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Biomedical subjects

J R Chen

Publications and source records attributed to J R Chen.

At least 73 records · Page 4Linked to original sources

Prevalence of familial systemic lupus erythematosus in Taiwan.

A survey of familial occurrence of systemic lupus erythematosus (SLE) was conducted among 728 first-degree relatives of 102 SLE patients. All of the patients were from the rheumatology ward or outpatient clinic of Kaohsiung Medical College. Ten familial members (9.80%) in the 102 patients with SLE suffered from the same disease. Among them, one (20%) was from the 5 male patient families and 9 (9.28%) were from the 97 female patient families. The overall prevalence of SLE in first-degree relatives of SLE patients was 1.37% (10/728).

Female↗

Intraoperative transesophageal echocardiography.

Intraoperative echocardiography in patients undergoing cardiac surgery was first described in 1972. Interest in intraoperative echocardiography has grown in recent years due to the extensive information provided by 2-dimensional (2-D) and color-flow Doppler imaging via the transesophageal approach. The value of this technique also has been verified in large clinical studies involving patients undergoing cardiac surgery. Intraoperative transesophageal echocardiography (TEE) is very useful in preoperative formulation of surgical plans and in immediate post-operative assessment of surgical results in patients undergoing valve surgery.

Echocardiography↗

Correlation of tumor necrosis factor alpha levels with disease activity of rheumatoid arthritis.

In this study, positive correlations were found between tumor necrosis factor alpha (TNF alpha) levels in the sera of rheumatoid arthritis (RA) patients and the duration of morning stiffness, joint tenderness count, the Ritchie articular index and erythrocyte sedimentation rate. Further, higher mean grades of disease activity of RA were accompanied by correspondingly higher levels of serum and synovial TNF alpha. In the longitudinal study, when the disease activity of RA decreased after treatment, serum TNF alpha levels also decreased. This suggests that the levels of serum and synovial TNF alpha correlate positively with RA disease activity. The levels of TNF alpha in synovial fluid were significantly higher in RA and acute gouty arthritis (GA) patients than in osteoarthritis (OA) patients. This suggests that joint inflammation in inflammatory arthritis related to local production of TNF alpha in the joint cavities. Serum TNF alpha levels in RA patients were significantly higher than those in the OA patients; no statistical difference was found between acute GA and OA patients.

Arthritis, Gouty↗

Polyamine catabolism in rodent and human cells in culture.

N1-Acetylspermidine (N1AcSpd) accumulates in late exponential phase, or after certain stresses such as heat shock, in both human tumour (A549) and rodent (HTC, CHO) cells, grown in medium containing an inhibitor of the FAD-dependent polyamine oxidase (PAO). Inhibition of PAO has little effect on cell growth or on the cellular content of the major polyamines, putrescine, spermidine or spermine, found in proliferating cells in culture, but decreases cellular putrescine content in heat shocked cells. Putrescine and spermidine are generated when N1AcSpd or N1-acetylspermine (N1AcSpm) respectively is added to either human or rodent cells depleted of the former amines by alpha-difluoromethylornithine. N1AcSpm is formed in polyamine-depleted human A549 cells when N1AcSpd is added to cultures treated with the PAO inhibitor. This reaction does not occur in either rodent line, suggesting that N1AcSpd can be converted directly into N1AcSpm in human, but not rodent, cells under specific conditions. The data presented demonstrate that a variety of human and rodent cells express PAO activity and catabolize polyamines by a mechanism which includes PAO. PAO activity is of little consequence to proliferating A549, HTC or CHO cells in culture, but does produce new putrescine in both late-exponential-phase and heat-shocked cells. These findings suggest that polyamine catabolism is part of a general response of both rodent and human cells to a variety of environmental and physiological stresses.

Animals↗

Proliferative responses of B cells from elderly humans: abnormalities in early responsiveness are related to alterations in B cell activation molecules.

Age-related changes are known to occur in the function of human T cells but less information is available about human B cells during aging. In this study, B cells obtained by negative selection from the peripheral blood of young and elderly subjects were stimulated in vitro with anti-IgM, Staphylococcus aureus Cowan strain I (SAC), or Staph protein A (SpA) from SAC. Their proliferative capabilities with and without lymphokines were quantitated by [3H]thymidine uptake. Stimulated B cells from elderly subjects were reduced in their overall ability to sustain normal levels of proliferation observed for B cells from young subjects. However, time course studies analyzing early proliferative responses revealed that B cells from one subset of elderly displayed persistent hyporesponsiveness whereas another subset demonstrated early hyperresponsiveness compared to B cells from young adults. Experiments to determine the frequencies of B cells with transferrin receptors (TfR) and low-affinity receptors for IgE (Fc epsilon RII/CD23) showed reductions in the expression of these two glycoproteins among stimulated B cells from elderly with the persistent decreases in proliferation. By contrast, unstimulated B cells of elderly subjects with early hyperresponsiveness displayed increased frequencies of TfR-positive cells, which became reduced after stimulation. Further, stimulated B cells from this group demonstrated greater frequencies of CD23 positive cells than young adults (13 vs. 8%). Thus two distinct profiles of proliferative abnormalities can be observed in early cohorts of activated B cells from elderly humans. The association of these abnormalities with differences in TfR and CD23 suggests that certain age-related defects occur relatively early during the B cell activation scheme.

Aged↗

Lactoferrin in rheumatoid arthritis and systemic lupus erythematous.

Systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) are prototypes of autoimmune diseases. In order to assess the inflammatory status in these conditions, lactoferrin, stored in specific granules of neutrophils, was measured in serum samples of patients with SLE and RA. In RA, the mean serum lactoferrin level (1221.397 +/- 289.476 ng/ml) was significantly higher than that in normal individuals (753.364 +/- 124.063 ng/ml). Surprisingly, there were no significant differences between active SLE (672.682 +/- 356.154 mg/ml) and inactive SLE (642.267 +/- 270.456 ng/ml). Still, no differences were found between normal volunteers, active SLE and inactive SLE. Serum lactoferrin in SLE correlated significantly with CRP (Rs = 0.4089, p less than 0.01), but not with complement level and ANA titers. Thus in RA serum lactoferrin was highly elevated and this indicated that PMN in systemic circulation was activated. In SLE the correlation of CRP with lactoferrin reflected the role of later protein in inflammation.

Adolescent↗

Polyamine regulation of heat-shock-induced spermidine N1-acetyltransferase activity.

The enzyme spermidine/spermine N1-acetyltransferase (N1-SAT) is rapidly induced by heat shock in CHO and A549 cells, with activity declining by 24 h. Depletion of intracellular polyamines by alpha-difluoromethylornithine, an inhibitor of ornithine decarboxylase, blocks this induction. Re-addition of putrescine to these cultures restores the response to heat shock, with a concomitant increase in intracellular N1-acetylspermidine. Diaminopropane is more than twice as effective as the naturally occurring diamine putrescine, suggesting that the propylamine moiety of spermidine is involved in the regulation of N1-SAT induction. Inhibitor studies indicate transcriptional activation and that the enzyme has an apparent half-life of 30-60 min. A second heat shock rapidly inhibits induced N1-SAT activity, which decays with a half-life of 2-3 min. Despite its induction by heat, N1-SAT is not a stable enzyme, suggesting that the activity observed is not due to a modification of an existing peptide, but is due to a transcriptional event, which may justify the inclusion of this enzyme in the family of heat-shock proteins.

Acetyltransferases↗

Subcutaneous injection of 99mTc pertechnetate at acupuncture points K-3 and B-60.

The acupuncture points are known to be morphologically related to the nerves and vessels. Yet the physiological role of blood vessels in the formation of acupuncture points remains unknown. With subcutaneous injection of 99mTc pertechnetate at the acupuncture points K-3 and B-60 and with intra-acupuncture point injection of 99mTc pertechnetate at K-3 and B-60, a lower-limb venography like what was obtained by intravenous injection of 99mTc macroaggregated albumin was demonstrated in the present study. It seems that some acupuncture points do play a role in drainage of tissue fluid from soft tissue into the veins.

Acupuncture Points↗

Estrogen induces the development of autoantibodies and promotes salivary gland lymphoid infiltrates in normal mice.

There are important bidirectional interactions between the immune and the endocrine system. Sex hormones influence the immune system throughout life including postnatal and prenatal stages. For example, we find that administration of estrogen to normal mice markedly augments the ability of CD5+ B cells to express their autoimmune potential by producing increased numbers of plaque-forming cells (APFC) to bromelain-treated mouse erythrocytes (Br-ME). The effect of sex hormones on immune function at the most critical stage of development, the prenatal period, remains unstudied. We hypothesize that an imbalance of the in utero sex hormone microenvironment critically influences the fetal immune system. We have termed this influence immunological imprinting. After birth this imprinting could contribute to immune-mediated disorders. To test this hypothesis, we developed a mouse model in which normal mice were prenatally exposed to estrogens. In preliminary experiments, these mice produced higher numbers of APFC to Br-ME, particularly in the peritoneal cavity cell exudates. Furthermore, mice prenatally exposed to estrogens had accelerated development of autoimmune salivary gland lesions indistinguishable from Sjögren's syndrome (SS) in humans. Further experiments are warranted to confirm these findings. The prenatal effects of estrogen may have relevance for familial and neonatal autoimmune syndromes.

Animals↗

Preformulation study of etoposide: identification of physicochemical characteristics responsible for the low and erratic oral bioavailability of etoposide.

Preformulation studies of etoposide, including pH-solubility profile, partition coefficient, pH-stability profile, and in vitro dissolution kinetics, were conducted to identify the responsible factor(s) for the low and erratic oral bioavailability of etoposide. A stability-indicating high-performance liquid chromatographic (HPLC) assay was used for drug monitoring. The equilibrium aqueous solubility of etoposide at 37 degrees C was low, 148.5-167.25 micrograms/ml, and did not vary over the pH range of 2 to 6. The pH-stability profile indicated rapid degradation of etoposide at pH 1.3 and 10, with degradation half-lives of 2.88 and 3.83 hr, respectively, at 25 degrees C. The half-life at pH 7.30 was 27.72 days. Maximum stability at 25 degrees C was reached at pH 5 to 6.15, with half-lives of 63 and 49.5 days, respectively. The intrinsic dissolution rate, determined on a Wood's apparatus, was slow, 0.0094 mg/min/cm2, while the etoposide partition coefficient between n-octanol and water was 9.94. Therefore, etoposide absorption appears to be dissolution rate limited rather than permeation rate limited. The low equilibrium aqueous solubility, slow intrinsic dissolution rate, and chemical instability at pH 1.3 could account for the low oral bioavailability.

Biological Availability↗

Erythrocyte complement receptor type 1 in patients with systemic lupus erythematosus.

Erythrocyte complement receptor type 1 (CR1) was measured in 71 patients with systemic lupus erythematosus (SLE) and 43 healthy controls. The level of erythrocyte CR1 in patients with SLE was significantly lower than that of controls and correlated with the disease activity of SLE. The more active the disease, the greater the decrease in erythrocyte CR1. The level of erythrocyte CR1 was inversely correlated with the level of circulating immune complexes (CIC) and was positively correlated with C3, CH50, factor B, and factor H. We also found lupus nephritis more frequently in patients with decreased erythrocyte CR1 than in those with normal levels of erythrocyte CR1. Our results suggest that the deficiency of erythrocyte CR1 in patients with SLE is acquired and may serve as a variable of clinical disease activity and may play a role in the pathogenesis of SLE.

Antigen-Antibody Complex↗

Stability-indicating high-performance liquid chromatography of etoposide at various pH conditions using a reversed-phase octyl column.

A stability-indicating reversed-phase high-performance liquid chromatographic assay of etoposide is described. Baseline resolution was achieved with an octyl column for etoposide and its four degradation products, including picrolactone. Peak homogeneity of etoposide was confirmed by quantitating etoposide in degraded samples at 230, 254 and 286 nm, respectively. The assay was reproducible with low within-day and between-day variations. Application of the assay for stability kinetic study was demonstrated. Etoposide in 0.1 M hydrochloric acid (pH 1.29) degraded with a half-life of 2.85 h, which may be responsible for the low oral bioavailability of etoposide.

Chromatography, High Pressure Liquid↗

Evoked potential changes and neuropsychological performance in Parkinson's disease.

Auditory brainstem responses (ABRs) and long latency exogenous and endogenous auditory evoked potentials (EPs) were investigated in 16 patients with Parkinson's disease and 11 control subjects. Parkinson's disease patients were impaired on mental status testing. While ABRs and the N1 component of the auditory EP were of normal latency in Parkinson patients, the endogenous components, N2 and P3, were prolonged. Prolongation of P3 latency in Parkinson's disease correlated with mental status decline, but not with severity of motoric disturbance. Thirteen PD patients also received neuropsychological evaluation. P3 latency was correlated with tests requiring learning or mental manipulation of information, but not with measures of verbal performance, immediate memory, or depression. P3 latency prolongation appears to have a selective relationship to intellectual changes in PD, and may be most sensitive to deficits requiring significant cognitive effort.

Aged↗