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At least 343 records · Page 19Linked to original sources
PubMed1993

Programmed lipid peroxidation of biomembranes generating kinked phospholipids permitting local molecular mobility: a peroxidative theory of fluidity management.

The lipid peroxidation profiles in the uterus of mature mice show cyclic alterations during the reproductive cycle. Similarly, during early pregnancy, alterations in lipid peroxidation are evident, keeping close pace with the superoxide anion radical levels and fluidity parameters reported elsewhere. This formulates a theory that a 'controlled' lipid peroxidation of biomembrane terminating at the accumulation of cyclic endoperoxides could rather enhance local molecular mobility because of the increased inter-molecular distance in these 'kinked-species'.

Animals↗
PubMed1998

A novel monoclonal antibody permitting recognition of NKT cells in various mouse strains.

By immunizing mouse lymphoma cell line tMK-2U derived from intermediate TCR cells of BALB/c nude mouse, U5A2-13 monoclonal antibody (mAb, a rat IgG2a) was established. U5A2-13 antigen (Ag) was expressed on around 65% of TCRint cells in the liver of the various mouse strains including both NK1.1- and NK1.1+ mouse strains, while NK1.1 Ag was expressed only in NK1.1+ C57BL/6 mouse strain. Among CD3+ cells, 26.3% cells co-expressed U5A2-13 Ag and NK1.1+ Ag, while small proportions of the CD3+ cells were U5A2-13+NK1.1- (9.2%) or U5A2-13-NK1.1+ (4.4%). Among NK1.1+ cells, 54.9% cells co-expressed CD3 and U5A2-13 Ag, while some proportions of the cells were U5A2-13+CD3- (19.4%) or U5A2-13-CD3+ (9.8%). It was found that approximately 85% of NK1.1+CD3+ cells coexpressed U5A2-13 Ag. U5A2-13 Ag with low fluorescence intensity was also expressed on 55% of NK1.1+CD3-NK cells. U5A2-13 Ag immunoprecipitated from tMK-2U cells consisted of three proteins, which were 65 kDa, 33 kDa and 32 kDa under both reducing and non-reducing conditions and these were apparently different from NK 1.1 Ag. These results indicated that U5A2-13 mAb was able to define a similar population to NK1.1+CD3+T cells and to 55% of NK1.1+CD3-NK cells in various strains, through recognizing a different molecule from NK1.1 Ag.

Animals↗
PubMed1993

Functional heterologous gap junctions in Fundulus ovarian follicles maintain meiotic arrest and permit hydration during oocyte maturation.

The physiological significance of heterologous gap junctions between granulosa cells and the oocyte was investigated in late vitellogenic ovarian follicles of the teleost Fundulus heteroclitus. Lucifer Yellow injected into the oocyte readily passed to the overlying granulosa cells, demonstrating effective dye-coupling. Passage of the fluorescent dye, and hence intercellular communication, was inhibited both by the tumor-promoting phorbol ester phorbol 12-myristate 13-acetate (PMA) and by 1-octanol, known uncouplers of gap junctions in a variety of invertebrate and vertebrate cell types. Octanol alone also initiated resumption of meiosis in follicle-enclosed oocytes, indicating that granulosa cells normally maintain meiotic arrest, as apparently occurs in mammalian and amphibian follicles. Both PMA and octanol also consistently inhibited the hydration process that normally accompanies meiotic maturation. These results support a previously suggested hypothesis that K+, which is the primary osmotic effector for oocyte hydration, is translocated via gap junction from granulosa cells to the maturing oocyte.

Analysis of Variance↗
PubMed1995

Limb bud mesenchyme permits seminiferous cord formation in the mouse fetal testis but subsequent testosterone output is markedly affected by the sex of the donor stromal tissue.

Mesonephric stromal cells have previously been shown to migrate into the genital ridge and to be necessary for seminiferous cord formation in organ culture. Here, we asked whether there is a specific requirement for mesonephric stromal cells or whether another source of mesonephric stromal cells can be substituted. Hindlimb buds were immersed in a vital stain and then grafted to male gonad primordia and cultured for 96 hr. Immunocytochemical staining of laminin was used to identify seminiferous cord formation. For Sertoli and Leydig cell differentiation, müllerian inhibiting substance and delta 5-3 beta-hydroxysteroid dehydrogenase were used, respectively. Testosterone secreted into the culture medium was assessed by radioimmunoanalysis. It was found that hindlimb stromal cells, like mesonephric stromal cells, migrate into the genital ridge and allow seminiferous cord formation. These results indicate that mesonephric stromal cells are not specifically required for seminiferous cord formation in the mouse fetal gonad. Furthermore, although Sertoli and Leydig cells differentiate in the gonads grafted to hindlimbs from either male or female embryos, testosterone production was considerably higher with hindlimbs from males. A similar stromal sex effect on subsequent testosterone output was also seen with mesonephric stromal cells.

Animals↗
PubMed1996

Deletion of integrin alpha 1 by homologous recombination permits normal murine development but gives rise to a specific deficit in cell adhesion.

Integrin alpha 1 is a receptor for laminin and collagen which is expressed widely and dynamically in embryogenesis and has been implicated in various developmental processes including establishment of the placenta and formation of the central and peripheral nervous system. In the adult it is the sole collagen receptor in smooth muscle and liver and is thought to be important for the stability of these tissues. We have generated a null allele of the alpha 1 gene in the germline of mice by homologous recombination in embryonic stem cells. Mice homozygous for the mutation are viable and fertile and have no overt phenotype, demonstrating that the molecule is not required for development. Embryonic fibroblasts derived from mutant animals are unable to spread on or migrate into substrata of collagen IV and are deficient in spreading on and migrating into laminin. Further in vitro analysis of cell spreading and migration suggests that alpha 1 beta 1 is not required for binding to collagen I and implicates a third receptor, possibly integrin alpha 3 beta 1, in collagen I binding.

Alleles↗
PubMed2001

The amino terminus of Smads permits transcriptional specificity.

Smad proteins transduce transforming growth factor-beta signals from the cell surface to the nucleus, regulating a variety of physiologic processes. In the nucleus, Smads control gene expression by binding to both DNA and transcription factors. Individual Smads regulate distinct subsets of target genes. The key residues important for this specificity are thought to reside in the carboxyl-terminal MH2 domain. To further examine Smad specificity in vivo, we undertook structure-function studies in Xenopus laevis embryos and found that truncated Smads containing the MH2 domain activate gene transcription. A striking finding revealed by the in vivo analyses was that the functional truncated Smads all behaved identically and had lost wild-type specificity. For most Smads, wild-type activity required the presence of an MH1 domain, either in cis or in trans. Of note, even heterologous MH1 domains could restore wild-type signaling specificity to effector MH2 domains. We found a possible mechanism to account for these observations, as Smad MH1 domains altered the binding of pathway-specific transcription factors to the MH2 domain. Thus, Smad MH1 domains are important to the regulation of transcriptional specificity.

Animals↗
PubMed1999

Poly(ADP-ribose) polymerase inhibition in oxidant-stressed endothelial cells prevents oncosis and permits caspase activation and apoptosis.

Endothelial cells (EC) are subject to oxidative-induced cell death. Activation of poly(ADP-ribose) polymerase (PARP) occurs early in oxidant-induced EC injury and putatively mediates cell death by depleting its substrate, NAD(+). In this study, the role of PARP in H(2)O(2)-induced EC death was investigated. EC were exposed to oxidant stress and viability continuously monitored using fluorescent dye exclusion. Inhibition of PARP with 1, 5-dihydroxyisoquinoline (DIQ) delayed the time course of oxidant-induced EC death. Concurrent addition of the protein synthesis inhibitor, cycloheximide, or the endonuclease inhibitor, aurintricarboxylic acid, to PARP-inhibited cells further delayed the onset and attenuated the extent of H(2)O(2)-induced cell lysis, consistent with an active mode of cell death. Caspase-3-like activity, a hallmark of apoptosis, was negligible in oxidant-treated EC alone, however, inhibition of PARP by 3-aminobenzamide or DIQ dramatically increased caspase-3-like activity. Morphological assessment confirmed that the primary mode of death in oxidant-stressed EC was oncosis. However, following PARP inhibition, the cells switched to apoptosis. Since inflammation is associated with oncosis and not apoptosis, the results presented here could explain the beneficial effects seen with PARP inhibition in various in vivo models of oxidant injury and provide a mechanism to manipulate this injury into a state of cell death that could ultimately be controlled.

Animals↗
PubMed1995

Conservative treatment of endometrial cancer permitting subsequent triplet pregnancy.

We report on a 28-year-old woman who received conservative treatment of endometrial carcinoma by curettage and progestins. After regression of endometrial lesions the patient's infertility was treated by gamete intrafallopian transfer (GIFT). Intact triplet pregnancy was diagnosed 3 weeks later. The patient was delivered of three infants by caesarean section following premature rupture of membranes at 30 weeks of gestation. Subsequent standard treatment of endometrial cancer by abdominal hysterectomy and bilateral salpingo-oophorectomy after 4 weeks revealed no clinical or histological evidence of persistent carcinoma. One year after surgery the patient remained without evidence of disease. We believe that individualized cancer therapy may be safely performed in carefully selected cases.

Adult↗
PubMed1996

Perceptual cues that permit categorical differentiation of animal species by infants.

Eight experiments were performed to determine the perceptual cues used by 3- and 4-month-old infants to categorically distinguish between perceptually similar natural animal species. These experiments provided evidence that information from the facial and head region, specifically, the internal features of the face and the external contour of the head, give the infant a necessary and sufficient basis to form a categorical representation for cats that excludes dogs. The results are discussed in terms of Johnson and Morton's (1991) theory of facial recognition and more general accounts of the information underlying categorical representations.

Animals↗
PubMed2001

Transaction costs and sequential bargaining in transferable discharge permit markets.

Market-type mechanisms have been introduced and are being explored for various environmental programs. Several existing programs, however, have not attained the cost savings that were initially projected. Modeling that acknowledges the role of transactions costs and the discrete, bilateral, and sequential manner in which trades are executed should provide a more realistic basis for calculating potential cost savings. This paper presents empirical evidence on potential cost savings by examining a market for the abatement of sediment from farmland. Empirical results based on a market simulation model find no statistically significant change in mean abatement costs under several transaction cost levels when contracts are randomly executed. An alternative method of contract execution, gain-ranked, yields similar results. At the highest transaction cost level studied, trading reduces the total cost of compliance relative to a uniform standard that reflects current regulations.

Agriculture↗
PubMed1995

Defects in the Drosophila myosin rod permit sarcomere assembly but cause flight muscle degeneration.

We have determined the molecular and ultrastructural defects associated with three homozygous-viable myosin heavy chain mutations of Drosophila melanogaster. These mutations cause a dominant flightless phenotype but allow relatively normal assembly of indirect flight muscle myofibrils. As adults age, the contents of the indirect flight muscle myofibers are pulled to one end of the thorax. This apparently results from myofibril "hyper-contraction", and leads to sarcomere rupture and random myofilament orientation. All three mutations cause single amino acid changes in the light meromyosin region of the myosin rod. Two change the same glutamic acid to a lysine residue and the third affects an amino acid five residues away, substituting histidine for arginine. Both affected residues are conserved in muscle myosins, cytoplasmic myosins and paramyosins. The mutations are associated with age-dependent, site-specific degradation of myosin heavy chain and failure to accumulate phosphorylated forms of flightin, an indirect flight muscle-specific protein previously localized to the thick filament. Given the repeating nature of the hydrophobic and charged amino acid residues of the myosin rod and the near-normal assembly of myofibrils in the indirect flight muscle of these mutants, it is remarkable that single amino acid changes in the rod cause such severe defects. It is also interesting that these severe defects are not apparent in other muscles. These phenomena likely arise from the highly organized nature and rigorous performance requirements of indirect flight muscle, and perhaps from the interaction of myosin with flightin, a protein specific to this muscle type.

Age Factors↗
PubMed1998

Temporal changes in tissue repair permit survival of diet-restricted rats from an acute lethal dose of thioacetamide.

Although, diet restriction (DR) has been shown to substantially increase longevity while reducing or delaying the onset of age-related diseases, little is known about the mechanisms underlying the beneficial effects of DR on acute toxic outcomes. An earlier study (S. K. Ramaiah et al., 1998, Toxicol. Appl. Pharmacol. 150, 12-21) revealed that a 35% DR compared to ad libitum (AL) feeding leads to a substantial increase in liver injury of thioacetamide (TA) at a low dose (50 mg/kg, i.p.). Higher liver injury was accompanied by enhanced survival. A prompt and enhanced tissue repair response in DR rats at the low dose (sixfold higher liver injury) occurred, whereas at equitoxic doses (50 mg/kg in DR and 600 mg/kg in AL rats) tissue repair in AL rats was substantially diminished and delayed. The extent of liver injury did not appear to be closely related to the extent of stimulated tissue repair response. The purpose of the present study was to investigate the time course (0-120 h) of liver injury and liver tissue repair at the high dose (600 mg TA/kg, i.p., lethal in AL rats) in AL and DR rats. Male Sprague-Dawley rats (225-275 g) were 35% diet restricted compared to their AL cohorts for 21 days and on day 22 they received a single dose of TA (600 mg/kg, i.p.). Liver injury was assessed by plasma ALT and by histopathological examination of liver sections. Tissue repair was assessed by [3H]thymidine incorporation into hepatonuclear DNA and proliferating cell nuclear antigen (PCNA) immunohistochemistry during 0-120 h after TA injection. In AL-fed rats hepatic necrosis was evident at 12 h, peaked at 60 h, and persisted thereafter until mortality (3 to 6 days). Peak liver injury was approximately twofold higher in DR rats compared to that seen in AL rats. Hepatic necrosis was evident at 36 h, peaked at 48 h, persisted until 96 h, and returned to normal by 120 h. Light microscopy of liver sections revealed progression of hepatic injury in AL rats whereas injury regressed completely leading to recovery of DR rats by 120 h. Progression of injury led to 90% mortality in AL rats vs 30% mortality in DR group. In the surviving AL rats, S-phase DNA synthesis was evident at 60 h, peaked at 72 h, and declined to base level by 120 h, whereas in DR rats S-phase DNA synthesis was evident at 36 h and was consistently higher until 96 h reaching control levels by 120 h. PCNA studies showed a corresponding increase in cells in S and M phase in the AL and DR groups. DR resulted in abolition of the delay in tissue repair associated with the lethal dose of TA in ad libitum rats. Temporal changes and higher tissue repair response in DR rats (earlier and prolonged) are the conduits that allow a significant number of diet restricted rats to escape lethal consequence.

Animals↗
PubMed1996

Definition of a human herpesvirus-6 betaherpesvirus-specific domain in glycoprotein gH that governs interaction with glycoprotein gL: substitution of human cytomegalovirus glycoproteins permits group-specific complex formation.

Formation of the glycoprotein gH/gL heterooligomer has important implications for understanding the pathology of human herpesvirus-6(HHV-6)-associated disease because this complex is essential for infectivity and fusogenic cell-to-cell spread. Definition of the HHV-6 gH domain involved in protein-protein interactions was addressed by targeting regions defined by conserved cysteines identified by alignment of gH amino acid sequences representative of all herpesvirus subfamilies. Studies using site-directed mutagenesis and transient cellular expression showed that the N-terminus of HHV-6 gH includes a 230-amino-acid domain required for interaction with HHV-6 gL encompassing residues conserved specifically amongst betaherpesviruses. Interestingly, the human cytomegalovirus (HCMV) homologues, UL75 (gH) or UL115 (gL), can substitute for HHV-6 glycoproteins and participate in heterologous complex formation. Furthermore, the region which governs this heterologous gL binding also maps to the N-terminal portion of HHV-6 gH. Although both proteins can functionally substitute for complex formation there are also specific differences. Surprisingly, further deletion of HHV-6 gH to 145-amino-acid-domain residues abolishes complex formation with HHV-6 gL but allows interaction with HCMV gL. This may be related to requirements in HHV-6 for homodimer formation before complex formation between gH and gL. Under nonreducing conditions HHV-6 gH and gL form multimeric complexes consistent with intra- and intermolecular dimer formation stabilised by disulphide bonds whereas for HCMV there is no evidence for dimer formation for gH and multimeric complexes have only been observed between gH and gL. In summary, both HHV-6 and HCMV glycoproteins can interact and the heterologous complex between HHV-6 gH and HCMV gL is possibly more stable. This may result in important biological consequences in vivo during cellular coinfections by facilitating spread of the viruses, with applications to altered cellular tropisms and effects on reactivation from the latently infected cell.

Base Sequence↗
PubMed1988

Suppressor deletion therapy: selective elimination of T suppressor cells in vivo using a hematoporphyrin conjugated monoclonal antibody permits animals to reject syngeneic tumor cells.

A MAb (B16G) which recognizes a constant epitope on TsC and their soluble factors in DBA/2 mice has been described previously. In this study, we show that when this MAb is covalently linked to the photoactivable molecule Hp, and injected i.v. into P815 tumor-bearing mice which were subsequently exposed to light, tumors undergo permanent regression in 10%-40% of these mice (depending on the individual experiment). All control animals died within an average of 22-24 days after tumor cell injection. It is suggested that tumor regression is attributable to immune mechanisms facilitated by the elimination of a population of TsC. When splenocytes of B16G-Hp-treated mice were assayed in vitro for the generation of CTL active against P815 tumor cells, it was found that 24 h after treatment, a significant increase in killer cell activity was noted but that this effect was gone by 48h. We also show that B16G-Hp conjugates are capable in vitro of specifically killing cells of a TsC hybridoma, A10 (which has been shown previously to secrete a T suppressor factor reactive with P815 cell surface antigens). This conjugate had no cytotoxic effect on P815 cells under conditions in which A10 cells were killed.

Animals↗
PubMed1986

Implantation of D-[3H]aspartate loaded gel particles permits restricted uptake sites for transmitter-selective axonal transport.

Intracerebral pressure injections of small molecular tracers such as D-[3H]aspartate are usually followed by considerable spread which makes it difficult to assess the effective uptake area and precludes analysis of short axonal connections. As an attempt to circumvent these problems, D-[3H]aspartate was adsorbed onto gel beads that were subsequently packed into glass capillaries and implanted in the brain. Model experiments suggested that the loaded beads gradually release the tracer to the nerve tissue. The implantations resulted in small and sharply circumscribed tracer deposits which enabled us to study long axonal projections, as well as short intrahippocampal and intraamygdaloid pathways that are not easily resolved after pressure injections.

Amygdala↗
PubMed1992

The Salmonella typhimurium RecJ function permits growth of P22 abc phage on recBCD+ hosts.

We describe recJ mutants of Salmonella typhimurium. The recJ gene maps between sufD and serA (min 62) and is transcribed counterclockwise. Unlike recJ mutants of Escherichia coli, recJ strains of S. typhimurium are sensitive to irradiation with UV light. This sensitivity is equivalent to or greater that that displayed by recBCD mutant strains. The residual ability of phage P22 abc (anti-recBCD) mutants to form plaques on recBCD+ strains is eliminated in recJ hosts. Thus host RecJ function appears to substitute for the anti-RecBCD functions of phage P22 and may serve to limit RecBCD activity.

Chromosome Mapping↗
PubMed1990

Agrobacterium tumefaciens T-DNA gene 6b stimulates rol-induced root formation, permits growth at high auxin concentrations and increases root size.

All Agrobacterium tumefaciens strains studied up to now transfer an active 6b gene to plant cells. However, the role of this gene in natural tumour induction is unknown. Various effects of 6b on plant cell growth have been described, but the precise mechanism by which 6b causes these effects has not been elucidated. Earlier experiments indicated that the 6b gene might increase auxin sensitivity as do the A. rhizogenes rol genes. The 6b gene from Tm4 (T-6b) was therefore compared with the rolB and rolABC genes. Although T-6b was unable to induce root formation, it strongly interfered with root induction and root elongation. In rolABC/T-6b coinfection experiments on carrots, T-6b-transformed cells stimulated root outgrowth of rolABC-transformed cells, indicating that the biologically active T-6b product is diffusible. Carrot rolABC roots containing the T-6b gene rapidly developed into unorganized calli. Nicotiana rustica roots with rolABC and T-6b continued their development, but became very large. Fragments of such roots formed callus at alpha-naphthaleneacetic acid concentrations which inhibited growth of rolABC and normal root fragments, suggesting that the role of 6b genes in natural tumour induction may be to reduce the inhibitory effects of high auxin levels and to keep cells in an undifferentiated state.

Cloning, Molecular↗