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Results for “Staining and Labeling”

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PubMed1995

Immunohistochemical evidence of alpha-, beta- and gamma 3-melanocyte stimulating hormone expression in cutaneous malignant melanoma of nodular type.

Opiomelanocortins are formed after cleavage of the larger precursor molecule, proopiomelanocortin (POMC), which contains several peptide residues, sharing certain amino acid homology, including adrenocorticotrophic hormone (ACTH) and alpha-, beta- and gamma-melanocyte stimulating hormone (MSH). The expressions of alpha-, beta- and gamma 3-MSH in human cutaneous malignant melanoma of nodular type are demonstrated. For the MSHs, the immunolabelling was concentrated mostly in the tumour cellular cytoplasm, with occasional cells displaying a nuclear staining. Labelled tumour cells were dispersed throughout the epidermis and dermis as individual cells or in so-called 'pearl-like nests', most of which consisted mainly of round or oval shaped cells as well as a few pleomorphic or spindle-shaped cells. The fluorescence intensity seemed to increase in accordance with the development of the tumours. All cases examined were clearly stained with protein S-100, which provided us with a definite diagnosis. Considering the overall MSHs-related staining intensity of each section, the general perception we got was that the closer to the centre of the tumour parenchyma, the stronger was the staining and, furthermore the larger/more poorly differentiated the cells, the stronger was the staining. We also found the MSHs expressions to appear in the peripheral part of the tumour and the perilesional tissues including epidermis, sweat glands, sebaceous glands as well as hair follicles. Neurohypertrophic features were encountered including increases in both the number of nerve fibres and their diameter. Our results presented here strongly support the viewpoint earlier proposed that MSH peptides, by an autocrine and/or paracrine production from melanoma cells, are engaged in the regulation of melanogenesis, growth and proliferation of the tumour cells. We also conclude that, although alpha-, beta- and gamma 3-MSH peptides do not provide as high a sensitivity for diagnosis as protein S-100, they appear as useful markers for supportive diagnosis and assessment of malignant melanoma.

Adult↗

PubMed1976

Fluorescent antibody localization of myosin in the cytoplasm, cleavage furrow, and mitotic spindle of human cells.

We have studied the distribution of myosin molecules in human cells using myosin-specific antibody coupled with fluorescent dyes. Rabbits were immunized with platelet myosin or myosin rod. They produced antisera which precipitated only myosin among all the components in crude platelet extracts. From these antisera we isolated immunoglobulin-G (IgG) and conjugated it with tetramethylrhodamine or fluorescein. We separated IgG with 2-5 fluorochromes per molecule from both under- and over-conjugated IgG by ion exchange chromatography and used it to stain acetone-treated cells. The following controls established the specificity of the staining patterns: (a) staining with labeled preimmune IgG; (b) staining with labeled immune IgG adsorbed with purified myosin; (c) staining with labeled immune IgG mixed with either unlabeled preimmune or immune serum; and (d) staining with labeled antibody purified by affinity chromatography. In blood smears, only the cytoplasm of platelets and leukocytes stained. In spread Enson and HeLa cells, stress fibers stained strongly in closely spaced 0.5 mum spots. The cytoplasm stained uniformly in those cells presumed to be motile before acetone treatment. In dividing HeLa cells there was a high concentration of myosin-specific staining in the vicinity of the contractole ring and in the mitotic spindle, especially the region between the chromosomes and the poles. We detected no staining of erythrocytes, or nuclei of leukocytes and cultured cells, or the surface of platelets and cultured cells.

Antibodies↗

PubMed1985

Early stages of Purkinje cell maturation demonstrated by Thy-1 immunohistochemistry on postnatal rat cerebellum.

The cell surface glycoprotein, Thy-1, is present on Purkinje cells at birth, so allowing Thy-1 immunohistochemistry to demonstrate the final stage of migration and the transition to dendritic growth of these cells. In the most caudal lobule of the cerebellar cortex of the newborn rat, migrating Purkinje cells are found. These have a prominent process (up to 50 micron long) from which fine filopodia project, presumably sensing the environment in front of the cell. These cells are orientated tangentially, at right angles to the radial orientation they assume for dendritic growth. Strong Thy-1 labelling is found not only on their surface, but also on a cytoplasmic cap above the presumed leading pole of the nucleus. More rostrally in the cerebellar cortex, Purkinje cells arrive up to 3 days before birth and are quiescent until the postnatal development of their dendritic tree. At birth and during early postnatal periods a rounded cell is found with little cytoplasm; Thy-1 staining labels its surface and the fine processes which emanate from it. Such cells coexist with other Thy-1-positive Purkinje cells with more developed surface orientated processes. Even as early as the day of birth these fine processes cross the molecular layer and contact the lower level of the external granule layer. Orientated dendritic growth appears to occur by a selective thickening of these processes and a massive apical protrusion of intensely Thy-1-positive cytoplasm. The whole of the Purkinje cell surface membrane exhibits high levels of Thy-1 throughout dendritic growth and synaptogenesis, and cytoplasmic antigen is prominent during the period of greatest growth. Thy-1 is also found on the neurons of the deep cerebellar nuclei, and is seen transiently on Golgi interneurons. High levels of the antigen are present on blood vessels and choroid plexus at birth but are lost from these structures over the first 2 postnatal weeks.

Animals↗

PubMed1988

Fluorescent vital stains for complementary labelling of protoplasts from Trichoderma spp.

In this study several fluorescent vital stains were evaluated for their ability to provide complementary vital staining of protoplasts of Trichoderma spp. for selection of heterokaryons following protoplast fusion. Tetramethyl rhodamine isothiocyanate and fluorescein isothiocyanate were rejected because they stained only a small proportion of protoplasts. Fluorescein diacetate stained all protoplasts, but the chromophore leaked rapidly from stained cells. A mixture of FluoroBora T and acriflavine stained all cells, but intensity was low and fading upon illumination was rapid. Nile red stained lipid bodies in all cells, but the stain was lost upon protoplast fusion in polyethylene glycol. Rhodamine 6G, on the other hand, stained all cells, fluoresced green, and was stable through fusion and upon illumination. Hydroethidine also stained all protoplasts, and staining was relatively stable through fusion and upon illumination. Hydroethidine fluoresced red and stained nuclei more prominently than the cytoplasm. Rhodamine 6G and hydroethidine were tested on a number of strains to determine whether they were toxic to protoplasts. No toxicity to any strain was noted with rhodamine 6G. Hydroethidine, however, was toxic at the higher concentrations tested, especially when stained protoplasts were exposed to light. When protoplasts were stained with the minimum concentration giving ready visualization and were incubated in darkness, hydroethidine also was nontoxic. Hydroethidine and rhodamine 6G are useful complementary vital stains of Trichoderma protoplasts for visualization of frequency and type (dicell, multicell) of fusion.

Fluorescent Dyes↗

PubMed2001

Neurotoxic effects of fluorinated glucocorticoid preparations on the developing mouse brain: role of preservatives.

Prenatal betamethasone (Celestene) therapy reduces the incidence of brain damage, whereas prenatal or neonatal dexamethasone (Soludecadron) increases the risk of brain lesions or neuromotor deficits. To determine whether this increase is ascribable to the sulfites used as preservatives in Soludecadron, we investigated the effects of 12 h of exposure to pure dexamethasone, Soludecadron, pure betamethasone, Celestene, and sulfites on in vitro and in vivo death of neurons cultured under basal conditions or with excitotoxic agents (N-methyl-D-aspartate or (S)-5-bromowillardiine) or hypoxia. Apoptotic features were quantitated using a fluorescent chromatin stain (Hoechst 33258). Neuronal viability was unaffected by pure dexamethasone, pure betamethasone, or Celestene. Soludecadron or sulfites significantly increased neuronal loss. Pure dexamethasone or pure betamethasone produced a 40-50% decrease in neuronal death induced by N-methyl-D-aspartate, (S)-5-bromowillardiine, or hypoxia, whereas Soludecadron had no effect and sulfites significantly increased the neurotoxicity of excitotoxic agents. In in vivo experiments involving terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling after several i.p. injections of fluorinated glucocorticoids, Soludecadron, but not pure dexamethasone, significantly increased the number of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-stained cells in neocortical layers and thalamus. These experimental findings suggest that injectable dexamethasone should be used with caution during the perinatal period.

Animals↗

PubMed1998

Apoptosis in the pathogenesis of cutaneous lupus erythematosus.

Defective regulation of apoptosis may play a role in the development of autoimmune diseases such as systemic lupus erythematosus, in which the skin is a prominent target. To our knowledge, however, the nature of epidermal changes in cutaneous lupus erythematosus (LE) has not previously been investigated. We investigated the involvement of apoptosis in cutaneous LE. A total of 44 lesional skin samples from patients with cutaneous LE, 44 skin samples from patients with scleroderma, five skin specimens from patients suffering from dermatomyositis, and 13 normal skin samples were stained immunohistochemically with monoclonal antibodies to Ki-67, p53 (DO-7), and bcl-2. The lesional skin from cutaneous LE, except LE profundus, showed a marked increase in Ki-67- and p53-positive keratinocytes, which were predominantly located in the basal layer of the epidermis and follicle, and a drastic reduction in the number of bcl-2-positive cells localized in the basal cell compartment. With TdT-mediated dUTP-biotin nick end-labeling staining, we demonstrated that extensive apoptosis occurred in almost the whole epidermis of cutaneous LE, except in cases of LE profundus. This abnormal expression of Ki-67, p53, and bcl-2 and the occurrence of apoptosis in the epidermis was also observed in epidermis from patients with dermatomyositis, but not in that from patients with scleroderma.

Apoptosis↗

PubMed2001

Tau filament formation in transgenic mice expressing P301L tau.

Mutations in the microtubule-associated protein tau, including P301L, are genetically coupled to hereditary frontotemporal dementia with parkinsonism linked to chromosome 17. To determine whether P301L is associated with fibril formation in mice, we expressed the longest human tau isoform, human tau40, with this mutation in transgenic mice by using the neuron-specific mouse Thy1.2 promoter. We obtained mice with high expression of human P301L tau in cortical and hippocampal neurons. Accumulated tau was hyperphosphorylated and translocated from axonal to somatodendritic compartments and was accompanied by astrocytosis and neuronal apoptosis indicated by terminal deoxynucleotidyl transferase-mediated biotinylated dUTP nick end-labeling staining. Moreover, P301L tau formed abnormal filaments. Electron microscopy of sarcosyl-insoluble protein extracts established that the filaments had a straight or twisted structure of variable length and were approximately 15 nm wide. Immunoelcecton microscopy showed that the tau filaments were phosphorylated at the TG3, AT100, AT8, and AD199 epitopes in vivo. In cortex, brain stem, and spinal cord, neurofibrillary tangles were also identified by thioflavin-S fluorescent microscopy and Gallyas silver stains. Together, our results show that expression of the P301L mutation in mice causes neuronal lesions that are similar to those seen in human tauopathies.

Actin Cytoskeleton↗

PubMed2001

Protective effect of heat preconditioning of rat liver graft resulting in improved transplant survival.

BACKGROUND: The protective effect of heat preconditioning of the liver against ischemia-reperfusion injury has been reported mostly in models of transient ischemia in relation to heat shock protein 70 (HSP70). We estimated the effect of heat preconditioning of liver grafts on the transplant survival rate and on apoptosis of sinusoidal endothelial cells (SEC) as well as hepatocytes in a rat model of liver transplantation. METHODS: Donor rats of the heat shock (HS) group were subjected to heat preconditioning 48 hr before graft harvest, and HSP70 levels were estimated by. Western blot analysis and immunohistochemistry. The liver isografts from the HS group and control (C) group were preserved in Euro-Collins solution for 6 or 8 hr and transplanted orthotopically. Serum hyaluronic acid and alanine aminotransferase were measured, and apoptosis of the SEC and hepatocytes was analyzed by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling staining and electron microscopy. RESULTS: HSP70 expression was detected not only in hepatocytes but also in SEC. In the 8-hr preservation model, the 1-week survival rate was 60% in the HS group and 0% in the C group. Serum hyaluronic acid and alanine aminotransferase levels in the HS group were significantly lower than those in the C group at 3 hr after reperfusion, and the number of terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling-positive SEC in the C group (35.2%) was markedly increased compared with the HS group (10.1%). Electron microscopic examination confirmed the features of apoptosis of SEC. CONCLUSIONS: Heat preconditioning of the graft improved the survival rate of the liver transplants. Induction of HSP70 in SEC as well as in hepatocytes might attenuate preservation-reperfusion injury by inhibiting apoptosis of SEC.

Alanine Transaminase↗

PubMed2001

[E-cadherin associated protein expression and its significance in invasive lobular carcinoma and invasive ductal carcinoma of breast].

OBJECTIVE: To study E-cadherin associated proteins alpha-, beta-, gamma-catenin expression and their significance in invasive lobular carcinoma (ILC) and invasive ductal carcinoma (IDC) of breast. METHODS: Immunohistochemistry staining (labeled streptavidin-biotin method) was used to detect alpha-, beta-, gamma-catenin expression in invasive breast carcinoma (19 cases of ILC and 32 cases of IDC ). RESULTS: The loss and reduction rate of alpha-, beta-, gamma-catenin expression in ILC was 78.9% (15 cases), 52.6% (10 cases) and 84.2% (16 cases), respectively. The rate of alpha-, beta-, gamma-catenin expression showing loss and reduction in IDC was 75.0% (24 cases), 43.8% (14 cases) and 81.3% (26 cases), respectively. The staining intensity of alpha-, beta-, gamma-catenin expression in invasive carcinoma of breast was weaker than that in foci of carcinoma in situ (semiquantitative grading). There was a positive relationship between the expression of alpha-catenin and beta-catenin in invasive breast carcinoma. No significant association was seen between reduced protein expression of alpha-, beta-, gamma-catenin and the development of lymph node metastasis. CONCLUSION: alpha-, beta-, gamma-catenin expression was almost identical in ILC and IDC of breast, showing significant loss and reduction of protein expression in the carcinoma cells of invasive breast carcinoma, suggesting that alpha-, beta-, gamma-catenin may lose their normal adherent ability in the pathogenesis of invasive breast carcinoma.

Adult↗

PubMed2004

Anti-actin antibodies generated against profilin:actin distinguish between non-filamentous and filamentous actin, and label cultured cells in a dotted pattern.

Actin polymerization is a prominent feature of migrating cells, where it powers the protrusion of the leading edge. Many studies have characterized the well-ordered and dynamic arrangement of filamentous actin in this submembraneous space. However, less is known about the organization of unpolymerized actin. Previously, we reported on the use of covalently coupled profilin:actin to study actin dynamics and presented evidence that profilin-bound actin is a major source of actin for filament growth. To locate profilin:actin in the cell we have now used this non-dissociable complex for antibody generation, and obtained monospecific anti-actin and anti-profilin antibodies from two separate immunizations. Fluorescence microscopy revealed drastic differences in the staining pattern generated by the anti-actin antibody preparations. With one, distinct puncta appeared at the actin-rich leading edge and sometimes aligned with microtubules in the interior of the lamella, while the other displayed typical actin filament staining. Labelling experiments in vitro demonstrated failure of the first antibody to recognize filamentous actin and none of the two bound microtubules. The two anti-profilin antibodies purified in parallel generated a punctated pattern similar to that seen with the first anti-actin antibody. All antibody preparations labelled the nuclei.

Actin Cytoskeleton↗

PubMed2006

Maternal folate deficiency affects proliferation, but not apoptosis, in embryonic mouse heart.

Low dietary folate and deficiency of methylenetetrahydrofolate reductase (Mthfr) were reported to increase the risk for congenital heart defects, but contributory mechanisms have not been elucidated. Because low folate and absent MTHFR activity were shown to affect proliferation and apoptosis in developing neural tissue, we examined these processes in the myocardium of embryos from Mthfr +/+ and Mthfr +/- mice fed control diets (CD) or folic acid-deficient diets (FADD). Mice consumed the designated diets for 8 wk, from weaning and through pregnancy until they were killed. Embryos were assessed on gestational day 12.5 for myocardial proliferation by 5-bromo-2'-deoxyuridine (BrdU) labeling and for apoptosis by TdT-mediated dUTP nick end labeling staining and caspase 3/7 activity assays. FADD-treated dams had significantly higher resorption rates than CD-treated dams. Embryonic lengths and weights from FADD-treated dams were significantly lower than those from CD-treated dams; the smallest embryos were those of the Mthfr +/- dams that consumed the FADD, with effect of genotype tending to be significant (P = 0.09). The thickness of cardiac ventricular compact walls of embryos from FADD-treated dams was significantly reduced, and embryonic myocardium from FADD-treated dams had significantly fewer BrdU-labeled cells compared with CD-treated dams, with no differences in apoptosis due to the diets. Genotype did not affect proliferation or apoptosis. Our results suggest that proliferation of embryonic myocardium is sensitive to maternal dietary folate and that folate supplementation during pregnancy is important for normal heart development and prevention of heart defects.

Animals↗

PubMed2005

Mild hypothermia decreases GSK3beta expression following global cerebral ischemia.

INTRODUCTION: The serine/threonine kinase glycogen synthase kinase 3beta (GSK3beta) is abundant in the central nervous system and is neuron-specific. GSK3beta plays a pivotal role in the regulation of numerous cellular functions (including phosphorylation) and, thereby, regulation of many metabolic, signaling, and structural proteins as well as transcription factors that can influence cell survival. This article reports that GSK3beta expression following global cerebral ischemia (GCI) is altered by the neuroprotectant, mild hypothermia (33 degrees C). METHODS: Male Sprague-Dawley rats were anesthetized and subjected to GCI; arterial blood pressure was reduced to 30 mmHg by blood withdrawal via the jugular vein, and both common carotid arteries were occluded with aneurysm clips for 8 minutes. Hypothermia (33 degrees C) was induced in half the rats 10 minutes prior to GCI and was maintained for 3 hours. Rats were killed 24 or 72 hours later to assess cell death and GSK3beta expression. RESULTS: At 72 hours post-GCI, levels of GSK3beta expression were significantly lower in hypothermic rats than in normothermic rats. This reduction in GSK3beta correlated with marked neuroprotection and reduced terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end labeling staining in hippocampal CA1 neurons. No significant changes in phosphorylated GSK3beta expression were observed. CONCLUSION: These data suggest that GSK3beta plays a role in GCI pathology that can be altered by mild hypothermia.

Animals↗

PubMed2004

Peyer's patch dendritic cells process viral antigen from apoptotic epithelial cells in the intestine of reovirus-infected mice.

We explored the role of Peyer's patch (PP) dendritic cell (DC) populations in the induction of immune responses to reovirus strain type 1 Lang (T1L). Immunofluorescence staining revealed the presence of T1L structural (sigma1) and nonstructural (sigmaNS) proteins in PPs of T1L-infected mice. Cells in the follicle-associated epithelium contained both sigma1 and sigmaNS, indicating productive viral replication. In contrast, sigma1, but not sigmaNS, was detected in the subepithelial dome (SED) in association with CD11c(+)/CD8alpha(-)/CD11b(lo) DCs, suggesting antigen uptake by these DCs in the absence of infection. Consistent with this possibility, PP DCs purified from infected mice contained sigma1, but not sigmaNS, and PP DCs from uninfected mice could not be productively infected in vitro. Furthermore, sigma1 protein in the SED was associated with fragmented DNA by terminal deoxy-UTP nick-end labeling staining, activated caspase-3, and the epithelial cell protein cytokeratin, suggesting that DCs capture T1L antigen from infected apoptotic epithelial cells. Finally, PP DCs from infected mice activated T1L-primed CD4(+) T cells in vitro. These studies show that CD8alpha(-)/CD11b(lo) DCs in the PP SED process T1L antigen from infected apoptotic epithelial cells for presentation to CD4(+) T cells, and therefore demonstrate the cross-presentation of virally infected cells by DCs in vivo during a natural viral infection.

Animals↗

PubMed1983

Immunoreactive vasoactive intestinal polypeptide is concentrated in the sacral spinal cord: a possible marker for pelvic visceral afferent fibers.

Previous descriptions of immunoreactive vasoactive intestinal polypeptide (VIP) in small-diameter dorsal root ganglion cells in the superficial dorsal horn implicated this 28 amino acid peptide in nociceptive transmission. In this study, we examined the distribution of immunoreactive VIP in the spinal cord and caudal medulla of cats and rats. The PAP method was used on paraffin and frozen sections of 4% paraformaldehyde-fixed tissue, using antibodies to VIP that were raised in rabbits. The distribution of immunoreactive VIP, while similar to that of substance P (SP), a putative primary afferent peptide neurotransmitter, is more restricted. VIP staining is found in sacral dorsal roots and densely in the Lissauer tract. Dorsal horn staining is concentrated in lamina I. In contrast to SP, lamina II is almost devoid of staining. Labeled VIP axons course along the lateral curvature of the dorsal horn and arborize across lamina V and around the central canal. A collateral branch of these fibers distributes to the sacral autonomic nucleus. A few fibers could be traced from the root entry zone to the contralateral central gray. VIP axons also terminate between ependymal cells of the central canal. Unlike SP, immunoreactive VIP was restricted, almost exclusively, to the sacral cord. The few fibers in the lumbar enlargement and in the coccygeal cord apparently derive from ascending and descending sacral primary afferents. In fact, the VIP pattern is almost identical to that reported for afferents from the pelvic viscera, including a discontinuous rostrocaudal distribution. Since the staining pattern is also very similar to that of A-delta high-threshold mechanoreceptors, the possibility is discussed that whereas VIP is not a general "somatic" primary afferent transmitter, it may transmit nociceptive input from the pelvic viscera.

Afferent Pathways↗

PubMed2001

Oxidative stress and neuronal DNA fragmentation mediate age-dependent vulnerability to the mitochondrial toxin, 3-nitropropionic acid, in the mouse striatum.

Oxidative stress is involved in the neuropathology of several neurodegenerative diseases and stroke, all of which are related to excitotoxicity. Age-dependent vulnerability is characteristic of these conditions. It is not clear whether apoptosis-related neuronal death is involved in age-dependent vulnerability to excitotoxicity. We evaluated whether apoptosis-related neuronal death after treatment with 3-nitropropionic acid (3-NP) is age-dependent in the mouse striatum. We have demonstrated that oxidative stress occurs early after 3-NP treatment and even more so in aged mice. DNA fragmentation with terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end labeling staining and gel electrophoresis occurred in an age-dependent fashion. Expression of the DNA repair enzyme, apurinic/apyrimidinic endonuclease, was more attenuated in old mice. Therefore, these results suggest that oxidative stress induces age-dependent neuronal apoptosis in the mouse striatum after 3-NP treatment, which in turn produces an age-dependent vulnerability to 3-NP.

Aging↗

PubMed2005

Loss of Gadd45a does not modify the pulmonary response to oxidative stress.

It is well established that exposure to high levels of oxygen (hyperoxia) injures and kills microvascular endothelial and alveolar type I epithelial cells. In contrast, significant death of airway and type II epithelial cells is not observed at mortality, suggesting that these cell types may express genes that protect against oxidative stress and damage. During a search for genes induced by hyperoxia, we previously reported that airway and alveolar type II epithelial cells uniquely express the growth arrest and DNA damage (Gadd)45a gene. Because Gadd45a has been implicated in protection against genotoxic stress, adult Gadd45a (+/+) and Gadd45a (-/-) mice were exposed to hyperoxia to investigate whether it protected epithelial cells against oxidative stress. During hyperoxia, Gadd45a deficiency did not affect loss of airway epithelial expression of Clara cell secretory protein or type II epithelial cell expression of pro-surfactant protein C. Likewise, Gadd45a deficiency did not alter recruitment of inflammatory cells, edema, or overall mortality. Consistent with Gadd45a not affecting the oxidative stress response, p21(Cip1/WAF1) and heme oxygenase-1 were comparably induced in Gadd45a (+/+) and Gadd45a (-/-) mice. Additionally, Gadd45a deficiency did not affect oxidative DNA damage or apoptosis as assessed by oxidized guanine and terminal deoxyneucleotidyl transferase-mediated dUTP nick-end labeling staining. Overexpression of Gadd45a in human lung adenocarcinoma cells did not affect viability or survival during exposure, whereas it was protective against UV-radiation. We conclude that increased tolerance of airway and type II epithelial cells to hyperoxia is not attributed solely to expression of Gadd45a.

Adenocarcinoma↗

PubMedDate not supplied

Clinicopathologic factors related to apoptosis in retinoblastoma.

PURPOSE: To investigate the presence of apoptosis in retinoblastoma and its correlation with other pathologic and prognostic factors. METHODS: The pathologic and admission records of 25 patients with a pathologically confirmed diagnosis of retinoblastoma were reviewed. TUNEL (TdT dUTP nick end labeling) staining was used to examine apoptosis in the pathologic slides of these 25 patients. The association between apoptosis and clinicopathologic factors was examined with chi-square, Fisher's exact, and Student's t tests. RESULTS: Of the 25 specimens tested, 11 were TUNEL stain-positive for the presence of apoptotic cells. Apoptosis was found more frequently in younger patients and within rosettes, although these associations were not statistically significant. Apoptosis was not associated with tumor invasion or metastasis. CONCLUSION: Apoptotic cells were found in 11 of 25 retinoblastoma specimens. Apoptosis tends to occur in young patients and be distributed within rosettes.

Apoptosis↗

PubMed2006

JNK1 is required to preserve cardiac function in the early response to pressure overload.

Cardiac stress consistently activates c-Jun NH(2)-terminal kinase (JNK) pathways, however the role of different members of the JNK family is unclear. In this study, we applied pressure overload (TAC) in mice with selective deletion of the three JNK genes (Jnk1(-/-), Jnk2(-/-), and Jnk3(-/-)). Following TAC, all three JNK knockout mouse lines developed cardiac hypertrophy similar to wild-type mice (WT), but only JNK1(-/-) mice displayed a significant reduction in fractional shortening after 3 and 7 days of pressure overload, associated with a significant increase in terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling staining and marked inflammatory infiltrate. After the acute deterioration stage, JNK1(-/-) mice underwent a slow recovery followed by a steady progression of cardiac dysfunction, becoming indistinguishable from WT after 12 weeks of TAC. These data suggest that JNK1 plays a protective role in response to pressure overload, preventing the early deterioration in cardiac function following an acute increase in afterload.

Animals↗