PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “light induction”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,009 records · Page 56Linked to original sources
PubMed1983

Immunologic unresponsiveness induced by topical application of hapten to PUVA-treated skin in guinea pigs.

Pretreatment by topical application of 8-methoxypsoralen and subsequent exposure to long-wave ultraviolet light (PUVA) on the induction site of contact sensitization to dinitrochlorobenzene (DNCB) significantly diminished the challenge reactions in guinea pigs. A single treatment with PUVA in a small area was enough to exhibit such an effect. Furthermore, the animals that had been first exposed to DNCB through PUVA-treated skin failed to become sensitized to the subsequent sensitization regimen of the same hapten even through previously untreated skin. The unresponsiveness in these animals was hapten-specific, since their capacity to become sensitized to an unrelated hapten, oxasolon, was not impaired. The intraperitoneal administration of cyclophosphamide at a dose of 200 mg/kg shortly before contact sensitization reversed the unresponsiveness in tolerant animals. These findings suggest that tolerance in these animals is a specific immunologic unresponsiveness mediated by suppressor cells.

Animals↗
PubMed1984

Secretion of gamma-interferon at the cellular level. Induction by Epstein-Barr virus.

Using a haemolytic plaque assay for gamma-interferon (IFN-gamma) secretion we found that in vitro Epstein-Barr virus (EBV) exposure of peripheral blood mononuclear cells from EBV immune individuals led to IFN-gamma secretion, which was apparent within 6 h after virus contact and peaked 12-24 h after induction. Live, ultraviolet-light-irradiated and heat-inactivated virions all caused IFN-gamma secretion. In contrast, blood mononuclear cells from EBV non-immune adults or neonates could not be activated to IFN-gamma production by EBV.

Cells, Cultured↗
PubMed1984

Renal vein thrombosis in stillborn infant of diabetic mother.

A second rare autopsy case of renal vein thrombosis in a stillborn female infant of a diabetic mother and the first after oxytocin induction is reported. Correlative light and electron microscopic studies were conducted. Extensive thrombosis from main to small cortical branches of the left renal vein was encountered causing hemorrhagic infarction of the left kidney. Newly formed hemorrhagic infarction and thrombosis of several small veins in the cortex of the right kidney were discovered. Hyperplasia of the pancreatic islets of Langerhans was observed. The literature was reviewed and the pathogenesis and clinical aspects were discussed.

Adult↗
PubMed1988

Induction of kappa transcription by interferon-gamma without activation of NF-kappa B.

The induction of immunoglobulin kappa light chain expression in 70Z/3 pre-B cells treated with bacterial lipopolysaccharide (LPS) requires the activation of the B cell-specific factor NF-kappa B, which binds to the kappa enhancer motif, GGGACTTTCC. This sequence alone can function as a tissue-specific enhancer for LPS-induced gene expression. A potent inhibitor of B lymphopoiesis [transforming growth factor-beta (TGF-beta)] was used to explore the mechanisms in the activation of kappa transcription by LPS and by interferon-gamma (IFN-gamma). TGF-beta inhibited LPS-induced kappa transcription but not the activation and in vitro binding of NF-kappa B. This indicates that NF-kappa B activation, while necessary, is not sufficient for LPS-induced kappa transcription. TGF-beta had no effect on IFN-gamma-induced kappa transcription, and NF-kappa B was not activated by IFN-gamma. These results reveal that LPS and IFN-gamma activate transcription through different mechanisms.

B-Lymphocytes↗
PubMed1988

A Study of 33 Bacteriophages of Rhizobium meliloti.

A total of 33 Rhizobium meliloti bacteriophages were studied. Of those, 21 were isolated in northern France from field soil in which Medicago sativa L. was grown. The other 12 phages were obtained by UV light and mitomycin C induction from 46 R. meliloti strains. Rhizobiophages were characterized by their morphology, host range, serological properties, restriction endonuclease patterns, DNA-DNA homologies, and DNA molecular weights. Five morphotypes were observed showing tailed phages with icosahedral heads. The categories of morphotypes included the Myoviridae (11 phages), Siphoviridae (3 morphotypes and 20 phages), and Podoviridae (2 phages). Type NM1 phage (Siphoviridae) is highly unusual because of the presence of transverse bars on the phage tail. Soil phages had broad host ranges, whereas phages isolated from bacterial cultures showed more or less narrow host ranges. Restriction endonuclease patterns and DNA-DNA hybridization experiments showed that the five phage type genomes were unrelated. Molecular weights of phage type DNAs were estimated, and they corresponded to values expected for capsid sizes, except for phage NM8. Type phiM11S (Siphoviridae) did not correspond to any other described Rhizobium phages and represents a new species.

Journal Article↗
PubMed1980

Control of phycobiliprotein proteolysis and heterocyst differentiation in Anabaena.

Phycobiliprotein degradation can be initiated in cultures of the cyanobacterium Anabaena by removal of combined nitrogen from the medium. Certain strains of Anabaena differentiate cells specialized for aerobic nitrogen fixation (heterocysts) under such conditions. We describe here a procedure for the preparation of extracts from heterocysts or vegetative cells that contain an activity capable of degrading only the phycobiliproteins in a mixture of soluble Anabaena proteins in vitro. This activity increased under nitrogen starvation conditions or in ammonia-replete cultures treated with the glutamine synthetase inhibitor methionine sulfoximine. The increase in activity induced by nitrogen starvation was prevented by chloramphenicol or by carbon starvation. Under all these conditions, phycobiliprotein degradative activity assayed in vitro was correlated with the loss of phycobiliprotein absorbance in vivo. Finally, starvation of a met auxotroph of Anabaena for methionine (in the presence of ammonia) did not induce phycobiliprotein degradation in vivo or the increase in proteinase activity. Together with direct measurements of ppGpp, these results indicate that proteolysis in Anabaena is not controlled by compounds associated with the stringent response in Escherichia coli. Since the increase in proteinase activity appears to be regulated by the same variables that control heterocyst differentiation, the activity should provide a useful biochemical marker for the early events of differentiation.

Adenosine Triphosphate↗
PubMed1990

In vitro susceptibility of T lymphocytes from chimpanzees (Pan troglodytes) to human herpesvirus 6 (HHV-6): a potential animal model to study the interaction between HHV-6 and human immunodeficiency virus type 1 in vivo.

The in vitro susceptibility of several nonhuman primate species to human herpesvirus 6 (HHV-6) was investigated. Only peripheral blood mononuclear cells from chimpanzees (Pan troglodytes) were found permissive to productive infection by HHV-6, indicating that the host range of HHV-6, albeit limited, may not be restricted to Homo sapiens. However, natural HHV-6 infection in chimpanzees, as well as in the other species tested, could not be documented by serological analysis. As previously observed with human cells, HHV-6 infection of chimpanzee peripheral blood mononuclear cells was highly cytopathic and the infected cells exhibited phenotypic features of activated T lymphocytes. Although in humans the majority of HHV-6-infected lymphocytes displayed the CD4 antigen, in chimpanzees a mixed CD4+ and CD8+ phenotype was observed. HHV-6 was also shown to productively coinfect individual chimpanzee T cells with human immunodeficiency virus type 1, resulting in an accelerated induction of cytopathicity. In light of these findings, we propose the utilization of chimpanzees as a potential animal model system to investigate the in vivo interaction between HHV-6 and human immunodeficiency virus type 1 and its relevance to the development of acquired immune deficiency syndrome.

Animals↗
PubMed1992

Extracellular Tax1 protein stimulates tumor necrosis factor-beta and immunoglobulin kappa light chain expression in lymphoid cells.

The human T-cell leukemia virus type I tax1 gene product is responsible for the increased expression of several cytokine and cellular genes that contain NF-kappa B regulatory sequences. Our laboratory has previously demonstrated that purified, extracellular Tax1 protein induced the nuclear accumulation of NF-kappa B binding activity in lymphoid cells. Since HTLV-I infection causes increased levels of lymphotoxin tumor necrosis factor-beta [TNF-beta] and immunoglobulin secretion, we have studied the interaction of NF-kappa B proteins from Tax1-stimulated cells with the TNF-beta and immunoglobulin kappa (Ig kappa) light chain genes. Tax1 induction of NF-kappa B occurred in the presence of cycloheximide, and Tax1 stimulation did not result in increased levels of NF-kappa B or c-rel RNA. These results indicate that new synthesis of NF-kappa B proteins was not required for induction of NF-kappa B-binding activity. With use of the Ig kappa NF-kappa B-binding site as a probe, two distinct NF-kappa B gel shift complexes were induced by the Tax1 protein. A slower-migrating complex, C1, was inhibited by the addition of purified I kappa B. In contrast, the faster-migrating C2 complex was not inhibited by I kappa B, but C2 was increased by detergent treatment of cytoplasmic extracts, suggesting that its binding activity was also regulated by an inhibitor. The Tax1-stimulated proteins that interacted with the NF-kappa B-binding sites in the Ig kappa and TNF-beta promoters were distinct. A 75-kDa protein preferentially associated with the Ig kappa NF-kappa B-binding site. In contrast, a 59-kDa protein associated with the TNF-beta NF-kappa B-binding site. Tax1 stimulation led to increased levels of TNF-beta and Ig kappa mRNA, as measured by reverse transcription and polymerase chain reaction analysis. These results represent the first experimental evidence that extracellular Tax1 can regulate the expression of endogenous cellular genes.

Animals↗
PubMed1990

Expression of the yeast PHR1 gene is induced by DNA-damaging agents.

The PHR1 gene of Saccharomyces cerevisiae encodes a photolyase which repairs specifically and exclusively pyrimidine dimers, the most frequent lesions induced in DNA by far-UV radiation. We have asked whether expression of PHR1 is modulated in response to UV-induced DNA damage and to DNA-damaging agents that induce lesions structurally dissimilar to pyrimidine dimers. Using a PHR1-lacZ fusion gene in which expression of beta-galactosidase is regulated by PHR1 5' regulatory elements, we found that exposure of cells to 254-nm light, 4-nitroquinoline-N-oxide, methyl methanesulfonate, and N-methyl-N'-nitro-N-nitrosoguanidine induced synthesis of increased amounts of fusion protein. In contrast to these DNA-damaging agents, neither heat shock nor exposure to photoreactivating light elicited a response. Induction by far-UV radiation was evident both when the fusion gene was carried on a multicopy plasmid and when it replaced the endogenous chromosomal copy of PHR1, and it was accompanied by an increase in the steady-state concentration of PHR1-lacZ mRNA. Northern (RNA) blot analysis of PHR1 mRNA encoded by the chromosomal locus was consistent with either enhanced transcription of PHR1 after DNA damage or stabilization of the transcripts. Neither the intact PHR1 or RAD2 gene was required for induction. Comparison of the region of PHR1 implicated in regulation of its expression with other damage-inducible genes from yeast cells revealed a common conserved sequence that is present in the PHR1, RAD2, and RNR2 genes and is required for damage inducibility of the latter two genes. These sequences may constitute elements of a damage-responsive regulon in S. cerevisiae.

Base Sequence↗
PubMed1994

Effect of muscular exercise on chronic relapsing experimental autoimmune encephalomyelitis.

We examined whether physical exercise affected the development of an autoimmune response, experimental autoimmune encephalomyelitis (EAE), which is a demyelinating disease leading to paralysis. EAE was inducted on day 0, in rats of both sexes, by injecting them with spinal cord tissue in adjuvant. From days 1 to 10 after injection, exercised rats (n = 55) ran on a treadmill (60-120 min/day) before the onset of the paralytic disease. Clinical signs of the disease (ataxia, paralysis, and body mass loss) were examined in exercised and control rats (n = 54). Three types of EAE were induced: monophasic, acute, and chronic relapsing (CR)-EAE (3 bouts of disease, CR-EAE 1, 2, and 3, separated by remissions). Exercise significantly delayed the onset of CR-EAE 1 (P = 0.001) and the 1st day of maximum severity of CR-EAE 1 (P = 0.001) and CR-EAE 2 (P = 0.002). Moreover, the duration of CR-EAE 1 was significantly decreased in exercised rats compared with control rats (P = 0.004). The peak severity of the different types of EAE was not modified by exercise. The present study indicates that endurance exercise during the phase of induction of EAE diminished lightly only one type of EAE (CR-EAE) and therefore did not exacerbate the autoimmune disease.

Animals↗
PubMed2003

Antisense targeting protein kinase A type I as a drug for integrated strategies of cancer therapy.

We have studied the role of protein kinase A (PKA) and its type I isoform (PKAI) in the transduction of mitogenic signaling, apoptosis, and angiogenesis. We have contributed to the development of selective inhibitors of PKAI, including a hybrid DNA/RNA mixed backbone oligonucleotide (AS-PKAI). We, and others, have demonstrated that AS-PKAI has a cooperative antitumor effect with a selected class of cytotoxic drugs and with radiotherapy in vitro and in vivo and that these effects can also be obtained following oral adinistration. Previously, we developed a series of therapeutic models based on the pleiotropic role played by PKAI in cell proliferation, apoptosis, and angiogenesis. On the basis of our former demonstration of functional and structural interactions of PKAI and the activated epidermal growth factor receptor (EGFR), we have shown that the combined blockade of both signaling molecules by AS-PKAI and either the monoclonal antibody C225 (erbitux) or the small molecule ZD1839 (gefitinib), results in a marked cooperative antitumor effect in a variety of human tumor models. A further cooperative antitumor effect can be obtained when AS-PKAI is used in combination with both EGFR inhibitors and either cytotoxic drugs or radiotherapy. The antitumor activity is associated with inhibition of growth factors and angiogenic factors production and to induction of apoptosis. In light of the recently demonstrated role of PKAI on the bcl-2-dependent apoptotic pathway, we have recently shown a synergistic antitumor, antiangiogenic, and proapoptotic effect of AS-PKAI in combination with antisense bcl-2 (oblimersen) or with a bispecific bcl-2/bcl-xL second generation antisense. A connection between COX-2, EGFR and PKAI was established, and we demonstrated that the combination of AS-PKAI with gefitinib and a COX-2 inhibitor, all adminstered orally, can result in a potent antitumor and antiangiogenic activity. These studies support the development of AS-PKAI as a novel anticancer agent and suggest its potentially relevant role when integrated with conventional treatments and/or other signaling inhibitors in novel therapeutic strategies.

Animals↗
PubMed2003

Evaluation of propofol and medetomidine-ketamine for short-term immobilization of Gulf of Mexico sturgeon (Acipenser oxyrinchus de soti).

Parenteral anesthetic protocols for short-term immobilization were evaluated in twenty 4-yr-old Gulf of Mexico sturgeon (Acipenser oxyrinchus de soti). An initial dose-response trial determined the efficacy of either propofol (3.5-7.5 mg/kg. i.v.) or combinations of medetomidine (0.03-0.07 mg/kg, i.m.)-ketamine (3-7 mg/kg, i.m.). A subsequent study evaluated the physiologic effects of propofol (6.5 mg/kg, i.v.)-induced anesthesia and anesthesia induced with a medetomidine (0.06 mg/kg, i.m.)-ketamine (6 mg/kg i.m.) combination. The effects of medetomidine were reversed at 30 min with atipamezole (0.30 mg/kg, i.m.). Both drug protocols provided adequate short-term immobilization for minor diagnostic procedures. Sturgeon receiving propofol were in a light plane of anesthesia within 5 min after drug administration, whereas only 30% of the medetomidine-ketamine group reached a light plane of anesthesia in the same time period. Both propofol and medetomidine-ketamine resulted in mild bradycardia and apparent respiratory depression, with propofol producing more profound effects. At the dosages used in this study, both propofol and the medetomidine-ketamine combination effectively induced a light plane of anesthesia. Induction times were shorter in the propofol group.

Anesthesia, Intravenous↗
PubMed2005

The mitotic checkpoint in cancer therapy.

The mitotic checkpoint is a key cell cycle control mechanism that ensures an accurate segregation of chromosomes during mitosis by delaying the onset of anaphase until all chromosomes are properly attached to a bipolar mitotic spindle. While complete loss of this checkpoint is lethal in vertebrates, a weakened mitotic checkpoint is frequently seen in cancer cells and it may contribute to tumorigenesis. Many anti-tumor drugs, including spindle assembly inhibitors and DNA damaging agents, can activate the mitotic checkpoint. However, since these drugs influence interphase events besides activating the mitotic checkpoint, the role of the mitotic checkpoint in drug-induced cell death remained unclear. Using a KSP antagonist that specifically acts on mitotic cells, we have recently shown that activation of the mitotic checkpoint followed by mitotic slippage or adaptation, activates Bax and initiates apoptosis. Notably, cells with a weakened mitotic checkpoint incur much less apoptotic death than their checkpoint-proficient counterparts, indicating the requirement of a competent mitotic checkpoint in the induction of apoptosis. In light of these findings and other recent reports, the potential influence of the mitotic checkpoint in response to chemotherapies, and the strategy to target the mitotic checkpoint for cancer therapeutics are discussed.

Animals↗
PubMed1976

Effect of hashish compounds on mouse peritoneal macrophages.

Light microscopy reveals an induction of extensive vacuolation in the macrophage after exposure to either delta 1-tetrahydrocannabinol or cannabidiol. Numerous small vacuoles appear in the cell periphery as early as 15 minutes after exposure (at 37degrees C.) to either of the compounds in 20 per cent newborn calf serum-Dulbecco's modified Eagle medium. The small lucent vacuoles coaleasce and yield enormous vacuoles which dominate the the cytoplasm. At approximately 3 hours, many of the vacuoles seem to burst with a concomitant expulsion of cell interior. The effect of hashish compounds on macrophages is essentially irreversible; exposure for 15 minutes to 10(-5) m of delta 1-THC or cannabidiol and a thorough wash in 20 per cent serum-medium, suffices to trigger the sequence of vacuolation and total cell death in the culture. Two major processes involving early reorganization of cellular membranes have been observed using electron microscopy. One relates to the formation of numerous autophagic vacuoles full of organelles, the other relates to the appearance of cytoplasmic inclusions representing extensive destruction of intracellular constituents. Both types of cytoplasmic change have been observed in alveolar macrophages of hashish smokers. Thus, the conditions in the in vitro studies are similar to conditions in people exposed to hashish smoke.

Animals↗
PubMedDate not supplied

[EPR study of electron transport in higher plant photosynthetic systems. II. Effect of temperature on the kinetics of photoinduced oxidation-reduction transformations of P700].

A sharp fall of ESR signal I is observed at temperature decrease while switching on light of 600 nm on the background of light of 707 nm; kinetics of the initiation of the signal under the illumination of light of 707 nm gets more complicated; the induction phase induced by previous illumination with the light of 600 nm increases.

Darkness↗
PubMed1990

Ultraviolet B light-induced alterations in epidermal Langerhans cells are mediated in part by tumor necrosis factor-alpha.

Acute, low-dose treatment of murine skin with ultraviolet B light (UVB) impairs the induction of contact hypersensitivity to dinitrofluorobenzene, and depletes the epidermis of normally appearing class II MHC positive Langerhans cells. Recent studies with inbred strains of mice have revealed that impairment of contact hypersensitivity by UVB is a polymorphic trait that is polygenically dictated by susceptibility alleles at the Lps and Tnf alpha loci. Since impairment of contact hypersensitivity by UVB has been associated with deleterious effects on Langerhans cells, we have tested the hypotheses that UVB and TNF alpha have similar effects on epidermal Langerhans cells and that TNF alpha is an important mediator of this UVB-induced effect. Our results confirm that both UVB and TNF alpha reduce the density of class II MHC-bearing epidermal cells and alter the morphology (shortened or absent dendrites, rounded shape) of the cells that remain. UVB- and TNF alpha-induced changes are prevented by systemic administration of neutralizing anti-TNF alpha antibodies. Circumstantial evidence, based on time of onset of numerical and morphologic changes among Langerhans cells following epidermal treatment, suggests that TNF alpha is the mediator of UVB-induced changes. Moreover, the ability of intradermally injected TNF alpha to alter Langerhans cells depends, in part, on whether the strain of mouse is of the UVB-susceptible or UVB-resistant phenotype as it pertains to the effect of UVB on contact hypersensitivity.

Animals↗
PubMed1975

In vivo erythrocyte sickling in the Japanese sika deer (Cervus nippon): methodology.

The Japanese sika deep (Cervus nippon) proved to be a suitable animal model for the study of acute phases of in vivo erythrocyte sickling. Ophthalmologic studies can be conducted during or after 1 to 6 hours of effective in vivo sickling. Intravenous administration of 1.75 to 3.5% sodium bicarbonate solution at a rate of 500 to 1,000 ml per hour produced a transient state of alkalosis and in vivo erythrocyte sickling in the sika deer. The percentage of sickled erythrocytes increased as the blood pH increased. Concurrently, the packed cell volume decreased. Sickling was enhanced by 100% oxygen ventilation after endotracheal intubation and light anesthetization. After the induction of erythrocyte sickling, a sickling-reversal phenomenon occurred despite continued bicarbonate administration. During the course of this reversal, the percentage of sickled erythrocytes steadily decreased, the venous blood pH decreased, and the packed cell volume slowly increased. Because of the sickling-reversal phenomenon, chronic erythrocyte sickling was not achieved.

Alkalosis↗