Protocatechuic acid impacts rotator cuff healing and reduces fatty degeneration in a chronic rotator cuff tear model in rats

The purpose of this study was to verify the effect of protocatechuic acid (PCA) on tendon healing and fatty degeneration in a chronic rotator cuff model. Methods: Twenty-eight Sprague-Dawley male rats were randomly allocated into two groups: Saline+repair (SR) and PCA+repair (PR). The right shoulder was used for experimental interventions, and the left served as a control. PCA (30 mg/kg/day) was administered intraperitoneally at the site of infraspinatus tendon detachment in rats in the PR group, and the same volume of saline was administered to the same site in the SR group. The torn tendon was repaired 4 weeks after infraspinatus detachment. Four weeks after repair, hematoxylin and eosin (H&E), S100, and CD68 stains were performed to evaluate the degree of fatty degeneration and H&E and Masson trichrome stains were performed to assess tendon healing. Superoxide dismutase (SOD) was measured to test the efficacy of PCA as an antioxidant. Results: Results from histological evaluation indicated that SOD and CD68 levels at the musculotendinous region and collagen fiber parallel to the orientation at the tendon-to-bone junction were not significantly different between the SR and PR groups. The mean load-to-failure of the PR group (20.32±9.37 N) was higher than that of the SR group (16.44±6.90 N), although this difference was not statistically significant (p=0.395). The SOD activity in the operative side infraspinatus muscle of the PR group was higher than that of the SR group, but the difference was not statistically significant (p=0.053). Conclusions: The use of PCA could improve tendon healing and decrease fatty degeneration after rotator cuff repair.

Effects of gamma-Aminobutyric Acid on Intrinsic Cholinergic Action in Exocrine Secretion of Isolated, Perfused Rat Pancreas

gamma-Aminobutyric acid (GABA) has been reported to enhance exocrine secretion evoked not only by secretagogues but also by intrinsic neuronal excitation in the pancreas. The pancreas contains cholinergic neurons abundantly that exert a stimulatory role in exocrine secretion. This study was undertaken to examine effects of GABA on an action of cholinergic neurons in exocrine secretion of the pancreas. Intrinsic neurons were excited by electrical field stimulation (EFS; 15 V, 2 msec, 8 Hz, 45 min) in the isolated, perfused rat pancreas. Tetrodotoxin or atropine was used to block neuronal or cholinergic action. Acetylcholine was infused to mimic cholinergic excitation. GABA (30microM) and muscimol (10microM), given intra-arterially, did not change spontaneous secretion but enhanced cholecystokinin (CCK; 10 pM) -induced secretions of fluid and amylase. GABA (3, 10, 30microM) further elevated EFS-evoked secretions of fluid and amylase dose-dependently. GABA (10, 30, 100microM) also further increased acetylcholine (5microM) -induced secretions of fluid and amylase in a dose-dependent manner. Bicuculline (10microM) effectively blocked the enhancing effects of GABA (30microM) on the pancreatic secretions evoked by either EFS or CCK. Both atropine (2microM) and tetrodotoxin (1microM) markedly reduced the GABA (10microM) -enhanced EFS- or CCK-induced pancreatic secretions. The results indicate that GABA enhances intrinsic cholinergic neuronal action on exocrine secretion via the GABAA receptors in the rat pancreas.

Roles of Gonadal Steroids on Exocrine Secretion of Isolated Perfused Rat Pancreas

To clarify the roles of gonadal steroids on pancreatic exocrine secretion, effects of progesterone and estradiol-17beta on spontaneous and secretagogue-induced exocrine response of isolated perfused rat pancreas were investigated. Intra-arterial infusion of progesterone resulted in significant increase of the spontaneous pancreatic fluid and amylase secretion dose-dependently. However, estradiol-17beta did not exert any influence on spontaneous pancreatic exocrine secretion. Exogenous secretin, cholecystokinin (CCK), and acetylcholine markedly stimulated pancreatic fluid and amylase secretion. Progesterone initially enhanced secretin-induced amylase secretion, but this stimulatory response declined thereafter to basal value. Moreover, secretin-induced fluid secretion was not affected by infusion of progesterone. Therefore, initial increase of secretion-induced amylase secretion by progesterone seems to be a non-specific action by washout effect of secretin. Estradiol-17beta failed to change the secretin-induced fluid and amylase secretion. Both progesterone and estradiol-17beta did not exert any influence on CCK-induced fluid and amylase secretion. Acetylcholine-induced exocrine secretion of isolated perfused pancreas also was not affected by intra-arterial infusion of progesterone or estradiol-17beta. It is concluded from the above results that progesterone could enhance the spontaneous pancreatic fluid and amylase secretion of isolated perfused rat pancreas through non-genomic short- term action, and that these effects could be masked by more potent stimulants such as secretin, CCK, and acetylcholine.

Effects of gamma-Aminobutyric Acid on Pancreatic Amylase Secretion Evoked by Sodium Oleate in Anesthetized Rats

gamma-Aminobutyric Acid (GABA) is contained in pancreatic islet beta-cells although its physiological role in pancreatic exocrine function is completely unknown at the present time. Recently, we have reported that exogenous GABA enhances secretagogue-evoked exocrine secretion in the isolated, perfused rat pancreas. This study was aimed to investigate an effect of exogenous GABA on pancreatic exocrine secretion in vivo evoked by intestinal stimulation. Rats were anesthetized with urethane (1.4 g/kg) after 24-h fast with free access to water. GABA (10, 30 and 100micromol/kg/h), given intravenously, did not change spontaneous pancreatic amylase secretion but dose-dependently elevated the amylase secretion evoked by intraduodenal sodium oleate (0.05 mmol/h). GABA (30micromol/kg/h) also further increased the amylase secretion stimulated by CCK+(30 pmol/kg/h) plus secretin (20 pmol/kg/h) but failed to modify the amylase secretion induced by secretin alone. GABA (10, 30 and 100micromol/kg/h) also dose-dependently elevated pancreatic amylase secretion evoked by CCK+alone. Bicuculline (100micromol/kg/h), a GABAA-receptor antagonist, markedly reduced the GABA-enhanced pancreatic responses to sodium oleate, CCK+plus secretin or CCK+alone. The results indicate that GABA enhances the sodium oleate-evoked pancreatic amylase secretion via GABAA-receptors in anesthetized rats, which may account for elevating the action of CCK+released by sodium oleate.

Influence of middle ear conditions on measurement of evoked otoacoustic emissions / 대한이비인후과학회지

BACKGROUND AND OBJECTIVES: Otoacoustic emissions (OAEs) are low level acoustic sounds of cochlear origin. They have several advantages over other methods in auditory testing, particularly in children. However, because of the crucial dependence of emission levels on the healthiness of the middle ear conduction system, some middle ear problems confound the interpretation of evoked OAEs (EOAEs). The purpose of this study is to evaluate the effects of middle ear condition (tympanometry) on DPOAEs and TEOAEs in normal hearers. Materials and Method : Tympanometry, TEOAEs and DPOAEs were measured in 42 subjects (68 ears) who were under 12 years old and have pure tone thresholds within 25 dB HL RESULTS: The OAEs pass rates for the three groups were as follows: 95 % for TEOAEs and 90 % for DPOAEs in the tympanogram type A group; 12 % for TEOAEs and 12 % for DPOAEs in the tympanogram type B group; 27.3 % for TEOAEs and 13.6 % for DPOAEs in the tympanogram type C group. The pass rate and sensitivity of EOAEs were much higher in the type A group than in the type B and C groups. CONCLUSION: OAEs are useful for screening the integrity of outer hair cells in the tympanogram type A group but not in the type B and C groups. Therefore, tympanometry that represents middle ear condition is recommended before the OAE test. In addition, if TEOAEs and DPOAEs are simultaneously performed, sensitivity will be increased.

Effects of p-chlorophenylalanine on the synthesis of pancreatic amylase in rats

Previously, we have reported that p-chlorophenylalanine (PCPA), a serotonin depletor, profoundly increased pancreatic fluid and bicarbonate secretion but remarkably inhibited pancreatic amylase secretion in anesthetized rats. The present study was performed to verify the detailed effects of PCPA on pancreatic amylase synthesis that is directly related to amylase exocrine secretion. PCPA significantly decreased pancreatic RNA and protein contents as well as the amylase activity. However, pancreatic DNA content, trypsin and chymotrypsin activities were not influenced by the treatment of PCPA. The rate of pancreatic amylase synthesis, which was assessed by the amount of incorporated (35S)-methionine into amylase for 1 h, was also significantly decreased by 44% in PCPA-treated rats. In order to determine whether the PCPA-induced decrease of amylase synthesis resulted from change in the level of amylase mRNA, Northern blot analysis was performed. The mRNA expression level of amylase was also decreased by 48% in the PCPA-treated rats, indicating that the inhibitory effect of PCPA on the synthesis of pancreatic amylase was mainly regulated at a step prior to translation. It was also revealed in SDS-polyacrylamide gel electrophoresis that the qualitative change of amylase was induced by PCPA. The 54 KDa amylase band seems to be degraded into small molecular weight protein bands in PCPA-treated rats, suggesting that the PCPA-induced decrease of amylase may be partly attributed to the degradation of synthesized amylase.

Ossification Patterns of Laryngeal Cartilage Using CT Scan / 대한이비인후과학회지

BACKGROUND AND OBJECTIVES: Cancer invasion of the laryngeal cartilage is mainly found in the ossified portion of cartilage and contraindication for conservation surgery of laryngopharyngeal cancer. Thus, it is an important factor to consider in planning the management of laryngopharyngeal cancer. Computed tomographic (CT) scan is an useful tool for the evaluation of laryngopharyngeal cancer, but it is difficult to distinguish cancer invasion from non-ossified cartilage regions by the CT scan. Knowledge of the precise ossification pattern will be useful to determine the cancer invasion of laryngeal cartilage. The purposes of this study include ossi6cation pattern according to age, symmetry of ossification and incidence of bone marrow formation. MATERIALS AND METHODS: Fifty-three cases of normal laryngeal CT scans which were reviewed by two radiologists. They were all males, ranging in the ages from 40 to 69 (mean age 53). Ossification degree (%) was measured from the inferior cornu in the thyroid cartilage and the superior border of the posterior lamina in the cricoid cartilage. Age relation and symmetry of ossification and incidence of bone marrow formation were evaluated. RESULTS: There were no correlation between age and degree of laryngeal cartilage ossification (p> 0.05). But there was symmetry and definite pattern of ossification. Symmetry of ossification was 84.9% in the thyroid cartilage. Incidence of bone marrow formation was 60.6% in the thyroid cartilage and 82.8% in the cricoid cartilage. CONCLUSION: This study reveals that there is no ossification-age relationship, but the symmetry and the definite pattern of ossification in the laryngeal cartilage are useful clues in determining the cancer invasion on CT scan.

Effects of GABA on pancreatic exocrine secretion of rats

Since GABA and its related enzymes had been determined in beta-cells of pancreas islets, effects of GABA on pancreatic exocrine secretion were investigated in the isolated perfused rat pancreas. GABA, given intra-arterially at concentrations of 3, 10, 30 and 100 microM, did not exert any influence on spontaneous or secretin (12 pM)-induced pancreatic exocrine secretion. However, GABA further elevated cholecystokinin (10 pM)-, gastrin-releasing peptide (100 pM)- or electrical field stimulation-induced pancreatic secretions of fluid and amylase, dose-dependently. The GABA-enhanced CCK-induced pancreatic secretions were completely blocked by bicuculline (10 microM), a GABAA receptor antagonist but not affected by saclofen (10 microM), a GABA(B) receptor antagonist. The enhancing effects of GABA (30 microM) on CCK-induced pancreatic secretions were not changed by tetrodotoxin (1 microM) but partially reduced by cyclo-(7-aminoheptanonyl-Phe-D-Trp-Lys-Thr[BZL]) (10 microM), a somatostatin antagonist. In conclusion, GABA enhances pancreatic exocrine secretion induced by secretagogues, which stimulate enzyme secretion predominantly, via GABA(A) receptors in the rat pancreas. The enhancing effect of GABA is partially mediated by inhibition of islet somatostatin release. GABA does not modify the activity of intrapancreatic neurons.

Distribution, content and molecular heterogeneity of gastrin-releasing peptide in rat pancreas

Although importance of intrapancreatic neurons containing gastrin-releasing peptide (GRP) in control of exocrine secretion has been raised, the nature of GRP in the pancreas is unclear Thus, the present study was undertaken to see distribution, content and molecular heterogeneity of immunoreactive GRP in the rat pancreas Content of immunoreactive GRP in the rat pancreas was 2 99 +/- 0.66 ng/g wet tissues determined by radioimmunoassay. Immunoreactive GRP was most abundantly expressed in the duodenal part among 3 parts of the pancreas, duodenal, body and splenic part. Vagotomy failed to change the content of immunoreactive GRP in the pancreas. Three distinct forms of immunoreactive GRP, very identical to GRP-27, bombesin-24 and neuromedin C, were observed in the rat pancreas by using reversed phase C18 HPLC and Sephadex G-50 superfine column chromatography. Cell bodies of neurons containing immunoreactive GRP were scattered in pancreatic connective tissues and their nerve fibers innerv ated pancreatic acini and large ducts as determined by immunohistochemistry. The present results suggest that three distinct forms of GRP exist in intrapancreatic GRPergic neurons, which exert a stimulatory role in pancreatic exocrine secretion in rats.

A role of endogenous somatostatin in exocrine secretion induced by intrapancreatic cholinergic activation

A role of endogenous somatostatin in pancreatic exocrine secretion induced by intrapancreatic cholinergic activation was studied in the isolated rat pancreas perfused with modified Krebs-Henseleit solution. Intrapancreatic neurons were activated by electrical field stimulation (EFS: 15 V, 2 msec and 8 Hz). Pancreatic exocrine secretion, including volume flow and amylase output, and release of somatostatin from the pancreas were respectively determined. Somatostatin cells in the islet were stained with an immunoperoxidase method. EFS significantly increased pancreatic volume flow and amylase output, which were reduced by atropine by 59% and 78%, respectively. Intraarterial infusion of either pertussis toxin or a somatostatin antagonist resulted in a further increase in the EFS-evoked pancreatic secretion. EFS also further elevated exocrine secretion in the pancreas treated with cysteamine, which was completely restored by intraarterial infusion of somatostatin. EFS significantly increased not only the number of immunoreactive somatostatin cells in the islet but also the concentration of immunoreactive somatostatin in portal effluent. It is concluded from the above results that intrapancreatic cholinergic activation elevates pancreatic exocrine secretion as well as release of endogenous somatostatin. Endogenous somatostatin exerts an inhibitory influence on exocrine secretion induced by intrapancreatic cholinergic activation via the islet-acinar portal system in the isolated pancreas of the rat.

Mechanism of action of pancreatic polypeptide (PP) on pancreatic exocrine secretion in isolated rat pancreas

Aim of this study was to investigate if pancreatic polypeptide (PP) reduced the insulin action via the intra-pancreatic cholinergic nerves in the isolated rat pancreas. The pancreas was isolated from rats and perfused with intra-arterial infusion of modified Krebs-Henseleit solution containing 2.5 mM glucose at a flow rate of 1.2 ml/min. Simultaneous intra-arterial infusion of insulin (100 nM) resulted in potentiation of the pancreatic flow rate and amylase output which were stimulated by cholecystokinin (CCK, 14 pM). These potentiating actions of insulin on the CCK-stimulated pancreatic exocrine secretion were completely abolished by administration of rat PP. Vesamicol, a potent inhibitor of vesicular acetylcholine storage, and tetrodotoxin (TTX) also significantly reduced the combined actions of insulin and CCK. Administration of carbamylcholine, an acetylcholine agonist, completely restored the vesamicol-or TTX-induced inhibition of the potentiation between insulin and CCK. Also rat PP failed to attenuate the restoring effect of carbamylcholine. Electrical field stimulation (15-30 V, 2 msec and 8 Hz) resulted in a significant increase in the pancreatic flow rate and amylase output in voltage-dependent manner. Effects of electrical field stimulation were augmented by endogenous insulin. Rat PP also suppressed the pancreatic exocrine secretion stimulated by electrical field stimulation. These observations strongly suggest that PP inhibits the potentiating actions of insulin on CCK-stimulated pancreatic exocrine secretion by suppression of the intra-pancreatic cholinergic activity in the isolated rat pancreas.

An Inhibitory Mechanism of Gastric Acid Secretion in Patients with Hyperthyroidism / 대한내분비학회지

BACKGROUND: Although hypochlorhydria, hypergastrinemia and antiparietal cell antibody have been well documented in the patients with hyperthyroidism, a cause of hypochlorhydria or hypergastrinemia is unknown at the present time. Therefore, in order to clarify an inhibitory mechansim of gastric acid secretion in the patients with hyperthyroidism, interrelationship among hypochlorhydria, hypergastrinemia and antiparietal cell antibody was investigated in this study. METHODS: The gastric secretory function, fasting and postprandial plasma concentrations of gastrin and titer of antiparietal cell antibody in the plasma were determined in the patients with hyperthyroidism and normal subjects. Immunoblot analysis was performed to identify the gastric membrane protein, a possible gastric antigen to antiparietal cell antibody. Using a immunocytochemical technique with electron microscopy, intracellular structure of the parietal cell reacted with antiparietal cell antibody was observed. RESULTS: The basal and pentagastrin-stimulated maximal acid output were reduced in the patients with hyperthyroidism. The fasting and postprandial plasma concentrations of gastrin were markedly elevated in the patients. The plasma gastrin concentration in the patients with the antiparietal cell antibody was higher than that of the norrnal subjects as well as the patients without the antibody not only in the fasting state but also in the postprandial state. However, the plasma gastrin concentration of the patients without the antiparietal cell antibody was elevated in the fasting state only. There was no difference in the gastrin content of the antral mucosa between the norrnal subjects and the patients. The antiparietal cell antibody was detected in 5 (38.5 %) out of 13 patients by using the indirect immunofluorescence method. Patient IgG dose-dependently inhibited rabbit gastric H (+),K (+)-ATPase activity. Among proteins of the rabbit gastric mucosa membrane, four high molecular weight proteins (91, 140, 170 and 210 K dalton) were reacted to the patient IgG. The patient IgG positive peroxidase-antiperoxidase (PAP) activity was electron microscopically detected on the intracellular cannalicular membrane of the parietal cell CONCLUSION: We conclude that hypochlorhydria and hypergastrinemia in the patients with hyperthyroidism are partially related to the antiparietal cell antibody and that the antigen to the antiparietal cell antibody may be H (+),K (+)-ATPase in the intracellular canalicular membrane of the parietal cell.

Morphological and functional changes of exocrine pancreas in genetic diabetic model mice / 대한해부학회지

No abstract available.