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Biomedical subjects

K Chung

Publications and source records attributed to K Chung.

At least 73 records · Page 4Linked to original sources

Comparison of the mutagenic specificity induced by four nitro-group-containing aromatic amines in Salmonella typhimurium his genes.

Four nitrated aromatic amines (2-nitro-p-phenylenediamine [2NPD], 3-nitro-o-phenylenediamine [3NPD], 4-nitro-o-phenylenediamine [4NPD] and 4,4'-dinitro-2-biphenylamine [DNBA]) are direct-acting mutagens in Salmonella typhimurium strain TA100. These compounds were tested further using the Xenometrix strains of S. typhimurium: TA7001, TA7002, TA7003, TA7004, TA7005, and TA7006, with and without S9 mix in the plate incorporation assay. The direct-acting mutagenicity of 2NPD, 4NPD, and DNBA was detected with TA7002, TA7004 and TA7005. 2NPD and DNBA showed some activity in TA7006; DNBA also showed some activity in TA7003. Mutagenicity was generally decreased in these strains when S9 was added. 3NPD was mutagenic in TA7004 without S9 and in TA7005 with and without S9. These data suggest that 2NPD, 4NPD and DNBA induced TA-->AT and CG-->AT transversions as well as GC-->AT transitions in the his gene. 3NPD induced CG-->AT transversions and GC-->AT transitions. 2NPD and DNBA also induced a small portion of CG-->GC transversions.

Amines↗

Effects of timing and heat treatment of silanated porcelain on the bond strength.

This study examined the effects of postsilanization interval and heat treatment on shear bond strength of composite resin to porcelain. One hundred and eighty square-shaped specimens were fabricated and sanded flat sequentially. The specimens were then randomly placed into six groups and 18 subgroups of 10 specimens each. An experimental and three commercially available silane systems, including two one-mix and one two-mix systems, were tested in this study. No silane treatment specimen was used as control. Specimens from the experimental and one of the Mirage groups were selected for heat treatment for 60 min at 60 degrees C. Three post-silanization intervals were scheduled. After incubation, a dual cure composite resin (Mirage FLC) was placed on the silanated surfaces and light-cured. All specimens were stored in 37 degrees C, 2% saline solution for 1 week and subjected to shear test using an Instron machine with cross-head speed of 5 mm/min. ANOVA and Scheffe tests were used to analyse data with confidence level at 95%. The mean values of the shear bond strengths ranged from 2.8 to 23.3 MPa. All groups showed significantly higher bond strength than the control group at the 3 min, 24 h and 1 week post-silanization periods (P < 0.05). Heat treatment groups recorded an increase in the shear bond strength and maintained significantly higher bond strength values (P < 0.05). In conclusion, bond strength of composite resin to porcelain resulting from silanization of porcelain increased after heat treatment and during the post-silanization periods. The bond strength also varied for different silane coupling agents tested in this study especially in the one-mix system.

Analysis of Variance↗

Differential response of obese gene expression from fasting in bovine adipose tissues.

To understand the molecular mechanism for intramuscular fat deposition, the expression of the obese gene was examined in response to fasting. Food deprivation for 48 h induced a decrease in the level of obese mRNA in pooled adipose tissues (abdominal, perirenal, subcutaneous, intermuscular and intramuscular). The expression of obese mRNA was examined for individual adipose tissue from several fat depots. It was highly expressed in perirenal adipose tissue, but fasting did not affect its expression level in this tissue. Moderate levels were detected in subcutaneous and intermuscular adipose tissues, and a fasting-induced decrease in obese mRNA was apparent in these tissues. The expression level of the obese gene in intramuscular adipose tissue was very low and did not respond to fasting.

Adipose Tissue↗

Ectopic discharges and adrenergic sensitivity of sensory neurons after spinal nerve injury.

At various times after spinal nerve injury, dorsal root ganglia (DRGs) from injured segments were removed with attached dorsal roots and spinal nerves. In an in vitro recording chamber, spontaneously active units were recorded from teased dorsal root fascicles. Sustained spontaneous activity could first be recorded at 13 h after the ligation, but adrenergic sensitivity did not develop until 24 h after the injury. Almost all recorded activity originated from the DRG. Thus, the DRG is the most common site for ectopic discharge generation after spinal nerve injury and separate mechanisms seem to be involved in the development of ectopic discharges and adrenergic sensitivity.

Action Potentials↗

Expression of neurotrophin mRNAs in the dorsal root ganglion after spinal nerve injury.

Neurotrophins have specificity toward distinct subpopulations of dorsal root ganglion (DRG) neurons with different neurotrophin receptors. It has been suggested that neurotrophins also play important roles in mature DRG neurons after injury. In the present study, we examined the expression of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin 3 (NT-3) mRNAs in the DRG after a peripheral nerve injury. The data showed that following a spinal nerve ligation, the level of NGF mRNA increased 4 times over the normal level and was maintained at a high level for a period of 3 weeks. The induction of BDNF mRNA was brief (lasting less than 3 days) and lesser in quantity ( approximately 1. 7 times increase) compared to NGF expression. The expression of NT-3 mRNA was not detected either in normal or nerve injured rats. Results suggest that different neurotrophins play different functional roles in the DRG after spinal nerve injury.

Animals↗

Endogenous lectin (RL-29) expression of the autonomic preganglionic neurons in the rat spinal cord.

Rat spinal neurons expressing lectin RL-29 are visualized immunohistochemically. RL-29 immunoreactive (RL-29 IR) neurons are found in the lateral parts of laminae V-VII, designated as the intermediolateral cell column (IML) in the thoracic cord, the sacral parasympathetic nucleus (SPN) in the lumbosacral cord, and the dorsomedial nucleus (DMN) of the ventral horn. The majority of RL-29 IR neurons in the SPN are also labeled by a retrograde tracer DAPI applied to the cut L6-S1 ventral roots. These data indicate that the majority of RL-29 IR neurons in the SPN are autonomic preganglionic neurons, thus suggesting that RL-29 can be a useful tool in marking this subpopulation of neurons. In addition, the presence of previously described RL-29 IR primary afferent fibers and terminals in the dorsal parts of the cord are confirmed.

Animals↗

Changes in trkA expression in the dorsal root ganglion after peripheral nerve injury.

Most of the biological effects of nerve growth factor (NGF) are mediated by TrkA, the high affinity receptor for NGF. Previous studies have shown that NGF levels in the dorsal root ganglia (DRG) fluctuate following a peripheral nerve injury. The present study examined changes of TrkA immunoreactivity and trkA mRNA expression in the DRG after segmental nerve ligation. In the normal L5 DRG of the rat, there were, on average, 4700 TrkA-immunoreactive (TrkA-IR) neurons, representing 42% of the total neuronal population. Following L5 spinal nerve ligation, the number of TrkA-IR neurons in the L5 DRG slowly declined, reducing by 25% at 1 week and 35% at 3 weeks postoperation (PO). In contrast, trkA mRNA in these ganglia showed a significant decrease from 3 days to 3 weeks PO and was followed by a full recovery at 2 months PO. The early decrease of trkA mRNA is likely due to deprivation of target-derived NGF, which is caused by nerve ligation, and the recovery might be because substitute sources of NGF become available. Despite the decline in trkA mRNA in the ganglion, 3000 injured DRG neurons sustain TrkA immunoreactivity, suggesting that exogenous NGF can still influence these TrkA expressing neurons, even though they are isolated from the periphery. Accordingly, the effects of endogenous NGF should be as well manifested by local administration of NGF to the ganglion as to the stump of the damaged nerve.

Animals↗

Different strains and substrains of rats show different levels of neuropathic pain behaviors.

This study compared and contrasted the manifestation of neuropathic pain behaviors in several strains of rats. These included ACI, Brown-Norway, Fischer 344, Lewis, Long-Evans, Sprague-Dawley, and Wistar-Furth, all obtained from Harlan Sprague-Dawley Inc. Comparison was also made between two substrains of Sprague-Dawley rats: one from Harlan and the other from Sasco. Neuropathic injury was produced by tightly ligating the left L5 and L6 spinal nerves with the animals under halothane anesthesia. Tests were conducted for 2 weeks to examine behavioral signs representing mechanical allodynia, cold allodynia, and spontaneous pain. There was no difference between strains in any of the tested behaviors before surgery. After neuropathic injury, rats in most groups developed high levels of behavioral signs of various components of neuropathic pain; however, some strains of rats showed weak behavioral signs of neuropathic pain. When a comparison was made between two substrains of Sprague-Dawley rats from two different sources, the ones from Sasco showed weaker behavioral signs than those from Harlan. When comparisons were made between different strains of rats from the same source (Harlan), Brown-Norway and Long-Evans rats showed the smallest magnitude of neuropathic pain behaviors. The data indicate that different strains and substrains of rats display different degrees of pain behaviors, suggesting that strains and substrains are important variables in the development of neuropathic pain after peripheral nerve injury.

Animals↗

Agricultural avermectins: an uncommon but potentially fatal cause of pesticide poisoning.

STUDY OBJECTIVE: Avermectins have been used in the control of parasites and insects; however, human data concerning poisoning are lacking. This study investigated the clinical spectrum of avermectin poisoning. METHODS: A retrospective study was conducted to evaluate patients with avermectin poisoning reported to a poison center from September 1993 through December 1997. RESULTS: Eighteen patients with abamectin (Agri-Mek; 2% wt/wt abamectin) exposure and 1 with ivermectin (Ivomec; 1% wt/vol ivermectin) ingestion were identified. There were 14 male and 5 female patients, ranging in age from 15 to 83 years. Most patients were exposed as a result of attempted suicide (14). Oral ingestion (15) was the most common route of exposure. Four patients were asymptomatic, and 8 had minor symptoms after a mean ingestion of 23 mg/kg abamectin (4.2 to 67 mg/kg), or after dermal and inhalation contact. Seven patients manifested severe symptoms, such as coma (7), aspiration with respiratory failure (4), and hypotension (3), after a mean ingestion of 100.7 mg/kg avermectin (15.4 mg/kg for ivermectin and 114.9 mg/kg for abamectin). All 7 patients received intensive supportive care; 1 patient died 18 days later as a result of multiple organ failure. CONCLUSION: Ingestion of a large dose of avermectin may be associated with life-threatening coma, hypotension, and subsequent aspiration.

Adolescent↗

Heritability of nociception II. 'Types' of nociception revealed by genetic correlation analysis.

Clinical pain syndromes, and experimental assays of nociception, are differentially affected by manipulations such as drug administration and exposure to environmental stress. This suggests that there are different 'types' of pain. We exploited genetic differences among inbred strains of mice in an attempt to define these primary 'types'; that is, to identify the fundamental parameters of pain processing. Eleven randomly-chosen inbred mouse strains were tested for their basal sensitivity on 12 common measures of nociception. These measures provided for a range of different nociceptive dimensions including noxious stimulus modality, location, duration and etiology, among others. Since individual members of inbred strains are identical at all genetic loci, the observation of correlated strain means in any given pair of nociceptive assays is an index of genetic correlation between these assays, and hence an indication of common physiological mediation. Obtained correlation matrices were subjected to multivariate analyses to identify constellations of nociceptive assays with common genetic mediation. This analysis revealed three major clusters of nociception: (1) baseline thermal nociception, (2) spontaneously-emitted responses to chemical stimuli, and (3) baseline mechanical sensitivity and cutaneous hypersensitivity. Many other nociceptive parameters that might a priori have been considered closely related proved to be genetically divergent.

Animals↗

Heritability of nociception I: responses of 11 inbred mouse strains on 12 measures of nociception.

It is generally acknowledged that humans display highly variable sensitivity to pain, including variable responses to identical injuries or pathologies. The possible contribution of genetic factors has, however, been largely overlooked. An emerging rodent literature documents the importance of genotype in mediating basal nociceptive sensitivity, in establishing a predisposition to neuropathic pain following neural injury, and in determining sensitivity to pharmacological agents and endogenous antinociception. One clear finding from these studies is that the effect of genotype is at least partially specific to the nociceptive assay being considered. In this report we begin to systematically describe and characterize genetic variability of nociception in a mammalian species, Mus musculus. We tested 11 readily-available inbred mouse strains (129/J, A/J, AKR/J, BALB/cJ, C3H/HeJ, C57BL/6J, C58/J, CBA/J, DBA/2J, RIIIS/J and SM/J) using 12 common measures of nociception. These included assays for thermal nociception (hot plate, Hargreaves' test, tail withdrawal), mechanical nociception (von Frey filaments), chemical nociception (abdominal constriction, carrageenan, formalin), and neuropathic pain (autotomy, Chung model peripheral nerve injury). We demonstrate the existence of clear strain differences in each assay, with 1.2 to 54-fold ranges of sensitivity. All nociceptive assays display moderate-to-high heritability (h2 = 0.30-0.76) and mediation by a limited number of apparent genetic loci. Data comparing inbred strains have considerable utility as a tool for understanding the genetics of nociception, and a particular relevance to transgenic studies.

Animals↗

Predominant presence of beta-arrestin-1 in small sensory neurons of rat dorsal root ganglia.

Reverse transcription-polymerase chain reaction and western immunoblot analyses were performed to demonstrate the presence of beta-arrestin-1 in rat dorsal root ganglion. beta-Arrestin-1 existed as two alternatively spliced variants, although predominantly in its untruncated form. Several factors affected the visualization of the truncated version on a sodium dodecyl sulfate-polyacrylamide gel; however, the isoform was clearly detected on a two-dimensional gel. We further localized beta-arrestin-1 immunoreactivity in the sensory neurons of the 5th lumbar dorsal root ganglia. Beta-arrestin-1-immunoreactive neurons accounted for approximately 60% of the sensory neurons, and approximately 88% of the beta-Arrestin-1 immunoreactive neurons fell into a category of small neurons having a diameter of 10-30 microm. Members of the arrestin superfamily play crucial roles in the desensitization of G protein-coupled receptors. Our data demonstrating the presence of beta-arrestin-1 in the rat dorsal root ganglion at both messenger RNA and protein levels support the idea that beta-arrestin- participates in receptor desensitization in the sensory neurons. Furthermore, because small-size neurons of dorsal root ganglion are often implicated in nociception, the predominant presence of beta-arrestin-1 immunoreactivity in small-size sensory neurons suggests that beta-arrestin-1 may have a role modulating nociceptive signals.

Alternative Splicing↗

Effect of water storage on the silanization in porcelain repair strength.

This study examined the long-term water storage affect of silanization on shear bond strength of composite resin to porcelain. One hundred and sixty square-shaped specimens were fabricated and sanded flat sequentially with silicone carbide papers. The specimens were then placed into four groups and 16 subgroups of 10 specimens each randomly. Four commercially available silane systems, two one-mix and two two-mix, were tested in this study. Teflon tubes with an internal diameter of 2.97 mm and 2 mm in height were filled with a dual cure composite resin (Mirage FLC), placed on the silanated surfaces and light-cured for 120 s. Specimens were stored in room temperature water and subjected to shear bond strength testing after 24 h, 1 week, 1 month and 3 month periods of immersion. An Instron Universal testing machine with a crosshead speed of 0.5 mm/min was used for the testing. The mean values of the shear bond strengths ranged from 4.38 MPa (24-h period) to 23.90 MPa (3-month period). ANOVA and Scheffe' tests were used to analyse data with confidence level at 95%. All groups recorded an increase in bond strength after one week as compared with the 24-h period (P<0.05). With the exception of a one-mix system, all systems showed significantly higher bond strength at 3 weeks as compared with the 24-h and 1-week water storage periods. In conclusion, bond strength of composite resin to porcelain resulting from silanization of porcelain increased during the experimental period. The bond strength also varied for different silanes used in this study.

Analysis of Variance↗

Effects of the solvents on bond strength of resin bonded porcelain.

Clinical trials of porcelain veneers for chairside colour modifications may require the use of a trial resin with various colours of tints. The bond strength effects of four different solvents used for removal of trial resin from etched porcelain specimens were investigated. Fifty-six porcelain specimens were fabricated, flattened by a metallurgically standard method, etched with hydrofluoric acid and silane treated. The specimens were divided into four groups at random. The trial resin material was cleaned with different solvents prior to bonding of a dual cure resin composite button. After bonding the specimens were stored in water at 37 degrees C for 7 days. Shear bond strength results were as follows: acetone (control) group, 12.9+/-2.9 MPa; ethanol group, 15.1+/-4.6 MPa; methanol group, 11.5+/-2.9 MPa; methylene chloride group, 11.3+/-2.4 MPa. No significant differences were measured (ANOVA, P>0.05). The results indicated that the resin-porcelain bond strengths were not affected by the type of solvent used to remove trial resin. This procedure is recommended for clinical cases when resin composite is used for the try-in of etched porcelain bonded restorations.

Acetone↗

Final report on public health practice linkages between schools of public health and state health agencies: 1992-1996.

Since 1988 there has been a call for enhanced linkages between schools of public health and public health agencies that has prompted schools of public health to develop public health practice initiatives. The University of Illinois at Chicago School of Public Health conducted surveys of schools of public health and of state public health agencies in 1992 to collect baseline data on practice initiatives undertaken by academe and governmental public health agencies to enhance collaboration; follow-up surveys were undertaken in 1993, 1994 and 1996. This article describes the trends and implications of this survey of practice linkages involving schools of public health and state health agencies.

Cooperative Behavior↗

Receptor subtype mediating the adrenergic sensitivity of pain behavior and ectopic discharges in neuropathic Lewis rats.

Receptor subtype mediating the adrenergic sensitivity of pain behavior and ectopic discharges in neuropathic Lewis rats. We attempted to identify the subtype of alpha-adrenergic receptor (alpha-AR) that is responsible for the sympathetic (adrenergic) dependency of neuropathic pain in the segmental spinal injury (SSI) model in the Lewis strain of rat. This model was chosen because our previous study showed that pain behaviors in this condition are particularly sensitive to systemic injection of phentolamine (PTL), a general alpha-AR blocker. We examined the effects of specific alpha1- and alpha2-AR blockers on 1) behavioral signs of mechanical allodynia, 2) ectopic discharges recorded in the in vivo condition, and 3) ectopic discharges recorded in an in vitro setup. One week after tight ligation of the L5 and L6 spinal nerves, mechanical thresholds of the paw for foot withdrawals were drastically lowered; we interpreted this change as a sign of mechanical allodynia. Signs of mechanical allodynia were significantly relieved by a systemic injection of PTL (a mixed alpha1- and alpha2-AR antagonist) or terazosin (TRZ, an alpha1-AR antagonist) but not by various alpha2-AR antagonists (idazoxan, rauwolscine, or yohimbine), suggesting that the alpha1-AR is in part the mediator of the signs of mechanical allodynia. Ongoing ectopic discharges were recorded from injured afferents in fascicles of the L5 dorsal root of the neuropathic rat with an in vivo recording setup. Ongoing discharge rate was significantly reduced after intraperitoneal injection of PTL or TRZ but not by idazoxan. In addition, by using an in vitro recording setup, spontaneous activity was recorded from teased dorsal root fibers in a segment in which the spinal nerve was previously ligated. Application of epinephrine to the perfusion bath enhanced ongoing discharges. This evoked activity was blocked by pretreatment with TRZ but not with idazoxan. This study demonstrated that both behavioral signs of mechanical allodynia and ectopic discharges of injured afferents in the Lewis neuropathic rat are in part mediated by mechanisms involving alpha1-ARs. These results suggest that the sympathetic dependency of neuropathic pain in the Lewis strain of the rat is mediated by the alpha1 subtype of AR.

Adrenergic alpha-Agonists↗

Intraventricular infusion of nerve growth factor as the cause of sympathetic fiber sprouting in sensory ganglia.

OBJECT: The results of previous clinical trials have indicated that intraventricular infusion of nerve growth factor (NGF) in patients with Alzheimer's disease is frustrated by the appearance of weight loss and diffuse back pain. The present study tested whether NGF induces sympathetic sprouting in sensory ganglia. Such sprouting has been implicated in previous studies as a possible mechanism of sympathetically maintained pain in neuropathic animals. METHODS: Nineteen Long-Evans rats underwent intraventricular infusion of either artificial cerebrospinal fluid (ACSF; seven animals) or NGF (12 animals). After 14 days of infusion, the sensory ganglia of the trigeminal nerve and the C-2, C-8, T-1, L-4, and L-5 dorsal roots were examined for sympathetic sprouting by using tyrosine hydroxylase immunohistochemical analysis. CONCLUSIONS: In the animals receiving NGF, 52 of 144 ganglia showed sympathetic fiber sprouting. In the control animals receiving ACSF, only two of 72 ganglia showed minor sympathetic fiber sprouting. A preferential sprouting of sympathetic fibers was demonstrated at lower lumbar ganglia compared with the cervical and thoracic ganglia. The data presented here demonstrate that in the rat intraventricular NGF infusion caused sympathetic sprouting in dorsal root ganglia (p < 0.01). These findings may have importance both for the treatment of Alzheimer's disease and the understanding of neuropathic pain.

Alzheimer Disease↗