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Biomedical subjects

J Yu

Publications and source records attributed to J Yu.

At least 829 records · Page 46Linked to original sources
PubMed1989

Neonatal enucleations reduce number, size, and acetylcholinesterase histochemical staining of neurons in the dorsal lateral geniculate nucleus of developing rats.

Previous studies have demonstrated that transient patterns of acetylcholinesterase (AChE) activity are characteristic of geniculo-recipient regions of rat cortical area 17 during the second and third postnatal weeks of life. Neonatal enucleation results in a marked reduction of this transiently expressed cortical AChE. Parallel studies have demonstrated that the dorsal lateral geniculate nucleus (dLGN) also expresses AChE transiently during development. The present study examines neuronal number and size as well as AChE histochemical staining in the dLGN of normal and neonatally enucleated rat pups to determine whether changes in dLGN neurons could account for the decreased visual cortical AChE staining that results from neonatal enucleation. Changes in 4 parameters in dLGN were noted after neonatal enucleation. First, a 26-37% shrinkage in the volume of dLGN occurred contralateral to enucleation. Second, enucleation resulted in a loss of 16-30% of AChE-stained neuronal somata. Third, remaining AChE-positive neuronal somata appeared shrunken by approximately 40%. Fourth, intensity of AChE histochemical staining of individual dLGN neurons was reduced by approximately 24% following neonatal enucleation. These data suggest that loss of transient AChE activity in cortical area 17 consequent to neonatal enucleation is secondary to enucleation-induced alterations in the dLGN; these alterations include loss of neurons, shrinkage of neurons, and an apparent decrease in the ability of neurons to synthesize AChE. These data support the hypothesis that geniculocortical projection neurons express AChE transiently during development of geniculocortical connectivity and indicate that normal afferent connections and/or activity are important for the transient expression of AChE by these neurons.

Acetylcholinesterase↗
PubMed1989

Intraocular injections of tetrodotoxin reduce transiently expressed acetylcholinesterase activity in developing rat visual cortex.

Geniculo-recipient layers of primary visual cortex in the rat display a transient pattern of acetylcholinesterase (AChE) activity during the second postnatal week of life. Previous work has demonstrated that neonatal enucleations markedly reduce the transient AChE activity in visual cortex. The present studies were undertaken to determine the effects of reduced afferent neural activity on expression of the transient pattern of AChE activity. Rat pups received intraocular injections of tetrodotoxin (TTX) on postnatal days (PND) 3, 5, 7, 9 and 11 and were sacrificed on PND 12. Some animals were enucleated on PND 3. Brain sections were processed for AChE histochemistry and analyzed by optical densitometry. These experiments show that uniocular injections result in a markedly decreased level of AChE activity in layer IV of the medial part of cortical area 17 contralateral to the injected eye. The degree of reduction of AChE activity from repeated TTX injections was similar to the degree of reduction following enucleation on PND 3. Binocular injections of TTX result in a reduction of AChE activity in layer IV throughout cortical area 17, similar to the effects of binocular enucleation on PND 3. Experiments combining injection of horseradish peroxidase along with TTX on PND 11 demonstrate that retinal ganglion cells of TTX injected eyes are still capable of anterograde axonal transport. These data demonstrate that normal innervation and afferent activity are necessary for the transient expression of AChE activity by geniculocortical neurons.

Acetylcholinesterase↗
PubMed1989

Preliminary studies on phospholipase A2-induced mouse paw edema as a model to evaluate antiinflammatory agents.

Phospholipase A2 (PLA2) is a key component of the inflammatory process because of its role in the generation of eicosanoids and platelet-activating factor (PAF). Manipulation of PLA2 activity offers a novel therapeutic approach for the development of antiinflammatory agents; however, there is a need for a suitable in vivo model. Injection of 1 microgram of snake venom PLA2 (A. piscivorus piscivorus, D-49) into the mouse hind footpad produced a significant three- to four-fold rise in paw edema within 10 min, compared to the saline control. Edema formation depended on enzyme concentration and appeared specific for PLA2 since edema was negated by enzyme pretreatment with p-bromophenacyl bromide, a nonspecific PLA2 inhibitor. Moreover, injection of a protein such as bovine serum albumin did not result in significant edema. Coinjection of phenidone (lipoxygenase inhibitor, 50 micrograms), indomethacin (cyclooxygenase inhibitor, 50 micrograms), cyproheptadine (antihistamine/antiserotonin, 50 micrograms), aristolochic acid (putative PLA2 inhibitor, 100 micrograms), or kadsurenone (PAF antagonist, 50 micrograms) with PLA2 (1 microgram/paw) resulted in partial reduction (44.5, 34.2, 54.7, 64, and 50% inhibition, respectively) of edema formation. Oral administration of cyproheptadine (10 mg/kg), indomethacin (10 mg/kg), BW 755c (100 mg/kg), or dexamethasone (1 mg/kg) 1-3 h before challenge also decreased PLA2-induced edema (63.0, 30.1, 47.8, or 62.5% inhibition, respectively). The data suggest that mouse paw edema resulting from PLA2 injection is a multicomponent event, influenced by both autacoids and lipid mediators of inflammation.

Animals↗
PubMed1989

Pharmacologic modulation of D-49 phospholipase A2-induced paw edema in the mouse.

Paw edema was produced in CD-1 mice by the injection of 0.3 micrograms of snake venom PLA2 (A.p. piscivorus D-49) into the hind paw. Edema peaked at 10 min, remained elevated until 60 min, and then declined slowly. The PLA2 inhibitors, luffariellolide and aristolochic acid, reduced the edema but only when coinjected with the PLA2. The histamine/serotonin antagonists were the most effective drug class against PLA2-induced paw edema. The PAF antagonists, CV-6202 (iv) and kadsurenone (coinjected) reduced the PLA2-induced edema, whereas high doses of the corticosteroids, dexamethasone and hydrocortisone, were also effective. NSAIDs only partially inhibited the paw edema. The LO/CO inhibitors yielded varying activities, with only BW755C and NDGA inhibiting the edema. These results suggest that PLA2 induces paw edema in the mouse via the action of several classes of inflammatory mediators.

Animals↗
PubMed1989

Failure to transfer a digging response to a detour problem in young rats with lesions to the "general learning system".

Recent lesion studies on young rats suggest that the components of the rodent's general learning system (GLS; a group of brain structures essential for normal acquisition of a wide range of laboratory tasks, include the regions of the caudatoputamen, globus pallidus, ventrolateral thalamus, substantia nigra, ventral tegmental area, superior colliculus, median raphe, and pontine reticular formation). The current study provides evidence that young GLS-lesioned rats, like mentally retarded humans, may be suffering from a disturbance in some superordinate ability (executive functioning) that controls the use of learning strategies in general and the transfer of learning in particular. Specifically, thirsty rats were initially trained to traverse a narrow runway to reach a goal box containing water. When a portion of the runway was blocked with sawdust, all of the sham-operated control rats succeeded in burrowing through the sawdust to gain access to the goal box, whereas most of our GLS-lesioned rats failed to do so even though they "knew how" to dig. Neocortically damaged rats showed a similar though significantly smaller deficit. Although other interpretations are possible, these data give tentative support to the view that this impairment in transfer reflects a defect in executive processing.

Animals↗
PubMed1989

Learning ability in young rats with single and double lesions to the "general learning system".

Previous lesion studies suggest that the dorsal caudatoputamen (DCP), globus pallidus, ventrolateral thalamus (VLT), substantia nigra, ventral tegmental area, superior colliculus (SC), median raphe, and pontine reticular formation are components of the general learning system (GLS) of the rat brain. The current study attempted to determine whether bilateral lesions to two components of the GLS (DCP/VLT, DCP/SC or VLT/SC) would produce greater deterioration of learning ability than bilateral lesions to only one component (DCP, VLT or SC). In all combinations examined, a second lesion added to the first led to a significantly greater learning decrement on a series of spatial reversal problems than that associated with the first lesion alone. These results are compatible with the view that the foregoing structures are elements of the same functional system concerned either directly or indirectly with general learning ability.

Animals↗
PubMed1989

Adjacent upstream activation sequence elements synergistically regulate transcription of ADH2 in Saccharomyces cerevisiae.

A 22-base-pair (bp) inverted repeat present in the ADH2 promoter is an upstream activation sequence (UAS1) which confers ADR1-dependent activation upon a heterologous Saccharomyces cerevisiae promoter. UAS1 was nonfunctional when placed within an intron 3' to the transcription start site. The 11-bp sequence which constitutes one-half of the UAS1 palindrome did not activate transcription in a single copy, as direct repeats, or in an inverted orientation opposite to that of ADH2 UAS1. Furthermore, two pairs of symmetrical point mutations within UAS1 significantly reduced activation. This result suggests that a specific orientation of sequences within UAS1 is necessary for ADR1-dependent activation. We determined that an ADR1-dependent complex was formed with UAS1 and, to a lesser extent, with the nonfunctional 11-bp half palindrome. However, the 11 bp did not confer UAS activity, suggesting that ADR1 binding is not sufficient for activation in vivo. ADR1 did not bind to mutant UAS1 sequences in vitro, indicating that their decreased activation is attributable to a reduced affinity of ADR1 for these sequences. We also identified an additional 20-bp ADH2 element (UAS2) that increased the expression of CYC1-lacZ 20-fold when combined with UAS1. UAS2 permitted ADR1-independent, glucose-regulated expression of the hybrid gene. Consistent with this observation, ADR1 did not form a detectable complex with UAS2. Deletion of UAS2 at the chromosomal ADH2 locus virtually abolished ADH2 derepression and had no effect on glucose repression.

Alcohol Dehydrogenase↗
PubMed1989

Pulmonary rapidly adapting receptors reflexly increase airway secretion in dogs.

We attempted to determine whether stimulation of pulmonary rapidly adapting receptors (RARs) increase tracheal submucosal gland secretion in anesthetized open-chest dogs. Electroneurographic studies of pulmonary afferents established that RARs but not lung C-fibers were stimulated by intermittent lung collapse during deflation, collapse being produced by removing positive end-expiratory pressure (PEEP, 4 cmH2O) or by applying negative end-expiratory pressure (NEEP, -4 cmH2O). We measured tracheal secretion by the "hillocks" method. Removing PEEP or applying NEEP for 1 min increased secretion from a base line of 6.0 +/- 1.1 to 11.8 +/- 1.7 and 22.0 +/- 2.8 hillocks.cm-2.min-1, respectively (P less than 0.005). After PEEP was restored, dynamic lung compliance (Cdyn) was 37% below control, and secretion remained elevated (P less than 0.05). A decrease in Cdyn stimulates RARs but not other pulmonary afferents. Hyperinflation, which restored Cdyn and RAR activity to control, returned secretion rate to base line. Secretory responses to lung collapse were abolished by vagal cooling (6 degrees C), by pulmonary vagal section, or by atropine. We conclude that RAR stimulation reflexly increases airway secretion. We cannot exclude the possibility that reduced input from slowly adapting stretch receptors contributed to the secretory response.

Afferent Pathways↗
PubMed1989

[Changes in serum FSH, LH and ovarian follicular growth during electroacupuncture for induction of ovulation].

Changes in serum FSH, LH and follicular sizes were observed in chronically anovulatory patients during electroacupuncture treatment (EAT) for induction of ovulation. 7 cases were diagnosed as PCOD, 3 as dysfunctional uterine bleeding, and 1 as hypogonadotropic amenorrhea. Among them 8 cases complained of infertility for 2.7 years on average. Ovulation was confirmed by pregnancy or the combination of biphasic BBT and ultrasonographic evidence. During one cycle with 3-day EAT on acupoints Ren 3, 4, Extra 16 and Sp 6, ovulation resulted in 5 patients (ovulatory group) and among the 5 cases, 3 of 4 infertile cases became pregnant. The other 5 cases remained in anovulation (anovulatory group); of them 3 cases got biphasic BBT, but no typical ovulatory signs were found on ultrasonography; 2 cases remained in monophasic BBT. Serum FSH, LH values were elevated in ovulatory group, and FSH pulsatile frequency increased significantly during EAT (from 2.10 +/- 0.42/4h to 3.70 +/- 1.64/4h), but not in anovulatory group. No apparent changes were found in serum LH pulsatile frequency and pulsatile amplitudes of FSH and LH in this study. In ovulatory group diameters of ovarian follicles increased markedly, while diameters of anovulatory group stopped to grow at 14-16 mm. It is suggested that ovulation may be induced by EAT via a regulation on hypothalamic-pituitary function leading to normal secretion of FSH and LH.

Acupuncture Therapy↗
PubMed1989

[Experimental studies on the relation of the kidney and reproduction].

To elucidate the mechanism of TCM in treating polycystic ovary syndrome, the authors tried to produce experimental PCO by sterilizing Kunming mice with 1 mg testosterone in various ages of day (5, 8, 11, 14, 17, 21 days). Every litter consisting of 10 young mice was divided into two groups: testosterone given group (T) and control group (C). At the age of 72-75 day, ovaries and uteri were weighed and all ovaries were investigated histologically. Mating was attempted in the two groups. 19 of the 20 ovaries in T5 group, but none of the other groups showed polycystic features. 4 of the 15 mice in T5 group and all of the other groups resulted in pregnancy (P less than 0.05). It was suggested that polycystic ovary was formed in the Kunming mice at age of less than 5 days administered with testosterone. For observation of tonifying Kidney drugs on the ovaries and uteri of the polycystic ovary model in Kunming mice, testosterone was given to Kunming mice of various age (2, 5, 8, 11, 14 days). The tonifying Kidney drugs for anovulatory menstrual disorder were separated into two parts, water soluble part(MS) and ester soluble part (ML). At the age of 56 days (8 weeks), two parts of the drug were given for 14 days to every group of the mice respectively. One day after the administration, uteri were weighed, ovaries were investigated microscopically, and mating was attempted in both groups. All uteri in mice taken water soluble drugs(MS) increased in weight (P less than 0.05), but not in the ML groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Characterization of the potentiation effect of activin on human erythroid colony formation in vitro.

Activin, also named FSH-releasing protein, was previously shown to induce hemoglobin accumulation in K562 cells and potentiate the proliferation and differentiation of CFU-E in human bone marrow cultures. Present studies indicate that the potentiation effect of activin is lineage specific. In addition to CFU-E, activin caused an increase in the colony formation of BFU-E from either bone marrow or peripheral blood. It had little effect on the colony formation of CFU-GM and the mixed colonies from CFU-GEMM. In serum-depleted culture, the effect of activin was shown to be dose-dependent with doses effective at picomolar concentrations. The potentiation effect of activin was exerted indirectly through mediation of both monocytes and T lymphocytes. Activin was also found to increase specifically the proportion of DNA-synthesizing erythroid progenitors from both bone marrow and peripheral blood. It had little effect on DNA synthesis in CFU-GM and in mitogen-stimulated lymphocytes. Addition of the monocytes or T lymphocytes to their respective depleted subpopulations of mononuclear cells reconstituted the enhancing effect of activin on the colony formation and DNA synthesis of erythroid progenitors. These results strongly suggest a specific role of activin in potentiating the proliferation and differentiation of erythroid progenitors in vitro.

Animals↗
PubMed1989

Electrophysiologic recovery of acute conduction block of rat tail nerve.

The recovery of experimental compression neuropathy with prolonged conduction block of the caudal nerve was studied electrophysiologically in 48 adult Sprague-Dawley albino rats divided equally into six groups. The pressure applied in groups A, B, C, D, E, and F was approximately 20kg/cm2 for 20 minutes, 20kg/cm2 for 10 minutes, 20kg/cm2 for 5 minutes, 10kg/cm2 for 20 minutes, 20kg/cm2 for 10 minutes, and 10kg/cm2 for 5 minutes, respectively. The motor nerve conduction velocity (NCV) and the amplitude of the evoked compound muscle action potential (CMAP) were measured before and periodically after nerve compression. The period of initial complete block was significantly longer in the high pressure groups than in the lower ones, and also significantly longer in the nerves compressed for 20 minutes than for those compressed for five or ten minutes. Thus, the severity of conduction block seems to be related to both pressure and duration of compression. Once the conduction block began to recover, the recovery rate of conduction block (recovery rate of amplitude ratio of CMAP, proximal/distal) was not significantly different. The recovery rate of demyelinative lesion (NCV recovery rate) was also not significantly different among the six groups. The degree of compression seems to determine the severity of the initial conduction block, but not the subsequent recovery rate of conduction.

Action Potentials↗