Biomedical subjects

K H Yang

Publications and source records attributed to K H Yang.

At least 91 records · Page 5Linked to original sources

PubMed1996

Frankel appliance type III: correct fabrication and case report of skeletal Class III malocclusion.

The functional Regulator was developed by Rolf Frankel of Zwickau, Germany in 1966. The Frankel appliance is used to effect changes in sagittal, transverse, and vertical jaw relationships and remove the abnormal muscle forces in the labial and buccal areas that restrict skeletal growth, thereby, providing an environment which maximizes skeletal growth. Four main types of functional regulators have been described by Frankel. They are the FR I, II, III and IV. One of these appliances, the FR-III, is used in the treatment of skeletal Class III malocclusion. This appliance is used during early mixed dentition stage to correct skeletal Class III malocclusion, characterized by maxillary skeletal retrusion and no mandibular prognathism. The correct fabrication of FR-III is required. In order to do it, one must pay attention to the following: mixing the alginate impression material in a thick consistency, optimum vestibular depth, oblique mounting of casts in the vertiiculator, minimum incisal vertical height of construction bite, sufficient working model trimming, rectangular wax relief of the occlusal margin area in the working cast and a palatal bow of 1.2 mm heavy wire. Finally one case is reported.

Child↗

PubMed1995

Induction of liver cytochrome P450 2B1 by beta-ionone in Sprague Dawley rats.

Induction of liver cytochrome P450 2B1 by beta-ionone was investigated in male and female Sprague Dawley rats. Administration of beta-ionone subcutaneously 72 and 48 hr before sacrificing the animals not only significantly induced the liver microsomal activity of pentoxyresorufin O-dealkylase, but also clearly increased in the level of cytochrome P450 2B1 protein. The induction of cytochrome P450 2B1 by beta-ionone was much greater in male rats than in female rats. A slot blot analysis showed that the mRNA level was increased from 6 hr after treatment with beta-ionone in male rats and from 12 hr after treatment in female rats. Taken together, the present results indicate for the first time that the induction of cytochrome P450 2B1 by beta-ionone might be regulated by the accumulation of mRNAs.

Animals↗

PubMed1995

Suppression of cytochrome P450 (Cyp1a-1) induction in mouse hepatoma Hepa-1C1C7 cells by methoxsalen.

Cultured mouse hepatoma cell line Hepa-1c1c7 cells were treated with methoxsalen to assess the role of methoxsalen in the process of Cyp1a-1 induction. Treatment of Hepa-1c1c7 cultures with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced Cyp1a-1, as indicated by analysis of 7-ethoxyresorufin O-deethylation (EROD) activity and P4501A1 protein. When methoxsalen and TCDD were both added to cultures, TCDD-inducible EROD activity was greatly suppressed by methoxsalen in a dose-dependent manner. We find that treatment of Hepa-1c1c7 cells with methoxsalen inhibited CYP1A1 mRNA induction by TCDD as well as the concomitant increase P4501A1 protein. Formation of DNA-protein complexes between the dioxin receptor and its DRE target was inhibited by methoxsalen, as determined by gel mobility shift assays using oligonucleotides corresponding to DRE 3 of the Cyp1a-1 gene. These results suggest that the inhibitory action of methoxsalen on TCDD induction of the Cyp1a-1 gene expression in Hepa-1c1c7 cells might be antagonism of the DNA binding potential of nuclear dioxin receptor.

Animals↗

PubMed1995

Cyclic AMP is an essential factor in immune responses.

In the present studies, cAMP, a secondary messenger historically viewed as a negative mediator of immune responses, was demonstrated to possess immunoenhancing activity at low concentrations. In parallel experiments the adenylate cyclase inhibitor, 2',3'-dideoxyadenosine, produced a marked inhibition of humoral and proliferative immune responses suggesting that cAMP at physiologically relevant concentrations acts as a critical second messenger in immune responses. Direct addition of dibutyryl cAMP (10-100 microM), a membrane permeable cAMP analog, to mouse spleen cell cultures produced a marked and dose-related increase (25-100%) in humoral immune responses as measured by the primary IgM antibody forming cell response to the antigen, sheep erythrocytes. Over a similar concentration range, dibutyryl cAMP (5-50 microM) also dose-dependently enhanced (25-50%) phorbol 12-myristate 13-acetate/ionomycin-stimulated lymphoproliferation. Incubation of spleen cells with 2',3'-dideoxyadenosine (40-80 microM), an adenylate cyclase inhibitor, for 30 min depressed significantly the basal level of intracellular cAMP. 2',3'-dideoxyadenosine treatment also significantly decreased both the antibody forming cell response and the proliferative response in a dose-dependent manner. Interestingly, the antibody forming cell response exhibited significantly greater sensitivity to inhibition by 2',3'-dideoxyadenosine than the lymphoproliferative responses. The critical role for cAMP as a positive immunoregulatory signal is further supported by the fact that the immunosuppression by 2',3'-dideoxyadenosine could be reversed completely in the antibody forming cell response to sheep erythrocytes through the addition of dibutyryl cAMP into the culture medium. Partial but not complete reversal of the inhibitory effects of 2',3'-dideoxyadenosine on lymphoproliferation was also demonstrated by dibutyryl cAMP. Taken together, these results suggest that cAMP acts as a positive regulatory signal for immune responses as indicated by the fact that depletion of intracellular cAMP induces a marked inhibition of humoral and proliferative responses.

Animals↗

PubMed1995

2-Acetylaminofluorene inhibits the activation of immune responses by blocking cell cycle progression at G1 phase.

2-Acetylaminofluorene (AAF) inhibited in a dose dependent manner mouse spleen cell blastogenesis in response to phorbol 12-myristate 13-acetate (PMA)/Ionomycin (Io) activation, the T-cell lectin, concanavalin A (Con A), and following stimulation by alloantigens as measured by the mixed lymphocyte response (MLR). AAF also markedly suppressed the T-cell dependent antibody forming cell (AFC) response to sRBC. AAF was most inhibitory on both the sRBC IgM AFC response and Con A stimulated proliferation when added during the first 24 h following initiation of culture. Direct addition of high concentrations of AAF (100 microM) to spleen cell cultures at 48 h following Con A stimulation produced a very modest inhibition (< 20%) of T-cell proliferation as compared to 90% when added at the time cultures were initiated. Similarly, AAF (75 and 100 microM) produced a greater than 80% inhibition of the in vitro AFC response when spleen cells were sensitized with antigen in presence of AAF. In contrast, no inhibition of the IgM AFC response was produced when AAF (75 microM) was added to spleen cell cultures 48 or 72 h after antigen sensitization. Con A-triggered cell-cycle progression was attenuated at the G1 stage by the addition of AAF (50 and 100 microM) with no inhibition of S to G2/M phase transition. These results suggest that the mechanism of AAF-mediated immune suppression is through a blockade of cell cycle progression from G1 to S phase.

2-Acetylaminofluorene↗

PubMed1995

Role of metabolism in cocaine-induced immunosuppression in splenocyte cultures from B6C3F1 female mice.

Cocaine has been reported to directly suppress the in vitro immune responses at very high concentrations. In the present study, the possible role of metabolism in cocaine-induced immunosuppression was investigated in splenocyte cultures isolated from B6C3F1 female mice. Since cocaine can be metabolized by both esterase and P-450 monooxygenase, we studied the direct effects of cocaine, benzoylecgonine and norcocaine on the in vitro T-dependent antibody response to SRBC. Direct exposure to cocaine only produced a modest (30%) but nonsignificant suppression of the antibody response, while benzoylecgonine, a primary product of metabolism by the esterase pathway, was devoid of activity. In contrast, direct exposure to norcocaine, the initial product of N-demethylation by the P-450 pathway, produced significant suppression at concentrations greater than or equal to 10 microM. Similar results were observed in studies measuring LPS and Con A mitogenicity. Furthermore, a significant suppression was observed when splenocytes were preincubated for 1 h with 1 mM cocaine in the presence of liver S-9 fractions isolated from phenobarbital-induced mice. Meanwhile, no suppression was obtained when splenocytes were preincubated in the presence of untreated S-9 fractions. To characterize the mechanism of our results, the capacity of both untreated and phenobarbital-induced microsomes to produce formaldehyde from cocaine was compared. The N-demethylation of cocaine was NADPH-dependent and phenobarbital-induced microsomes produced approx. 6-times higher amounts of formaldehyde, indicating a greater portion of cocaine could be metabolized through the P-450 pathway to its toxic metabolites. Finally, because benzoylecgonine shares with cocaine the presence of a methyl group on the tropane nitrogen, we also compared the ability of N-demethylation from cocaine and benzoylecgonine in mouse liver microsomes. Our results indicated that benzoylecgonine could not be demethylated as determined by a failure to generate any formaldehyde. These results offer further support that the N-demethylation pathway is a critical step to cause its immunotoxicity.

Animals↗

PubMed1995

Research in biomechanics of occupant protection.

This paper discusses the biomechanical bases for occupant protection against frontal and side impact. Newton's Laws of Motion are used to illustrate the effect of a crash on restrained and unrestrained occupants, and the concept of ride down is discussed. Occupant protection through the use of energy absorbing materials is described, and the mechanism of injury of some of the more common injuries is explained. The role of the three-point belt and the airbag in frontal protection is discussed along with the potential injuries that can result from the use of these restraint systems. Side impact protection is more difficult to attain but some protection can be derived from the use of padding or a side impact airbag. It is concluded that the front seat occupants are adequately protected against frontal impact if belts are worn in an airbag equipped vehicle. Side impact protection may not be uniform in all vehicles.

Accidents, Traffic↗

PubMed1995

The strength of Achilles tendon repair: an in vitro study of the biomechanical behavior in human cadaver tendons.

Eighteen fresh frozen human Achilles tendons were used to test the ultimate strength of repaired tendon "ruptures." Three methods, the Kessler, the Bunnell, and the locking loop, were used to test the initial strength of Achilles tendon repair. The Kessler and Bunnell methods are current standard clinical configurations described for Achilles tendon repair. Under uniform and standardized laboratory conditions, the specimens were loaded to failure. The locking loop suture method was substantially stronger than either of the other two standard configurations. The latter two did not differ significantly from each other. The results of this study may be clinically relevant in terms of the choice of the repair method for surgically treated Achilles tendon ruptures.

Achilles Tendon↗

PubMed1995

Significance of fracture gap in open tibial fracture.

The healing pattern of medial and lateral cortical gap in open transverse or short oblique tibial fractures were retrospectively reviewed in 2 groups; In group A, 16 patients were treated by Judet external fixator in rigid mode. In group B, 6 patients were treated in biocompressive mode, which allowed predominantly longitudinal axial motion. The characteristic healing pattern in group A was gap healing without or with minimal periosteal callus. The healing time and time for consolidation per 1mm gap were significantly longer in medial cortices than lateral ones (p < 0.036, p < 0.024 respectively). In group B, the fractures were healed with periosteal callus. There was no difference in the healing time and the time for consolidation per 1mm gap between the two cortices. The consolidation time per 1mm gap in the medial cortices was significantly longer in group A than group B (p < 0.020). The longitudinal axial motion in open transverse tibial fractures seems to shorten the healing time effectively in the medial cortex.

Adolescent↗

PubMed1995

Effects of putative cannabinoid receptor ligands, anandamide and 2-arachidonyl-glycerol, on immune function in B6C3F1 mouse splenocytes.

Anandamide (arachidonylethanolamide), isolated from the porcine brain, and 2-arachidonyl-glycerol (2-Ara-Gl), derived from the canine gut, are two recently identified putative endogenous cannabinoid receptor ligands. Both ligands have been reported to possess binding affinity for cannabinoid receptor subtypes, CB1 and CB2. The objective of the present studies was to investigate the immunomodulatory effects of both of these ligands in B6C3F1 mouse splenocytes. 2-Ara-Gl produced a marked and dose-related inhibition of the mixed lymphocyte response, anti-CD3 mAb-induced T-cell proliferation and LPS-induced B-cell proliferation, whereas having no inhibitory effect on phorbol-12-myristate-13-acetate/ionomycin-induced cell proliferation. Interestingly, the inhibitory effects by 2-Ara-Gl on proliferation were at least dependent in part on cell density. At high cell density, 2-Ara-Gl enhanced lymphoproliferation whereas exhibiting marked inhibitory activity at low cell density. Similarly, in vitro primary immunoglobulin M antibody-forming cell responses which are dependent on high cell density also were found to be enhanced by 2-Ara-Gl. Conversely, anandamide exhibited no inhibitory effects on cell proliferative responses to stimulation by anti-CD3 mAb, lipopolysaccharide or phorbol-12-myristate-13-acetate/ionomycin treatment. Anandamide also showed no effect on the in vitro sheep erythrocyte antibody-forming cell response. Although shown previously to markedly inhibit forskolin-stimulated cyclic AMP accumulation, 2-Ara-Gl exhibited no effect on basal adenylate cyclase activity in splenocytes. Additionally, anandamide showed negligible inhibitory effects at extremely high concentrations on forskolin-stimulated adenylate cyclase activity and no effect on basal adenylate cyclase activity in splenocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗

PubMed1994

Suppression of the humoral immune response by cannabinoids is partially mediated through inhibition of adenylate cyclase by a pertussis toxin-sensitive G-protein coupled mechanism.

Cannabinoid compounds, including the major psychoactive component of marihuana, delta 9-tetrahydrocannabinol (delta 9-THC), have been widely established as being inhibitory on a broad array of humoral and cell-mediated immune responses. The presence of cannabinoid receptors has been identified recently on mouse spleen cells, which possess structural and functional characteristics similar to those of the G-protein coupled cannabinoid receptor originally identified in rat brain. These findings, together with those demonstrating that delta 9-THC inhibits adenylate cyclase in splenocytes, strongly suggest that certain aspects of immune inhibition by cannabinoids may be mediated through a cannabinoid receptor-associated mechanism. The objective of the present studies was to determine whether inhibition of adenylate cyclase is relevant to mouse spleen cell immune function and, if so, whether this inhibition is mediated through a Gi-protein coupled mechanism as previously described in neuronal tissue. Spleen cell activation by the phorbol ester phorbol-12-myristate-13-acetate (PMA), plus the calcium ionophore ionomycin, produced a rapid but transient increase in cytosolic cAMP, which was inhibited completely by immunosuppressive concentrations of delta 9-THC (22 microM) and the synthetic bicyclic cannabinoid CP-55940 (5.2 microM), which produced no effect on cell viability. Inhibition by cannabinoids of lymphocyte proliferative responses to PMA plus ionomycin and sheep erythrocyte (sRBC) IgM antibody-forming cell (AFC) response, was abrogated completely by low concentrations of dibutyryl-cAMP (10-100 microM). Inhibition of the sRBC AFC response by both delta 9-THC (22 microM) and CP-55940 (5.2 microM) was also abrogated by preincubation of splenocytes for 24 hr with pertussis toxin (0.1-100 ng/mL). Pertussis toxin pretreatment of spleen cells was also found to directly abrogate cannabinoid inhibition of adenylate cyclase, as measured by forskolin-stimulated accumulation of intracellular cAMP. These results indicate that inhibition of the sRBC AFC response by cannabinoids is mediated, at least in part, by inhibition of adenylate cyclase through a pertussis toxin-sensitive Gi-protein coupled cannabinoid receptor. Additionally, these studies further support the premise that cAMP is an important mediator of lymphocyte activation.

Adenylate Cyclase Toxin↗

PubMed1994

Role of hydrocortisone in dimethylnitrosamine-induced suppression of antibody response in the mixed culture of murine hepatocytes and splenocytes.

We have previously reported that the hormone-supplemented culture condition for primary hepatocytes is required in dimethylnitrosamine (DMN)-induced suppression of antibody response to sheep erythrocytes in the mixed cultures of murine hepatocytes and splenocytes. In the present investigation, the components of the hormone supplement were screened to identify the component(s) responsible for the increased ability of hepatocytes to activate DMN to its immunosuppressive form. The presence of hydrocortisone in the hepatocyte culture media had the primary role in DMN activation in the co-culture system. Other components of the hormone supplement showed slight or no effects. The effects of hydrocortisone were clearly confirmed through the dose-response study of both DMN and hydrocortisone. To characterize whether the effect of hydrocortisone is glucocorticoid-dependent we tested another potent glucocorticoid, dexamethasone (DEX), and determined if the activity by hydrocortisone could be reversed by RU 486. It was found that hepatocytes cultured in DEX-containing media could also activate DMN to its immunosuppressive form. However, the activity by hydrocortisone to increase DMN-induced immunosuppression was not reversed by RU 486. Furthermore, a possible direct interaction between DMN and hydrocortisone was ruled out. Finally, we transferred DMN-pre-treated culture supernatant from hepatocytes to spleen cell cultures, and found that the metabolite of DMN was very unstable, and that DMN-induced suppression of T-dependent antibody response was hepatocyte-dependent. The present results suggest that glucocorticoids, including hydrocortisone and DEX, in hepatocyte culture media can affect DMN-induced immunosuppression in the hepatocyte/splenocyte co-culture system via a pathway which does not appear to be related to the glucocorticoid receptor.

Animals↗

PubMed1994

Parathyroid hormone-related protein: evidence for isoform- and tissue-specific posttranslational processing.

Parathyroid hormone-related protein (PTHrP) is expressed by malignant tumors and leads to the syndrome of humoral hypercalcemia of malignancy. It is also expressed by a wide variety of nonmalignant tissues, in which it appears to play distinct paracrine and/or autocrine roles. The human PTHrP gene encodes three cDNA-predicted initial translational products of 139, 141, and 173 amino acids. Most human cell lines contain mRNAs encoding all three PTHrP isoforms. The physiological rationale for the existence of these three highly similar transcripts is unknown. In order to determine whether the protein products derived from these three transcripts differ, we transfected Chinese hamster ovary (CHO) cells and rat insulinoma (RIN) cells individually with cDNAs encoding human PTHrP(1-139), PTHrP(1-141), and PTHrP(1-173). Cell extracts and conditioned medium were then chromatographed using reversed-phase HPLC and analyzed using region-specific PTHrP immunoassays. As we had previously observed in SKRC-1 (renal cell carcinoma) and RIN(1-141) cells, multiple amino-terminal PTHrP species as well as a separate midregion PTHrP species were identified in all six cell lines. In addition, both CHO and RIN cell lines transfected with the PTHrP(1-139) construct contained a previously unrecognized carboxy-terminal fragment that reacted with a PTHrP(109-138) antiserum. This carboxy-terminal fragment was physically distinct from the midregion fragment discovered earlier and was also present in conditioned medium, indicating that it is a secretory form, rather than a biosynthetic intermediate or a degradation product.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗

PubMed1994

Investigation of how different halos influence pin forces.

STUDY DESIGN: This study investigated the effect of the size and material of halo rings on the pin force produced at the halo pin-calvarium complex. SUMMARY OF BACKGROUND DATA: Loosening of halo pins has been a problem with using the halo-vest apparatus to stabilize cervical spine fractures. METHODS: One standard halo pin and seven different halo rings were used to test the anterior pin hole of each ring at a constant torque of 8 inch-pounds (0.9 Nm). RESULTS: Pin force fluctuated from halo to halo, and decreased as the nut was tightened. CONCLUSIONS: Identical torques applied to different halos will not guarantee the same magnitude of pin force for halo fixation.

Alloys↗

PubMed1994

Recovery of dimethylnitrosamine-induced immunosuppression by pargyline in the mixed cultures of murine hepatocytes and splenocytes.

To investigate the role of monoamine oxidase (MAO) in dimethylnitrosamine (DMN)-induced suppression of the antibody response to sheep erythrocytes, the effect of an MAO inhibitor, pargyline, was studied in mixed cultures of murine hepatocytes and splenocytes. When pargyline was added simultaneously with DMN during the coculture, DMN-induced immunosuppression was clearly recovered dose-dependently. Cyclophosphamide was used as a comparative control in these studies. Surprisingly, pargyline also reversed cyclophosphamide-induced suppression of the antibody response in the coculture system. The results with cyclophosphamide were not consistent with a role by MAO, and suggested that pargyline may not be selective for MAO. To confirm our hypothesis, the ability of pargyline to inhibit three cytochrome P-450 (P-450) isozyme-specific monooxygenase activities in vitro was studied using mouse liver microsomes. Pargyline, under the same concentration ranges that we used in the coculture studies, clearly inhibited the P-450IIE1-specific p-nitrophenol hydroxylase activity and P-450IIB1-specific pentoxyresorufin O-dealkylase activity. Taken together, our present results indicate that pargyline inhibits P-450 activity and is not selective for MAO. Although further studies are required to confirm a possible role by MAO in DMN-induced immunosuppression, our results suggest that pargyline may recover DMN-induced immunosuppression by primarily inhibiting the ability of P-450 enzymes in hepatocytes to activate DMN to its immunosuppressive metabolite(s).

Animals↗

PubMed1994

Acute focal bacterial nephritis presented as acute renal failure and hepatic dysfunction in a renal transplant recipient.

We describe acute focal bacterial nephritis (AFBN) presented as acute renal failure and hepatic dysfunction in a renal transplant recipient. He had received a renal transplantation 5 years previously and maintained good renal function without an episode of acute rejection or any urinary abnormalities. He had been an HBsAg carrier and showed mild elevation of liver enzymes after renal transplantation. For 5 days before admission, the patient suffered from fever, graft kidney swelling, tenderness and oliguria. On admission, renal biopsy was performed and solumedrol pulse therapy was started under the impression of acute rejection. The following laboratory findings revealed acute renal failure and hepatic dysfunction. From the abdomen CT and renal biopsy findings this case was confirmed as AFBN in a grafted kidney. With successive hemodialysis and antibiotic therapy clinical symptoms and renal function improved promptly. In acute hepatic dysfunction we discontinued cyclosporine (CsA) to prevent irreversible fulminant hepatic failure until the normalization of liver function. It should be considered that AFBN must be included in the differential diagnosis of acute rejection, and the early diagnosis and treatment of AFBN is important to save the grafted kidney. In addition, early withdrawal of CsA is essential to prevent irreversible hepatic failure when infection triggers hepatic dysfunction in HBsAg-positive renal transplant recipients.

Acute Kidney Injury↗

PubMed1994

Primary aldosteronism detected after renal transplantation.

A 44-year old female was admitted to our hospital for evaluation of uncontrolled hypertension. She received renal transplantation 3 months ago and suffered from a tingling sensation and weakness on both hands. Laboratory findings (low serum potassium, low plasma renin activity and elevated plasma aldosterone level) was consistent with primary aldosteronism. Through the postural study for plasma aldosterone and the adrenal CT finding we diagnosed this case as adrenal adenoma, which was confirmed by surgical removal. A retrospective review of medical records showed that characteristic findings in primary aldosteronism (hypokalemia and low plasma renin activity) were masked by renal failure and became evident after successful renal transplantation. It was suggested that impaired urinary potassium excretion and excess release of renin from the ischemic kidney masked the characteristic findings of primary aldosteronism. To our knowledge, this is the first report documenting the change of renin-angiotensin-aldosterone system after renal transplantation in a case of coexistence of primary aldosteronism and chronic renal failure.

Adrenal Cortex Neoplasms↗

PubMed1994

Parathyroid hormone-related protein as a prohormone: posttranslational processing and receptor interactions.

Since the elucidation of the structures of the three human PRHrP isoforms in 1987, information has rapidly accured which indicates that the role of PTHrP in normal physiology will prove to be crucial as well as exceedingly complex. The importance of the role of PTHrP in normal physiology is underscored by its broad tissue expression, by its intense evolutionary conservation, by its extremely early expression after fertilization of the ovum, and by the lethal consequences of PTHrP gene disruption. The complexity of the role of PTHrP in normal physiology increases almost monthly. This complexity is reflected in the broad tissue distribution of the peptide, its complex transcriptional regulation and mRNA instability motifs, and its multiple transcripts and isoforms. It is now clear that additional complexity exists at the level of posttranslational processing. Expression of the PTHrP gene leads to the tissue-specific processing and secretion of an increasingly complex family of derivative peptides, each with its own repertoire of cognate receptors, signal transduction pathways, and physiological consequences. Further elucidation of the posttranslational processing pathways and mechanisms can be anticipated in the coming years, coupled with a corresponding elucidation of multiple PTHrP receptors, their specific signal transduction pathways, and their unique physiological roles. The role of PTHrP in causing HHM is now clearly established. Work in the coming decade will focus on the normal physiological roles played by PTHrP.

Amino Acid Sequence↗