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Biomedical subjects

K Ishihara

Publications and source records attributed to K Ishihara.

At least 271 records · Page 15Linked to original sources

Existence of voltage-dependent Ca2+ channels in vestibular dark cells: cytochemical and whole-cell patch-clamp studies.

To determine whether functional Ca2+ channels are present in vestibular dark cells, changes in intracellular Ca2+ concentration ([Ca2+]i) due to K+ applications were measured using the Ca(2+)-sensitive dye (fura-2) and patchclamp whole-cell recordings were made in dark cells isolated from the ampullae of the semicircular canal of the guinea pig. Exchange of the external solution with a buffer medium containing a high K+ concentration (80 mM K+ or 150 mM K+) caused a concentration-dependent increase in [Ca2+]i in vestibular dark cells. Application of 1 microM nifedipine as a Ca2+ channel antagonist completely blocked the increase in [Ca2+]i. Further treatment with 10 microM BAY K 8644 as a Ca2+ channel agonist caused an increase in [Ca2+]i. In the patch-clamp whole-cell recordings a 1-s depolarizing pulse given into the dark cell in the presence of a high barium concentration (50 mM Ba2+) induced an inward current. In determining the current-voltage relationship, a current was detected at a potential that depolarized at-50 mV and was maximal at +10 mV. This inward current was completely blocked by 1 mM La3+ as a Ca2+ channel antagonist. These findings suggest the presence of voltage-dependent Ca2+ channels in dark cells, which have a presumed function in the regulation of [Ca2+]i in the vestibular endolymph.

Animals↗

Recovery of mucin content in surface layer of rat gastric mucosa after HCl-aspirin-induced mucosal damage.

Quantitative changes in mucin (mucus glycoprotein) in different layers of rat gastric mucosa after mucosal damage induced by acidified acetylsalicylic acid (HCl-aspirin; 0.15N HCl, 20-200 mg acetylsalicylic acid/kg body weight) were studied. More than 50 mg/kg HCl-aspirin led to a significant increase in macroscopic gastric injury (expressed as ulcer index) at 3 h, compared with control (no aspirin) and there was a significant recovery at 7 h. Three h after dosing with 50 mg/kg acidified aspirin, there was superficial mucosal damage and decreased mucin content in the surface mucosal layer. Mucin production recovered 7 h after the administration of 50 mg/kg acidified aspirin. Doses of acidified aspirin higher than 100 mg/kg decreased mucin content in the surface and deep corpus mucosal layers and no recovery was seen 7 h after the administration. Physiological damage after the administration of 50 mg/kg HCl-aspirin was limited mainly to surface epithelial mucus cells. An experimental model in which superficial erosion was induced in rat gastric mucosa was established with low-dose HCl-aspirin.

Animals↗

Adherence of oral streptococci to an immobilized antimicrobial agent.

An antimicrobial agent, 3-(trimethoxysilyl)-propyldimethyloctadecyl ammonium chloride, was immobilized on silica. Interaction between the material (termed) OAIS) and various oral bacterial species were then studied. Seven species of Streptococcus and two Actinomyces were investigated for their ability to adhere to this biomaterial. Cell-surface hydrophobicity and zeta-potential were examined as well. Analysis of extracted hydrophobic proteins which adhered to OAIS revealed that the adherence of these micro-organisms was closely related to the hydrophobicity of their cell surfaces. The results of zeta-potential assays indicated that negative charge on the cell surface inhibited adherence to OAIS. Gel electrophoresis revealed that OAIS could absorb cell-surface hydrophobic proteins from all bacterial species tested. Preadsorption of hydrophobic components on the cell surface inhibited adherence of the Strep. mutans strain to OAIS in a dose-dependent manner. The results indicate that OAIS adsorption of these oral bacteria was dependent on the degree of hydrophobicity of their surfaces. A major component of this adherence was hydrophobic cell-surface proteins.

Absorption↗

Behavioral LTP during learning in rat hippocampal CA3.

Behavioral long-term potentiation (LTP) of the potentials with the advance of learning were investigated in hippocampal mossy fiber (MF)-CA3 synapses. In both acute and chronic experiments, control and test groups of rats were used. Daily learning tasks in the radial arm maze were given to animals in the test groups. Complete acquisition of learning was observed on day 5. In acute experiments, when MF stimulation-induced population spikes (PS) were examined on day 7 of learning task, relatively higher PS were observed in the test group than those in the control group, and tetanic stimulation (TS)-induced LTP was still observed from the increased PS before TS in the test groups. In chronic experiments, in which the MF stimulation-induced PS were recorded daily after the learning tasks with implanted electrodes, amplitude of PS of the test groups, but not the control, increased concomitantly with the progress in learning. The PS potentiation persisted steadily from day 4 to day 7 of training. The fact that LTP in the MF-CA3 system coincided well with the advance of learning suggests that the MF-CA3 system is involved in the acquisition of learning and/or memory storage.

Anesthesia↗

Protection of ischemic hippocampal neurons by ginsenoside Rb1, a main ingredient of ginseng root.

Our previous study showed that the oral administration of red ginseng powder before but not after transient forebrain ischemia prevented delayed neuronal death in gerbils, and that a neuroprotective molecule within red ginseng powder was ginsenoside Rb1. However, it remains to be clarified whether or not ginsenoside Rb1 acts directly on the ischemic brain, and the mechanism by which ginsenoside Rb1 protects the ischemic CA1 neurons is not determined. Without elucidation of the pharmacological property of ginsenoside Rb1, the drug would not be accepted as a neuroprotective agent. The present study demonstrated that the intracerebroventricular infusion of ginsenoside Rb1 after 3.5 min or 3 min forebrain ischemia, precluded significantly the ischemia-induced shortening of response latency in a step-down passive avoidance task and rescued a significant number of hippocampal CA1 neurons from lethal ischemic damage. The intracerebroventricular infusion of ginsenoside Rb1 did not affect hippocampal blood flow or hippocampal temperature except that it caused a slight increase in hippocampal blood flow at 5 min after transient forebrain ischemia. Furthermore, ginsenoside Rb1 at concentrations of 0.1-100 fg/ml (0.09-90 fM) rescued hippocampal neurons from lethal damage caused by the hydroxyl radical-promoting agent FeSO4 in vitro, and the Fenton reaction system containing p-nitrosodimethylaniline confirmed the hydroxyl radical-scavenging activity of ginsenoside Rb1. These findings suggest that the central infusion of ginsenoside Rb1 after forebrain ischemia protects hippocampal CA1 neurons against lethal ischemic damage possibly by scavenging free radicals which are overproduced in situ after brain ischemia and reperfusion. The present study may validate the empirical usage of ginseng root over thousands of years for the prevention of cerebrovascular diseases.

Animals↗

Platelet-derived growth factor prevents ischemia-induced neuronal injuries in vivo.

Platelet-derived growth factor (PDGF) has been considered to be a neuroprotective factor candidate on the basis of several in vitro studies. However, the in vivo effect of PDGF on ischemic neurons has not been determined. In the present study, the effect of PDGF-BB on the ischemia-induced disability of passive avoidance task and hippocampal CA1 neuron death in normothermic gerbils, whose the brain temperature was kept at 37.0 +/- 0.2 degrees C during 3-min occlusion of the common carotid arteries was investigated. When PDGF-BB was continuously infused for 7 days into the cerebral ventricles of gerbils with transient forebrain ischemia, response latency time in a passive avoidance task was significantly prolonged. Subsequent histological examinations showed that PDGF-BB effectively increased the number of viable pyramidal neurons in the hippocampal CA1 region as well as synapses within the strata moleculare, radiatum and oriens of the region in comparison with the numbers of neurons and synapses in vehicle-treated ischemic gerbils. In situ detection of DNA fragmentation (TUNEL staining) revealed that TUNEL-positive neurons in the hippocampal CA1 field of vehicle-treated ischemic gerbils were much more numerous than those in the field of PDGF-BB-treated ischemic animals after 7 days ischemia. These findings suggest that the present ischemic animal model exhibits a more delayed neuronal degeneration of the hippocampal CA1 field than the conventional 5-min ischemic model and that the 7-day infusion of PDGF-BB, starting 2 h before ischemic insult, not only prevents delayed neuronal death in the hippocampal CA1 field at 7 days after forebrain ischemia but also inhibits a slowly progressive neuronal degeneration occurring thereafter.

Animals↗

Access to emergency care under TennCare: do patients understand the system?

STUDY OBJECTIVE: To determine patient understanding of how to properly gain access to urgent and emergency medical care under TennCare, a government-mandated managed health care initiative designed to replace Medicaid in Tennessee. METHODS: We prospectively surveyed a convenience sample of ED patients at university hospital ED with an annual census of 50,000 during two periods (summer 1994 and summer 1995). In 1994, 250 TennCare patients were enrolled (part 1). In 1995, 199 were enrolled (part 2). RESULTS: Patients from seven different TennCare managed care organizations (MCOs) were interviewed. Thirty-eight percent of part 1 patients and 37% of part 2 patients did not have or did not know the names of their primary care physicians (PCPs). Fifty-eight percent of the part 1 patients who knew their PCPs' names had never visited them. This figure had decreased to 25% by the time part 2 patients were surveyed. Seventy-three percent of part 1 patients interviewed did not call their PCPs before coming to the ED. This figure had decreased to 48% by the time part 2 patients were interviewed. Thirty-two percent of part 1 patients were aware that they were supposed to contact the PCP before visiting the ED, whereas 94% of part 2 patients were aware of this requirement. Thirty-one percent of part 1 patients and 40% of part 2 patients who tried to contact their PCPs were unsuccessful, most often because of a delay on the part of PCPs in returning calls. Fifty-six percent of part 1 patients and 69% of part 2 patients did not know that they might be held responsible for the bill if an ED visit was not considered a true emergency and was not approved by the MCO. CONCLUSION: Improvements in communication of pertinent information must be implemented in managed care systems such as TennCare to better inform participants of the proper use of the system. MCOs will not reduce inappropriate use of the ED if patients are not aware of their responsibilities and do not know their PCPs or how to gain access to them. PCP responsiveness to patients must also be improved.

Adult↗

Characterization of the gene for pyruvate,orthophosphate dikinase from rice, a C3 plant, and a comparison of structure and expression between C3 and C4 genes for this protein.

To investigate the molecular changes that might have occurred in genes for pyruvate,orthophosphate dikinase (PPDK) during the evolution of C4 plants from C3 plants, we isolated a full-length cDNA and the corresponding gene for a C4-like PPDK from rice, a C3 gramineous plant and compared their structures and promoter activities to those of the corresponding gene from maize, a C4 gramineous plant. As in maize, there are at least two ppdk genes in rice and one of them was very similar to the maize C4-type ppdk. The deduced amino acid sequence of the rice PPDK was 88% homologous to the maize C4-type PPDK in the mature peptide region and 56% homologous in the transit peptide region. The C4-like ppdk in rice contained 21 exons, which were interrupted by twenty introns, and the positions of the introns were essentially the same as those in the gene from maize, with the except in that the gene from rice had two extra introns. Such extra introns were also found in the C4-type ppdk from a dicot, Flaveria, at the same positions. These results strongly suggest that the two introns were present in an ancestral gene before the divergence of monocot and dicot plants. The C4-like ppdk in rice contained two functionally independent promoters had generated a larger transcript with the transit peptide region and a smaller transcript without this region. The unusual dual-promoter system for transcription has been conserved in the C4-type ppdk gene from maize, indicating that the dual-promoter system is a common feature of ppdk genes in both C3 and C4 plants. The patterns of expression of the two transcripts in rice were different: the larger transcript was expressed exclusively in green leaves at a low level whereas the smaller transcript was expressed in some reproductive organs at a high level. Essentially the same patterns of expression were observed in maize, but the level of expression of the larger transcript in maize green leaves was much higher than that in green leaves of rice. The promoter activities of the rice and maize genes for PPDK were examined directly in a transient expression assay in maize mesophyll protoplasts after electroporation with promoter::beta-glucuronidase chimeric genes. The rice promoter for the smaller transcript was very active in the protoplasts but the rice promoter for the larger transcript had relatively low activity. By contrast, both promoters of the maize gene had high activity. Taken together, these results demonstrate that the rice C4-like ppdk is very similar to the maize C4-type ppdk, not only in terms of primary structure but also in terms of the regulation of expression, with the exception that the strength of the maize promoter for the larger transcript is higher. The results strongly suggest that the genetic alterations required to give rise to the C4-type ppdk gene were relatively limited.

Amino Acid Sequence↗

Amplification of BCR protein associated with oncogenesis in human hepatocellular carcinoma.

The BCR gene is located on human chromosome 22. The normal cellular BCR gene encodes a 160,000-dalton phosphoprotein associated with a serine/threonine kinase activity. The BCR protein is involved in signal transduction. We investigated the expression of the BCR protein in hepatocellular carcinoma (HCC), surrounding noncancerous liver tissue, liver cirrhosis (LC), chronic hepatitis (CH), and normal liver with immunohistochemistry and a western blot analysis. BCR immunoreactivity was detected using a monoclonal antibody. In normal liver, and both CH and LC without association of HCC, the immunoreactivity of the BCR protein was minimal. In contrast, 73% (22 of 30) of noncancerous liver tissue adjacent to the HCC and 40% (12 of 30) of HCC expressed BCR protein; this difference was statistically significant (P < 0.01). The expression of the BCR protein expression correlated with the degree of histological differentiation of HCC (P < 0.05). In addition, the amplification of BCR protein in noncancerous cells was supported by the detection of specific protein using a western blot analysis. In two cases, the expression of BCR protein occurred only in overtly malignant HCC cells. As a result, the expression of the BCR protein may be associated with oncogenesis in human HCC.

Aged↗

Structural requirements for roxatidine in the stimulant effect of rat gastric mucin synthesis and the participation of nitric oxide in this mechanism.

1. The structural requirements of the histamine H2-receptor antagonist, roxatidine (2-acetoxy-N-(3-[m-(1-piperidinylmethyl)phenoxy]-propyl)acetamide hydrochloride), for the stimulant effect on mucin biosynthesis and their relation to histamine H2-receptor antagonism were identified by considering the structural analogues of this drug using an organ culture system of the rat stomach and competition studies with [125I]iodoaminopotentidine ([125I]-APT) binding to membranes of the guinea pig striatum. 2. [3H]Glucosamine incorporation into mucin during 5 h incubation period was stimulated by roxatidine and its structural analogues A (2-hydroxy-N-(3-[m-(1-piperidinylmethyl)phenoxy]-propyl)acetamide) and B (N-(3-[m-(1-piperidinylmethyl)phenoxy]-propyl)acetamide). This effect was seen in mucosal cultures of the corpus, but not antrum, region. 3. Structural analogues, in which the length of the flexible chain between the benzene ring and the amide structure differs from that of roxatidine, failed to activate mucin synthesis. No significant change in mucus synthesis occurred with the addition of analogues in which the piperidine ring attached to the benzene ring via a methylene bridge was changed. 4. Specific [125I]-APT binding to the histamine H2 receptor of guinea pig brain membranes was inhibited by roxatidine and all structural analogues used in this study, except F (N-(3-[m-(N, N-dimethyl-aminomethyl)phenoxy]-propyl)acetamide). 5. Ranitidine at 10(-4) M did not suppress the roxatidine-induced increase in [3H]glucosamine incorporation into mucin. 6. Roxatidine-induced stimulation of [3H]glucosamine incorporation into mucin was completely blocked by the addition of either NG-nitro-L-arginine (10(-5) M) or 2-(4-carboxyphenyl)-4,4,5,5,-tetramethylimidazoline-1-oxyl-3-oxide sodium salt (10(-5) M). The inhibitory action of NG-nitro-L-arginine was totally reversed by L-arginine (5 x 10(-3) M). 7. These results suggest that the cardinal chemical features of roxatidine for the activation of mucin biosynthesis in the corpus region of the rat stomach are the appropriate length of the flexible chain between the amide structure and the aromatic ring system bearing the methylpiperidinyl group at the meta position. The activity of roxatidine and its analogues to stimulate mucin synthesis is not related to their histamine H2 receptor antagonistic activity. Roxatidine-induced activation of mucin biosynthesis in the corpus tissue is mediated by nitric oxide.

Animals↗

Time-dependent outward currents through the inward rectifier potassium channel IRK1. The role of weak blocking molecules.

Outward currents through the inward rectifier K+ channel contribute to repolarization of the cardiac action potential. The properties of the IRK1 channel expressed in murine fibroblast (L) cells closely resemble those of the native cardiac inward rectifier. In this study, we added Mg2+ (0.44-1.1 mM) or putrescine (approximately 0.4 mM) to the intracellular milieu where endogenous polyamines remained, and then examined outward IRK1 currents using the whole-cell patch-clamp method at 5.4 mM external K+. Without internal Mg2+, small outward currents flowed only at potentials between -80 (the reversal potential) and approximately -40 mV during voltage steps applied from -110 mV. The strong inward rectification was mainly caused by the closed state of the activation gating, which was recently reinterpreted as the endogenous-spermine blocked state. With internal Mg2+, small outward currents flowed over a wider range of potentials during the voltage steps. The outward currents at potentials between -40 and 0 mV were concurrent with the contribution of Mg2+ to blocking channels at these potentials, judging from instantaneous inward currents in the following hyperpolarization. Furthermore, when the membrane was repolarized to -50 mV after short depolarizing steps (> 0 mV), a transient increase appeared in outward currents at -50 mV. Since the peak amplitude depended on the fraction of Mg(2+)-blocked channels in the preceding depolarization, the transient increase was attributed to the relief of Mg2+ block, followed by a re-block of channels by spermine. Shift in the holding potential (-110 to -80 mV), or prolongation of depolarization, increased the number of spermine-blocked channels and decreased that of Mg(2+)-blocked channels in depolarization, which in turn decreased outward currents in the subsequent repolarization. Putrescine caused the same effects as Mg2+. When both spermine (1 microM, an estimated free spermine level during whole-cell recordings) and putrescine (300 microM) were applied to the inside-out patch membrane, the findings in whole-cell IRK1 were reproduced. Our study indicates that blockage of IRK1 by molecules with distinct affinities, spermine and Mg2+ (putrescine), elicits a transient increase in the outward IRK1, which may contribute to repolarization of the cardiac action potential.

Action Potentials↗

CD79 alpha/CD79 beta heterodimers are expressed on pro-B cell surfaces without associated mu heavy chain.

During B cell development, the surface expression of CD79 alpha/CD79 beta heterodimers had been thought to begin in the pre-B cell stage where the heterodimers constitute pre-B cell receptors together with mu heavy and surrogate light chains. Thereafter, in mature B cells, CD79 alpha/CD79 beta associates with surface Ig to form B cell antigen receptors. In this study, we revealed by using newly established mAb that CD79 beta was expressed on the surface of pro-B cells which had not undergone the productive Ig gene rearrangement. Biochemical analysis showed that CD79 beta on pro-B cells existed either as monomers or as disulfide-linked heterodimers with CD79 alpha, non-covalently associated with four unidentified membrane molecules. Our finding that CD79 beta is expressed on earlier B-lineage cells than previously expected coincides with the recent study in which CD79 beta-deficient mice exhibit a blockade of B cell differentiation at the pro-B cell stage. Thus, it is speculated that the CD79 beta-containing complexes on pro-B cell surfaces may function to induce early B cell differentiation.

Animals↗

Effects of histamine on mucin biosynthesis in rat gastric mucosa.

Mucin biosynthesis is stimulated by gastrin during the process of glycosylation in the corpus mucosa of the rat stomach. The purpose of this study was to clarify, using an organ culture technique, whether biosynthetic responses to histamine in the rat gastric mucin are the same as that to gastrin. Radiolabeled mucin was obtained from the corpus and antral mucosa of the rat stomach after in vitro incubation for 5 h with [3H]glucosamine (GlcN), [14C]threonine (Thr), and [35S]sulfate. Addition of histamine (10(-7)-10(-5) M) to the culture medium increased [3H]GlcN-labeled mucin in the corpus tissue in a concentration-dependent manner. In the antrum, there was no significant change in the biosynthetic activity of mucin in response to histamine. Histamine at 10(-5) M also increased the incorporation of both [35S]sulfate and [14C]Thr into the corpus mucin. These results indicate that histamine stimulates the biosynthesis of the mucin peptide, as well as the glycosylation step in the corpus, and suggest that the effect of histamine on mucin synthesis is distinct from that of gastrin.

Animals↗

Genetic control of immune response to a synthetic fimbrial antigen of Actinobacillus actinomycetemcomitans.

The incidence of infection by Actinobacillus actinomycetemcomitans, one of the important pathogens in human periodontal diseases, has been reported to be associated with racial background and genetic factors. We attempted to determine the genetic regulation of immune responses to A. actinomycetemcomitans fimbriae, an attachment factor, using various inbred strains of mice. For this purpose, we synthesized an oligopeptide antigen using the amino acid sequence of the fimbriae and conjugated this antigen to branched lysine polymer resin beads. After immunization with the synthetic A. actinomycetemcomitans fimbrial antigen, serum antibody levels and the delayed-type hypersensitivity (DTH) reaction to the antigen were measured by enzyme-linked immunosorbent assay (ELISA) and footpad swelling responses, respectively. The strains of mice found to be high-IgG responders to the antigen were B10.HTT, B10.RIII, B10.A (5R) and B10.S (9R). These results indicate that mice with E(beta s):E(alpha k), E(beta r):E(alpha r) and E(beta b):E(alpha k) respond strongly to the synthetic peptide. All of the high-IgG responders showed a high DTH response. A cell transfer experiment confirmed that CD4 T cells mediated with DTH response to the synthetic peptide. Thus, the results of this study demonstrate that the immune responses to A. actinomycetemcomitans fimbriae are genetically controlled.

Aggregatibacter actinomycetemcomitans↗

Role for the S-layer of Campylobacter rectus ATCC33238 in complement mediated killing and phagocytic killing by leukocytes from guinea pig and human peripheral blood.

OBJECTIVE: The role of the S-layer of Campylobacter rectus ATCC 33238 in complement-mediated killing and interaction with leukocytes of the intraperitoneal cavity from guinea pigs and human peripheral blood was studied in vitro. MATERIALS AND METHODS: Rabbit polyclonal anti-serum to whole C. rectus cells, a monoclonal antibody which recognizes 150 KDa S-layer protein antigen and a monoclonal antibody against lipopolysaccharide (LPS) were prepared. Sensitivities of C. rectus cells against complement mediated killing and phagocytic killing by peritoneal leukocytes of guinea pig and human peripheral leukocytes were examined in the presence or absence of a specific antibody. RESULTS: C. rectus ATCC 33238 cells were moderately sensitive to complement mediated killing in the presence of rabbit polyclonal antibody against whole cells, and slightly sensitive in the presence of monoclonal antibody against S-layer. Ingestion and phagocytic killing of C. rectus cells by leukocytes were enhanced by the rabbit anti-serum and monoclonal antibody against S-layer, but not by the monoclonal antibody against LPS, pre-immune rabbit serum or control ascites. Viability of leukocytes was dependent on the number of ingested C. rectus cells. CONCLUSIONS: The present study demonstrates that S-layer possessing C. rectus cells are resistant to complement mediated killing and phagocytic killing by leukocytes in the absence of specific antibody.

Animals↗

Cloning, expression, and sequencing of a protease gene from Bacteroides forsythus ATCC 43037 in Escherichia coli.

We have isolated and characterized an N-benzoyl-Val-Gly-Arg-p-nitroanilide-specific protease gene, designated prtH, from Bacteroides forsythus ATCC 43037. Nucleotide sequencing of the DNA insert from the clone (hereafter referred to as clone FST) revealed that the protease activity corresponded to an open reading frame consisting of 1,272 bp coding for a 47.8-kDa protein. When plasmid pFST was used as a probe in Southern hybridization, Sau3AI-digested chromosomal DNA of B. forsythus ATCC 43037 as well as the chromosomal DNAs of the isolated strains Ta4, TR5, and YG2 showed 0.6- and 0.8-kb hybridizing bands. The cell-free extracts of clone FST showed hemolytic activity on human blood cells. The hydrolytic activity of cell extracts of the pFST clone was inhibited by p-toluenesulfonyl-L-lysine chloromethyl ketone hydrochloride, leupeptin, N-ethylmaleimide, iodoacetic acid, iodoaceteamide, and EDTA.

Amino Acid Sequence↗

Stimulation of mucin metabolism in rat gastric mucosa by histamine.

We examined the effects of histamine on mucin localized in the different regions and layers of rat gastric mucosa by determining the changes in the content as well as the biosynthetic activity of the mucin. In vivo administration of 0.8 mg/kg of histamine, which could not induce a concomitant gastric acid secretion, caused a significant increase in the mucin content in the corpus mucosa, but not in the antral mucosa. This increase was due to a significant accumulation of the mucin in the mucus gel and surface mucosa of the corpus region, whereas that in the deep mucosa did not significantly change. In the in vitro incubation system of rat gastric mucosa, histamine and dibutyryl cyclic AMP significantly increased [3H]-labeled mucin in the corpus. The histamine-induced acceleration of mucin biosynthesis was suppressed by ranitidine, but not pyrilamine. In the antrum, the biosynthetic activity showed no significant change by histamine. These results suggest that histamine promotes mucin metabolism via histamine H2 receptors in the surface mucosal layer of the corpus.

Animals↗

Evaluation of the frictional properties of an elastomer with enhanced lipid-adsorbing ability.

Wear particle production in load-bearing orthopaedic implants is one of the major factors currently limiting the service life of the implant. Most of the research carried out to date in attempting to solve this problem has used the approach of finding more wear-resistant biocompatible material pairs. In contrast, other researchers have attempted to reduce wear by encouraging elastohydrodynamic film formation through the use of elastomeric bearing surfaces. Unfortunately, these elastomeric bearing surfaces have poor tribological properties when a fluid film is not present. Boundary lubrication of an elastomeric orthopaedic bearing may alleviate some of these difficulties. The purpose of this research was to fabricate and characterize an elastomeric material that had a surface capable of specifically adsorbing a naturally occurring boundary lubricant. Dipalmitoyl phosphatidylcholine (DPPC) has been previously shown to be able to act as a boundary lubricant at stresses that occur in human load-bearing joints such as the hip and knee; therefore, DPPC was chosen for use in this study. It was expected that in an aqueous liposome suspension the static coefficient of friction microseconds of such a material would be lower, and increase less quickly over time, than a similar material without an ability to adsorb specifically DPPC when articulated against a polished chrome steel ball bearing. The lipid-adsorbing elastomer did not possess the desired tribological properties. This result was attributed to the polymer adsorbing the DPPC in the liposome phase and not in the bilayer phase, and interaction among the polymeric surface, DPPC and water. This approach to lubricating orthopaedic bearings was shown to have some merit, but a great deal of work needs to be done before such an approach can be used on a clinically available material.

1,2-Dipalmitoylphosphatidylcholine↗