Biomaterials in cardiopulmonary bypass.
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Biocompatible Materials↗
Biomedical subjects
X Zhao
Publications and source records attributed to X Zhao.
Nitric oxide production during endotoxin-induced mastitis in the cow.
Nitric oxide production was measured during endotoxin-induced mastitis. One hour after morning milking, the right hind quarters of 15 cows were infused with saline containing Escherichia coli endotoxin. Left hind control quarters were infused with saline only. At varying intervals before and after infusion, diagnostic markers of mastitis were recorded and nitric oxide production was evaluated by measuring nitrite plus nitrate levels in milk. In endotoxin-infused quarters, a significant increase in nitrite plus nitrate concentrations was observed 3 h postinfusion; concentrations decreased to preinfusion levels within 48 h. This change indicates that significant amounts of nitric oxide are released during endotoxin-induced mastitis. At 3 different time points, somatic cells were harvested from milk samples, plated, and maintained in culture for 24 h. The concentration of nitrite plus nitrate in medium from cells harvested 12 h postinfusion was increased, suggesting that nitric oxide is released, at least in part, by milk somatic cells. In a second set of experiments, we evaluated nitric oxide production when animals were infused with endotoxin and aminoguanidine, a specific inhibitor of the inducible form of nitric oxide synthase. In cows treated with aminoguanidine, the increase in nitrite plus nitrate observed after endotoxin infusion was prevented. These results suggest that nitric oxide production during endotoxin-induced mastitis resulted from the activity of the inducible form of nitric oxide synthase. They also support a possible involvement for nitric oxide in the inflammatory reaction observed during mastitis.
Animals↗
Ethanol inhibits lung clearance of Pseudomonas aeruginosa by a neutrophil and nitric oxide-dependent mechanism, in vivo.
Pseudomonas aeruginosa (P. aeruginosa) is an opportunistic pathogen that can be found in individuals in which the immune system has been suppressed by HIV/AIDS or chronic alcoholism. We evaluated the role of inducible nitric oxide synthase (NOS II) as a modulator of lung concentrations of P. aeruginosa in normal rats and rats given a single dose of ethanol (ETOH). Rats were pretreated with either sterile saline (PBS, 0.1 ml/kg, i.v.) or the NOS II inhibitor L-N6-iminoethyl lysine (LNIL, 10 mg/kg, i.v.) 15 min before intraperitoneal administration of either PBS (4.5 ml/kg) or ETOH (4.5 g/kg). Thirty min after administration of PBS or ETOH the rats were placed in inhalation chambers and exposed to 45 min of an aerosol containing P. aeruginosa (5 x 10(4) colony forming units, CFU). A group of rats (n = 5-6/treatment/time period) were killed immediately (0 hr) or 4 hr after inhalation of P. aeruginosa. The lungs were homogenized and the P. aeruginosa were grown in nutrient broth to determine the number of viable CFU remaining in the lung. The NOS II and TNFalpha mRNA and protein content lung alveolar macrophages (AM) and neutrophils (PMN) were measured with RT-PCR and Western blot. The concentration of nitrate and nitrite anion in the bronchoalveolar lavage fluid (BALf) and ex vivo incubates of PMN were also measured. The CFU of P. aeruginosa present in the lungs of the four groups of rats at 0 hr did not differ. The CFU of P. aeruginosa in the lung increased (p < 0.05) in rats pretreated with ETOH when compared with that obtained from rats pretreated with PBS. However, pretreatment of rats with LNIL decreased (p < 0.05) the 4 hr lung content of P. aeruginosa. Coadministration of LNIL and ETOH to rats augmented the CFU of P. aeruginosa in lungs to amounts which did not differ from that of rats pretreated with ETOH. Inhalation of P. aeruginosa increased NOS II mRNA and protein in rat AM and PMN. Pretreatment of rats with ETOH alone, or in combination with LNIL, inhibited P. aeruginosa-induced NOS II transcription and translation and AM and PMN nitrate and nitrite generation whereas pretreatment with LNIL alone only inhibited nitrate and nitrite generation. Pretreatment of rats with ETOH suppressed P. aeruginosa stimulated PMN recruitment into the lung whereas LNIL enhanced (p < 0.05) P. aeruginosa-stimulated PMN recruitment into the lung. ETOH-induced increases of the lung content of P. aeruginosa were associated with increased PKC delta isozyme in the membrane of the PMN but could not be explained by altered plasma concentrations of hydrocortisone or ETOH. The data demonstrate that selective inhibition of NOS II-derived NO by LNIL decreases the lung content of P. aeruginosa whereas ETOH inhibits the lung clearance of P. aeruginosa. Speculatively, the difference between these effects of LNIL and ETOH may result from differences in drug-induced changes in lung recruitment of PMN.
Animals↗
Eimeria from bats of Bolivia: two new species from vespertilionid bats.
Between 1985 and 1987, fecal samples were collected from 71 bats representing 14 species (Desmodontidae, Molossidae, Noctilionidae, Phyllostomidae, Vespertilionidae) from 8 localities in 3 states (Beni, Pando, Santa Cruz) in Bolivia, South America. Of these, 2 black myotid bats (Vespertilionidae), Myotis nigricans, and 1 tent-making bat (Phyllostomidae), Uroderma magnirostrum, had oocysts in their feces that represent undescribed species of Eimeria. The new species from M. nigricans (2/4, 50%) has sporulated oocysts that are subspheroidal, 18.9 x 16.9 (17-23 x 14-20) microm, without a micropyle; oocyst residuum of 6-8 spheroidal globules and 1 highly refractile polar granule are present. The oocyst wall has 2 layers (approximately 1.3 microm thick), with a rough outer layer. Ovoidal sporocysts are 10.1 x 7.4 (7-14 x 5-10) microm, with a Stieda body, substieda body, and a sporocyst residuum. The new eimerian species from U. magnirostrum (1/2, 50%) has sporulated oocysts that are subspheroidal to ellipsoidal, 23.8 x 20.8 (20-26 x 19-24) microm, without micropyle or oocyst residuum, but 1-3 polar granules are present. The oocyst wall has 2 layers (approximately 1.5 microm thick), with a rough, mammilated outer layer. Ovoidal sporocysts are 11.6 x 8.6 (10-12 x 7-10) microm, with a Stieda body, substieda body and a sporocyst residuum.
Animals↗
Effects of the oxadiazine insecticide indoxacarb, DPX-MP062, on neuronal nicotinic acetylcholine receptors in mammalian neurons.
The effects of the novel oxadiazine insecticide DPX-MP062 and its metabolite (DCJW) on neuronal nicotinic acetylcholine receptors (AChRs) were investigated using the whole-cell patch clamp technique in rat embryonic cerebral cortical neurons in primary culture. DPX-MP062, applied at concentrations of 1 and 10 microM to the bath, reduced the peak amplitude of ACh-induced, rapidly decaying currents to 46.8+/-8.8% (n=9) and 15.7+/-5.0% (n=4) of the control, respectively. The effect was irreversible after washing with drug-free solution. DCJW at either 1 microM or 10 microM had similar actions but the potency was much less than that of DPX-MP062. The slowly desensitizing currents induced by low concentrations of ACh (0.1-10 microM) were augmented and those induced by high concentrations of ACh (100-1000 microM) were inhibited by 10 microM DPX-MP062 with great acceleration of the current decay in a time-dependent manner. These effects were use independent and reversible after washing with drug-free solution. In contrast, DCJW at 10 microM did not show significant effects on peak amplitude and decay phase of the slowly desensitizing ACh-induced current in cortical neurons. These results indicate that the oxadiazine insecticide DPX-MP062 has potent modulating actions on neuronal nicotinic AChRs. The neuronal nicotinic AChR could be one of the primary target sites of the insecticide in mammals.
Acetylcholine↗
Effects of ethanol on neutrophil recruitment and lung host defense in nitric oxide synthase I and nitric oxide synthase II knockout mice.
BACKGROUND: Ethanol (ETOH) inhibits Escherichia coli endotoxin [lipopolysaccharide (LPS)]-mediated induction of nitric oxide (NO) synthase (NOS) transcription and translation in macrophages and neutrophils [polymorphonuclear (PMN) cells] within the lung. ETOH also inhibits PMN recruitment into the lung and enhances NOS I-mediated production of NO. The contribution of the individual NOS isozymes to ETOH-mediated suppression of the host defense response to lung infection has not been defined. METHODS: We evaluated the role of constitutive NOS I and NOS II in ETOH-mediated inhibition of PMN recruitment into the lung and ETOH-mediated suppression of lung clearance of inhaled Klebsiella pneumonia (K. pneumoniae) in female, homozygous transgenic mice deficient in the genes for NOS I (nNOS-KO) or NOS II (iNOS-KO) and their wild-type controls (WT). RESULTS: Four hours after intratracheal administration of LPS or aerosol inhalation of K. pneumoniae, the lung content of PMNs obtained by bronchoalveolar lavage from WT mice was significantly reduced when compared with that obtained from the lungs of nNOS-KO and iNOS-KO mice. Pretreatment of WT mice with the NOS II inhibitor L-N6-iminoethyllysine (L-NIL; 10 mg/kg, i.p.) or with the NOS I inhibitor 7-nitroindazole (7-NI) (10, 25, or 40 mg/kg, i.p.) 30 min before LPS administration enhanced the lung content of PMNs recoverable by bronchoalveolar lavage. However, pretreatment of iNOS-KO with L-NIL did not affect lung recruitment of PMNs. Moreover, administration of 25 or 40 mg/kg, i.p. of 7-NI to nNOS-KO mice resulted in death of all the animals within 10 min. Pretreatment of nNOS-KO with 7-NI (10 mg/kg) did not affect LPS-stimulated PMN recruitment. Pretreatment of mice with ETOH (4.5 g/kg, i.p.) produced a greater inhibition of LPS-stimulated lung recruitment of PMNs in iNOS-KO mice than in WT mice. In contrast, pretreatment of nNOS-KO with ETOH produced little inhibition of LPS-stimulated lung recruitment of PMNs when compared with that measured in WT mice. Finally, 4 hr after aerosol inhalation of K. pneumoniae, lung clearance of this bacteria was enhanced in iNOS-KO when compared with WT and inhibited in nNOS-KO when compared with WT mice. ETOH-mediated suppression of lung clearance of K. pneumoniae was unaffected in nNOS-KO mice and enhanced in the iNOS-KO mice, when compared with that obtained in WT mice. ETOH-stimulated the production of NOS I-derived nitrate and nitrite production by rat brain and lung and inhibited LPS-induced NOS II mRNA, protein, and production of nitrate and nitrite anion. Finally, inhibition of NOS I and NOS I deletion inhibited the in vivo metabolism of ETOH. CONCLUSIONS: We conclude that constitutive NOS I is involved in protection of the lung from stressor-induced lung injury. NOS I within the PMNs may limit PMN recruitment into the lung. Speculatively, NOS II-derived NO may also limit PMN-induced lung damage at the expense of a slower clearance of the bacterial burden.
Animals↗
Inhibition of DNA synthesis in isolated human endometrial cells by a levonorgestrel-releasing intrauterine device.
OBJECTIVE: To estimate the effect of an intrauterine device (IUD) releasing 20 micrograms levonorgestrel (LNG) per 24 hours on DNA synthesis in human endometrial cells before and after 12 months of use. STUDY DESIGN: Endometrial specimens were collected from the anterior or posterior wall of the miduterus from 6 females on cycle day 10-12 before insertion of the IUD and after 12 months of use. RESULTS: Previous results from our group did not reveal any influence on endometrial DNA cell content when a levonorgestrel IUD releasing 2 micrograms/24 h was used for 12 months in a group of fertile females. In this study, the IUD release rate, 20 micrograms LNG/24 h, was statistically significantly different from the results in the previous studies. The effect of the levonorgestrel IUD on endometrial proliferation was dose dependent, and a significant correlation could be found between continuous exposure to LNG and inhibition of DNA synthesis in endometrial cells. CONCLUSION: Inhibition of proliferative activity in endometrial cells seems to be reflected by a decrease in DNA synthesis per cell nucleus and contributes to the clinical performance of the LNG-releasing IUD.
Adult↗
Clinical analysis on the treatment of HIV/AIDS by traditional Chinese medicine.
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AIDS-Related Complex↗
[Phorbol-12-myristate-13-acetate and interferon-gamma synergistic induction of B7-1 expression in ovary carcinoma cells and immunological value].
OBJECTIVE: To investigate the therapeutic potential of phorbol-12-myristate-13-acetate(PMA) and interferon-gamma(IFN-gamma) by induction of expression of adhesion molecule in mucious cystadenocarcinoma of ovary (MCAS) and other tumor cells. METHODS: Expression of costimulatory signals(B7-1), major histocompatibility complex(MHC-I, MHC-II) was analysed with flow cytometry. Cytotoxic T lymphocytes(CTL) killing activity and T cell proliferation induced with expression of B7-1 were evaluated by 4-h 51Cr release assay and standard 3HTdR incorporation and scintitation counting. RESULTS: Pretreatment with PMA and then treated with IFN-gamma was able to enhance B7-1 expression on the tumor cell lines with the constitutive B7-1 expression or on B7-1-transfected tumor cells and to induce B7-1 expression on MCAS and some tumor cell lines without constitutive B7-1 expression. However, treatment with IFN-gamma alone failed to induce B7-1 expression on the tumor cell lines. The synergistic effect of PMA combined with IFN-gamma in the induction of B7-1 expression can be anatagonised by H7 [1-(5-isoquinolinesulfonyl)-2-methyl-Piperazine dihydrochloride]. In addition, treatment with PMA combined with IFN-gamma simultaneously induced or enhanced the expression of MHC class I/II on these tumor cell lines. The tumor cells treated by PMA combined with IFN-gamma were able to induce CTL killing activity and T cell proliferation, which is involved in the expression of B7-1. CONCLUSIONS: The enhancement or induction of B7-1 expression by IFN-gamma may be dependent on the prior activation of protein kinase by PMA and the induced B7-1 expression on tumor cells may have some therapeutic potential.
B7-1 Antigen↗
[Relationship between the bone marrow cell proliferation and the prognosis in childhood acute lymphoblastic leukemia].
OBJECTIVE: To study the expression of proliferative antigens in leukemic cells and the relationship between the cell proliferation activity and the prognosis. METHODS: The labeling index (LI) of CD71, Ki-67 and PCNA in normal and leukemic cells were measured by flow cytometry. RESULTS: In normal children, the LI of CD71, Ki-67 and PCNA was (32.18 +/- 16.66)%, (4.82 +/- 9.27)% and (19.69 +/- 25.11)%, respectively, while in ALL children, which was (33.66 +/- 21.52)%, (32.14 +/- 23.59)% and (47.46 +/- 30.96)%, respectively. The PCNA LI of leukemia cells was (47.46 +/- 30.96)% and (27.28 +/- 12.51)% when patients was at presentation and remitted for 3 years, respectively, and was (52.59 +/- 32.00)% and at presentation in 28 CCR children and and (26.94 +/- 14.48)% in 7 high-risk group ALL children (F = 8.877, P < 0.01), respectively. CONCLUSIONS: The proliferation, LI of leukemic cells was higher than that of normal cells, and reduced to normal level after treatment. The higher PCNA proliferation of untreated cells was a favourable marker for prognosis.
Adolescent↗
Electrophoresis of creatine kinase isoforms: a highly sensitive fluorescence scanning method.
OBJECTIVE: To develop an agarose electrophoretic method for creatine kinase (CK) isoforms, using highly sensitive fluorescence scanning. METHODS: A discontinuous buffer system was used. Electrophoresis on agarose gel was performed under constant current and low voltage. CK isoforms were separated within 30 minutes and detected by fluorescence scanning. RESULTS: There were no significant differences when the activities of CK-MM were between 853.0 U/L and 14.0 U/L and those of CK-MB between 152.0 U/L and 2.4 U/L. The detection limits of stain method for CK-MM and CK-MB isoforms were 36.0 U/L and 12.3 U/L, respectively; while those of fluorescence method were 12.0 U/L and 2.1 U/L. The experimental results showed good precision for CK-MM isoforms, as well for CK-MB isoforms and isoenzymes. CONCLUSION: An agarose electrophoretic method has been developed to measure CK isoenzymes and isoforms clinically. This method is rapid, simple, sensitive, highly reproducible and inexpensive. It is suitable for general laboratories.
Creatine Kinase↗
[Effects of NGF and CNTF on NO level in brain of burn rats].
OBJECTIVE: To investigate the injurious effects of NO to the brain and protective effect of NGF and CNTF following burn injury in rats. METHODS: Following intubation of the lateral cerebroventricle, the rats were divided into four groups:sham burn, burn, burn + NGF, burn + CNTF. The contents of NO in various parts of brain in rats with 30% TBSA third degree scald were measured. RESULTS: The contents of NO were increased in burned rats. NGF and CNTF could lower the contents of NO. CONCLUSION: The brain injury caused by burns may be associated with increase of NO. The protective effect of NGF and CNTF on the brain of burn rats may be related to lowering of NO.
Animals↗
Non-invasive assessment of myocardial risk and infarct area in canine model of myocardial reperfusion by intravenous contrast echocardiography.
OBJECTIVE: To evaluate the newly developed perfluoropropene-filled echo-contrast agent (FCT-188) in non-invasive assessment of risk areas (RA) and infarct areas (IA) with intravenous myocardial contrast echocardiography (MCE) in canine model of ischemia followed by reperfusion. METHODS: Eight chest-opened Beagle dogs with a 90-minute ischemia followed by a 240-minute reperfusion were studied. MCE was performed after a bolus injection of FCT-188 (0.025 ml/kg, i.v.) into a superficial vein of the forelimb at baseline, 20 minutes after occlusion, and 4 h after reperfusion to non-invasively assess the left ventricular myocardium area (LVMA), myocardial ischemic risk area (RA), and infarct area (IA) in a short-axis view of left ventricle. The accuracy of detecting myocardial perfusion with intravenous MCE was further assessed by in vitro myocardial staining of the matched cross-sections. Both RA and IA were expressed as percent of LVMA. RESULTS: LVMA, RA, IA, and IA/RA ratio were accurately assessed by MCE (LVMA: 6.60 cm2 +/- 0.76 cm2; RA: 35.7% +/- 6.68%; IA: 21.0% +/- 13.2%; IA/RA: 60.3% +/- 31.4%; n = 7) as compared with those of the matched cross-section (LVMA: 6.81 cm2 +/- 0.73 cm2, P = 0.062; RA: 35.3% +/- 9.9%, P = 0.84; IA: 25.10% +/- 14.5%, P = 0.07; IA/RA: 68.0% +/- 22.2%, P = 0.28, respectively). There was a significant correlation of MCE-assessed IA/RA ratio and its corresponding pathologically determined finding in vitro (Y = 1.21 x -21.6, r = 0.73, P = 0.015). No significant changes of electrocardiogram (ECG), mean artery pressures (MAP), pulmonary artery pressures (PAP), and pulmonary artery wedge pressures (PAWP) were found between pre- and post-intravenous injection of FCT-188 at each time point. CONCLUSION: These indicate that FCT-188 can be used to assess risk areas and infarct areas accurately and non-invasively with intravenous MCE in the canine model of a 90-minute ischemia followed by a 240-minute reperfusion and might have potential significance for non-invasive assessment of myocardial reperfusion clinically.
Animals↗
Correlation of cell proliferation inhibition and apoptosis induction with expression of human beta 5 integrin on hematopoietic cells.
OBJECTIVE: To investigate the function of the alpha v beta 5 integrin in hematopoietic cells. METHODS: Tissue culture, integrin expression vectors, gene transfer, polymerase chain reaction (PCR), apoptosis analyses and cytometic analysis were made on hematopoietic cells. RESULTS: The beta 5 integrin cDNA was not expressed in hematopoietic cells following exposure to the beta 5 integrin retrovirus vector pG beta 5CHT. Unbalanced expression of the alpha v beta 3 and alpha v beta 5 integrins occurred during apoptosis induced by serum depletion and upon differentiation. The treatment of hematopoietic cells with anti-alpha v beta 5 monoclonal antibody inhibited apoptosis induced by serum depletion. Inducible expression of the beta 5 integrin cDNA in the hematopoietic cell line K562 caused cellular proliferation inhibition. CONCLUSION: The alpha v beta 5 integrin cDNA in hematopoietic cells can inhibit the proliferation of the hematopoietic cell, cause the differentiation of the hematopoietic cells and induce the apoptosis of the hematopoietic cells.
Apoptosis↗
Surgical treatment of DeBakey type I aortic dissection using the "elephant trunk technique".
OBJECTIVES: To review the indications, operative methods and postoperative management of the "elephant trunk technique", and to report two cases of DeBakey type I aortic dissection treated with the "elephant trunk technique". METHODS: Two cases of DeBakey type I aortic dissection were operated with selective cerebral perfusion via the right subclavian artery. At the first stage, a tubular dangling aortic graft prosthesis ("elephant trunk") was inserted into the distal aorta while replacing the ascending aorta and aortic arch. The distal elephant trunk prosthesis was then used at the second stage involving the replacement of the sections of the distal aorta via a left-sided thoracotomy. RESULTS: The two operations were successful. Ultrafast computed tomograph (UFCT) showed that the two patients were cured after the first stage operation, and the second stage procedure could have been avoided. CONCLUSIONS: The "elephant trunk technique" is a multiple stage approach in the treatment of extensive aneurysmal diseases of the aorta. The procedure is indicated for patients who have combined diseases of both ascending aorta plus aortic arch segments and descending aortic aneurysm. It can also be used for patients with DeBakey type I aortic dissection. Some patients can be cured after the first stage operation.
Aortic Dissection↗
[An analysis of autologous peripheral stem cell transplantation for hematological malignancies].
OBJECTIVE: To summarize the data of autologous peripheral stem cell transplantation (APBSCT) for 49 hematological malignancies patients. METHODS: Forty-nine patients, 18 with acute myeloid leukemia, (AML) 10 acute lymphoblastic leukemia(ALL), 14 multiple myeloma(MM), 6 non-Hodgkin's lymphoma(NHL) and 1 myelodysplastic syndrome(MDS RAEB-t) received APBSCT were retrospectively analyzed. RESULTS: Comparing to conventional chemotherapy, APBSCT can prolong the patients' disease-free survival(DFS) and overall survival (OS). The 3 and 5-year OS rates were 74.78% and 83.33% for AML/NHL; 38% and 19% for MM; 40% and 0 for ALL, respectively. The time of hematopoietic reconstitution was influenced by G-CSF administration significantly. The mean time of neutrophil recovering to 0.5 x 10(9)/L after APBSCT was +17.7 days in no G-CSF group, and +11.14 days in G-CSF group. Up to now, of the 49 patients, no APBSCT related death occur, 23 have died and 22 of them died of relapse. The most common transplantation related complications were fever, liver dysfunction and hypopotassemia, all of which can be cured by proper treatment. CONCLUSION: APBSCT can be safely performed in hematological malignancies.
Acute Disease↗
Effects of diabetes on creatine kinase activity in streptozotocin-diabetic rats.
OBJECTIVE: To study the effect of diabetes on the creatine kinase (CK) activity in different tissues of streptozotocin-induced diabetic rats. METHODS: Serum samples, heart, extensor digitorum longus, brain and bladder were collected from both streptozotocin-induced diabetic rat and control group. Ck was measured by enzymologic method. RESULTS: The body weight, heart weight and brain weight were reduced significantly compared with control group (P < 0.001), but bladder weight was increased significantly (P < 0.001). CK activity in serum and extensor digitorum longus in diabetic rat was significantly lower (P < 0.001); CK activity in diabetic heart was lower (P < 0.01); and in brain also lower (P < 0.05). A higher CK activity in diabetic bladder was found (P < 0.001). CONCLUSIONS: Diabetes can result in a lower CK activity in serum, heart, brain and extensor digitorum longus that may affect the energy metabolism in the tissues. A higher CK activity in diabetic bladder may reflect a functional compensatory mechanism.
Animals↗
[Apoptosis of ovarian carcinoma cell line induced by amiloride].
OBJECTIVE: To investigate induction of apoptosis and its possible mechanism in amiloride-treated ovarian carcinoma cell line. METHODS: Morphological changes of apoptotic cells were investigated by light and fluorescence microscopy. DNA fragmentation was analysed by agarose gel electrophoresis. In addition, the number of hypodiploid cells (apoptotic cells) was quantitatively assessed by flow cytometry and intracellular pH was also analysed. RESULTS: Amiloride-treated ovarian carcinoma cells showed morphological characteristics of apoptosis. A ladder-like pattern of DNA fragmentation was demonstrated on agarose gel electrophoresis. Amiloride at 0.01-5 mumol/L could induce apoptosis in 18.7%-61.6% of ovarian carcinoma cells. The apoptosis-inducing effect of amiloride was dose- and time-dependent. In addition, amiloride induced intracellular acidification in a subpopulation of the treated cells. Furthermore, these isolated acidified cells revealed chromatin condensation as well as DNA degradation with characteristics of apoptosis. There was good correlation between apoptotic cells and acidic cells. CONCLUSION: Amiloride triggers apoptosis of ovarian carcinoma cells; intracellular acidification may be involved in the mechanism of apoptosis.
Amiloride↗