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Biomedical subjects

C L Lu

Publications and source records attributed to C L Lu.

At least 109 records · Page 6Linked to original sources
PubMed1993

Effects of chemical stimulation in the periaqueductal gray on vocalization in the squirrel monkey.

Twenty-nine agonists and 32 antagonists of more than 10 transmitters known to be present in the periaqueductal gray (PAG) have been injected into the squirrel monkey's PAG in order to test their effects on spontaneous vocalization at sites yielding vocalization with electrical stimulation. Vocalization could be elicited with the glutamate agonists sodium-L-glutamate, L-aspartic acid, L-homocysteic acid, N-methyl-D-aspartic acid, quisqualic acid, and kainic acid, the cholinergic agonists acetylcholine, carbachol, and muscarine, the monoaminergic agonist histamine, and the GABA antagonists bicuculline and picrotoxin. No vocalizations could be obtained with agonists of dopamine, noradrenaline, adrenaline, serotonin, GABA, glycine, nicotinic receptors, and endogenous opioids, as well as with antagonists of glutamate, acetylcholine, dopamine, noradrenaline, adrenaline, serotonin, histamine, glycine, GABA-B, delta- and mu-receptors. Blocking of spontaneous vocalization was obtained with the nonspecific glutamate antagonist kynurenic acid and the GABA-A receptor agonist muscimol. The results indicate that the production of vocalization depends upon the activation of glutamatergic synapses in the PAG. GABAergic afferents seem to have a tonic inhibitory control on the periaqueductal vocalization mechanism, while acetylcholine and histamine seem to exert only a transient modulatory control.

Acetylcholine↗
PubMed1993

A preliminary study of the fixation mechanism of collagen reaction with a polyepoxy fixative.

A new biomaterial has been developed by fixing native collagens with a polyepoxy compound (PC) fixative. Prior studies have shown that this biomaterial has comparable properties as compared to collagen fixed with glutaraldehyde (GA) and thus has a great promise for use as an implantable bioprosthesis. The purpose of this study was to understand the mechanism of the amino acids-PC reactions in the fixation process. Bovine arteries were fixed with PC under various pH, concentration and temperature conditions as a function of fixation time. Individual amino acid components in the fresh and the fixed arteries were assayed using a Beckman amino acid analyzer to determine the degree of tanning. The denaturation temperature (Td) was also measured on each sample. Since the denaturation temperature is a direct indication of cross-linking of individual amino acids with the fixative, the difference in the degree of tanning for the same increase in Td may be indicative of the quantity of the masked, non-cross-linked amino acids. The fixation reaction data indicated that not all amino acids were cross-linked upon contacting the PC fixative. Masking appeared to be more substantial with a fixation at higher pH values.

Amino Acids↗
PubMed1993

Hepatic actinomycosis with portal vein thrombosis mimicking hepatocellular carcinoma: a case report.

A fatal case of hepatic actinomycosis with portal vein thrombosis is reported. The diagnosis of actinomycosis was delayed because of its rarity in Taiwan. This 63-year-old man was admitted due to body weight loss and poor appetite. No fever was noted before admission. Liver biochemical test showed a decreased serum albumin level with elevated serum levels of globulin and alkaline phosphatase. He was not a hepatitis B carrier and his serum level of alfafetoprotein was within normal range. Image studies (abdominal sonography and computed tomography) showed a hepatic mass over the medial segment of the left lobe with involvement of right lobe of the liver. Main portal vein thrombosis was also seen. Because of profound cachexia, he died of aspiration pneumonia and disseminated intravascular coagulation on the 11th day after admission. An autopsy revealed hepatic actinomycosis. High index of suspicion for early diagnosis and treatment is emphasized.

Actinomycosis↗
PubMed1992

Role of NMDA receptors in hypothalamic facilitation of feline defensive rage elicited from the midbrain periaqueductal gray.

The present study tested the hypothesis that the pathway from the medial hypothalamus to the midbrain periaqueductal gray (PAG) subserving defensive rage behavior in the cat facilitates the occurrence of this response when elicited from the PAG by utilizing excitatory amino acids as a neurotransmitter or neuromodulator. Cannula electrodes were implanted into the PAG for the elicitation of defensive rage behavior as well as for microinjections of excitatory amino acid antagonists and N-methyl-D-aspartic acid (NMDA). Monopolar stimulating electrodes were also implanted into the medial hypothalamus from which this response could also be elicited and, when stimulated at subthreshold levels for elicitation of behavior, could also facilitate the occurrence of PAG elicited defensive rage. Initially, dual stimulation of the PAG and medial hypothalamus facilitated the occurrence of defensive rage elicited from the PAG. Then, the identical dual stimulation paradigm was repeated with the same current parameters following the infusion of various antagonists for different receptors into the PAG defensive rage sites. The results indicate that infusion of either kynurenic acid [(0.1-2.0 nmol), a non-selective excitatory amino acid receptor antagonist] or D-2-amino-7-phosphonoheptanoic acid (AP7) [(0.1-2.0 nmol), a specific NMDA receptor antagonist], produced a dose and time dependent blockade of the facilitatory effects of medial hypothalamic stimulation. In contrast, microinjections of relatively larger doses of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) [(4 nmol), a non-NMDA receptor (quisqualate and kainate) antagonist] or atropine [(4.4 nmol), a muscarinic receptor antagonist] had little effect upon medial hypothalamically elicited facilitation of the PAG response. In a second experiment, NMDA [0.1-1.0 nmol] was microinjected directly into PAG defensive rage sites in the absence of medial hypothalamic stimulation. In these animals, drug infusion mimicked the effects of dual stimulation by producing a dose and time dependent decrease in response latencies. A third experiment was designed to further test the hypothesis by neuroanatomical methods. Here, the retrograde label, Fluoro-Gold, was microinjected into defensive rage sites within the PAG and following a survival time of 5-6 days, the animals were sacrificed. The brains were then processed for immunocytochemical analysis of cells that immunoreact positively for aspartate and glutamate. The results indicated the presence of many retrogradely labelled and immunocytochemically positive cells within the rostro-caudal extent of the medial hypothalamus as well as others that were double labelled.(ABSTRACT TRUNCATED AT 400 WORDS)

2-Amino-5-phosphonovalerate↗
PubMed1991

An enkephalinergic mechanism involved in amygdaloid suppression of affective defence behavior elicited from the midbrain periaqueductal gray in the cat.

A series of recent studies in our laboratory have provided evidence that opioid peptides powerfully suppress feline affective defense behavior at the level of the midbrain periaqueductal gray (PAG). In the present study, we tested the hypothesis that the central (CE) nucleus of the amygdala constitutes a significant inhibitory input to the PAG which utilizes enkephalins as its neurotransmitter or neuromodulator. Cannula-electrodes were implanted into the PAG for the elicitation of affective defense behavior as well as for infusion of opioid antagonists. Monopolar stimulating electrodes were also implanted into the central, lateral and medial amygdaloid nuclei from which suppression or facilitation of affective defense behavior could be obtained. Initially, 4 trials of concurrent, subseizure stimulation of the CE or lateral amygdala at very low (100 microA, 60 Hz) currents and PAG resulted in an immediate suppression of this response which displayed a time dependent decline after 30 min. In the next stage of the experiment, naloxone (2.7, 18.9 and 27.5 nM) was microinjected through the cannula-electrode into the PAG affective defense site and the experimental procedures noted above were repeated. Naloxone treatment (at 27.5 and 18.9 nM) blocked the suppressive effects of CE and lateral amygdaloid stimulation in a dose and time dependent manner. Further analysis revealed that this effect is likely mediated via the mu receptor since the suppressive effects of amygdaloid stimulation were blocked by the selective mu antagonist, beta-Funaltrexamine (0.05 and 0.2 nM) but not by the selective delta-antagonist, ICI 174,864 (0.7 nM).(ABSTRACT TRUNCATED AT 250 WORDS)

Affect↗
PubMed1991

Affective defense behavior elicited from the feline midbrain periqueductal gray is regulated by mu and delta opioid receptors.

The present study sought to identify specific opioid receptor subtypes involved in the modulation of affective defense behavior (AD) at the level of the midbrain periaqueductal gray (PAG). Cannula electrodes were utilized for eliciting AD from the PAG as well as for microinjecting mu, delta and kappa agonists and antagonists into these sites. Following microinjections of morphiceptin, D-Pen2,D-Pen5 enkephalin (DPDPE), or U-488H into sites from which AD was elicited, threshold values were determined. The results indicated that morphiceptin and DPDPE significantly suppressed AD in a dose- and time-dependent manner. Pretreatment with mu and delta opioid antagonists, B-FNA and ICI 174,864, completely blocked the suppressive effects of morphiceptin and DPDPE, respectively. Microinjections of morphiceptin and DPDPE failed to alter response thresholds for circling behavior also elicited from electrical stimulation of dorsal PAG. Administration of the selective kappa agonist, U-488H, or vehicle alone, did not alter the threshold for AD. The results of this study indicate that opioid peptides interact with mu and delta receptors within the midbrain PAG to powerfully suppress AD.

Affect↗
PubMed1991

Dopaminergic regulation of quiet biting attack behavior in the cat.

The present study provides evidence for the involvement of dopamine in the regulation of quiet biting attack behavior. Utilizing monopolar electrodes, quiet biting attack was elicited by electrical stimulation of lateral hypothalamus in five cats. After stable baseline response latency values were established, the nonselective dopamine agonist, apomorphine, was administered peripherally (IP, 1.0, 1.4 and 1.8 mg/kg), and its effects upon the attack response were identified. Apomorphine significantly facilitated the occurrence of quiet biting attack in a dose- and time-dependent manner. Conversely, quiet biting attack behavior was also suppressed in a dose- and time-dependent manner by the selective D2 antagonist, spiperone (0.2, 0.4 and 0.8 mg/kg), but not by the selective D1 antagonist, SCH 23390 (0.8 mg/kg). Moreover, pretreatment with spiperone (0.2 mg/kg) completely blocked the facilitatory effects of 1.4 mg/kg of apomorphine, while SCH 23390 (0.8 mg/kg) pretreatment failed to alter apomorphine-induced facilitation of the attack response. In addition, neither apomorphine nor spiperone altered response latencies for hypothalamically elicited circling behavior. The results suggest that dopamine plays a significant role in the regulation of quiet biting attack behavior.

Aggression↗
PubMed1989

Antigenic analysis between BCG and tumor cells by BCG-monoclonal antibodies.

Antigenic relation between Mycobacterium bovis strain BCG and experimental animal tumor cells was analyzed with BCG monoclonal antibodies (BCG-MoAbs). Four BCG-MoAbs of 602, 603, 609, and 612 were successfully established and applied for the antigenic analysis of Meth A, RL male 1, colon tumor 26 of mouse, and line 10 of guinea pig tumor. MoAb 602 showed broad reactivity against all types of tumor cells. BCG antigen(s) was clearly recognized as small granules on the tumor cell surface under the fluorescence microscope, indicating that the animal tumor cells shared the common antigen(s) with BCG.

Animals↗
PubMed1986

Characteristics of egg yolk phosvitin as an antioxidant for inhibiting metal-catalyzed phospholipid oxidations.

A study was conducted to determine the antioxidant activity of phosvitin in an egg yolk phospholipid emulsion system. Various inorganic and organic metals (Fe2+, Cu2+, and hemin) in several different concentrations were added individually to the emulsions to induce lipid oxidation. Characteristics of phosvitin for inhibiting these metal-catalyzed lipid oxidations were investigated. The effect of heat treatments, both pasteurization (61.1 C, 4 min) and autoclaving (121.1 C, 10 min), on phosvitin was examined to find out if there was any effect on its antioxidant characteristics. Lipid oxidations were measured by thiobarbituric acid assays. Phosvitin effectively inhibited Fe2+ and Cu2+-catalyzed phospholipid oxidations as shown by low malondialdehyde values over the entire reaction period; however, it did not exert similar effects on the hemin-catalyzed oxidation reaction. Phosvitin demonstrated higher capacity to inhibit iron catalysis of phospholipid oxidations (up to 30:1 Fe2+-to-phosvitin molar ratio) than copper catalysis (1:1 molar ratio). Pasteurization did not change the antioxidant activities of phosvitin; however, autoclaving decreased phosvitin's inhibitory capacity on iron catalysis.

Antioxidants↗
PubMed1983

Metabolic clearance rate and half-time disappearance rate of human N-terminal and adrenocorticotropin of pro-opiomelanocortin in the rat: a comparative study.

In metabolic clearance rate (MCR) and plasma half-time disappearance rate (t 1/2) of human N-terminal (1-76) and adrenocorticotropin(hACTH 1-39) of pro-opiomelanocortin were compared after intravenous bolus injection of both peptides simultaneously into rat. The level of immunoreactive (IR) hNT and IR-ACTH in plasma and urine samples were measured by specific and homologous radioimmunoassays (RIAs). The MCR and hNT and hACTH were 3.01 +/- 0.20 ml/min (M +/- S.D., N = 4) and 2.04 +/- 0.06 ml/min, respectively (p less than 0.05), The curve for the disappearance rate of IR-hNT was triphasic (rapid t 1/2 = 0.96 +/- 0.39 min, intermediate t 1/2 = 6.7 +/- 2.25 min, and slow t 1/2 = 74 +/- 15.8 min), while that of IR-ACTH was biphasic (rapid t 1/2 = 3.3 +/- 0.68 min, and slow t 1/2 = 41.5 +/- 3.03 min) as analyzed by the non-linear least-squares methods. Statistically significant difference (p less than 0.01) was found between IR-hNT and IR-hACTH in the rapid t 1/2 and in the slow t 1/2. Subsequent analysis of pooled plasma sample (30 min post-injection) by molecular sieve chromatography on Sephadex G-50 superfine column revealed that the majority of IR-hNT (90-95%) and IR-ACTH (60-70%) are co-chromatographed with [125I]iodo hNT and [125I]iodo ACTH respectively. Similarly, gel filtration of pooled urine sample (120 min post-injection) on Sephadex G-50 superfine revealed that 80-90% of IR-hNT and less than 50% of IR-ACTH co-eluted with [125I]iodo hNT and [125I]iodo ACTH, respectively. Smaller molecular forms of IR-hNT and IR-ACTH were definitely apparent in the urine sample. In conclusion, hNT has a larger MCR and a longer half-time disappearance rate (t 1/2) than IR-hACTH in rat plasma and it appears that hNT is more resistant to degradation by plasma and by kidney than hACTH.

Adrenocorticotropic Hormone↗
PubMed1983

Corticotropin (ACTH) and the N-terminal fragment of pro-opiomelanocortin are located in the same granules in cells of rat pituitary gland.

The localization of corticotropin (ACTH) and of the N-terminal fragment (NTF) of pro-opiomelanocortin were assessed by light and electron microscope immunochemistry. Using the unlabeled technique of Sternberger at the light microscope level, a strongly positive reaction for both NTF and ACTH antisera was observed in all secretory cells of the pars intermedia. In the pars distalis, immunostaining with ACTH antiserum was localized in stellate cells dispersed throughout the lobe. As observed in serial, consecutive sections, the NTF antiserum stained exactly the same cells. At the electron microscope level, using the protein A-gold technique, all the secretory granules of the cells of the pars intermedia showed a positive reaction with both antisera. In the pars distalis, after exposure to either of the antisera, gold particles were found over secretory granules of typical stellate corticotrophs. Making use of the possibility of reacting both faces of a fine section with gold particles of different sizes, it was found that the same secretory granules in all the cells of the pars intermedia and in corticotrophs of the pars distalis contained particles of both sizes. These results indicate that ACTH and NTF are contained in the same secretory granules and released together in the circulation where NTF is found in high amounts.

Adrenocorticotropic Hormone↗
PubMed1982

Distribution pattern in the human pituitary and hypothalamus of a new neuropeptide: the C-terminal glycoprotein-fragment of human pro-pressophysin (CPP).

The distribution pattern of CPP-containing neurons and fibers in the human pituitary and hypothalamus was studied with a specific antiserum to human CPP and the unlabeled antibody technique. Immunoreactive CPP was found in the magnocellular neurons of the supraoptic nucleus (SON), the paraventricular nucleus (PVN) and in neurons scattered in the supraoptic hypophyseal tract. CPP-containing parvocellular neurons were found in the suprachiasmatic nucleus (SCN). The CPP-containing fibers from the magnocellular neurons formed a tract coursing through the median eminence and the pituitary stalk to the posterior lobe of the hypophysis. In contrast, no such fibers from the SCN projected to SON, PVN and the median eminence. This pattern is identical to that of vasopressin and its associated neurophysin-containing neurons and fibers and strongly supports the concept that CPP is a part of the common precursor for vasopressin and neurophysin II. The biological importance of human CPP other than being a precursor fragment remains to be elucidated.

Arginine Vasopressin↗
PubMed1982

Immunohistochemical localization of human pituitary glycopeptide (HPGP)-like immunoreactivity in the hypothalamus and pituitary of normal and homozygous diabetes insipidus (Brattleboro) rats.

Sections of the hypothalami and pituitary glands of normal (Sprague-Dawley) and homozygous diabetes insipidus (Brattleboro) rats were stained with antiserum to a human pituitary glycopeptide (HPGP) by using the immunohistochemical peroxidase-antiperoxidase method at the light microscopic level. Our results show in normal rats that immunoreactive HPGP was localized in the perikarya of the magnocellular neurons of the hypothalamus, in the posterior pituitary, and in the nerve fibers distributed in the median eminence (ME) and in the areas between the supraoptic nuclei (SON), paraventricular nuclei (PVN), and median eminence and also in the suprachiasmatic nuclei (SCN), a part of the parvocellular system. In the Brattleboro rats, however, no staining was found either in the hypothalami or pituitary glands. The present data strongly support our previous hypothesis that HPGP, a 39 residue glycopeptide isolated from human neurohypophysis, may be part of the precursor of arginine-vasopressin and its neurophysin II (Pro-NP-AVP).

Animals↗
PubMed1982

Corticotropin releasing factor (CRF): effects on the release of pro-opiomelanocortin (POMC)-related peptides by human anterior pituitary cells in vitro.

The effect of synthetic ovine corticotropin-releasing factor (oCRF), alpha-melanotropin (alpha-MSH) and arginine-vasopressin (AVP) on the release of pro-opiomelanocortin (POMC)-related peptides (beta-endorphin, beta-lipotropin, adrenocorticotropin, and the 12K N-terminal) was studied in primary cultures of human anterior pituitary (HAP) cells. The peptides released into the medium were measured by specific radioimmunoassays. HAP cells responded to oCRF at concentrations as low as 10 ng/ml by significantly increasing peptide secretion (p less than 0.005). AVP was also effective, but, it is only 0.1% as potent as oCRF. alpha-MSH was ineffective even at a dose of 10 micrograms/ml. Immunoreactive (IR)-beta EP, IR-beta LPH, IR-ACTH, and IR-HNT were released in approximately equimolar ratios. Partial characterization of the peptides released by HAP cells with gel chromatography on Sephadex G-50 superfine revealed two peaks of IR-beta EP (as beta EP and beta-LPH), two peaks of IR-beta LPH (as beta-LPH and gamma-LPH), one peak of IR-ACTH, and two peaks of IR-HNT. In conclusion, oCRF is a potent secretagogue for the equimolar release of ACTH, HNT and related peptides in the human pituitary gland.

Adrenocorticotropic Hormone↗