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At least 991 records · Page 55Linked to original sources

Direct cutaneous arterial supply to the tail in dogs.

Cutaneous arterial blood supply to the tail was evaluated in 12 dogs. Subtraction radiography of internal iliac artery and distal aorta angiography in 3 of these dogs was used to determine arterial blood supply to the tail from the median sacral and lateral caudal arteries. Dissection of the tail in 8 canine cadavers revealed bilateral subcutaneous location of lateral caudal arteries following tail amputation. An axial pattern flap based on the lateral caudal arteries contributed to the reconstruction of a large caudodorsal cutaneous defect in a dog. An axial pattern flap based on the lateral caudal arteries following tail amputation may be indicated to aid reconstruction of large caudodorsal cutaneous defects of the trunk in dogs.

Amputation, Surgical↗

Interactions of sigma and phencyclidine receptor ligands with the norepinephrine uptake carrier in both rat brain and rat tail artery.

The interaction of several sigma and PCP receptor ligands with the norepinephrine uptake carrier was investigated in the rat tail artery and brain. These ligands include haloperidol; (+)- and (-) 3-(3-hydroxy- phenyl)-N-(1-propyl)piperidine (3-PPP), (+/-)-BMY 14802, [(+/-) alpha-(4-fluoro- phenyl)-4-(5-fluoro-2-pyrimidinyl)-1-piperazine butanol]; (+)-SKF 10047, [(+/-)-N-allyl-N-normetazocine]; 1,3-di-ortho-tolyl-guanidine; rimcazole (BW 234U), [cis-9-[3-(3,5-dimethyl-1-piperazinyl)propyl] carbazole dihydrochloride]; and MK 801, [(+)-5-methyl-10,1 1-dihydro-5H-dibenzo[a, d]cyclohepten-5, 10-imine maleate]. Our results show that all ligands used, except 1,3-di-ortho-tolyl-guanidine, inhibit both neuronal [3H]norepinephrine accumulation in the rat tail artery and specific [3H] desmethylimipramine binding in the rat brain. Except for (+)-SKF 10047, the order of potency of the ligands used for inhibiting neuronal [3H]norepinephrine accumulation in the rat tail artery was similar to that measured for inhibition of specific [3H]desmethylimipramine binding in the rat brain. Despite these similarities, our results also suggest that haloperidol, (+)- and (-)3-PPP, MK 801, rimcazole and cocaine interact with the [3H]norepinephrine site in the rat tail artery and with the [3H]desmethylimipramine binding site in the rat brain in a complex fashion. These studies demonstrate an important action on the norepinephrine carrier by these sigma and PCP ligands in the rat tail artery and brain.

Animals↗

Origin of the avian glycogen body: I. Effects of tail bud removal in the chick embryo.

The tail bud was removed from chick embryos at stage 16-17 in a first study directed to learn of the origin of the glycogen body in the lumbosacral spinal cord of birds. Results of tail bud removal and chorio-allantoic grafting of caudal portions of the embryo containing the tail bud or the neural tube suggest that the glycogen body does not arise from the tail bud, but from the preexisting neural tube craniad or anterior to the tail bud. The stem cells of the glycogen body are most likely among those components of the anterior portion of the lumbosacral neural tube derived from primary neurulation.

Allantois↗

Serotonin mimics tail shock in producing transient inhibition in the siphon withdrawal reflex of Aplysia.

Tail shock-induced modulation of the siphon withdrawal reflex of Aplysia has recently been shown to have a transient inhibitory component, as well as a facilitatory component. This transient behavioral inhibition is also seen in a reduced preparation in which a cellular reflection of the inhibitory process, tail shock-induced inhibition of complex EPSPs in siphon motor neurons, is observed. The biogenic amine serotonin (5-HT) is known to play a role in the facilitatory aspects of sensitization in Aplysia. The aim of this article was to examine whether 5-HT might also contribute to the inhibitory effects of tail shock in the siphon withdrawal reflex. To examine this question, we carried out two kinds of experiments. First, in the isolated abdominal ganglion, we recorded intracellularly from siphon motor neurons and examined the effects of 5-HT on (1) complex (polysynaptic) EPSPs, produced by siphon nerve stimulation, and, simultaneously, (2) monosynaptic EPSPs from siphon sensory neurons. We found that, paralleling the effects of tail shock in the reduced preparation, 5-HT produced transient inhibition of the complex EPSP; the monosynaptic EPSP was facilitated by 5-HT. Second, we examined the behavioral effects of 5-HT on siphon withdrawal in a reduced preparation. We found that 5-HT again paralleled tail shock by producing transient inhibition of the siphon withdrawal reflex. Our results suggest that, in addition to its well-established facilitatory role in reflex modulation in Aplysia, 5-HT might play an important inhibitory role, as well.

Animals↗

[Application of mouse tail artery for the study of alpha adrenoceptor agonists and antagonists and calcium antagonists].

Isolated mouse tail artery strip was used for the study of alpha 1-, alpha 2-adrenoceptor agonists and antagonists. NA (alpha 1 and alpha 2 agonist) was shown to have greater activity in contracting tail artery. Phenylephrine (alpha 1 agonist) and clonidine (alpha 2 agonist) exhibited the same contractile action but much weaker than NA. Prazosin (alpha 1 antagonist) and yohimbine (alpha 2 antagonist) greatly diminished the contraction induced by phenylephrine and clonidine. These results indicate that mouse tail artery is rich in postsynaptic alpha 1- and alpha 2-adrenoceptor. In addition, mouse tail artery preparation was shown to be a useful tool for screening calcium agonists and antagonists. This model has advantages of being simple and easy to prepare, short equilibrium time and more economic in comparison with the helical strips of isolated rat tail artery.

Adrenergic alpha-Agonists↗

A study of tail tip necrosis in young fattening bulls on slatted floors.

A questionnaire sent to 78 producers revealed that tail tip necrosis was seen only in units with fattening bulls housed on slatted floors. Out of 43 such units, 20 (46.5 per cent) reported that tail tip necrosis was a herd problem. All 43 herds were visited, owners were interviewed and housing and management data recorded. It is concluded that tail tip necrosis is a multifactorial disease. The initial lesion is caused by tramping, but the following factors are essential in the development and severity of the disease, i) slatted concrete floors, ii) close confinement, iii) hot season and iv) body weight above 200 kg. The stocking density (expressed as kg bodyweight per square meter pen) was significantly higher in problem herds (210 kg/m2) than in control herds (165 kg/m2). There was a close relationship between high environmental temperature and tail tip necroses. The majority of incidents occurred during the warm season (May through September), very few cases were seen during the colder months. The general morbidity and mortality rates were significantly higher in problem herds than in control herds. Microbiology of affected tails revealed mixed infections in most cases, with Corynebacterium pyogenes and Bacteroides melaninogenicus as the most frequently isolated organisms. Principles of treatment and prevention are discussed. There is evidence to assume that a 10-20 per cent reduction in stocking density could be an efficient prophylactic measure.

Animals↗

Relationship between timing of posterior neuropore closure and development of spinal neural tube defects in mutant (curly tail) and normal mouse embryos in culture.

The relationship between timing of closure of the posterior neuropore (PNP) and development of spinal neural tube defects (NTD) has been studied in individual mutant curly tail mouse embryos maintained in culture. Moderate delay in PNP closure results in development of tail flexion defects whereas extreme delay of PNP closure is associated with development of open NTD. Experimental enlargement of the PNP at the stage of 25 to 29 somites leads to delayed PNP closure and development of tail flexion defects in 36% and 38% respectively of non-mutant A/Strong embryos. In curly tail embryos, the effect of experimental enlargement of the PNP summates with the genetic predisposition to produce an increased incidence of spinal NTD among which open defects are proportionately more common. These results indicate that a causal relationship exists between delay in PNP closure and development of spinal NTD in mouse embryos. The method described for distinguishing between prospective normal and abnormal curly tail embryos at a stage prior to the appearance of malformations provides an opportunity to study the morphogenetic processes that precede the development of genetically determined spinal NTD.

Animals↗

Critical role of the capsaicin-sensitive nerve fibers in the development of the causalgic symptoms produced by transecting some but not all of the nerves innervating the rat tail.

We investigated the role of capsaicin-sensitive small diameter fibers in the development of the thermal and mechanical allodynia in a new rat model for neuropathic pain, produced by transecting some but not all of the nerves innervating the tail. Capsaicin (50 mg/kg, s.c.) injected neonatally prior to the nerve injury produced thermal hypoalgesia in the tail the degree of which was variable across individual rats, presumably as a result of variable degeneration of the small diameter fibers. When subjected to the nerve injury, the animals with moderate thermal hypoalgesia exhibited signs of pain (e.g., tail flick) to normally innocuous mechanical stimuli applied to the tail with von Frey hairs (4.9 mN or 19.6 mN bending force), but not to thermal stimuli given by immersion of the tail into cold (4 degrees C) or warm (40 degrees C) water. The animals with marked thermal hypoalgesia, on the other hand, exhibited no signs of pain either to the mechanical or to the thermal stimuli. These results suggest that the capsaicin-sensitive fibers are critical in the development of both the mechanical and thermal allodynia. It is hypothesized that the destruction of A delta- and C-nociceptive fibers by capsaicin prevented activities induced in these fibers by the nerve injury from producing a central sensitization and thus allodynia.

Animals↗

Effect of levofloxacin and ciprofloxacin injection on permeability of the tail vein in mice and skin microvasculature in rats.

We examined the effects of levofloxacin (LVFX) and ciprofloxacin (CPFX) on the permeability of the tail vein in mice and skin microvasculature in rats after a single intravenous and intracutaneous injection, respectively, with 125I-human serum albumin. In addition, the effect of an H1 histamine antagonist, diphenhydramine, on the hyperpermeability induced by quinolone injections was examined, and the injections were also performed into the tail vein of WBB6F1 (mast cell-deficient) mice. LVFX and CPFX significantly increased the permeability of the mouse tail vein at injection concentrations of 0.2% and 0.05% of more, respectively, and both quinolones increased the permeability of rat skin microvasculature by 0.5% or more. Diphenhydramine concomitantly injected with quinolones completely blocked the hyperpermeability induced by LVFX and CPFX at 0.5% in the mouse tail vein and rat skin microvasculature. Neither quinolone increased the tail vein permeability in WBB6F1 mice. These results suggest that LVFX and CPFX increase vascular permeability through the induction of histamine release from mast cells in rodents.

Animals↗

Distributed input to the tail-siphon withdrawal circuit in Aplysia from neurons in the J cluster of the cerebral ganglion.

Plasticity in the circuits for the withdrawal reflexes has been correlated with several simple forms of nonassociative and associative learning in Aplysia, and biochemical, biophysical, and molecular mechanisms of plasticity in these circuits have been described. In order to examine network features of this plasticity, we identified and characterized a component of the modulatory circuitry for the tail-siphon withdrawal circuit. Activation of mechanoafferent neurons in the J cluster of the cerebral ganglion produced strong and distributed input to the tail-siphon withdrawal circuit. Stimulation of the J cells led to excitatory and inhibitory effects in the sensory neurons in the pleural ganglion, the tail motor neurons in the pedal ganglion, and several classes of interneurons in the pleural ganglion, including the multifunctional neuron LPI17. Activation of the J cells produced both fast and slow post-synaptic potentials in neurons of the tail-siphon withdrawal circuit. Of particular interest was the ability of the J cells to produce slow EPSPs in the pleural sensory neurons. These slow EPSPs were associated with an increase in the excitability of the sensory neurons, but no effect of the J cells on spike duration in the sensory neurons was observed. The J cells appear to mediate both sensory and modulatory inputs to the circuit for tail withdrawal.

Action Potentials↗

Compartmentalization, processing and redistribution of the plasma membrane protein CE9 on rodent spermatozoa. Relationship of the annulus to domain boundaries in the plasma membrane of the tail.

Western blotting, immunofluorescence and immunogold electron microscopy were used to examine the compartmentalization, processing and redistribution of the integral plasma membrane protein CE9 on the spermatozoa of rats, mice and hamsters. In each species examined, spermatozoal CE9 was found to undergo endoproteolytic processing followed by a net redistribution from the posterior-tail domain into the anterior-tail domain of the plasma membrane during epididymal maturation. Compared to spermatozoa of the rat and mouse, those of the hamster were found to express a greater proportion of their CE9 within the anterior-tail plasma membrane domain at all stages of maturation. As a consequence, CE9 was judged to be a suitable marker for two different spermatozoal plasma membrane domains: the posterior-tail plasma membrane domain (spermatozoa from the testis and caput epididymidis of the rat and mouse) and the anterior-tail domain (spermatozoa from the cauda epididymidis of the hamster). Immunogold electron microscopy was used to pinpoint the positions of the boundaries of these CE9-containing plasma membrane domains at a high level of resolution. In each case, the position of the CE9 domain boundary was found to be strongly correlated with that of the subplasmalemmal electron-dense ring known as the annulus. The precise spatial relationship between the CE9 domain boundary and the annulus was, however, found to differ significantly among species and/or as a function of maturation.

Animals↗

Inhibition of alpha1-adrenoceptor-mediated contractions in isolated tail arteries and aorta of the rat by alpha2-adrenoceptor agonists.

The effects of alpha2-adrenoceptor agonists, clonidine, tizanidine and UK-14304 on alpha1-adrenoceptor-mediated contractile responses were studied in isolated tail arteries and thoracic aorta of the rat. When applied during sustained contractile responses to almost maximum concentration (10 microM) of phenylephrine, clonidine (0.3 microM to 100 microM) produced concentration-dependent relaxations in both tissues. The maximum relaxation was smaller in tail arteries than in thoracic aorta. Clonidine up to 100 microM failed to relax both tissues precontracted with KCl (60 microM) or U-46619 (1 microM), a thromboxane mimetic. The clonidine-induced relaxation in tail arteries, was reversed by alpha2-adrenoceptor antagonists, yohimbine and idazoxane. Effects of the alpha2-adrenoceptor antagonists were concentration-dependent (0.1 microM to 1 microM), but not in a competitive manner. On the other hand, the relaxation in thoracic aorta was not significantly antagonized by these alpha2-adrenoceptor antagonists. Tizanidine and UK-14304 also relaxed both tail arteries and thoracic aorta precontracted with phenylephrine. The characteristics of the relaxation and their antagonism by yohimbine in both arteries were similar to those induce by clonidine. In tail arteries, NG-nitro-L-arginine, a nitric oxide synthase inhibitor, at a concentration that completely inhibited acetylcholine-induced relaxations did not significantly affect the relaxation induced by clonidine. In contrast, the relaxation of thoracic aorta in response to clonidine was partly reduced in the presence of NG-nitro-L-arginine. These results indicate that the alpha2-adrenoceptor agonists selectively inhibit the contractions induced by phenylephrine in both tissues. Regional differences in the modes of the inhibition by the alpha2-adrenoceptor agonists exist.

Acetylcholine↗

[Inflammation of the tail in swine. Slaughter-house findings during 1972, 1973, and 1974 (author's transl)].

In the Public Salughter-House of Utrecht, a percentage increase in the number of pigs with inflammation of the tail, which had or had not healed, was observed during the period from 1972 to 1974 inclusive. The most common secondary symptoms of inflammation consisted in embolic pneumonia, osteomyelitis of the vertebrae and abscess formation in other parts of the body, particularly the semimebranosus muscles. Osteomyelitis was found to be the most common complication in pigs in which the inflammation of the tail had healed, whereas this usually consisted in embolic pneumonia in those cases in which the inflammation of the tail had not healed. The bacteriological examination carried out in accordance with the Meat Inspection Regulations was positive in 21.7 per cent, 13.5 per cent of the cases respectively in 1972, 1973 and 1974. Micro-organisms were isolated much more frequently from the kidney than they were from the spleen and meat. There was no relationship between the presence of inflammation of the tail and climatological conditions during the fattening period. The losses at slaughter from inflammation of the tail in the Netherlands are estimated at 3-4 million guilders per annum.

Animals↗

Postnatal differentiation of the ductus deferens, tail of the epididymis, and distal body of the epididymis in goats occurs independently of rete testis fluid.

Observations from extratesticular rete-ligated, mature goats indicated that epithelial morphology in the tail of the epididymis can be maintained without any input from testicular fluid (Goyal et al., Acta Anat., 1994;150: 127-135). Hence, the objective of this study was to determine whether the tail of the epididymis and/or other regions of the male excurrent ducts can differentiate prior to the appearance of lumen in the seminiferous tubules, which is an indicator for the onset of seminiferous tubular fluid secretion. Based on age and scrotal circumference (SC), 20 male goats were divided into four groups of five animals each: 1-4 weeks (SC, 6.5-7.5 cm), 7-10 weeks (SC, 8.5-11.0 cm), 12-15 weeks (SC, 11.0-14.0 cm), and 15-25 weeks (SC, 16.0-19.0 cm). Tissues were collected from the testis, six regions of the epididymis (proximal, middle and distal head; proximal and distal body; and tail), and the ductus deferens, and were processed for light and electron microscopic examination. Changes in epithelial height and cytological features associated with absorption (microvilli, pinocytotic and coated vesicles) and protein secretion (RER, Golgi body) were used as markers for differentiation. Differentiation of all of these features was comparable to that observed in the 15-25-week-old animals in the ductus deferens by > or = 1 week, in the tail of the epididymis by > or = 7 weeks, in the distal body of the epididymis by > or = 12 weeks, and in the proximal body of the epididymis and all three regions of the head of the epididymis by > or = 15 weeks. Seminiferous tubules developed lumens between 12 and 15 weeks. In conclusion, epithelial differentiation in the ductus deferens, tail of the epididymis, and distal body of the epididymis follows a time-dependent, spatial, ascending order and is achieved before lumen formation in the seminiferous tubules. Conversely, epithelial differentiation in all three regions of the head and the proximal body of the epididymis occurs simultaneously and after lumen formation in the seminiferous tubules.

Age Factors↗

Changes in poly(A) tail length of maternal transcripts during in vitro maturation of bovine oocytes and their relation with developmental competence.

Molecules of mRNA are stored in the oocyte cytoplasm in order to be used during the initial phases of embryonic development. The storage takes place during oocyte growth and the extent of poly(A) tail at the 3' end of the transcripts has emerged as an important regulatory element for determining their stability. The objective of the present study was to analyse changes in polyadenylation levels of mRNA transcripts, stored in bovine oocytes, during in vitro maturation and their possible relation with developmental competence. Oocyte developmental competence was predicted on the basis of the morphological appearance of their originating ovary as previously established (Gandolfi et al. 1997a. Theriogenology 48:1153-1160) and were divided into groups H (high competence) and L (low competence). The length of the poly(A) tail of the following genes, beta-actin (beta-Act), connexin 43, glucose transporter type 1, heat shock protein 70, oct-4, plakophilin, pyruvate dehydrogenase phosphatase (PDP), and RNA poly(A) polymerase, was determined at the germinal vesicle (GV) and metaphase II (MII) stage. The results indicated that the poly(A) tail of all genes except for beta-Act and PDP, is shorter after in vitro maturation (IVM) in both groups. Moreover, group L oocytes showed a shorter poly(A) tail than group H oocytes in all genes except for beta-Act and PDP, both at GV and MII stage. We conclude that most of the examined transcripts follow the default deadenylation pattern described during oocyte maturation in other species and that a shorter poly(A) tail is correlated with low developmental competence.

Animals↗

Blood groups of pig-tailed macaques (Macaca nemestrina).

The human-type A-B-O blood groups of 57 pig-tailed macaques (Macaca nemestrina) were determined and the calculated gene frequencies, O = 0.8908, A = 0.0825 and B = 0.0267, gave excellent fit with the hypothesis of inheritance by triple allelic genes. In tests for simian-type blood groups with rhesus, baboon and crab-eating macaque immune antisera, it was shown that the red cells of pig-tailed macaques are polymorphic for several simian-type specificities defined by those cross-reacting sera. Pig-tailed macaques share with other macaque species the complex Drh-graded blood group system, which seems to occupy a special role among red cell antigens of macaques. Normal sera of three female macaques contained spontaneous isoagglutinins which selectively agglutinated the red cells of some pig-tailed as well as stump-tailed macaques.

ABO Blood-Group System↗

T cell receptor alpha-chain tail is required for protein kinase C-mediated down-regulation, but not for signaling.

Antigen stimulation through the T cell receptor (TCR) induces phosphorylation of the associated CD3 gamma delta epsilon- and zeta-chain cytoplasmic tails. These events lead to the induction of the intracellular signaling pathways with concomitant receptor down-regulation. The TCR is down-regulated from the cell surface by the activation of protein kinase, C (PKC) and subsequent serine phosphorylation of the CD3 gamma-chain. We report here that the TCR alpha-chain cytoplasmic tail is also necessary for PKC-mediated internalization of the TCR complex. The requirement for the TCR alpha-chain cytoplasmic tail is specific for internalization of the TCR complex, since down-regulation of CD4 is still intact in hybridoma cells expressing a tailless TCR alpha-chain. The absence of TCR internalization directly correlates with defective PKC-mediated phosphorylation of the CD3 gamma-chain. Despite deficient PKC-mediated TCR down-regulation, the tailless alpha beta TCR still transduces antigenic signals resulting in the production of interleukin-2. Although the TCR tails are not obviously required for signal transduction, the TCR alpha-tail may serve as a targeting domain for PKC-mediated down-regulation of the TCR complex.

Amino Acid Sequence↗

Disassembly of in vitro formed lamin head-to-tail polymers by CDC2 kinase.

The nuclear lamina is an intermediate filament-type network underlying the inner nuclear membrane. At the onset of mitosis it depolymerizes, presumably in response to phosphorylation of the lamin proteins. Recently, cdc2 kinase, a major regulator of the eukaryotic cell cycle, was shown to induce lamina depolymerization when incubated with isolated nuclei. Here, we have analysed the structural consequences of lamin phosphorylation by cdc2 kinase using lamin head-to-tail polymers reconstituted in vitro from bacterially expressed chicken lamin B2 protein as a substrate. The effects of phosphorylation were monitored by both a pelleting assay and electron microscopy. We show that lamin B2 head-to-tail polymers disassemble in response to phosphorylation of specific sites that are phosphorylated also during mitosis in vivo. These sites are located within SP/TP motifs N- and C-terminal to the central alpha-helical rod domain of lamin proteins. Subsequent dephosphorylation of these sites by purified phosphatase 1 allows reformation of lamin head-to-tail polymers. The relative importance of N- and C-terminal phosphorylation sites for controlling the assembly state of nuclear lamins was assessed by mutational analysis. Polymers formed of lamin proteins carrying mutations in the C-terminal phosphoacceptor motif could still be disassembled by cdc2 kinase. In contrast, a single point mutation in the N-terminal site (Ser16----Ala) rendered head-to-tail polymers resistant to disassembly. These results emphasize the importance of the N-terminal end domain for lamin head-to-tail polymerization in vitro, and they demonstrate that phosphorylation-dephosphorylation is sufficient to control the longitudinal assembly of lamin B2 dimers.

Adenosine Triphosphate↗