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Biomedical subjects

S L Chang

Publications and source records attributed to S L Chang.

At least 55 records · Page 3Linked to original sources
PubMed1998

The commissioning of a flexible low-cost multipurpose X-ray beamline at SRRC.

A low-cost multipurpose X-ray beamline has been commissioned at the bending magnet B15 of the Synchrotron Radiation Research Center (SRRC). The beamline is constructed in such a way to accommodate the various needs of small research consortia, from universities or research institutes, whose requirements of a beamline facility are quite diverse while under limited funding support. Flexibility is the special feature of this beamline. It is capable of performing quick test measurements without a prolonged reviewing process. Switching between different techniques, such as white-beam irradiation, EXAFS and X-ray scattering, can be achieved within 1 h. Novel experiments, such as energy-dispersive small-angle scattering experiments and energy-dispersive reflectivity measurements, can also be performed.

Journal Article↗
PubMed1998

Role of type III collagen in bladder filling.

The function of the urinary bladder is to store urine at low pressure and expel it periodically. To accomplish this, it must have the appropriate structural properties to accommodate slow but continuous volume changes. While much is presently known about the functional measurements of compliance, relatively little is known about the structural basis of compliance. In the present study, immunohistochemistry has been used to localize type III collagen fibers in the bladder wall at different intravesical volumes. To improve the resolution of these fibers, confocal microscopy was utilized to determine the changes in type III collagen fiber orientation and correlate them with the degree of mechanical distension of the bladder wall at partial and full capacity. We demonstrate that there were significant changes in both the orientation and conformation of type III collagen fibers during bladder filling. These observations support the view that volume accommodation in the bladder is achieved by changes in the arrangement of type III collagen. These data suggest that abnormal deposition or arrangement of type III collagen fibers can have an impact on normal bladder function.

Animals↗
PubMed1998

Cocaine infusion increases interferon-gamma and decreases interleukin-10 in cocaine-dependent subjects.

The effects of cocaine infusion (40 mg) on interferon-gamma (IFN-gamma) and interleukin-10 (IL-10) cytokine secretion were examined in 15 cocaine-dependent subjects. Pre- and postcocaine infusion peripheral blood mononuclear cells (PBMC), stimulated with phytohemagglutinin A, were cultured for 48 h and the cytokines in the supernatant measured by enzyme-linked immunosorbent assay. Cocaine infusion, but not saline infusion, increased IFN-gamma secretion and decreased IL-10 secretion, while, in PBMC collected simultaneously from control subjects, secretion of these cytokines was unaltered. Baseline IFN-gamma levels were lower and IL-10 levels higher in addicted subjects compared to those in control subjects. White blood cell and lymphocyte number and CD4(+) and CD8(+) counts were all increased following cocaine infusion. In vitro cocaine treatment of PBMC from addicted subjects suppressed both IL-10 and IFN-gamma secretion. These data suggest that acute cocaine administration, via both central and peripheral effects, may enhance Th1-type immune responses and inhibit Th2-type responses.

Adult↗
PubMed1998

Cocaine enhances monocyte migration across the blood-brain barrier. Cocaine's connection to AIDS dementia and vasculitis?

Cocaine has wide-ranging effects on the immune and neuroendocrine systems (Fiala et al., 1996) resembling an inflammatory "stress" response with upregulation of pro-inflammatory cytokines and stimulation of the HPA axis (Gan et al., 1997). Cocaine abuse has also been associated with vascular pathology, including vasculitis, vasospasm and hemorrhage. These effects suggest that cocaine could perturb the function of endothelial cells, including the blood-brain barrier, and influence the progression to AIDS in HIV-infected individuals (Shapshak et al., 1997; Goodkin et al., 1997). In order to understand clinical consequences of cocaine abuse, it is important to gain insight into molecular and cellular basis of cocaine's effects on immune and endothelial cells. Cocaine's in vitro effects on (a) permeability, (b) immune cell migration, (c) adhesion molecules, and (d) cytokine expression were investigated in a blood-brain barrier model constructed with brain microvascular endothelial cells and fetal astrocytes with the following results: (a) cocaine and tumor necrosis factor-alpha (TNF-alpha) increased the model's permeability to inulin similarly in a dose-responsive fashion; (b) cocaine (10(-4) to 10(-8_ M) enhanced monocyte migration across the barrier with the maximum increase, approximately 100%, by 10(-5) M cocaine; (c) cocaine treatment also increased the expression of endothelial adhesion molecules, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecules-1 (VCAM-1) and platelet/endothelial cell adhesion molecule-1 (PECAM-1); (d) although the cocaine in vitro effects on cytokine production by mononuclear cells have been difficult to assess due to a heterogeneity in the degree of responsiveness between individuals, the data suggest that mononuclear cells from cocaine addicts are sensitized to in vitro cocaine challenge with hypersecretion of inflammatory cytokines. Cocaine's in vivo manifestations are compatible with these in vitro effects: (A) chronic cocaine treatment of rats significantly increased rolling white blood cell flux, leukocyte-endothelium adhesion, and ICAM-1 expression in the mesentery (House et al., 1996); (B) cocaine injection to cocaine-dependent subjects tipped the balance of cytokine secretion by mononuclear cells to Th1-type (Gan et al., 1997), and (C) cocaine injection stimulated the hypothalamic-pituitary axis (HPA) to increase both anti- and pro-inflammatory hormonal secretion. Collectively, these results suggest that the immune effects of cocaine on endothelial, immune and neuroendocrine cells impair the function of the blood-brain, barrier, increase cell emigration from the blood vessels, in particular into the brain, and may cause vasculitis. These effects could also increase importation of HIV-1 into the brain.

AIDS Dementia Complex↗
PubMed1998

The effects of interaction between morphine and interleukin-1 on the immune response.

The findings presented here clearly indicate an association between opioid- and cytokine-dependent systems. Exposure to exogenous opioids can produce profound effects on IL-1-mediated immune responses. Chronic exposure to morphine appears to disrupt the brain-immune axis by desensitizing the IL-1 activation of the HPA axis, and consequently potentiate the LEA response to IL-1. On the other hand, endogeneous IL-1, secreted in response to disease or stress, may alter the endogenous opioid pathway by inducing the expression of opioid receptors in endothelial cells. Clinically, the potential impact on the body's defense mechanisms resulting from the interaction between opioids, such as morphine, and cytokines, such as IL-1, can be substantial. Further investigation of this interaction is essential to understanding the extent of damage in human body caused by drugs of abuse, such as morphine.

Animals↗
PubMed1998

Interleukin-1 induces the expression of mu opioid receptors in endothelial cells.

Immunocytokines, such as interleukin-1 (IL-1), have been shown to be involved in the activation and/or induction of a variety of transcription factors which may modulate the expression of genes possessing DNA binding sites on which these transcription factors act. The promoter DNA sequence of the mu opioid receptor gene contains IL-1 response elements such as NF-IL6, and, therefore, the receptor gene may be responsive to IL-1. To investigate the effect of IL-1 on the opioid receptor gene, the in vitro expression of mu opioid receptor mRNA in neural microvascular endothelial cells (NMVEC) was determined before and after IL-1 treatment. PCR analysis revealed that there was virtually no mu opioid receptor expression at basal levels and no increase after either IL-1alpha or IL-1beta treatment. However, simultaneous treatment with both IL-1alpha and IL-1beta increased mu opioid receptor expression. This upregulation of mu opioid receptor expression provides direct evidence of a relationship between opioid and cytokine actions, and suggests that opioid-dependent pathways may be modulated in the disease state.

Cells, Cultured↗
PubMed1998

Dose reconstruction for residents living in 60Co-contaminated rebar buildings.

The first 60Co-contaminated rebar building was discovered in Taipei city in 1992. As of 18 July 1997, 144 buildings with 1,327 housing units were confirmed to contain 60Co-contaminated rebars. All these reinforced concrete buildings were constructed between 1982 and 1984. Thousands of residents have been exposed to ionizing radiation of various degrees. Preliminary assessments by the Atomic Energy Council showed that the accumulated maximal doses ranged from a few mSv to several Sv. The purpose of this work was to reconstruct more reliable individual doses for epidemiologic and medical uses. This reconstruction provided the best estimated doses as well as conceivable upper and lower bounds. The variation of residential day-life activities by individual members in a family was considered according to their sex, age, profession, etc. Intensive data on exposure rates were collected using thermoluminescent dosimeters positioned at 1 m height and 1 m x 1 m intersections with additional measurements at special locations such as bed, sofa, dining table, etc. Thermoluminescent dosimeter measurements were performed in all 24 residences studied in this work. This showed that the Atomic Energy Council maximal doses were 2-6 times higher than the present best estimated doses. Among all family members, elders and housewives received the highest doses; children received the lowest doses. The difference in doses among all family members belonging to different cohort categories is within a factor of two.

Adolescent↗
PubMed1998

Transdermal iontophoretic delivery of hydrocortisone from cyclodextrin solutions.

Enhanced skin penetration of hydrocortisone can be desirable for treatment of several diseases. Transdermal iontophoretic delivery of hydrocortisone solubilized in an aqueous solution of hydroxypropyl-beta-cyclodextrin (HP-beta-CyD) was investigated and compared with chemical enhancement of co-solvent formulations. The passive permeation of hydrocortisone through human cadaver skin was higher when delivered from propylene glycol than when delivered after solubilization in an aqueous solution of HP-beta-CyD. However, the iontophoretic delivery of the 1% hydrocortisone-9% HP-beta-CyD solution was higher than the amount delivered passively by the 1% hydrocortisone-propylene glycol formulation, even if oleic acid was used as a chemical enhancer. Iontophoretic delivery of 1% hydrocortisone with 3% or 15% HP-beta-CyD was lower than that of the 9% HP-beta-CyD solution. These data suggest that free hydrocortisone rather than complexes is predominantly delivered iontophoretically through the skin and the HP-beta-CyD complex serves as a carrier to replenish depletion of hydrocortisone. HP-beta-CyD prevents hydrocortisone from forming a skin reservoir. Iontophoresis provides better enhancement of transdermal delivery of hydrocortisone than the chemical approach when just sufficient HP-beta-CyD is added to solubilize the hydrocortisone.

Administration, Cutaneous↗
PubMed1998

Early patterning of prelimbic cortical axons to the striatal patch compartment in the neonatal mouse.

The striatum receives excitatory input from virtually the entire cerebral cortex. In the adult, this input is segregated into two functionally distinct compartments of the striatum, the patch (striosome) and matrix regions. This study determined whether the patterning of corticostriatal afferents from the prelimbic cortex to the striatal patch compartment develops during the early period of collateral formation or instead at the time of peak synaptogenesis. Initial formation of corticostriatal axon collaterals was observed by embryonic day (E) 19. Quantification of corticostriatal collaterals revealed a significant increase in the number and complexity of collateral branches at postnatal day 6 as compared to E19. Concomitant with the increase in collateral branching, a heterogeneous pattern of collateralization consisting of parallel rows of corticostriatal collaterals was observed in the medial striatum. In addition to the rows, clusters of corticostriatal axons occurred more laterally. These clusters colocalized with patches of dense tyrosine hydroxylase-positive fibers, a marker for the striatal patch compartment in the neonatal mouse. Together, these data indicate that corticostriatal patterning occurs during the period of early axon collateralization resulting in a segregation of corticostriatal axon collaterals from the prelimbic cortex to the striatal patch compartment.

Animals↗
PubMed1998

Temporal expression of elastic fiber components in bladder development.

Fetal and postnatal bovine bladders were examined for expression of elastic fiber components by immunohistochemistry as well as by measurement of steady state mRNA levels. Expression of fibrillin-1, microfibril-associated glycoprotein (MAGP) and elastin during the fetal period were compared with that of postnatal two year old animals (heifers) and adults. Each bladder was separated into two distinct tissue samples: 1) the outer smooth muscle layer (detrusor) and 2) the inner epithelium (urothelium) lined lamina propria (urotherial-lamina propria). Each of these samples was analyzed separately. Distribution of the elastic fiber components, determined by immunohistochemistry with matrix-specific antibodies, was different depending upon the region of the bladder wall examined and its developmental stage. In particular, MAGP and fibrillin-1 were conspicuously present in the urothelium during the later fetal stages. RNA products of elastic fiber genes were detectable both in the detrusor smooth muscle and urothelial-lamina propria fractions. The highest level of expression occurred in the urothelial-lamina propria fraction during the late second-early third trimester. Elastin expression was different from that of MAGP and fibrillin-1. The highest levels of steady-state elastin mRNA occurred at the earliest developmental stages examined and then progressively decreased through term. A high level of elastin expression occurred within the inner or lamina propria layer of the bladder. Since this layer is the functional capacitance layer within the bladder, its flexibility is likely related to the structural integration of elastin and associated microfibrillar components.

Animals↗
PubMed1998

Cocaine opens the blood-brain barrier to HIV-1 invasion.

Cocaine abuse has been associated with vasculitis and stroke, and is suspected to influence the progression of AIDS dementia. Cocaine may enhance HIV-1 neuroinvasion by actions directed at the blood-brain barrier. HIV-1 appears to penetrate the human brain microvascular endothelial cell barrier by a paracellular route breached by tumor necrosis factor-alpha (TNF-alpha). Cocaine's effects on the blood-brain barrier were investigated using human brain microvascular endothelial cells and peripheral blood monocytes. Cocaine (10(-5) M and 10(-6) M) increased molecular permeability of the barrier and viral invasion by the macrophage-tropic HIV-1(JR-FL) into the brain chamber. Cocaine also augmented apoptosis of brain endothelial cells and monocytes, increased secretion of four chemokines (interleukin-8, interferon-inducible protein-10, macrophage inflammatory protein-1alpha, and monocyte chemoattractant protein-1) and the cytokine, TNF-alpha, by human monocytes. TNF-alpha enhanced invasion of the brain compartment by macrophage-tropic, lymphotropic, and bitropic HIV-1 strains. These data indicate that HIV-1 neuroinvasion can be increased by (a) cocaine's direct effects on brain microvascular endothelial cells and (b) paracrine effects of cocaine-induced pro-inflammatory cytokines and chemokines on the blood-brain barrier.

Apoptosis↗
PubMed1997

Chronic exposure to morphine, but not ethanol, attenuates the expression of interleukin-1 beta converting enzyme in rat spleen.

IL-1 beta converting enzyme (ICE), a proteolytic enzyme that converts the inactive precursor of interleukin-1 beta (IL-1 beta) to its mature active form, has been abundantly detected in the IL-1 beta producing cells in the spleen. Since IL-1 beta is a potent neuro-endocrine-immuno modulator, alterations in the production of IL-1 beta by an exogenous factor, such as morphine or ethanol, may have deleterious effects on the system as a whole. In this study, we examined the expression of ICE in the spleens of rats given chronic treatment with morphine versus ethanol using reverse transcriptase-polymerase chain reaction (RT-PCR). The expression of ICE in the spleen of rats given chronic morphine was clearly less than that of the animals given placebo, however, it was similar for both rats on ethanol and control diets. These data suggest that chronic use of morphine, but not ethanol, attenuates the expression of ICE in the spleen.

Animals↗
PubMed1997

Developmental expression of interstitial collagen genes in fetal bladders.

Bovine bladders at 3 stages during fetal development were examined for expression of collagens by immunohistochemistry as well as by measurement of steady state mRNA levels. Expression of type I and type III collagens during the fetal period was compared with that of adult cows as well as a young animal (heifer). Each bladder was separated into a detrusor and a urothelial-lamina propria sample which were then analyzed separately. Distribution and fiber arrangement of types I and III collagens were different depending upon the region of the bladder wall examined. Type III collagen, in particular, has a "coiled" appearance which is especially prominent within the lamina propria. Collagen gene expression showed a distinctive pattern which was different for both type I and type III collagen. While type I collagen gene expression peaked during the late second to early third trimester, type III collagen expression progressively decreased throughout the fetal period. In addition, expression of both collagens was greater in the urothelial-lamina propria fractions. These data demonstrate that the pattern of collagen gene expression in the developing bladder is developmentally regulated and is unique to each of the two major structural layers.

Animals↗
PubMed1997

Inflammatory fibroid polyp of the jejunum causing intussusception.

Inflammatory fibroid polyp of jejunum is a very rare nonneoplastic lesion of gastrointestinal tract. We reported a 66-year-old male who presented with abdominal fullness, colicky pain, and vomiting for 4 days. Plain abdomen showed intestinal obstruction with dilated small bowel loops. The exploratory laparotomy was performed under the clinical impression of intussusception caused by small bowel tumor. The diagnosis of an inflammatory fibroid polyp causing jejunojejunal intussusception was confirmed after surgery.

Aged↗
PubMed1996

FOS expression induced by interleukin-1 or acute morphine treatment in the rat hypothalamus is attenuated by chronic exposure to morphine.

Interleukin-1 (IL-1) is a cytokine involved in a variety of biological activities. It has been hypothesized that the immunomodulatory effects of IL-1 are the result of both direct action on immune cells and indirect action on a regulatory cascade mediated through the hypothalamus. Chronic exposure to substances of abuse, such as morphine, appears to modulate immunoresponsiveness by mechanisms not yet defined. The expression of FOS, the protein product of the c-fos proto-oncogene, has been widely used as an anatomical marker for monitoring neuronal activity. We have previously shown that acute treatment with either morphine or IL-1 induces FOS immunoreactivity in the rat brain, including the paraventricular (PVN) and supraoptic (SON) nuclei of the hypothalamus. In this study, using immunocytochemical staining of FOS, we demonstrate that chronic exposure to morphine attenuates the cellular responsiveness to IL-1 and to morphine in the PVN and SON, whereas pretreatment with naloxone, an opiate receptor antagonist, does not reverse the effect of IL-1 on FOS expression. The results not only confirm that the PVN and SON are neuroanatomical sites where the actions of both morphine and IL-1 converge, but also indicate that chronic exposure to morphine may desensitize the cellular response involved in hypothalamic functions through an IL-1-dependent pathway.

Animals↗
PubMed1996

The role of acidic amino acid residues in the structural stability of snake cardiotoxins.

We have recently shown that membrane-related activities of cardiotoxin V from Naja naja atra (CTX A5) are diminished at acidic pH although the overall beta-sheet structure of the molecule is maintained. In order to understand more about the mechanism of inactivation of CTX at acidic pH, we studied the effect of pH and denaturing reagents on the structural stability of CTX. We found, first, pH-induced structural transitions occurred in CTX A5 at two pH values as judged by the CD ellipticity around 195 nm: an increase in the beta-sheet content occurred around pH 4 and followed by a decrease, therein, around pH 2. The pKa of three acidic amino acid residues in CTX A5, i.e., Glu-17, Asp-42, and Asp-59, were determined to be 4.0, 3.2, and below 2.3, respectively, by NMR spectroscopy. The low pKa value of Asp-59 implies salt bridge formation between Lys-2 and Asp-59. Thus, electrostatic interaction may stabilize the three loop structure in addition to the hydrogen bonds between N- and C-termini of CTX molecule. Second, 2,2,2-trifluoroethanol (TFE) and guanidinium chloride (GdmHCI) were found to induce alpha-helical and random coil formation, respectively, in CTX A5 and eight other beta-sheet CTXs. Comparison of the relative potencies of TFE and GdmHCI to induce structural changes suggests that the amino acid residue located at position 17 plays a role in the structural stability. Specifically, CTXs containing negatively charged Glu-17 are least stable. It is suggested that Glu-17 may perturb the interaction between Lys-2 and Asp-59, and thus the overall stability of beta-sheet, in the presence of denaturing reagent. In conclusion, the perturbed structural stability of CTXs may partially explain the lower activity CTX exhibits at acidic pH. A structural model to account for the unfolding and refolding of CTX molecules without the breaking of disulfide bonds is also proposed.

Amino Acid Sequence↗