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Biomedical subjects

C D Han

Publications and source records attributed to C D Han.

33 records · Page 2Linked to original sources

Molecular cloning and characterization of iojap (ij), a pattern striping gene of maize.

Iojap (ij) is a recessive striped mutant of maize affecting the development of plastids in a local and position-dependent manner on the leaves. The ij-affected plastids are transmitted to some of the progeny even when the function of the nuclear gene is restored. Developmental defects during embryogenesis and leaf proliferation are other phenotypic characteristics of ij. The extent of striping and the degree of developmental arrest in ij depend upon genetic background. To understand the diverse and unique phenotypic expression of ij, a transposon tagging experiment has been conducted using Robertson's Mutator (Mu). A new ij mutant was obtained from crosses of the reference allele of (ij-ref) to Mu lines. Subsequent genetic and molecular studies showed that the mutant carried a new ij allele (ij-mum1) from the Mu lines and contained a Mu1 element that cosegregated with the iojap phenotype. A 6.0 kb EcoRI genomic DNA fragment containing the Mu1 element was cloned. ij-ref is unstable, and revertants (Ij-Rev) have been obtained. Using the flanking DNA from the genomic clone as a probe, DNA polymorphisms were detected between ij-ref and these revertants. Further, transcripts were restored to the normal level in Ij-Rev seedlings. Comparison of genomic DNA clones from ij-ref, ij-mum1 and Ij indicated that the ij-ref allele contained 1.5 kb of additional DNA related to a transposable element, Ds. Germinal and somatic revertant alleles were derived by excision of this 1.5 kb element from ij-ref. The structure of the Ij gene and the DNA sequence of its transcribed region were determined. The Ij gene encodes a 24.8 kDa protein that showed no significant sequence similarity with proteins listed in databases.

Alleles↗

Pyogenic arthritis of the hip due to Campylobacter fetus--a case report.

Septic arthritis of the hip caused by Campylobacter fetus subsp. fetusis very rare. The authoris isolated C. fetus subsp. fetus from a specimen of the left hip. The patient was a 53-year old man with a history of heavy drinking, diabetes, and chronic hepatitis, and had been suffering from avascular necrosis of both femoral heads. It was considered that the organism invaded already damaged tissue of the joint. The patient was treated with intravenous antibiotics and later received successful total hip replacement.

Arthritis, Infectious↗

Blood gas and electrolyte changes after tourniquet application in total knee replacement surgery.

The tourniquet is widely used in upper and lower extremity surgery in orthopedic practice. However, safe working guidelines for the application of the tourniquet are not clearly defined. The use of a tourniquet is an important step in performing total knee arthroplasty, and it seems plausible that mechanical damage is directly related to the height and the duration of the pressure of the tourniquet applied. Even the tourniquet pressure which is widely accepted in clinical practice, if it is applied for several hours, would permanently damage not only tissues directly under the tourniquet but also the muscles and the nerves distal to the tourniquet. The resultant ischemia to limb produces local changes including hypoxemia, acidosis and hyperkalemia. Relatively little is known about the systemic effects of tourniquet release when the patient is undergoing total knee replacement surgery under a general anesthesia. Therefore, we studied the systemic effects. The results were as follows: 1) Approximately five minutes after the tourniquet was released there was a statistically significant increase in mean heart rate.: 2) Serum potassium levels tended to increase significantly until five minutes while the serum sodium level rose significantly only one minute, and the lactate level rose significantly for only two minutes after tourniquet released; 3) PaCO2 increased for five minutes after tourniquet release and remained elevated for 30 minutes; 4) PaO2 did not change significantly two minutes after tourniquet release; 5) The mean pH dropped to 7.34 and remained low for over five minutes.

Aged↗

An experimental intraarticular implantation of woven carbon fiber pad into osteochondral defect of the femoral condyle in rabbit.

The defects of the articular cartilage structure are not replaced unless the subchondral plate has been breached. However, following the creation of a defect in the subchondral plate, the area is filled in with a fibrous tissue which gradually transforms to hyaline cartilage. The porous nontoxic materials of both biologic and synthetic origin have reportedly been used as matrices for repairing bone and cartilage. Following implantation, carbon fibre, chemically inert and well-tolerated by the body, induces a proliferation of ordered fibrous tissue. We implanted carbon fiber pads in osteochondral defects in rabbits. Those repairs were compared to control holes with no implants. The pads appeared to induce the gross appearance of a restored joint surface, mechanically strong to loading for periods from 2 to 6 weeks. Also, carbon fiber pads promoted the healing of the osteochondral defects in the rabbit femoral condyle, supplying well-organized cartilagenous tissue over repaired subchondral bone. The use of carbon fiber pads as implant material is suggested for the restoration of articular surface in osteoarthritis and osteochondritis dissecans.

Animals↗

Effect of sodium hyaluronate on prevention of osteoarthritis.

The changes in the surface of articular cartilage of femoral condyle from rabbits were evaluated after degenerative changes were made by the technique advocated by Hulth. The medial collateral and both cruciate ligaments were excised, and a medial menisectomy was done. Then the right knee joint was injected with 1 ml of Na-hyaluronate gel every two weeks. The animals were sacrificed at two, four, six, eight, or sixteen weeks postoperatively. After sacrifice, the medial femoral condyle was excised and prepared for the light microscopic and scanning electron microscopic study. At eight to sixteen weeks, there were chondrocyte clones with clefts to the radial zone and increased loss of the height of articular cartilage on the control side; but, on the experimental side there was a significant delay and lessening of the arthritic response. The biocompatibility and the protective effect of joint degeneration of this device make this material a valuable adjuvant in the treatment of osteoarthritis and the traumatized joints.

Animals↗

Interaction of subtype-selective antagonists with alpha 1-adrenergic receptor binding sites in rat tissues.

(+)-Niguldipine inhibited specific 125I-BE 2254 binding more potently in membrane preparations from rat tissues enriched in the alpha 1A subtype (hippocampus and vas deferens) than those with the alpha 1B subtype (liver and spleen). Inhibition curves for (+)-niguldipine were better fit by a two-site model in most tissues, although Kl values for each site varied markedly between tissues. The potency of this lipophilic drug was highly dependent on tissue concentration, probably accounting for most of this variability. Pretreatment of membranes with chloroethylclonidine (CEC) to inactivate the alpha 1B subtype did not completely eliminate the low affinity sites for (+)-niguldipine, particularly in heart. Saturation analysis showed that (+)-niguldipine competitively inhibited both alpha 1A and alpha 1B subtypes. However, substantial non-competitive inhibition was also observed in several tissues. Analysis of inhibition curves for 5-methylurapidil gave similar proportions of alpha 1A and alpha 1B receptor sites as were calculated for (+)-niguldipine in various tissues. Although (+)-niguldipine and 5-methylurapidil revealed variable proportions of low affinity sites in CEC-pretreated hippocampus and heart, this was not observed with inhibition curves for WB 4101 and phentolamine. These results are generally consistent with the previously defined alpha 1A and alpha 1B subtypes. 5-Methylurapidil currently appears to be the best antagonist for discriminating these subtypes; (+)-niguldipine shows similar selectivity but is complicated by a high lipophilicity. However, the persistence of low affinity sites for 5-methylurapidil and (+)-niguldipine after CEC pretreatment and the noncompetitive effects of (+)-niguldipine in some tissues raise the possibility of an additional subtype(s) of alpha 1-adrenergic receptors in rat tissues.

Adrenergic alpha-Antagonists↗

Hypotension- and endotoxin-induced alterations in calcitonin gene-related peptide: modulation by dexamethasone.

Plasma levels of calcitonin gene-related peptide (CGRP) were studied in anesthetized rats during and after recovery from hemorrhagic hypotension as well as following administration of bacterial endotoxin. Hypotension of 35-40 mmHg maintained for 2 hr resulted in significant (P less than .05) elevation of plasma CGRP levels. Plasma levels at 120 min of hypotension were 49.5 +/- 5.9 pg/ml, over 4-fold above average control levels (11.1 +/- 1.1 pg/ml). Plasma CGRP levels at 90 min of hypotension (20.2 +/- 2.4 pg/ml) or before were not more than 2.5-fold above control levels. Ninety minutes after the return of shed blood in the 30 min group, blood pressure (83 +/- 3 mmHg) and CGRP (17.2 +/- 2.2 pg/ml) were not different from saline controls (88 +/- 3 mmHg and 15.1 +/- 1.7 pg/ml CGRP). However, if hypotension was maintained for 120 min before the return of shed blood, blood pressure following 90 min recovery was significantly lower (59 +/- 5 mmHg) and CGRP levels significantly higher (39.2 +/- 5.6 pg/ml) than saline control values (82 +/- 5 mmHg and 19.5 +/- 2.7 pg/ml). Dexamethasone treatment of the 120 min hypotension group when shed blood was returned resulted in CGRP values not different from saline treated, but hypotension persisted. Administration of bacterial endotoxin (16.7 mg/kg) to anesthetized rats caused significant elevations (P less than .05 vs. saline treatment at 3 hr) in plasma CGRP levels from aorta (82.2 +/- 5.0 pg/ml), vena cava (79.4 +/- 12.9), and portal vein (117.7 +/- 29 pg/ml) compared to levels in saline-treated control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Changes in the hyaline articular cartilage after air exposure.

UNLABELLED: The changes of hyaline articular cartilage from rabbits after air exposure were evaluated. The knee joints were exposed to air for periods of thirty minutes to two hours. The animals were killed periodically, at three days, one week and three weeks postoperatively. After sacrifice, the cartilage was removed and prepared for study by light microscopy and electron microscopy. Exposure to room air for thirty minutes produced chondrocyte necrosis in the upper third of the cartilage, and exposure for 60 minutes or longer produced chondrocyte necrosis of the entire thickness of articular cartilage at three days after arthrotomy. But, three weeks after arthrotomy, we could not find any chondrocyte necrosis in any rabbits at varying periods of air exposure. There was no significant change in proteoglycan content between the aired and control cartilage. CLINICAL RELEVANCE: Exposing cartilage to air can cause transient and reversible cartilage damage. If these changes are not reversible, the orthopedic surgeon should consider avoiding the prolonged exposure of articular cartilage to air, since complete matrix disintegration is known to occur months after chondrocyte necrosis.

Air↗

The effect of experimental trypsin on the regeneration of hyaline articular cartilage.

There is evidence from other studies that some degree of cartilage healing may take place after the initiation of an inflammatory response. It is postulated that the induction of the platelet-cartilage interaction may eventuate in cartilage repair. The treatment of fresh articular cartilage with proteolytic enzymes rendered the tissue active as a platelet aggregant. During platelet aggregation a host of active substances are released which are known to play a role in the inflammatory response (Thompson 1975). This study was undertaken to evaluate the effects of trypsin on the surface injury of rabbit hyaline cartilage. The results were as follows: 1) Hyaline cell regeneration was observed only in the group treated with trypsin and blood; 2) Hyaline cartilage regeneration did not occur in the group treated with a single injection of trypsin or blood; 3) There was no significant damage to the healthy articular cartilage by the single injection of trypsin or blood, or both; and 4) Platelets do not adhere to cartilage and superficial damaged cartilage does not induce platelet aggregation.

Animals↗

Autolysed antigen-extracted allogeneic bone for repair of diaphyseal bone defects in rabbits.

Autolysed antigen-extracted allogeneic bone (AAA bone) was used to bridge a large osteoperiosteal gap in the diaphysis of the radius of 50 rabbits. Periodic observations of the graft were made clinically, radiologically and histologically every week up to fourteen weeks. The continuity of the radius was evaluated macroscopically and histologically. The AAA bones were progressively resorbed and replaced by the new bone. The bone remodelled to the mature tubular bone and did not undergo absorption during the experimental period. The AAA bone proceeded to be an osteoinductive and osteoconductive material. There were no appreciable histologic signs of immune or foreign body reaction.

Animals↗

Alpha 1-adrenergic receptor subtypes and formation of inositol phosphates in dispersed hepatocytes and renal cells.

The ability of alpha 1a- and alpha 1b-adrenergic receptor subtypes to stimulate [3H]inositol phosphate [( 3H]InsP) formation was examined in collagenase-dispersed hepatocytes and renal cells. alpha 1-Adrenergic receptor binding sites were labeled with 125I-BE 2254, and the proportion of alpha 1a and alpha 1b subtypes was determined with chloroethylclonidine (CEC) and WB 4101. Hepatocytes contained only alpha 1b-adrenergic receptors, whereas renal cells had approximately equal proportions of both subtypes. Pretreatment of renal cells with CEC selectively inactivated the alpha 1b subtype, leaving a homogeneous population of alpha 1a receptors. Norepinephrine stimulated [3H]InsP accumulation to a similar extent in both hepatocytes and renal cells. Pretreatment with CEC inactivated this response completely in hepatocytes but only partially in renal cells. WB 4101 was 1000-fold more potent in inhibiting the [3H]InsP response in renal cells than hepatocytes; however, some of this difference was due to rapid metabolism of WB 4101 by hepatocytes. After correction for metabolism, WB 4101 was still 11-fold more potent in inhibiting norepinephrine-stimulated [3H]InsP formation in hepatocytes (alpha 1b) than in CEC-pretreated renal cells (alpha 1a). These results demonstrate that both alpha 1a- and alpha 1b-adrenergic receptor subtypes activate formation of [3H]InsP, although the molecular mechanisms by which these responses occur remain to be determined.

Animals↗