An established rat hypoxia-ischemia model was used by ligation of the right common carotid artery of 7-day-old pups, followed by 90 minute of hypoxia (8% 02 and 92% N2) at 37°C. Animals were divided into three groups: control, hypoxia-ischemia, and hypoxia-ischemia plus rhEPO treatment. In rhEPO treated pups, 300 units rhEPO was administered intraperitoneally 24 hours before hypoxia. rhEPO treatment (300 units) was administered daily for an additional 2 days. ELISA and immunohistochemistry examined the expression of EPO and EPOR. Brain weight, morphology, TUNEL assay, and DNA laddering evaluated brain protection. rhEPO abolished mortality (from 19% to 0%) during hypoxia insult, increased brain weight from 52% to 88%, reduced DNA fragmentation, and decreased TUNEL-positive cells. Real-time RT-PCR, Western blot, and immunohistochemistry revealed an enhanced expression of heat shock protein 27 (HSP27) in ischemic brain hemisphere. Double labeling of TUNEL with HSP27 showed most HSP27 positive cells were negative to TUNEL staining. rhEPO reduces brain injury, especially apoptotic cell death after neonatal hypoxia-ischemia, partially mediated by the activation of HSP27.

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Bikbova, Guzel, Toshiyuki Oshitari, Takayuki Baba, and Shuichi Yamamoto. "Combination of Neuroprotective and Regenerative Agents for AGE-Induced Retinal Degeneration: In Vitro Study." BioMed Research International 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/8604723.

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To determine the most effective combination of neuroprotective and regenerative agents for cultured retinal neurons from advanced glycation end products- (AGEs-) induced degeneration, retinal explants of 7 adult Sprague-Dawley rats were three-dimensionally cultured in collagen gel and incubated in serum-free media and in 7 media; namely, AGEs, AGEs + 100 μM citicoline, AGEs + 10 ng/mL NT-4, AGEs + 100 μM TUDCA, AGEs + 100 μM citicoline + TUDCA (doublet), and AGEs + 100 μM citicoline + TUDCA + 10 ng/mL NT-4 (triplet) were examined. The number of regenerating neurites was counted after 7 days of culture, followed by performing TUNEL and DAPI staining. The ratio of TUNEL-positive cells to the number of DAPI-stained nuclei was calculated. Immunohistochemical examinations for the active form of caspase-9 and JNK were performed. All of the neuroprotectants increased the number of neurites and decreased the number of TUNEL-positive cells. However, the number of neurites was significantly higher, and the number of TUNEL-positive cells and caspase-9- and JNK-immunopositive cells was fewer in the retinas incubated with the combined three agents. Combination solutions containing citicoline, TUDCA, and NT-4 should be considered for neuroprotective and regenerative therapy for AGE-related retinal degeneration.

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Matsushita, Kohji, Wei Meng, Xiaoying Wang, Minoru Asahi, Kazuko Asahi, Michael A. Moskowitz, and Eng H. Lo. "Evidence for Apoptosis After Intracerebral Hemorrhage in Rat Striatum." Journal of Cerebral Blood Flow & Metabolism 20, no. 2 (February 2000): 396–404. http://dx.doi.org/10.1097/00004647-200002000-00022.

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The overall hypothesis that cell death after intracerebral hemorrhage is mediated in part by apoptotic mechanisms was tested. Intracerebral hemorrhage was induced in rats using stereotactic infusions of 0.5 U of collagenase (1-μL volume) into the striatum. After 24 hours, large numbers of TUNEL-positive stained cells with morphologies suggestive of apoptosis were present in the center and periphery of the hemorrhage. Double staining with Nissl and immunocytochemical labeling with antibodies against neuronal nuclei and glial fibrillary acidic protein suggested that these TUNEL-positive cells were mostly neurons and astrocytes. Electrophoresis of hemorrhagic brain extracts showed evidence of DNA laddering into ∼200-bp fragments. Western blots showed cleavage of the cytosolic caspase substrate gelsolin. The density of TUNEL-positive cells at 24 and 48 hours after hemorrhage was significantly reduced by treatment with the broad-spectrum caspase inhibitor zVADfmk. It was unlikely that apoptotic changes were due to neurotoxicity of injected collagenase because TUNEL-positive cells and DNA laddering were also obtained in an alternative model of hemorrhage where autologous blood was infused into the striatum. Furthermore, equivalent doses of collagenase did not induce cell death in primary neuronal cultures. These results provide initial evidence that apoptotic mechanisms may mediate some of the injury in brain after intracerebral hemorrhage.

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Grigaitienė, Jūratė, Irena Marčiukaitienė, Audra Blažienė, and Anželika Chomičienė. "Study of apoptosis in normal skin tissues." Medicina 43, no. 4 (January 21, 2007): 301. http://dx.doi.org/10.3390/medicina43040037.

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The aim of the study was to investigate the apoptosis in normal human skin by examination of all epidermal layers. Material and methods. The normal skin epidermis of 15 healthy subjects was investigated by TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP-X nick end labeling) technique. Apoptotic cells were evaluated in the germinative and differential compartments and stratum corneum. Only highly TUNEL-positive cells with typical morphological DNA fragmentation signs were calculated. Results. In vital strata (except stratum corneum) of normal skin epidermis, 37.5% of all TUNEL-positive cells were observed in the germinative compartment and 41.7% in the granular layer of differential compartment. Conclusions. The study showed that apoptosis occurs in all layers of normal skin epidermis. It demonstrates that apoptosis is highly important in the renewal of cells and formation of epidermal structure within all compartments.

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Kang, Peter M., and Seigo Izumo. "Apoptosis in heart failure: Is there light at the end of the tunnel (TUNEL)?" Journal of Cardiac Failure 6, no. 1 (March 2000): 43–46. http://dx.doi.org/10.1016/s1071-9164(00)80005-6.

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Loureiro, Bárbara, Amber Mary Brad, and Peter James Hansen. "Heat shock and tumor necrosis factor-α induce apoptosis in bovine preimplantation embryos through a caspase-9-dependent mechanism." Reproduction 133, no. 6 (June 2007): 1129–37. http://dx.doi.org/10.1530/rep-06-0307.

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Heat shock and tumor necrosis factor-α (TNF-α) induce apoptosis through different mechanisms, with heat shock acting to cause mitochondrial depolarization and caspase-9 activation, while TNF-α acts through a receptor-mediated process to activate caspase-8. In some cells, however, TNF-α can also cause mitochondrial depolarization and caspase-9 activation. In the present study, we tested the hypothesis that heat shock at 41 °C and TNF-α induce apoptosis in bovine preimplantation embryos through a caspase-9-dependent mechanism. Treatment of embryos with either heat shock (41 °C) or TNF-α increased the proportion of blastomeres that were TUNEL positive and the proportion of embryos exhibiting elevated caspase-9 activity. Furthermore, the caspase-9 inhibitor, z-LEHD-fmk, blocked the increase in TUNEL-positive nuclei caused by both heat shock and TNF-α. For embryos at day 6 after insemination, for example, the percent of blastomeres positive for TUNEL was 3.6% for control embryos, 11.1% for embryos cultured at 41 °C, and 15.1% for embryos cultured with 10 ng/ml TNF-α. In the presence of z-LEHD-fmk, the percent of cells positive for TUNEL was 3.7% for control embryos, 6.1% for embryos cultured at 41 °C, and 8% for embryos cultured with 10 ng/ml TNF-α. Although TNF-α did not cause a measurable increase in caspase-8 activity, there was a tendency (P= 0.07) for treatment of embryos with z-IETD-fmk, an inhibitor of caspase-8, to partly reduce the magnitude of the increase in TUNEL-positive cells caused by TNF-α. The percent of cells that were TUNEL positive was increased by TNF-α from 9.7 to 19.7% in the absence of inhibitor and from 13.0 to 15.6% in the presence of z-IETD-fmk. Results indicate that induction of apoptosis by both heat shock and TNF-α involve activation of caspase-9-dependent pathways. It is likely that TNF-α also activates apoptotic pathways involving caspase-8 but that the degree of activation is small and caspase-9-dependent pathways are required for full activation of apoptosis.

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Austgulen, Rigmor, Lisa Chedwick, Christina Vogt Isaksen, Lars Vatten, and Catherine Craven. "Trophoblast Apoptosis in Human Placenta at Term as Detected by Expression of a Cytokeratin 18 Degradation Product of Caspase." Archives of Pathology & Laboratory Medicine 126, no. 12 (December 1, 2002): 1480–86. http://dx.doi.org/10.5858/2002-126-1480-taihpa.

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Abstract Context.—Apoptosis occurs in the normal placenta. The monoclonal antibody M30 is directed against a novel epitope of cytokeratin 18 (CK18) that is formed by caspase cleavage early in the apoptotic cascade, and this antibody may therefore be useful for evaluating trophoblast apoptosis. Objective.—We undertook the present study to evaluate the use of monoclonal antibody M30 to assess trophoblast apoptosis in placenta at term. Methods.—We stained paraffin-embedded placental tissues from 15 deliveries at term with M30. We compared positive M30 staining and CK18 staining (as detected by a monoclonal antibody directed against CK18) of trophoblasts in serial slides. We also compared apoptotic rates as detected by M30 and TUNEL (terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick end labeling) in 7 of the placentas. Results.—In fields of villous tissue, most M30-positive cells were CK18-positive syncytiotrophoblasts. Approximately half of M30-positive cells occurred as focal positive staining in the syncytial layer, and half occurred as abundant staining of syncytiotrophoblasts in areas with increased intervillous or perivillous fibrinoid. We found very few M30-positive cells in villous stroma. In decidual/basal plate tissues, most (two thirds) of the M30-positive cells were CK18-positive extravillous trophoblasts, whereas one third were syncytiotrophoblasts of anchoring villi. Since TUNEL detects apoptosis in both epithelial and nonepithelial cells, more cells were positively stained with TUNEL than with M30 in some tissue fields. However, our observations suggest that M30 was more sensitive than TUNEL in recognizing apoptotic trophoblasts and had less nonspecific staining than TUNEL. Conclusion.—We recommend the use of monoclonal antibody M30 for apoptosis studies in placental tissues. This antibody is easy to handle, the staining obtained seems specific, and the nonspecific staining seems negligible.

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Holmin, Staffan, and Tiit Mathiesen. "Intracerebral administration of interleukin-1β and induction of inflammation, apoptosis, and vasogenic edema." Journal of Neurosurgery 92, no. 1 (January 2000): 108–20. http://dx.doi.org/10.3171/jns.2000.92.1.0108.

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Object. The proinflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor—α (TNFα) are produced intracerebrally in brain disorders such as trauma, ischemia, meningitis, and multiple sclerosis. This investigation was undertaken to analyze the effect of intracerebral administration of IL-1β and TNFα on inflammatory response, cell death, and edema development.Methods. Intracerebral microinjections of these cytokines were administered to rats. The animals were killed 24 or 72 hours after the injections, and their brains were analyzed by using deoxynucleotidyl transferase—mediated deoxyuridine triphosphate nick-end labeling (TUNEL) with digoxigenin-labeled deoxyuridine triphosphate, immunohistochemical studies, and brain-specific gravity measurement. The IL-1β induced a transient inflammatory response (p < 0.001) and TUNEL staining (p < 0.001), indicating cell death, in intrinsic central nervous system (CNS) cells and infiltrating inflammatory cells. In 73.8 ± 6.77% of the TUNEL-positive cells, small, fragmented nuclei were found. All TUNEL-positive cells expressed the proapoptotic gene Bax, and 69.6 ± 4.6% of the TUNEL-positive cells expressed the antiapoptotic gene Bcl-2; the Bax expression was stronger than the Bcl-2 expression. Taken together, the data indicate that cell death occurred via the apoptotic pathway. The TNFα did not induce inflammation or DNA fragmentation within the analyzed time period. Both IL-1β (p < 0.001) and TNFα (p < 0.01) caused vasogenic edema, as measured by specific gravity and albumin staining. The edematous effect of TNFα persisted 72 hours after injection (p < 0.01), whereas the IL-1β—treated animals had normalized by that time.Conclusions. Intracerebral inflammation, death of intrinsic CNS cells, and vasogenic edema can be mediated by IL-1β, and TNFα can cause vasogenic edema. Suppression of these cytokines in the clinical setting may improve outcome.

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Jamnicki-Abegg, Marina, Dorothee Weihrauch, Paul S. Pagel, Judy R. Kersten, Zeljko J. Bosnjak, David C. Warltier, and Martin W. Bienengraeber. "Isoflurane Inhibits Cardiac Myocyte Apoptosis during Oxidative and Inflammatory Stress by Activating Akt and Enhancing Bcl-2 Expression." Anesthesiology 103, no. 5 (November 1, 2005): 1006–14. http://dx.doi.org/10.1097/00000542-200511000-00015.

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Background Volatile anesthetics attenuate apoptosis. The underlying mechanisms remain undefined. The authors tested whether isoflurane reduces apoptosis in cardiomyocytes subjected to oxidative or inflammatory stress by enhancing Akt and B-cell lymphoma-2 (Bcl-2). Methods Adult and neonatal rat ventricular myocytes and atrial HL-1 myocytes were exposed to hypoxia, hydrogen peroxide, or neutrophils with or without isoflurane pretreatment. The authors assessed cell damage and investigated apoptosis using mitochondrial cytochrome c release, caspase activity, and TUNEL assay. They determined expression of phospho-Akt and Bcl-2 and tested their involvement by blocking phospho-Akt with wortmannin and Bcl-2 with HA14-1. Results Isoflurane significantly reduced the cell damage and apoptosis induced by hypoxia, H2O2, and neutrophils. Isoflurane reduced hypoxia-induced mitochondrial cytochrome c release in HL-1 cells by 45 +/- 12% and caspase activity by 28 +/- 4%; in neonatal cells, it reduced caspase activity by 43 +/- 5% and TUNEL-positive cells by 50 +/- 2%. Isoflurane attenuated H2O2-induced caspase activity in HL-1 cells by 48 +/- 16% and TUNEL-positive cells by 78 +/- 3%; in neonatal cells, it reduced caspase activity by 30 +/- 3% and TUNEL-positive cells by 32 +/- 7%. In adult cardiomyocytes exposed to neutrophils, isoflurane decreased both mitochondrial cytochrome c and caspase activity by 47 +/- 3% and TUNEL-positive cells by 25 +/- 4%. Isoflurane enhanced phospho-Akt and Bcl-2 expression. Wortmannin and HA14-1 prevented the action of isoflurane (53 +/- 8% and 54 +/- 7% apoptotic cells vs. 18 +/- 1% without blockers). Conclusions Isoflurane protects cardiomyocytes against apoptosis induced by hypoxia, H2O2, or activated neutrophils through Akt activation and increased Bcl-2 expression. This suggests that a reduction in apoptosis contributes to the cardioprotective effects of isoflurane.

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Sliesoraitis, Sarunas, Amy L. Collinsworth, Jose Gilberto Trevino, Robert Zlotecki, Xiaomin Lu, Judith L. Lightsey, Carmen Joseph Allegra, et al. "Effect of neoadjuvant treatment with gemcitabine with nab-paclitaxel on SPARC and Ki-67 in patients with resectable pancreatic adenocarcinoma." Journal of Clinical Oncology 33, no. 3_suppl (January 20, 2015): 322. http://dx.doi.org/10.1200/jco.2015.33.3_suppl.322.

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322 Background: Nab-paclitaxel (nab-P) and gemcitabine (Gem) improve survival in metastatic pancreatic cancer (PCa). We sought to determine the impact of nab-P and Gem on the primary tumor and associated microenvironment in neoadjuvant treatment (NAT). Methods: All patients in the GAIN-1 study (NCT01470417) received NAT with nab-P and Gem with or without radiation depending on risk status. A comparator group without NAT was matched for age, sex, race, resection status, smoking, primary tumor site, and tumor size. Surgical specimens of tumor, associated stroma and lymph nodes were analyzed. Routine immunohistochemistry (IHC) for Ki-67 and TUNEL was performed. Immunolabeling was assessed using anti-SPARC antibody (Invitrogen) with scoring consistent with prior reports: Negative = intensity absent to weak (+) with extent <10%; Positive = intensity moderate (++) to strong (+++) with extent ≥ 10%. For Ki-67 and TUNEL, the percentage of positive tumor cells was averaged over four HPF/specimen. Study was conducted with IRB approval. Results: A total of 30 unique patients were included in this analysis, 8 NAT cases and 22 matched controls. Clinical outcomes have been previously reported. Minimal to no SPARC expression was noted in either group of tumor cells. However, stromal SPARC expression was markedly reduced in NAT group (mean 2.88 ± 0.69%) compared to controls (28.43 ± 5.80%; p = 0.0002). Ki-67 was reduced in NAT group compared to controls (10.5 ± 2.83% vs. 36.76 ± 4.32%; p = 0.0004). TUNEL stain revealed a trend toward lower levels in NAT group (mean 1.13 ± 0.30% vs. 1.62 ± 0.31%; p = 0.574). SPARC, Ki-67 and TUNEL did not correlate with survival. Conclusions: SPARC expression in pCa primary tumors is low. Neoadjuvant nab-P and Gem significantly decreased stromal SPARC and tumor Ki-67. There was no change in TUNEL expression, indicating a population of residual viable cells. Additional stromal microenvironment change analysis in response to treatment is ongoing.

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Kanno, Haruo, Hiroshi Ozawa, Kyoichi Handa, Taishi Murakami, and Eiji Itoi. "Changes in Expression of Receptor-Interacting Protein Kinase 1 in Secondary Neural Tissue Damage Following Spinal Cord Injury." Neuroscience Insights 15 (January 2020): 263310552090640. http://dx.doi.org/10.1177/2633105520906402.

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Introduction: Necroptosis is a form of programmed cell death that is different from apoptotic cell death. Receptor-interacting protein kinase 1 (RIPK1) plays a particularly important function in necroptosis execution. This study investigated changes in expression of RIPK1 in secondary neural tissue damage following spinal cord injury in mice. The time course of the RIPK1 expression was also compared with that of apoptotic cell death in the lesion site. Methods and Materials: Immunostaining for RIPK1 was performed at different time points after spinal cord injury. The protein expressions of RIPK1 were determined by western blot. The RIPK1 expressions in various neural cells were investigated using immunohistochemistry. To investigate the time course of apoptotic cell death, TUNEL-positive cells were counted at the different time points. To compare the incidence of necroptosis and apoptosis, the RIPK1-labeled sections were co-stained with TUNEL. Results: The RIPK1 expression was significantly upregulated in the injured spinal cord. The upregulation of RIPK1 expression was observed in neurons, astrocytes, and oligodendrocytes. The increase in RIPK1 expression started at 4 hours and peaked at 3 days after injury. Time course of the RIPK1 expression was similar to that of apoptosis detected by TUNEL. Interestingly, the increased expression of RIPK1 was rarely observed in the TUNEL-positive cells. Furthermore, the number of RIPK1-positive cells was significantly higher than that of TUNEL-positive cells. Conclusions: This study demonstrated that the expression of RIPK1 increased in various neural cells and peaked at 3 days following spinal cord injury. The temporal change of the RIPK1 expression was analogous to that of apoptosis at the lesion site. However, the increase in RIPK1 expression was barely seen in the apoptotic cells. These findings suggested that the RIPK1 might contribute to the pathological mechanism of the secondary neural tissue damage after spinal cord injury.

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Tang, Ling-Hua, Zhong-Yuan Xia, Bo Zhao, Xiao-Dong Wei, Tao Luo, and Qing-Tao Meng. "Phosphocreatine Preconditioning Attenuates Apoptosis in Ischemia-Reperfusion Injury of Rat Brain." Journal of Biomedicine and Biotechnology 2011 (2011): 1–4. http://dx.doi.org/10.1155/2011/107091.

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Phosphocreatine (PCr) is an endogenous compound containing high-energy phosphate bonds. It has been confirmed that PCr is effective in preventing and treating cardiac and renal ischemia-reperfusion injury. In this study, rat cerebral ischemia-reperfusion injury models were constructed. Apoptotic cells in the cortex region were measured by TUNEL method. Malondialdehyde (MDA) content was detected by chromatometry, and calmodulin (CaM) activity was detected by ELISA. Compared with sham-operated group (sham group), TUNEL-positive cells, MDA, and level of CaM activity increased in ischemia-reperfusion group (I/R group) and PCr preconditioning group (PCr group); compared with I/R group, TUNEL-positive cells, MDA content, and level of CaM activity decreased in PCr group. This study indicated that PCr can decrease the morphological damage and the neuron apoptosis of the ischemia-reperfusion injury brain through attenuating abnormalities of calcium balance and production of oxygen free radicals.

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Rohwer, Forest, and Farooq Azam. "Detection of DNA Damage in Prokaryotes by Terminal Deoxyribonucleotide Transferase-Mediated dUTP Nick End Labeling." Applied and Environmental Microbiology 66, no. 3 (March 1, 2000): 1001–6. http://dx.doi.org/10.1128/aem.66.3.1001-1006.2000.

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ABSTRACT Numerous agents can damage the DNA of prokaryotes in the environment (e.g., reactive oxygen species, irradiation, and secondary metabolites such as antibiotics, enzymes, starvation, etc.). The large number of potential DNA-damaging agents, as well as their diverse modes of action, precludes a simple test of DNA damage based on detection of nucleic acid breakdown products. In this study, free 3′-OH DNA ends, produced by either direct damage or excision DNA repair, were used to assess DNA damage. Terminal deoxyribonucleotide transferase (TdT)-mediated dUTP nick end labeling (TUNEL) is a procedure in which 3′-OH DNA ends are enzymatically labeled with dUTP-fluorescein isothiocyanate using TdT. Cells labeled by this method can be detected using fluorescence microscopy or flow cytometry. TUNEL was used to measure hydrogen peroxide-induced DNA damage in the archaeonHaloferax volcanii and the bacterium Escherichia coli. DNA repair systems were implicated in the hydrogen peroxide-dependent generation of 3′-OH DNA ends by the finding that the protein synthesis inhibitors chloramphenicol and diphtheria toxin blocked TUNEL labeling of E. coli and H. volcanii, respectively. DNA damage induced by UV light and bacteriophage infection was also measured using TUNEL. This methodology should be useful in applications where DNA damage and repair are of interest, including mutant screening and monitoring of DNA damage in the environment.

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Laychock, Suzanne G., Shawn M. Sessanna, Mei-Hui Lin, and Lucy D. Mastrandrea. "Sphingosine 1-Phosphate Affects Cytokine-Induced Apoptosis in Rat Pancreatic Islet β-Cells." Endocrinology 147, no. 10 (October 1, 2006): 4705–12. http://dx.doi.org/10.1210/en.2006-0456.

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Cytokines mediate pancreatic islet β-cell apoptosis and necrosis, leading to loss of insulin secretory capacity and type 1 diabetes mellitus. The cytokines, IL-1β and interferon-γ, induced terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling (TUNEL) staining of rat islet cells within 48 h by about 25–30%, indicative of apoptosis and/or necrosis. Sphingosine 1-phosphate (S1P) at nanomolar concentrations significantly reduced islet cell cytokine-induced TUNEL staining. Similar effects were observed in INS-1 cells. The dihydro analog of S1P also reduced the percentage of TUNEL stained islet and INS-1 cells, whereas the S1P receptor antagonist BML-241 blocked the protective effects. Pertussis toxin did not affect the S1P protective response. In the presence of a phospholipase C antagonist, U73122, there was significant inhibition of the S1P protective effects against apoptosis/necrosis. S1P stimulated INS-1 cell protein kinase C activity. Carbamylcholine chloride acting through muscarinic receptors also inhibited cytokine-induced TUNEL staining in pancreatic islet cells. S1P and/or dihydro-S1P also antagonized cytokine-induced increases in cytochrome c release from mitochondria and caspase-3 activity in INS-1 cells, which are indicative of cell apoptosis vs. necrosis. S1P failed to affect nitric oxide synthase activity after 48 h. Thus, the evidence suggests that S1P acting on S1P receptors coupled to Gq mediates protective effects on islet β-cells against cytokine-induced apoptosis.

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Rodriguez, Valeria, Gabriela Diaz de Barboza, Ruben Ponce, Valeria Merico, Silvia Garagna, and Nori Tolosa de Talamoni. "Spermatocyte apoptosis, which involves both intrinsic and extrinsic pathways, explains the sterility of Graomys griseoflavus × Graomys centralis male hybrids." Reproduction, Fertility and Development 22, no. 2 (2010): 478. http://dx.doi.org/10.1071/rd09106.

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Spermatogenic impairment and the apoptotic pathways involved in establishing sterility of male hybrids obtained from crossing Graomys griseoflavus females with Graomys centralis males were studied. Testes from G. centralis, G. griseoflavus and hybrids were compared at different ages. Terminal transferase-mediated dUTP nick-end labelling assay (TUNEL), Fas, Bax and cytochrome c labelling were used for apoptosis evaluation, and calbindin D28k staining as an anti-apoptotic molecule. In 1-month-old animals, spermatocytes were positive for all apoptotic markers, but moderate TUNEL (+) spermatocyte frequency was only found in G. centralis. At subsequent ages, the apoptotic markers were downregulated in testes from parental cytotypes, but not in hybrid testes. TUNEL (+) spermatocytes were present at 78% and 44% per tubule cross-section in 2- and 3-month-old hybrid animals, respectively. Pachytene spermatocyte death in adult hybrids occurs via apoptosis, as revealed by high caspase-3 expression. Calbindin was highly expressed in spermatocytes of adult hybrids, in which massive cell death occurs via apoptosis. Calbindin co-localisation with TUNEL or Fas, Bax and cytochrome c was very limited, suggesting an inverse regulation of calbindin and apoptotic markers. Hybrid sterility is due to breakdown of spermatogenesis at the pachytene spermatocyte stage. Both extrinsic and intrinsic pathways are involved in apoptosis of spermatocytes, which are the most sensitive cell type to apoptotic stimuli.

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Journal articles on the topic 'TUNEL'

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