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Biomedical subjects

S Sun

Publications and source records attributed to S Sun.

At least 235 records · Page 13Linked to original sources
PubMed1996

Dual function of Drosophila cells as APCs for naive CD8+ T cells: implications for tumor immunotherapy.

With unseparated mouse spleen cells as responders, Drosophila cells expressing MHC class I (L(d)) molecules alone lead to peptide-specific responses of CD8+ cells in the absence of exogenous cytokines. Under these conditions, DNA released from dying cells stimulates the B cells in spleen to up-regulate costimulatory molecules; these activated B cells then provide bystander costimulation for CD8+ cells responding to class I-peptide complexes on the Drosophila APCs. By stimulating B cells and presenting antigen to T cells, Drosophila cells thus serve two different functions in promoting primary responses of CD8+ cells in vitro. With this system, we show that Ld-transfected Drosophila cells are able to induce autologous spleen cells to respond to a tumor-specific peptide in vitro and, after transfer, cause tumor rejection in vivo.

Animals↗
PubMed1996

Effects of various carotenoids on cloned, effector-stage T-helper cell activity.

Astaxanthin, a carotenoid without provitamin A activity, enhances murine T-helper (Th) cell clone-mediated antibody (Ab) production with suboptimal antigen (Ag) challenges. It also suppresses interferon-gamma (IFN-gamma) production by cloned murine Th1 cells. beta-Carotene is less effective than astaxanthin. This study evaluates the effects of various carotenoids with various relative polarity, provitamin A activity, and antioxidant activity. Carotenoids tested include astaxanthin, cantaxanthin, zeaxanthin, lutein, and lycopene, and their effects were tested at a concentration at which astaxanthin's effect was most potent. A.E7 and CDC35 cells are used as representative type 1 and type 2 Th cell (Th1 and Th2) clones, respectively. In the Th1 clone, astaxanthin, but not other carotenoids, suppressed IFN-gamma production and increased the number of Ab-secreting cells with the use of primed spleen cells. With cultures of Th1 cells and unprimed spleen cells, astaxanthin and zeaxanthin augmented the number of immunoglobulin M Ab-secreting cells. In the cultures of Th2 clone and primed spleen cells, astaxanthin, but not other carotenoids, enhanced the number of Ab-secreting cells. With unprimed spleen cells, lycopene suppressed Th2 clone-mediated Ab production. Interleukin-5 production by the Th2 clone was not significantly altered with the carotenoids tested, irrespective of the use of unprimed or primed spleen cells. Carotenoid actions on Th cells may vary in each carotenoid and do not seem to be closely associated with carotenoid antioxidant activity or relative polarity.

Animals↗
PubMed1996

An orally supplemented mononucleotide mixture prevents the decrease in T cell-dependent humoral immunity in C57BL/6 mice fed a nucleotide-free diet.

T-cell-dependent humoral immune responses are lower in mice fed a nucleotide-free (NF) diet. In a previous study, a mononucleotide and nucleoside mixture prevented the decrease in humoral immune responses in mice fed a NF diet when a total of seven doses [2100 micromol/(kg x dose)] were administered intraperitoneally. In the present study, C57BL/6 (B6) mice were fed a NF diet for 3 wk with or without mononucleotide mixture (MM) supplementation. The MM was given at the levels of 14 or 70 micromol/(kg x d) by daily gavage feeding for 3 wk. Control mice were fed a NF diet without supplements (negative control) or a NF diet plus the mononucleotide/nucleoside mixture administered intraperitoneally (positive control). Both doses of MM prevented the decrease in T-dependent antibody (Ab) production in mice fed a NF diet as effectively as positive controls. T-helper (Th) spleen cells from mice of each diet group were enriched, mixed with Th cell-depleted spleen cells from each diet group, and antigen-primed in the culture. The number of Ab-secreting cells formed was higher with Th cells from mice with oral MM supplements or from positive controls than with those from mice without nucleotide supplement. The source of Th cell-depleted spleen cells did not influence the number of Ab-secreting cells. Thus, orally supplemented nucleotides can prevent the suppression of Th cell-dependent humoral immunity in mice fed a NF diet with doses likely to be provided by dietary sources.

Animals↗
PubMed1996

Effects of buffer agents on postresuscitation myocardial dysfunction.

OBJECTIVES: Earlier studies demonstrated that hypertonic buffer agents administered during cardiopulmonary resuscitation (CPR) altered neither myocardial pH nor cardiac resuscitability. The rationale for the routine use of buffer agents for CPR has therefore been challenged. However, when these buffer agents are administered during CPR, they may have favorable effects on the postresuscitation course. Postresuscitation myocardial dysfunction has more recently emerged as a potentially fatal complication after successful cardiac resuscitation. Options for prevention and management of this complication have prompted the present studies, in which the effects of buffer agents administered during CPR are evaluated as to their effects on postresuscitation myocardial function and survival. DESIGN: Prospective, randomized, controlled animal study. SETTING: University animal laboratory. SUBJECTS: Forty male Sprague-Dawley rats (450 to 570 g). INTERVENTIONS: Ventricular fibrillation was induced electrically. Mechanical Ventilation and percordial compression were initiated after either a 4- or an 8-min interval of untreated cardiac arrest. Sodium bicarbonate as a CO2-generating buffer, Carbicarb and tromethamine as CO2-consuming buffers, or hypertonic saline placebo were injected as a bolus into the right atrium during CPR. Defibrillation after 10 mins of cardiac arrest and CPR was successful in each instance. No differences in the electric power required for successful resuscitation were documented. Left ventricular pressure, rate of left ventricular pressure increase measured at a left ventricular pressure of 40 mm Hg (dP/dt40), rate of left ventricular pressure decline (-dP/dt), and end-tidal PCO2 were continuously measured for 240 mins after successful resuscitation. MEASUREMENTS AND MAIN RESULTS: Decreases in coronary perfusion pressure were observed after each buffer or placebo injection. As anticipated, end-tidal PCO2 increased after bicarbonate and decreased after Carbicarb or tromethamine. Postresuscitation left ventricular function was significantly decreased in all animals. However, there was significantly less depression in rate of left ventricular pressure increase measured at a left ventricular pressure of 40 mm Hg (dP/dt40), rate of left ventricular pressure decline (-dP/dt), and a lower left ventricular diastolic pressure with both Carbicarb and tromethamine in association with significant increases in postresuscitation survival rate. When the duration of untreated cardiac arrest was increased to 8 mins, the severity of postresuscitation left ventricular dysfunction was magnified and postresuscitation myocardial function and survival were significantly improved with both CO2-generating and CO2-consuming buffer agents. CONCLUSION: Although buffer agents may not improve the success of resuscitation when administered during CPR, they may ameliorate postresuscitation myocardial dysfunction and thereby improve postresuscitation survival.

Animals↗
PubMed1996

Both amino- and carboxyl-terminal sequences within I kappa B alpha regulate its inducible degradation.

Nuclear expression and consequent biological action of the eukaryotic NF-kappa B transcription factor complex are tightly regulated through its cytoplasmic retention by an ankyrin-rich inhibitory protein termed I kappa B alpha. I kappa B alpha specifically binds to and masks the nuclear localization signal of the RelA subunit of NF-kappa B, thereby effectively sequestering this transcription factor complex in the cytoplasm. Specific cellular activation signals lead to the rapid proteolytic degradation of I kappa B alpha and the concomitant nuclear translocation of NF-kappa B. However, the precise biochemical mechanisms underlying the inhibitory effects of I kappa B alpha on RelA and its inducible pattern of degradation remain unclear. By using HeLa cells transfected with various cDNAs end-coding epitope-tagged mutants of I kappa B alpha, our studies demonstrate the following: (i) sequences within the 72-amino-acid N-terminal region of I kappa B alpha are required for tumor necrosis factor alpha (TNF-alpha)-induced degradation but are fully dispensable for I kappa B alpha binding to and inhibition of RelA; (ii) serine residues located at positions 32 and 36 within the N-terminal region of I kappa B alpha represent major sites of induced phosphorylation (substitution of these serine residues with alanine abrogates TNF-alpha-induced degradation of I kappa B alpha); (iii) the C-terminal 40 residues of I kappa B alpha (amino acids 277 to 317), which include a PEST-like domain, are entirely dispensable for TNF-alpha-induced degradation and inhibition of RelA; (iv) a glutamine- and leucine-rich (QL) region of I kappa B alpha located between residues 263 and 277 and overlapping with the sixth ankyrin repeat is required for both inducible degradation and inhibition of RelA function; (v) regulation of I kappa B alpha degradation by this QL-rich region appears to occur independently of phosphorylation at serines 32 and 36. These findings thus indicate that I kappa B alpha is generally organized within distinct modular domains displaying different functional and regulatory properties. These studies have also led to the identification of a novel class of dominant-negative I kappa B alpha molecules that retain full inhibitory function on NF-kappa B yet fail to undergo stimulus-induced degradation. These molecules, which lack N-terminal sequences, potently inhibit TNF-alpha-induced activation of the human immune deficiency virus type 1 kappa B enhancer, thus indicating their possible use as general inhibitors of NF-kappa B.

Amino Acid Sequence↗
PubMed1996

Breathing and brain blood flow during sleep in patients with chronic mountain sickness.

Chronic mountain sickness (CMS) patients have lower arterial O2 saturation (SaO2) during sleep compared with healthy high-altitude residents, but whether nocturnal arterial O2 content (CaO2) and brain O2 delivery are reduced is unknown. We measured SaO2, CaO2, sleep-disordered breathing (SDB), and internal carotid artery flow velocity in 8 CMS patients, 8 age-matched healthy CMS controls, 11 healthy younger-aged Han, and 11 healthy younger-aged Tibetan male residents of Lhasa, Tibet (3,658 m). CMS patients spent a greater portion of the night in SDB (total no. of episodes of apnea, hypopnea, and hypoventilation) than did the CMS controls, young Han, or young Tibetans (15% vs. 5, 1, and 1%, respectively; P < 0.05) because of more frequent apnea and hypoventilation episodes and longer duration of all types of episodes. SDB and unexplained arterial O2 desaturation caused nocturnal SaO2 to be lower and more variable in CMS patients than in CMS controls or in younger-aged Han or Tibetan men. Average CaO2 was similar, but the CMS patients spent 29%, whereas the other groups spent < 4%, of the night at values < 18 ml O2/100 ml whole blood. Internal carotid artery flow velocity during wakefulness was similar in CMS patients and CMS controls despite higher end-tidal PcO2 values in the CMS patients. When contiguous sleep stages are compared, flow velocity rose from stage 2 to rapid-eye-movement sleep in both groups. Whereas flow velocity remained elevated from awake to rapid-eye-movement sleep in the CMS controls, it fell in the CMS patients. During episodes of SDB, internal carotid flow velocity increased in CMS controls but did not change in the CMS patients such that values were lower in the CMS patients than in CMS controls at the end and after SDB episodes. We concluded that SDB and episodes of unexplained desaturation lowered nocturnal SaO2 and CaO2, which, together with a lack of compensatory increase in internal carotid artery flow velocity, likely decreased brain O2 delivery in CMS patients during a considerable portion of the night.

Adult↗
PubMed1996

[Role of PCR and dot bolt hybridization in the detection of human papillomavirus of the penile cancer].

Human papillomavirus (HPV), a oncogenicpotential, may be carcinogenic effectors in variety of genital tract malignancies. We examined the association of human papillomavirus type 16 and 18 in 28 penile cancers by the highly sensitive polymerase chain reaction and dot bolt hybridization. Human papillomavirus type 16 was found in 14 of 28 penile cancers (50%), whereas type 18 was identified in 3 of 28 penile cancers (10.6%). Our results suggest humanpapillomavirus type 16 may play a role in the development of this tumor and associate with smoking and ages of patients.

Adult↗
PubMed1996

[Computed tomography of the ethmoid labyrinth and adjacent structures].

In order to study the relation of ethmoid labyrinth to the adjacent structures, continuous axial CT scan of the ethmoid labyrinth was performed on 9 normal subjects. Meanwhile, coronal and axial CT scans of ethmoid labyrinth were obtained in 20 normal subjects. On an average, 22 scan sections were done on each subject. The relation of ethmoid labyrinth to adjacent structures was observed and the remarkable intersubject variations in this anatomic area were noted. The relation of posterior ethmoid cells or sphenoid sinus to the optic canal, and the relation of internal carotid artery to the sphenoid sinus were clearly demonstrated on axial scans. The detailed anatomic structure of the ostiomeatal complex and the anatomic relation of ethmoid labyrinth to orbit and anterior skull base were revealed by coronal CT scans. CT scan of the paranasal sinuses was of great importance in clinical practice for the purpose of etiological analysis of sinusitis, design of endoscopic sinus surgery and prevention of complication.

Adolescent↗
PubMed1995

Epinephrine increases the severity of postresuscitation myocardial dysfunction.

BACKGROUND: Epinephrine has been the mainstay for cardiac resuscitation for more than 30 years. Its vasopressor effect by which it increases coronary perfusion pressure is likely to favor initial resuscitation. Its beta-adrenergic action, however, may have detrimental effects on postresuscitation myocardial function when administered before resuscitation because it increases myocardial oxygen consumption. In the present study, our focus was on postresuscitation effects of epinephrine when this adrenergic agent was administered during cardiopulmonary resuscitation. Postresuscitation myocardial functions were compared with those of a selective alpha-adrenergic agent, phenylephrine, when epinephrine was combined with a beta 1-adrenergic blocking agent, esmolol, and saline placebo. METHODS AND RESULTS: Ventricular fibrillation was induced in 40 Sprague-Dawley rats. Mechanical ventilation and precordial compression was initiated either 4 or 8 minutes after the start of ventricular fibrillation. The adrenergic drug or saline placebo was administered as a bolus after 4 minutes of precordial compression. Defibrillation was attempted 4 minutes later. Left ventricular pressure, dP/dt40, and negative dP/dt were continuously measured for an interval of 240 minutes after successful cardiac resuscitation. Except for saline placebo, comparable increases in coronary perfusion pressure were observed after each drug intervention. The number of countershocks required for restoration of spontaneous circulation was significantly greater for epinephrine-treated animals (10 +/- 8) when compared with phenylephrine-treated animals (1.8 +/- 0.4, P < .01) and with animals treated with epinephrine combined with esmolol (1.6 +/- 0.9, P < .01). After resuscitation, dP/dt40 and negative dP/dt were significantly decreased and left ventricular end-diastolic pressure was significantly increased in each animal when compared with prearrest levels. However, the greatest impairment followed epinephrine, and this was associated with significantly greater heart rate and the shortest interval of postresuscitation survival of 8 +/- 4 hours, whereas placebo controls survived for 12 +/- 11 hours. Phenylephrine-treated animals survived for 41 +/- 10 hours (P < .01 versus epinephrine), and animals that received a combination of epinephrine and esmolol survived for 35 +/- 11 hours (P < .01 versus epinephrine). When the duration of untreated cardiac arrest was increased from 4 to 8 minutes, the severity of postresuscitation left ventricular dysfunction was magnified, but disproportionate decreases in postresuscitation survival were again observed with placebo and epinephrine when compared with alpha-adrenergic agonists. CONCLUSIONS: In an established rodent model after resuscitation following cardiac arrest, epinephrine significantly increased the severity of postresuscitation myocardial dysfunction and decreased duration of survival. More selective alpha-adrenergic agonist or blockade of beta 1-adrenergic actions of epinephrine reduced postresuscitation myocardial impairment and prolonged survival.

Adrenergic Agonists↗
PubMed1995

Plasticity of vascular smooth muscle alpha-actin gene transcription. Characterization of multiple, single-, and double-strand specific DNA-binding proteins in myoblasts and fibroblasts.

Transcriptional activity of the mouse vascular smooth muscle (VSM) alpha-actin promoter was governed by both cell type and developmental stage-specific mechanisms. A purine-rich motif (PrM) located as -181 to -176 in the promoter was absolutely required for activation in mouse AKR-2B embryonic fibroblasts and partially contributed to activation in undifferentiated mouse BC3H1 myoblasts. Transcriptional enhancer factor 1 recognized the PrM and cooperated with other promoter-binding proteins to regulate serum growth factor-dependent transcription in both myoblasts and fibroblasts. Two distinct protein factors (VAC-ssBF1 and VAC-ssBF2) also were identified that bound sequence-specifically to single-stranded oligonucleotide probes that spanned both the PrM and a closely positioned negative regulatory element. VAC-ssBF1 and BF2 binding activity was detected in undifferentiated myoblasts, embryonic fibroblasts, and several smooth muscle tissues in the mouse and human. A myoblast-specific protein (VAC-RF1) also was detected that bound double-stranded probes containing a CArG-like sequence that previously was shown to impart strong, cell type specific repression. The binding activity of transcription enhancer factor 1, VAC-RF1, and VAC-ssBF1 was significantly diminished when confluent BC3H1 myoblasts differentiated into myocytes and expressed VSM alpha-actin mRNA after exposure to serum-free medium. The results indicated that cell type-specific control of the VSM alpha-actin gene promoter required the participation of multiple DNA-binding proteins, including two that were enriched in smooth muscle and had preferential affinity for single-stranded DNA.

Actins↗
PubMed1995

Improved small intestinal preservation after lazaroid U74389G treatment and cold storage in University of Wisconsin solution.

The small intestine (SI) is highly sensitive to oxygen free radical-induced injury. The most common preservation solution, University of Wisconsin (UW) solution, does not adequately prevent free radical-induced injury. Lazaroids, and U74389G in particular, are a new class of compound that are potent inhibitors of superoxide-mediated lipid peroxidation. We studied the added influence of U74389G to 18-hr cold preservation of rat SI in UW solution. Three groups of rats were studied. In group 1, SI was excised and reperfused immediately. In group 2, SI was stored in UW solution at 4 degrees C for 18 hr. In group 3, U74389G was given to the SI graft before storage and again before reperfusion. Blood reperfusion of the grafts was achieved via connection to the superior mesenteric artery and portal vein of support rats. Functional recovery was assessed using a maltose tolerance test. Weight changes were calculated and histologic studies done. After 30 and 60 min of reperfusion, maltose uptake in group 3 was significantly better than that of the group 2, and returned to control levels. Significantly more tissue swelling was noted in group 3 over control, but the magnitude was less than that of group 2. Less transmural necrosis and villous blunting were noted in group 3 versus group 2; the appearance of the mucosa in group 3 approached that of group 1. We conclude that the use of U74389G treatment in addition to cold storage in UW solution improves recovery of graft function and minimizes morphologic damage to the small intestinal mucosa.

Adenosine↗
PubMed1995

Reduced representation approach to protein tertiary structure prediction: statistical potential and simulated annealing.

A reduced representation model has been developed and used to predict the folded structures of proteins from their primary sequences and random starting conformations. The molecular structure of each protein is reduced to its backbone atoms (with ideal fixed bond lengths and valence angles) and each side chain approximated by a single virtual united atom. The co-ordinate variables are the backbone dihedral angles phi and psi. A statistical potential function, which includes local and non-local interactions and is computed from known X-ray elucidated protein structures, is used in the structure minimization. Simulated annealing method of energy minimization is employed to search for folded conformations. Simulations using the reduced representation model reproduce many structural features of the studied proteins.

Computer Simulation↗
PubMed1995

Dynamics surrounding Cys-34 in native, chemically denatured, and silica-adsorbed bovine serum albumin.

We report the steady-state and time-resolved fluorescence of 6-acryloyl(dimethylamino)naphthalene (acrylodan) covalently attached to Cys-34 in bovine serum albumin (BSA). For this conceptually simple system, complicated fluorescence intensity and anisotropy decay kinetics are observed. The steady-state and time-resolved results demonstrate the presence of an excited-state reaction for the BSA-acrylodan system. Additional analysis shows that dipolar relaxation of the environment surrounding acrylodan within BSA is responsible for most of the observed time-dependent evolution of the emission spectrum. The effects of temperature, chemical denaturation, and protein adsorption to a bare silica substrate are also investigated. These results demonstrate the complexity of the changes within a protein/biorecognition element that affect the signal from a single fluorescent reporter group.

2-Naphthylamine↗
PubMed1995

Protein kinase-C mediates chicken vasoactive intestinal peptide stimulated prolactin secretion and gene expression in turkey primary pituitary cells.

This set of experiments investigated the role of protein kinase-C (PKC) as a second messenger in vasoactive intestinal peptide (VIP)-stimulated prolactin (PRL) secretion and PRL mRNA abundance. Dispersed anterior pituitary cells (5 x 10(5) or 10(6) cells/tube) were isolated from laying turkeys and incubated in 1.0 ml of M-199. In Experiment 1, 10(-7) M VIP increased PRL secretion three- to fivefold. Prolactin mRNA abundance was higher in VIP-treated cells (11.45 +/- 2.11 arbitrary optical unit; AOU) than control cells (4.59 +/- 1.2 AOU). In Experiment 2, the addition of 10(-12), 10(-10), 10(-8), and 10(-6) M phorbol 12-myristate 13-acetate (PMA; PKC agonist) increased PRL release from 8.5 +/- 0.7 to 14.9 +/- 1.1, 17.2 +/- 1.3, 18.1 +/- 2.2, and 18.7 +/- 2.8 micrograms/10(6) cells, respectively. PRL mRNA abundance was significantly (P < 0.01) increased in only 10(-6) M PMA treatment. In Experiment 3, PKC desensitization decreased VIP-stimulated PRL release from 10.0 +/- 2.3 to 4.2 +/- 0.6 micrograms/5 x 10(5) cells and PMA-induced release from 7.1 +/- 1.3 to 2.7 +/- 0.3 micrograms/5 x 10(5) cells. VIP and PMA up-regulated PRL mRNA abundance was decreased two- to fourfold by PKC desensitization. In Experiment 4, 10(-6) M staurosporine (ST; PKC antagonist) decreased both 10(-7) M VIP-stimulated PRL secretion from 7.86 +/- 2.9 to 2.43 +/- 0.5 micrograms/5 x 10(5) cells and 10(-8) M PMA-stimulated PRL secretion from 4.26 +/- 0.2 to 2.23 +/- 0.3 micrograms/5 x 10(5) cells (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗