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Biomedical subjects

C H Moon

Publications and source records attributed to C H Moon.

At least 19 recordsLinked to original sources
PubMed2004

Comparison of the immunogenicity of recombinant VP2 and VP3 of infectious pancreatic necrosis virus and marine birnavirus.

Recombinant proteins of truncated viral protein-2 (VP2) (aa 79-359) and VP3 of infectious pancreatic necrosis virus (IPNV) and marine birnavirus (MABV) were expressed in E. coli and their immunogenicities in fish were investigated. The recombinant proteins from IPNV were used to immunize rainbow trout and those from MABV to immunize flounder. The sera from the immunized fishes were assayed for antibody by ELISA and a neutralization test. Both the recombinant VP2 and VP3 produced antibodies in fish but the VP3 antibody titers were higher than that of the VP2 of IPNV and MABV. These results indicate that the recombinant VP3 is more immunogenic than the recombinant VP2.

Animals↗
PubMed2001

Differential roles of cyclooxygenase isoforms after kainic acid-induced prostaglandin E(2) production and neurodegeneration in cortical and hippocampal cell cultures.

Prostaglandins, which are cyclooxygenase (COX) products, are pathologically up-regulated, and have been proven to be closely associated with neuronal death. In this study, we investigated a role of COX isoforms (COX-1 and COX-2) in kainic acid-induced neuronal death in cultured murine cortical or hippocampal neurons. In primary cortical neurons, both indomethacin (COX-1/-2 nonselective inhibitor) and aspirin (COX-1 preferential inhibitor) reduced basal and kainic acid-induced PGE(2) production significantly and prevented neuronal cell death after kainic acid treatment. In contrast, NS398 (COX-2 selective inhibitor) had no effect on kainic acid-induced neuronal cell death. In hippocampal neurons, however, COX-2 inhibitors prevented both kainic acid-induced neuronal death and PGE(2) production. COX-2 expression was remarkably up-regulated by kainic acid in hippocampal neurons; whereas in cortical neurons, COX-2 expression was comparatively less significant. Astrocytes were unresponsive to kainic acid in terms of PGE(2) production and cell death. In conclusion, we suggest that the release of PGE(2) induced by kainic acid occurred through COX-1 activity rather than COX-2 in cortical neurons. The inhibition of PGE(2) release by COX-1 inhibitors prevented kainic acid-induced cortical neuronal death, while in the hippocampal neurons, COX-2 inhibitors prevented kainic acid-induced PGE(2) release and hippocampal neuronal death.

Animals↗
PubMed2001

Rutaecarpine, a quinazolinocarboline alkaloid, inhibits prostaglandin production in RAW264.7 macrophages.

In order to delineate the mechanism involved in the anti-inflammatory activity of rutaecarpine, its effects on the production of prostaglandin (PG) and therein involved enzymes were examined. Rutaecarpine reduced the production of PGE(2) in RAW264.7 cells treated with lipopolysaccharide (LPS) in a dose dependent manner when added to the culture media at the time of stimulation. However, the inhibition of total cellular cyclooxygenase (COX) activity under the same experimental condition was observed only at high concentrations of rutaecarpine. Rutaecarpine did not affected the levels of COX-2 mRNA and protein in macrophages stimulated with LPS. Calcium ionophore A23187 induced-PG production and [(3)H]-arachidonic acid release were significantly decreased by the pretreatment of rutaecarpine for 30 minutes. With the same treatment schedule, however, rutaecarpine failed to alter the activities of cellular COX-1 and COX-2. Collectively, our data suggest that anti-inflammatory effect of rutaecarpine is, at least in part, ascribed to the diminution of PG production through inhibition of arachidonic acid release albeit the nature of its effects on PLA(2) activity remains to be elaborated.

Alkaloids↗
PubMed2000

High glucose enhances IL-1beta-induced cyclooxygenase-2 expression in rat vascular smooth muscle cells.

The changes in vascular prostaglandin production are implicated in the derangement of vascular reactivity in diabetes. However, the mechanism of altered prostaglandin (PG) production in diabetes is largely unknown. In this study, we investigated the effect of high glucose on IL-1beta-induced PG production and the possible underlying mechanism in cultured vascular smooth muscle cell (VSMC). High glucose evoked an augmentation of IL-1beta-induced PG synthesis in a dose dependent manner and enhanced cyclooxygenase (COX) activity, which reached to maximum at 8-12 hours after stimulation. Western blot analysis supported the activity data. Protein kinase C (PKC) inhibitors, H-7 and chelerythrine, significantly inhibited the enhancement of IL-1beta-induced COX-2 expression by high glucose. The activation of PKC by PMA resulted in marked increase of PG production in low glucose group, whilst this was not the case in high glucose group. Furthermore, glucose-enhancing effect was significantly suppressed by zopolrestat, an aldose reductase inhibitor, and sodium pyruvate. These results suggest that the augmenting effect of high glucose on IL-1beta-induced PG production and COX-2 expression is, at least in part, due to increased glucose metabolism via sorbitol pathway following PKC activation.

Animals↗
PubMed2000

4-1BB: still in the midst of darkness.

4-1BB is a member of the tumor necrosis factor receptor superfamily. The receptor functions mainly as a costimulatory molecule in T lymphocytes. In addition, several lines of evidence have shown that interactions between 4-1BB and its ligand are involved in the antigen presentation process and the generation of cytotoxic T cells. Recent studies, however, have demonstrated that 4-1BB plays more diverse roles: Signals through 4-1BB are important for long-term survival of CD8+ T cells and the induction of helper T cell anergy. Clinically, there is great interest in 4-1BB, because T-cell activation induced by anti-4-1BB monoclonal antibodies is highly efficient in the eradication of established tumor cells in mice. Now, since mice deficient in 4-1BB or the 4-1BB ligand are available, subtle roles played by 4-1BB may be revealed in the near future.

4-1BB Ligand↗
PubMed2000

An animal model of neuropathic pain employing injury to the sciatic nerve branches.

The present study was conducted to develop a new animal model of neuropathic pain employing injury to the distal sciatic nerve branches. Under halothane anesthesia, the tibial, sural, and/or common peroneal nerves were injured and neuropathic pain behaviors were compared among different groups of rats. Different types of injury produced different levels of neuropathic pain. Rats with injury to the tibial and sural nerves showed the most vigorous mechanical allodynia, cold allodynia, and spontaneous pain. These neuropathic pain behaviors were not relieved by functional sympathectomy using guanethidine. The results suggested that injury to the tibial and sural nerves, while leaving the common peroneal nerve intact, can be used as a new animal model of neuropathic pain and that this model represents sympathetically independent pain (SIP). The present animal model is very simple to produce injury and can produce profound and reliable pain behaviors. These features enable the new animal model to be a useful tool in elucidating the mechanisms of neuropathic pain, especially SIP.

Animals↗
PubMed2000

Mechanism for antiplatelet effect of onion: AA release inhibition, thromboxane A(2)synthase inhibition and TXA(2)/PGH(2)receptor blockade.

Antiplatelet actions of aqueous extract of onion were investigated in rat and human platelet. IC(50)values of onion extract for collagen-, thrombin-, arachidonic acid (AA)-induced aggregations and collagen-induced thromboxane A(2)(TXA(2)) formation were 0.17 +/- 0. 01, 0.23 + 0.03, 0.34 +/- 0.02 and 0.12 +/- 0.01 g/ml, respectively. [(3)H]-AA release induced by collagen (10 microg/ml) in rat platelet was decreased by onion compared to control (22.1 +/- 2.13 and 5.2 +/- 0.82% of total [(3)H]-AA incorporated, respectively). In fura-2 loaded platelets, the elevation of intracellular Ca(2+)concentration stimulated by collagen was inhibited by onion. Onion had no cytotoxic effect in platelet. Onion significantly inhibited TXA(2)synthase activity without influence on COX activity. Platelet aggregation induced by U46619, a stable TXA(2)mimetic, was inhibited by onion, indicating its antagonism for TXA(2)/PGH(2)receptor. These results suggest that the mechanism for antiplatelet effect of onion may, at least partly, involve AA release diminution, TXA(2)synthase inhibition and TXA(2)/PGH(2)receptor blockade.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2000

Outcome from injury: general health, work status, and satisfaction 12 months after trauma.

OBJECTIVE: We evaluated outcomes 12 months after trauma in terms of general health, satisfaction, and work status. METHODS: Two hundred forty-seven patients without severe neurotrauma were evaluated by interview during admission and by mailed self-report 6 and 12 months after trauma. Data were obtained from the Trauma Registry, interviews, and survey instruments. Baseline assessment was obtained with the Short Form 36 (SF36) and the Sickness Impact Profile (SIP) work scale. Outcome measures were the SF36, SIP work scale, Brief Symptom Inventory (BSI) depression scale, the Civilian Mississippi Scale for Posttraumatic Stress Disorder (PTSD), and a satisfaction questionnaire. Three regressions were determined for outcome. The dependent variables were general health and work status (linear) and satisfaction (logistic). Each regression controlled for baseline status and mental health, Injury Severity Score (ISS), and 12-month SF36 physical function before evaluating the effect of outcome mental health. RESULTS: Follow-up data were available for 75% of the patients at 6 months and 51% at 12 months. The mean age of patients was 37.2 +/- 0.9 years (+/-SEM), and 73% were male. Their average ISS was 13.9 +/- 0.6. Seventy percent of injuries were blunt force, 13.5 % were penetrating, and 16.5 % were burn injuries (mean total body surface area, 13.3 +/- 1.5%). Sixty-four percent of the patients had returned to work at 12 months. Follow-up SF36 mental health was associated with the dependent outcome in each regression. After controlling for baseline status and mental health, ISS, and outcome SF36 physical function, outcome mental health was associated with outcome SF36 general health (p < 0.001), SIP work status (p = 0.017), and satisfaction with recovery (p = 0.005). Outcome SF36 mental health was related to baseline mental health, 12-month PTSD and BSI depression scores, and increased drug and alcohol use. CONCLUSIONS: Twelve months after trauma, patients' work status, general health, and overall satisfaction with recovery are dependent on outcome mental health. This dependency persists despite measured baseline status, ISS, or physical recovery. The mental disease after trauma is attributable to poor mental health, the development of symptoms of PTSD and depression, and increased substance abuse. Trauma centers that fail to recognize, assess, and treat these injury-related mental health outcomes are not fully assisting their patients to return to optimal function.

Activities of Daily Living↗
PubMed1999

Systemically administered capsazepine prevents the capsaicin-induced functional desensitization and loss of substance P-like immunoreactivity (SP-LI) in guinea-pig bronchi.

In this study, we investigated whether the systemically administered capsazepine can prevent the capsaicin-induced desensitization ex vivo in guinea-pig bronchi. Pretreatment with capsaicin (2.5, 5 and 10 mg/kg, s.c.) induced the functional desensitization and the loss of substance P-like immunoreactivity (SP-LI) with a similar potency (ED50: 3.31 +/- 0.57 and 4.81 +/- 0.89 mg/kg, respectively) in isolated guinea-pig bronchi. Capsazepine (30 mg/kg, s.c.) co-administered with capsaicin (5 mg/kg, s.c.) prevented the capsaicin (5 mg/kg, s.c.)-induced functional desensitization and loss of SP-LI. These results suggest that capsazepine can antagonize systemically the desensitizing action of capsaicin at the level of receptor, preventing the loss of SP-LI and the establishment of functional desensitization in guinea-pig bronchi.

Animals↗
PubMed1999

Posttraumatic stress disorder after injury: impact on general health outcome and early risk assessment.

OBJECTIVE: To evaluate prospectively components of general health outcome after trauma and to report on the further validation of the Michigan Critical Events Perception Scale (MCEPS), an instrument that predicts increased risk for posttraumatic stress disorder (PTSD). METHODS: Adults without neurologic injury admitted to a Level I trauma center in 1997 were interviewed during hospitalization. Baseline data included demographics, injury mechanism, Injury Severity Score, the Short Form 36 (SF36), and the MCEPS, which measures peri-traumatic dissociation (the sense of depersonalization or derealization during an injury event). Surveys sent by mail and completed 6 months later included the SF36 and civilian Mississippi Scale for PTSD. RESULTS: A total of 140 patients were interviewed; the 70% (n = 100 patients) who completed the 6-month assessment form the study group. Injuries were categorized as 71% blunt, 13% penetrating, and 16% burn. Mean Injury Severity Score was 13.7+/-0.52. PTSD at 6 months occurred in 42% of the patients and was directly related to MCEPS dissociation (p = 0.001; odds ratio = 3.1; 95% confidence interval, 1.6, 5.9). A stepwise linear regression explains 40% of the variance in 6-month SF36 general health outcome (adjusted R2 = 0.402). The model controls for individual factors related to dissociation, PTSD, and general health outcome. Development of PTSD was independently and inversely related to general health outcome as measured by the SF36 at 6 months (p < 0.001, beta = -0.404). The R2 change of 0.132 for PTSD (vs. 0.082 for 6-month physical function) illustrates that PTSD contributes more to the patient's perceived general health at 6 months than the degree of physical function or injury severity. CONCLUSIONS: Within hours of injury, the MCEPS identifies patients who are three times more likely to develop PTSD. PTSD compromises self-reported general health outcome in injured adults independent of baseline status, Injury Severity Score, or degree of physical recovery. These data suggest that psychological morbidity is an important part of the patient's perceived general health.

Adult↗
PubMed1999

Posttraumatic stress disorder in injured adults: etiology by path analysis.

OBJECTIVE: Posttraumatic Stress Disorder (PTSD) impairs outcome from injury. We present a path analysis of factors related to the development of PTSD in injured adults. METHODS: A prospective cohort of 250 patients without severe neurotrauma was evaluated by interview during admission and by mailed self-report 6 months later. Data were gathered from the trauma registry (age, injury mechanism, and Injury Severity Score), social history (gender, income, education, and social support), and survey instruments. Baseline assessment used the Michigan Critical Events Perception Scale (peritraumatic dissociation and subjective threat to life), the Life Experience Survey (stressful exposure history), and the SF36 (general and mental health). PTSD at 6 months was identified with the civilian Mississippi Scale for PTSD. Data are listed as mean +/- SEM or percent (%). Path analysis was conducted by linear regression and significant (p<0.05) variables are shown. Factors are listed with the standardized beta. A negative beta suggests a protective effect. RESULTS: The 176 patients (72%) who completed the 6-month follow-up were 37.7+/-0.88 years old; 75% were men; and blunt (70%), penetrating (13.5%), and burn (16.4%) mechanisms caused the injuries. Assault was involved in 14.5% of the cases. Average income was $44,300+/-2,700/yr, education was 13.0+/-0.15 years, and Injury Severity Score was 13.9+/-0.50. A total of 42.3% of the patients developed PTSD. The 39.7% of the variance in PTSD explained by the model was due to intentional injury (beta = 0.27), male gender (beta = -0.21), age (beta = -0.20), peritraumatic dissociation (beta = 0.174), baseline mental health (beta = -0.21), and prior life-threatening illness (beta = -0.29). Peritraumatic dissociation was due to the patient's sense of threat to life (beta = -0.47), and threat was related to Injury Severity Score (beta = 0.2), assault(beta = 0.14), education (beta = -0.15), and age (beta = -0.19). Baseline SF36 mental health was related to social support (beta = 0.27) and income (beta = 0.21). Income was contingent on education (beta = 0.21). CONCLUSION: PTSD occurred in 42.3% of injured adults 6 months after trauma and was related to assault, dissociation, female gender, youth, poor mental health, and prior illness. By modeling PTSD, we may learn more of the etiology, risk stratification, and potentials for the treatment of this common and important morbidity of injury.

Adaptation, Psychological↗
PubMed1999

Protein kinase C inhibitors abolish the increased resistance of diabetic rat heart to ischemia-reperfusion injury.

Protein kinase C (PKC) has been implicated in ischemic preconditioning, but whether it plays a role in the cardioprotection observed in the diabetic heart is not known. We assessed the possible role of PKC by investigating whether the inhibition of PKC with staurosporine (Stau, 0.01 microM) or chelerythrine (Chel, 1 microM) can abolish the increased resistance to ischemia (25 min)-reperfusion (30 min) injury in Langendorff perfused hearts from streptozotocin-induced 4-week diabetic rats. In the diabetic heart, pre-ischemic left ventricular developed pressure (LVDP), double product (DP: LVDPxheart rate/1,000), +/- dP/dt(max) and coronary flow rate (CFR) were all reduced compared to the control. The pretreatment with Stau or Chel significantly improved these parameters. The post-ischemic contractile function was recovered to a greater extent in the diabetic heart (116.9 +/- 20.5% of pre-ischemic DP) than in the control (23.3 +/- 2.3% of pre-ischemic DP), indicating the increased resistance of the diabetic heart to ischemia-reperfusion injury. The treatment with Stau or Chel abolished the enhanced recovery in the diabetic heart (36.0 +/- 14.6 and 54.1 +/- 12.8% of pre-ischemic DP, respectively). The reduction in post-ischemic end diastolic pressure (EDP) and lactate dehydrogenase (LDH) release in diabetes (13.5 +/- 2.5 mmHg and 27.2 +/- 6.2 U/g heart) compared to the control (55.8 +/- 2.9 mmHg and 60. 3 +/- 5.7 U/g heart) was significantly (p<0.05) increased by pretreatment with Stau (39.0 +/- 4.9 mmHg and 53.1 +/- 7.6 U/g heart) or Chel (36.2 +/- 3.0 mmHg and 48.8 +/- 4.3 U/g heart). Neither Stau nor Chel had any influence on the post-ischemic values of LVDP, DP, +/- dP/dt(max), EDP and LDH release in the control heart. In the conclusion, the present results suggest that PKC activation may, at least in part, contribute to the increased resistance of the diabetic heart to ischemia-reperfusion injury.

Alkaloids↗
PubMed1999

Can you spot the signs of elder mistreatment?

The incidence of elder mistreatment is expected to increase as the baby boom generation ages and more elderly people are living or receiving care at home. Despite increased awareness and reporting of other forms of domestic abuse and neglect, recognition and management of elder abuse lag far behind actual incidents. Drs Kruger and Moon describe the signs of mistreatment as well as the physician's role in reporting and management.

Aged↗
PubMed1998

Capsaicin-induced desensitization is prevented by capsazepine but not by ruthenium red in guinea pig bronchi.

In isolated guinea pig bronchi, the influence of ruthenium red, capsazepine and extracellular Ca2+ on capsaicin-induced desensitization was examined to investigate whether this desensitization was mediated via a specific receptor coupled with an ion channel. Pre-exposure of tissues to capsaicin (1, 3 or 10 microM) caused a dose-dependent desensitization to the second application of capsaicin. However, the contractile responses to exogenous tachykinins were not changed after pre-exposure of tissues to capsaicin. This capsaicin-induced desensitization was prevented by capsazepine (30 microM), but not by ruthenium red added to tissues 20 min before pretreatment with capsaicin (3 microM). While the excitatory contractile response to capsaicin was markedly reduced in the absence of extracellular Ca2+, the desensitization induced by capsaicin was not changed by the removal of extracellular Ca2+. In summary, the results from the present study suggest that in vitro functional desensitization induced by capsaicin in guinea pig bronchi may involve changes in the vanilloid receptor and occur through a ruthenium red-insensitive pathway.

Animals↗
PubMed1998

Molecular cloning of a novel GTP-binding protein induced in fish cells by rhabdovirus infection.

We have cloned and sequenced a cDNA encoding GTP-binding protein from a fish cell, CHSE-214. The clone was 1493 bp long and contained an open reading frame encoding 364 amino acids. It has the five sequence motifs G1-G5 that are conserved in all GTP-binding proteins. Its amino acid sequences are strikingly different from those of the well-characterized G-proteins. However, sequences closely related to this protein are found in various kinds of species including human, Arabidopsis, Drosophila and archaebacteria, suggesting a novel subfamily within the superfamily of the GTP-binding proteins. Northern analysis indicates that this gene is constitutively expressed at a low level in normal cells but is induced by fish rhabdovirus infection at about 24 h post infection and disappears thereafter. Based on these observations, we propose that this protein represents an evolutionarily conserved novel subfamily of GTP-binding proteins which may play an important role in fish rhabdovirus infection.

Amino Acid Sequence↗