Biomedical subjects

C E Lee

Publications and source records attributed to C E Lee.

At least 37 records · Page 2Linked to original sources

PubMed1999

Physical performance: differences in men and women with and without low back pain.

OBJECTIVE: To determine the extent to which there may be major differences in scores on a battery of physical performance tasks among men with nonspecific, mechanical low back pain (LBP), women with LBP, healthy men, and healthy women. DESIGN: Case series survey. SETTING: A referral-based orthopedic clinic. PATIENTS: Thirty-three men and 46 women with LBP. Control Subjects: Twenty-one men and 25 women healthy controls. INTERVENTION: Completion of six clinician-assessed physical performance tasks and self-report inventories. MAIN OUTCOME MEASURE: Performance scores on distance walked in 5 minutes, 50-foot walk at fastest speed, repeated sit-to-stand, repeated trunk flexion, loaded forward reach, and the Sorensen fatigue tasks. RESULTS: Discriminant function analysis revealed that the four groups of subjects performed the physical tasks significantly different in two major ways: (1) healthy control subjects outperformed LBP patients, irrespective of gender, on tasks involving trunk control, coordination, and stability while withstanding heavy or quickly changing loads on the spine; (2) men outperformed women, irrespective of patient or nonpatient status, on tasks involving anthropometric features of limb length. The findings provide guidance on reasonable performance expectations for men and women patients with LBP. Future studies of treatment effectiveness also will be able to assess physical performance change in terms of the intersection between standards set by the men and women healthy control subjects and those of men and women patients. However, whether a return to nonpatient status is an appropriate treatment goal is left to future research.

Adult↗

PubMed1999

Causes and consequences of recent freshwater invasions by saltwater animals.

Transitions from marine to freshwater habitats constitute dramatic shifts between 'adaptive zones' that have initiated the radiation and speciation of many taxa. As recently as 10?000 years ago, deglaciation resulted in marine fauna being trapped in freshwater lakes. In modern times, human activity has caused the acceleration of freshwater invasions from marine or brackish habitats, leading to serious environmental problems. The rapid pace of these invasions provides ideal opportunities for examining initial responses to environmental change and mechanisms involved in habitat transitions. Despite conservation implications and evolutionary applications, recent transitions to fresh water remain inadequately explored.

Journal Article↗

PubMed1999

Assessment of metered dose inhaler technique in family health service patients in Singapore.

OBJECTIVE: To assess the metered-dose inhaler technique in polyclinic patients with chronic lung disease. METHOD: A cross-sectional study was conducted in three polyclinics. The inhalation technique was assessed in six steps. RESULTS: Only 7.1% of patients could perform all six steps correctly. Percentage of patients performing each of the following steps correctly were: preparation (89.1%), exhalation (53.8%), lip closure (69.2%), inhalation (57.7%), breath-holding (32.1%) and puff interval (35.4%). CONCLUSION: This study showed a high incidence of incorrect usage of metered dose inhaler amongst polyclinic patients.

Adolescent↗

PubMed1998

Psychometric characteristics and clinical usefulness of physical performance tests in patients with low back pain.

STUDY DESIGN: The psychometric properties and clinical use of a battery of physical performance measures were tested on 44 patients with low back pain and 48 healthy, pain-free control subjects. OBJECTIVES: Reliability, validity, and clinical use of nine physical performance measures were evaluated. SUMMARY OF BACKGROUND DATA: Although physical performance measures have potential use in evaluation, treatment planning, and determination of treatment outcome, there is sparse systematic investigation of their reliability, validity, and clinical use. METHODS: Forty-four subjects with low back pain and 48 healthy pain-free subjects participated. The following physical performance measures were tested: distance walked in 5 minutes; 50-foot walk at fastest speed; 50-foot walk at preferred speed; 5 repetitions of a sit-to-stand task; 10 repetitions of a repeated trunk flexion task; timed up-and-go task; unloaded forward reach task; loaded forward reach task; and Sorensen fatigue test. Subjects were assessed twice on 2 days. RESULTS: All measures had excellent intertester reliability (intraclass correlation coefficient [ICC]1,1 > 0.95). Test-retest (within session) reliability was adequate for all measures (ICC1,1 > 0.83) except repeated trunk flexion (ICC1,1 > 0.45) in the low back pain group. Test-retest (day-to-day) reliability ranged between 0.59 and 0.88 in the low back pain group and between 0.46 and 0.76 in the control group. Day-to-day reliability improved when the averages of two trials of repeated trunk flexion and sit-to-stand were used (0.76-0.91 low back pain group and 0.62-0.89 control group). Results of a multivariate analysis of variance showed a significant effect of group (F10,65 = 3.52, P = 0.001). Results of univariate analyses showed significant group differences on all measures except the 50-foot walk at preferred speed and unloaded forward reach. Self-report of disability was moderately correlated with the performance tasks (r = 0.400 to -0.603). CONCLUSIONS: The results provide support for the use of these physical performance measures as a complement to patient self-report.

Activities of Daily Living↗

PubMed1998

Differences in delta opioid receptor antinociception, binding, and mRNA levels between BALB/c and CXBK mice.

Mu and delta opioid receptors have been demonstrated to mediate supraspinal opioid antinociception. Whereas the recombinant inbred CXBK mouse is notably deficient in mu opioid receptor antinociception, binding density, and mRNA (MOR-1) levels, little is known about delta opioid receptor processes in this strain. The present study thus compared CXBK mice and their BALB/c strain progenitors with respect to delta opioid antinociception, whole-brain receptor binding levels, and mRNA (DOR-1) levels. Following intracerebroventricular injections of the selective delta1 and delta2 opioids DPDPE and [d-Ala2]deltorphin II, respectively, CXBK mice displayed relatively lower antinociception on the tail-flick test, resulting in significantly increased ED50 values for both agonists in this strain. Decreased whole-brain specific binding of [3H][d-Ala2]deltorphin II, but not [3H]DPDPE, was also observed in CXBK mice. Solution hybridization with a probe for the DOR-1 revealed increased transcript levels in the caudate-putamen, frontal cortex, and spinal cord of this strain. The present data demonstrate a deficiency in delta1 and delta2 opioid antinociception in CXBK mice concomitant with reductions in whole-brain delta2 receptor binding and regional increases in DOR-1. Whether these observations are causally related remains to be clarified.

Analgesics↗

PubMed1998

Chronic naltrexone differentially affects supraspinal delta-opioid receptor-mediated antinociception.

The effects of chronic treatment with naltrexone, an opioid receptor antagonist, on delta1- and delta2-opioid receptor agonist-induced antinociception and ligand binding were investigated in mice. Antinociception by intracerebroventricular (i.c.v.) [D-Pen2,5]enkephalin (DPDPE) and [D-Ala2]deltorphin II, agonists selective for delta1- and delta2-opioid receptors, respectively, was blocked following subcutaneous (s.c.) implantation of a naltrexone pellet (7.5 mg) for 7 days. Removal of the naltrexone pellet was followed 24 h later by a decrease of 7.5-fold in the ED50 value of [D-Ala2]deltorphin II, but not that of DPDPE. In a whole brain homogenate the binding of [3H][D-Ala2]deltorphin II was increased twice as much as that of [3H]DPDPE. Chronic naltrexone treatment also produced an 8.6-fold decrease in the ED50 value of i.c.v. administered morphine. The increase in morphine potency was reversed to a control (placebo-treated mice) value by the selective delta2-opioid receptor antagonist, naltriben (25 pmol, i.c.v.). Thus, chronic naltrexone selectively increases delta2-opioid receptor-mediated antinociception, supporting the existence of delta opioid receptor subtypes with distinct adaptive characteristics. The data also indicate that delta2-opioid receptors are critically involved in the expression of morphine supersensitivity.

Analgesics↗

PubMed1998

Interferon-gamma-induced factor binding to the interleukin-4-responsive element of CD23b promoter in human tonsillar mononuclear cells: role in transient up-regulation of the interleukin-4-induced CD23b mRNA.

Stimulation of human tonsillar mononuclear cells with interleukin-4 (IL-4) and interferon-gamma (IFN-gamma) rapidly induced the activation of distinct nuclear factors with different mobilities, both of which bind the IL-4 response element (IL-4RE) of CD23b promoter as examined by electrophoretic mobility shift assays (EMSA). Co-treatment of IL-4 and IFN-gamma induced, in addition to the two distinct complexes, a new complex with an intermediate mobility. The IL-4-induced complex reacted with anti-STAT (signal transducers and activators of transcription) 6, resulting in a supershift whereas the formation of the IFN-gamma-induced complex was inhibited by anti-STAT 1. The intermediate complex appeared to react with both anti-STAT 6 and anti-STAT 1. Although IFN-gamma alone did not induce CD23 mRNA transcription, Northern blot analysis revealed a transient up-regulation of the IL-4-induced CD23 mRNA by IFN-gamma within 2 h of IFN-gamma treatment in these tonsillar cells. The results suggest that the IL-4RE of the IL-4-inducible gene can accommodate both IL-4- and IFN-gamma-activated factors, such as STAT 6 and STAT 1, either in homodimeric or heterodimeric forms and the binding of these different proteins to the respective promoter may play a potential regulatory role in the IL-4-inducible gene expression.

Animals↗

PubMed1997

Identification and activation mechanism of the interleukin-4-induced nuclear factor binding to the CD23(b) promoter in human B lymphocytes.

CD23 is a B cell activation antigen involved in B cell proliferation and production of IgE, of which two isoforms are known. While CD23(a) is constitutively expressed in B cells, the expression of CD23(b) is specifically induced by interleukin-4 (IL-4) or selected mitogenic stimuli. We have previously shown that CD23(b) is a primary response gene rapidly activated by IL-4 in resting human B cells. We now report the identification of a nuclear factor binding to the IL-4-response element (IL-4RE) in CD23(b) promoter in purified human tonsillar B cells. Activation of this factor, named NF-IL-4/CD23, occurred within 5 min after IL-4 treatment in a cycloheximide-insensitive manner. The activation was sensitive to phosphatases and inhibitors of protein tyrosine kinases, but it was not sensitive to inhibitors of protein kinase C. This behavior, in fact, closely correlates with the IL-4-induced activation mechanism of CD23 gene expression. In transformed B cell line Raji, where the IL-4-induced CD23 mRNA expression was hardly detected, no activation of NF-IL-4/CD23 was noted. The activation was also observed that although a sequence highly homologous to the IL-4RE of the CD23(b) promoter is present in the CD23(a) promoter, the IL-4-induced factor did not bind the sequence. These results strongly suggest that NF-IL-4/CD23 acts as an IL-4 signal transducer leading to CD23(b) gene activation in human B cells. Further characterization of this factor is now in progress, including comparison with STAT6, recently shown to be involved in IL-4 signal transduction and transcriptional activation.

B-Lymphocytes↗

PubMed1997

Luteinizing hormone-releasing hormone gene expression differs in young and middle-aged females on the day of a steroid-induced LH surge.

LHRH mRNA levels were examined in young and middle-aged female rats at 4 times (10:00 h, 14:00 h, 18:00 h and 20:00 h) on the day of a steroid-induced LH surge by in situ hybridization with a digoxigenin-labeled riboprobe. Young, but not middle-aged females, exhibited dynamic temporal changes in the number of LHRH mRNA positive neurons detected in the organum vasculosum of the lamina terminalis-preoptic area (OVLT-POA) continuum. Specifically, fewer LHRH mRNA positive neurons were detected at 18:00 h compared with the number detected at 14:00 h and 20:00 h (P < 0.01) in the OVLT-POA of young females. All LHRH mRNA positive neurons present in 4 anatomically matched sections through the rostral POA of young and middle-aged animals were digitized for detailed computer-assisted analysis of the hybridization reaction product. The mean hybridization area (P < 0.00025) and integrated optical density per cell (P < 0.006) were reduced in middle-aged compared to young females consistent with a relative age-related decline in LHRH mRNA levels. Moreover, an age-related reduction in cellular and/or regional hybridization area was noted at each of the time points examined (P < 0.05-P < 0.001). These data confirm earlier reports of dynamic changes in LHRH mRNA levels on the day of an LH surge. Furthermore, they support a role for age-related alterations in LHRH gene expression in the disruption of regular estrous cyclicity in middle-aged females.

Aging↗

PubMed1997

Blockade of morphine supersensitivity by an antisense oligodeoxynucleotide targeting the delta opioid receptor (DOR-1).

An antisense oligodeoxynucleotide (ODN) targeting 20 bases of the coding sequence of the cloned delta opioid receptor (DOR-1), a mismatched ODN (different from the antisense ODN at 4 bases) or saline was administered to 3 groups of CD-1 mice implanted with naltrexone pellets (7.5 mg) for 7 days. Morphine supersensitivity (i.e., increased potency as defined by decreased morphine ED50 values) was observed 24 h after pellet removal (day 8) in mice treated with saline or mismatch ODN, but not in antisense ODN treated mice. Antisense ODN alone had no effect on basal nociceptive thresholds or morphine analgesia but reduced the analgesic potency of the delta, opioid agonist [D-Ala2]deltorphin II. These data suggest that the delta2 opioid receptor system participates in the adaptive changes contributing to increased morphine potency following chronic naltrexone treatment.

Analgesics↗

PubMed1997

Effect of supraspinal antisense oligodeoxynucleotide treatment on delta-opioid receptor mRNA levels in mice.

Studies in vivo demonstrate that antisense oligodeoxynucleotide (ODN) treatment specifically reduces the functions mediated by numerous central nervous system (CNS) receptors, including opioid receptors. However, the effects of antisense ODN on the opioid receptor mRNA target, itself are rarely examined. In the present study, the effect of supraspinal antisense ODN administration on delta-opioid receptor (DOR) mRNA levels in selected CNS regions, was investigated in mice. ODN targeting a 20-nucleotide sequence of the DOR mRNA transcript was administered by intracerebroventricular (i.c.v.) injection twice daily for 3 days. First, to confirm that antisense ODN treatment decreases DOR function in this system, antinociception produced by DOR-selective agonist [D-Ala2]deltorphin II was assessed on day 4. A 2-fold reduction in [D-Ala2]deltorphin II potency was revealed in antisense ODN-treated mice compared to mice receiving control treatments. DOR mRNA levels in selected CNS regions which either mediate antinociception; medial thalamus (MThal), periaqueductal gray (PAG), frontal cortex (FCtx) and spinal cord (SpC) or exhibit relatively high levels of DOR mRNA; nucleus accumbens (Acb) and caudate-putamen (CPu) were then quantitated by solution hybridization. Levels of DOR mRNA in antisense ODN-treated mice were not different from levels in mice treated with saline vehicle, which ranged from 0.07 pg/microg total RNA in MThal and PAG to 0.26 pg/microg total RNA in CPu. These results are both consistent with previous reports that antisense oligodeoxynucleotide (ODN) treatment down-regulates DOR protein in vivo and indicate that this down-regulation is not associated with altered DOR mRNA levels.

Animals↗

PubMed1996

An antisense oligodeoxynucleotide to the delta opioid receptor (DOR-1) inhibits morphine tolerance and acute dependence in mice.

Pharmacological data from several laboratories support a modulatory role for the delta opioid receptor in morphine analgesia, tolerance, and physical dependence. We examined the role of the delta opioid receptor in these processes using an in vivo antisense strategy in mice. Intracerebroventricular administration of a 20mer antisense or a mismatch control oligodeoxynucleotide (ODN) targeting the mRNA of the cloned delta opioid receptor (DOR-1) for 3 days did not affect baseline nociceptive thresholds or morphine analgesia compared to untreated or saline-treated mice. However, dose-response studies indicate that the induction of morphine tolerance following 3 days of chronic morphine administration was blocked in antisense but not mismatch ODN or saline-treated mice. Antisense ODN treatment also blocked the development of acute morphine dependence, whereas similar protection was not afforded to mice treated with saline or mismatch ODN. This study demonstrates the relevance of the cloned DOR-1 in morphine tolerance and dependence and provides new evidence for a modulatory role of the delta opioid receptor using this novel approach.

Animals↗

PubMed1995

Reconstructions of populations of luteinizing hormone releasing hormone neurons in young and middle-aged rats reveal progressive increases in subgroups expressing Fos protein on proestrus and age-related deficits.

Fos expression has been used as a marker of activation of neuroendocrine cells including LHRH neurons. In this study, Fos protein was localized within LHRH neurons in young and middle-aged rats to trace the temporal and spatial pattern of LHRH neuronal activation associated with the preovulatory LH surge. Animals were killed during the late morning, afternoon, and evening of proestrus. Dual immunocytochemical protocols localized LHRH and LHRH/Fos neurons, and computer-assisted methods were used to reconstruct forebrain populations of single- and double-labeled LHRH neurons. Although a significant increase in the number of LHRH/Fos neurons was noted by evening in both age groups, a greater increase was observed in young (12% in morning, 28% in afternoon, and 62% by evening) compared with aging females (5% in morning, 10% in afternoon, and 40% by evening). Reconstructions of LHRH and LHRH/Fos neurons revealed time- and age-dependent differences in Fos expression within LHRH neurons. In young females, LHRH/Fos neurons were restricted to central regions of the population of LHRH neurons on the morning of proestrus. By evening, Fos expression was also observed in more peripheral and caudal LHRH neurons. In middle-aged females, Fos expression was restricted to ventral subgroups of LHRH neurons on the afternoon of proestrus. By evening, more LHRH neurons contained Fos protein, however, few were located in the dorsal aspect of the population. These data trace the progressive increase in activation of LHRH neurons during the preovulatory LH surge in young females and reveal deficits in this pattern of activation by middle age.

Aging↗

PubMed1994

A reduced proportion of luteinizing hormone (LH)-releasing hormone neurons express Fos protein during the preovulatory or steroid-induced LH surge in middle-aged rats.

Results of previous studies suggest that altered patterns of LHRH neurosecretion contribute to attenuated LH surges and the eventual cessation of ovulation in aging female rats. The present study compared evidence of LHRH neuronal activation in conjunction with the preovulatory and steroid-induced LH surge in young and middle-aged animals to determine whether age-related alterations could be detected. Double immunocytochemical protocols were used to colocalize LHRH and the protein product of the proto-oncogene c-fos, which increases within the nucleus of LHRH neurons in association with spontaneous or induced LH surges. The mean proportion of LHRH neurons containing immunoreactive Fos was higher in the brains of young compared to middle-aged females in association with both the preovulatory (p < 0.01) and the steroid-induced LH surge (p < 0.001). The time course of activation of LHRH neurons was delayed in the brains of aging females, and the proportion of double-labeled LHRH neurons remained elevated longer in the brains of young compared to middle-aged steroid-treated females. Moreover, regional differences in LHRH neuronal activation were observed both within and between age groups. The data presented suggest that reduced LHRH neuronal activation may contribute to the attenuation and eventual loss of preovulatory LH surges in middle-aged female rats.

Aging↗

PubMed1994

Electrical injury--clinical report of 67 cases.

We have reviewed 67 patients of electrical burns treated at Linkou Burn Center of Chang Gung Memorial Hospital from January 1988 to April 1992. There were 2086 acute burn admissions during this period with the proportion of electrical injuries being 3.2%. Their age ranged from 13 to 68 years, with 61% in the age group of 20 to 40 years. Sixty-two (92.5%) of our patients were males. Over 60% of these injuries were work-related. The proportion of high voltage electrical injuries was over 60% in our series. All deceased patients and those patients with major complications were in the high voltage electrical injuries group. Low voltage injuries did not leave any major sequelae. In a mean follow-up of 2 years, 83% of our patients could return to the previous job or change to another work. The overall mortality was 6%.

Accidents, Occupational↗

PubMed1993

Interleukin-4 signals regulating CD23 gene expression in human B cells: protein kinase C-independent signaling pathways.

Signal transduction by IL-4 leading to the activation of CD23(Fc epsilon RII) gene expression using human tonsillar B cells was studied. IL-4 stimulated CD23 mRNA transcription within hours (1-4 hr) which preceded the later induction of cell surface CD23. The induction of CD23 gene transcription by IL-4 was not adversely affected by cycloheximide, suggesting that post-translational modifications are accounted for the gene activation. PKC activators (PMA, diacylglycerol, indolactam) were effective inducers of CD23 gene expression, whereas calcium ionophores were not. PMA and IL-4 also displayed similar induction kinetics for CD23 mRNA. However, the signaling pathways utilized by the two agents appear distinct as shown by (1) cotreatment of IL-4 and PMA caused CD23 gene expression over the maximum level inducible by each agent alone and (2) unlike the PMA-induced CD23 expression, the IL-4-induced expression was not affected by PKC inhibitors. These results strongly suggest that IL-4 signals leading to CD23 gene activation are mediated via a PKC-independent pathway. A possible role of tyrosine kinases in the regulation of CD23 expression is discussed.

B-Lymphocytes↗

PubMed1993

Mechanism of interferon-gamma down-regulation of the interleukin 4-induced CD23/Fc epsilon RII expression in human B cells: post-transcriptional modulation by interferon-gamma.

It has been reported that the interleukin 4 (IL-4) specific induction of cell surface CD23 (Fc epsilon RII) is down-regulated by interferon-gamma (IFN-gamma) in monocytes and B cells. However, the molecular level at which the inhibition occurs seems to vary depending on the cell types. In normal human B cells, IFN-gamma inhibits the IL-4 induced de novo synthesis of CD23 at the level of gene expression. Analysis of inhibition kinetics suggested a rapid signal transmission by IFN-gamma. Yet the inhibitory action of IFN-gamma on CD23 mRNA accumulation appeared as a secondary response requiring a new protein synthesis. Through nuclear run-on transcription and mRNA stability studies, we further demonstrate that the IL-4 induced CD23 gene expression is down-regulated by IFN-gamma mainly at post-transcriptional levels by decreasing mRNA stability.

B-Lymphocytes↗

PubMed1992

Interleukin-6 is released in the cutaneous response to allergen challenge in atopic individuals.

The mechanisms responsible for cutaneous response to antigen are complex. Interleukin-1 (IL-1) and interleukin-6 (IL-6) are proinflammatory cytokines that share many properties. Previous studies with a blister-chamber model have demonstrated IL-1 to be produced in the cutaneous response to antigen. Since IL-2 production by activated T cells and IL-6 production by macrophages are both stimulated by IL-1, we hypothesized that IL-2 and IL-6 may be involved in the cutaneous late-phase response (LPR) to antigen. We examined antigen-challenged sites for IL-2 immunoreactivity (ELISA) but found no difference between antigen- and diluent-challenged skin sites (N = 4). Since IL-2 has been demonstrated to be produced in response to IL-1 and IL-1 activity has been demonstrated to be greatest between hours 10 and 12, we speculated that IL-2 might not be detected until after hour 12. We were unable to demonstrate any increase in IL-2 production, even by extending our studies to 24 hours in two subjects. Antigen-challenged, skin blister-chamber fluids from atopic subjects demonstrated the appearance of IL-6 (ELISA) in pooled samples representing hours 1 1/2, 3 1/2, 5 1/2, and 7, but not at diluent control sites (p less than 0.05; N = 6). IL-6 reached a median peak of 0.66 ng/ml at 3 1/2 hours. Median levels of IL-6 fell to baseline at 8 hours, followed by a second peak of 0.25 ng/ml at hour 10. Three distinct patterns of IL-6 release were noted: early release of IL-6 followed by a sustained slower rise that peaked at hour 9 before declining to baseline levels at 12 hours, early release of IL-6 followed by a fall to baseline levels at hours 7 to 9 with a second smaller peak at hours 9 to 11, and isolated early release of IL-6. Early IL-6 production correlated with late histamine production (R = 0.801; p = 0.06), and late IL-6 production correlated with eosinophil influx (R = 0.813; p = 0.05). The area of the LPR at skin test sites correlated with early IL-6 peak levels (R = 0.977; p = 0.004) and with total early IL-6 production (R = 0.885; p = 0.05), but not with late IL-6 production.(ABSTRACT TRUNCATED AT 400 WORDS)

Allergens↗