Vibrio parahaemolyticus CadC regulates acid tolerance response to enhance bacterial motility and cytotoxicity.

Pathogens adapted to sub-lethal acidic conditions could increase the virulence and survival ability under lethal conditions. In the aquaculture industry, feed acidifiers have been used to increase the growth of aquatic animals. However, there is limited study on the effects of acidic condition on the virulence and survival of pathogens in aquaculture. In this study, we investigated the survival ability of Vibrio parahaemolyticus at lethal acidic pH (4.0) after adapted the bacteria to sub-lethal acidic pH (5.5) for 1 hr. Our results indicated that the adapted strain increased the survival ability at lethal acidic pH invoked by an inorganic (HCl) or organic (citric) acid. RNA-sequencing (RNA-seq) results revealed that 321 genes were differentially expressed at the sub-lethal acidic pH including cadC, cadBA and groES/groEL relating to acid tolerance response (ATR), as well as genes relating to outer membrane, heat-shock proteins, phosphotransferase system and flagella system. Quantitative real-time polymerase chain reaction (qRT-PCR) confirmed that cadC and cadBA were upregulated under sub-lethal acidic conditions. The CadC protein could directly regulate the expression of cadBA to modulate the ATR in V. parahaemolyticus. RNA-seq data also indicated that 113 genes in the CadC-dependent way and 208 genes in the CadC-independent way were differentially expressed, which were related to the regulation of ATR. Finally, the motility and cytotoxicity of the sub-lethal acidic adapted wild type (WT) were significantly increased compared with the unadapted strain. Our results demonstrated that the dietary acidifiers may increase the virulence and survival of V. parahaemolyticus in aquaculture.

Mechanism of Action of Veverimer: A Novel, Orally Administered, Nonabsorbed, Counterion-Free, Hydrochloric Acid Binder under Development for the Treatment of Metabolic Acidosis in Chronic Kidney Disease.

Current management of metabolic acidosis in patients with chronic kidney disease (CKD) relies on dietary intervention to reduce daily endogenous acid production or neutralization of retained acid with oral alkali (sodium bicarbonate, sodium citrate). Veverimer is being developed as a novel oral treatment for metabolic acidosis through removal of intestinal acid, resulting in an increase in serum bicarbonate. Veverimer is a free-amine polymer that combines high capacity and selectivity to bind and remove hydrochloric acid (HCl) from the gastrointestinal (GI) tract. In vitro studies demonstrated that veverimer had a binding capacity of 10.7 ± 0.4 mmol HCl per gram of polymer with significant binding capacity (>5 mmol/g) across the range of pH values found in the human GI tract (1.5-7). Upon protonation, veverimer bound chloride with high specificity but showed little or no binding of phosphate, citrate, or taurocholate (<1.5 mmol/g), which are all anions commonly found in the human GI tract. Administration of veverimer to rats with adenine-induced CKD and metabolic acidosis resulted in a significant increase in fecal chloride excretion and a dose-dependent increase in serum bicarbonate to within the normal range compared with untreated controls. Absorption, distribution, metabolism, and excretion studies in rats and dogs dosed with 14C-labeled veverimer showed that the polymer was not absorbed from the GI tract and was quantitatively eliminated in the feces. Acid removal by veverimer, an orally administered, nonabsorbed polymer, may provide a potential new treatment for metabolic acidosis in patients with CKD. SIGNIFICANCE STATEMENT: Metabolic acidosis is a complication of chronic kidney disease (CKD) as well as a cause of CKD progression. Veverimer is a high-capacity, selective, nonabsorbed, hydrochloric acid-binding polymer being developed as a treatment for metabolic acidosis. Veverimer binds and removes hydrochloric acid from the gastrointestinal tract, resulting in increased serum bicarbonate and the correction of metabolic acidosis. Veverimer is not an ion-exchange resin and does not deliver sodium or other counterions, and so it may be appropriate for patients with CKD with and without sodium-sensitive comorbidities.

Triaminopyrimidine derivatives as transmembrane HCl transporters.

Small synthetic molecules capable of inducing transmembrane anion transport have received a lot of attention as potential anti-cancer agents due to their ability to interfere with intracellular pH homeostasis. A series of triaminopyrimidine-based anion transporters have been synthesised, and they are found to diminish proton gradients across lipid bilayers at physiologically relevant pH. The compounds have pKa values (≈7.2) that allow protonation/deprotonation processes coupled with anion binding/unbinding events in physiologically relevant conditions. Synthetic vesicle transport experiments as well as solid state structures indicate synergistic binding of HCl. Cell assays show that the transporters induce apoptosis in various cancerous cell lines.

Physiologically Based Absorption Modeling of Salts of Weak Bases Based on Data in Hypochlorhydric and Achlorhydric Biorelevant Media.

Physiologically based absorption modeling has been attracting increased attention to study the interactions of weakly basic drug compounds with acid-reducing agents like proton-pump inhibitors and H2 blockers. Recently, standardized gastric and intestinal biorelevant media to simulate the achlorhydric and hypochlorhydric stomach were proposed and solubility and dissolution data for two model compounds were generated. In the current manuscript, for the first time, we report the utility of these recently proposed biorelevant media as input into physiologically based absorption modeling. Where needed, data collected with the biorelevant gastrointestinal transfer (BioGIT) system were used for informing the simulations in regard to the precipitation kinetics. Using two model compounds, a HCl salt and a semi-fumarate co-crystal which as expected dissolve to a greater extent in these media (and in gastric and intestinal human aspirates) compared to what the pH-solubility profile of the free form would suggest, we demonstrate successful description of the plasma concentration profiles and correctly predicted the lack of significant interaction after administration with pantoprazole or famotidine, respectively. Thus, the data reported in this manuscript represent an initial step towards defining biorelevant input for such simulations on interactions with acid-reducing agents.

Enhancement of hydrolysis of Chlorella vulgaris by hydrochloric acid.

Chlorella vulgaris is considered as one of the potential sources of biomass for bio-based products because it consists of large amounts of carbohydrates. In this study, hydrothermal acid hydrolysis with five different acids (hydrochloric acid, nitric acid, peracetic acid, phosphoric acid, and sulfuric acid) was carried out to produce fermentable sugars (glucose, galactose). The hydrothermal acid hydrolysis by hydrochloric acid showed the highest sugar production. C. vulgaris was hydrolyzed with various concentrations of hydrochloric acid [0.5-10 % (w/w)] and microalgal biomass [20-140 g/L (w/v)] at 121 °C for 20 min. Among the concentrations examined, 2 % hydrochloric acid with 100 g/L biomass yielded the highest conversion of carbohydrates (92.5 %) into reducing sugars. The hydrolysate thus produced from C. vulgaris was fermented using the yeast Brettanomyces custersii H1-603 and obtained bioethanol yield of 0.37 g/g of algal sugars.

ENaC inhibition stimulates HCl secretion in the mouse cortical collecting duct. I. Stilbene-sensitive Cl- secretion.

Inhibition of the epithelial Na(+) channel (ENaC) reduces Cl(-) absorption in cortical collecting ducts (CCDs) from aldosterone-treated rats and mice. Since ENaC does not transport Cl(-), the purpose of the present study was to explore how ENaC modulates Cl(-) absorption in mouse CCDs perfused in vitro. Therefore, we measured transepithelial Cl(-) flux and transepithelial voltage in CCDs perfused in vitro taken from mice that consumed a NaCl-replete diet alone or the diet with aldosterone administered by minipump. We observed that application of an ENaC inhibitor [benzamil (3 µM)] to the luminal fluid unmasks conductive Cl(-) secretion. During ENaC blockade, this Cl(-) secretion fell with the application of a nonselective Cl(-) channel blocker [DIDS (100 µM)] to the perfusate. While single channel recordings of intercalated cell apical membranes in split-open CCDs demonstrated a Cl(-) channel with properties that resemble the ClC family of Cl(-) channels, ClC-5 is not the primary pathway for benzamil-sensitive Cl(-) flux. In conclusion, first, in CCDs from aldosterone-treated mice, most Cl(-) absorption is benzamil sensitive, and, second, benzamil application stimulates stilbene-sensitive conductive Cl(-) secretion, which occurs through a ClC-5-independent pathway.

ENaC inhibition stimulates HCl secretion in the mouse cortical collecting duct. II. Bafilomycin-sensitive H+ secretion.

Epithelial Na(+) channel (ENaC) blockade stimulates stilbene-sensitive conductive Cl(-) secretion in the mouse cortical collecting duct (CCD). This study's purpose was to determine the co-ion that accompanies benzamil- and DIDS-sensitive Cl(-) flux. Thus transepithelial voltage, VT, as well as total CO2 (tCO2) and Cl(-) flux were measured in CCDs from aldosterone-treated mice consuming a NaCl-replete diet. We reasoned that if stilbene inhibitors (DIDS) reduce conductive anion secretion they should reduce the lumen-negative VT. However, during ENaC blockade (benzamil, 3 µM), DIDS (100 µM) application to the perfusate reduced net H(+) secretion, which increased the lumen-negative VT. Conversely, ENaC blockade alone stimulated H(+) secretion, which reduced the lumen-negative VT. Application of an ENaC inhibitor to the perfusate reduced the lumen-negative VT, increased intercalated cell intracellular pH, and reduced net tCO2 secretion. However, benzamil did not change tCO2 flux during apical H(+)-ATPase blockade (bafilomycin, 5 nM). The increment in H(+) secretion observed with benzamil application contributes to the fall in VT observed with application of this diuretic. As such, ENaC blockade reduces the lumen-negative VT by inhibiting conductive Na(+) absorption and by stimulating H(+) secretion by type A intercalated cells. In conclusion, 1) in CCDs from aldosterone-treated mice, benzamil application stimulates HCl secretion mediated by the apical H(+)-ATPase and a yet to be identified conductive Cl(-) transport pathway; 2) benzamil-induced HCl secretion is reversed with the application of stilbene inhibitors or H(+)-ATPase inhibitors to the perfusate; and 3) benzamil reduces VT not only by inhibiting conductive Na(+) absorption, but also by stimulating H(+) secretion.

Acid-generated soy protein hydrolysates and their interfacial behavior on model surfaces.

The present work attempts to provide data to warrant the consideration of soy proteins (SP) as potentially useful biomolecules for practical chemical and surface applications. Despite their sundry properties, SP use has been limited by their high molecular weight. In response to this limitation, we analyze acid hydrolysates of soy proteins (0.1 N HCl, 70 °C) for surface modification. Techniques typical in protein (SDS-PAGE) as well as colloidal (charge demand and electrophoretic mobility) analyses were used to follow the effects of molecular changes that occur upon hydrolysis. Adsorption experiments on hydrophobic (polypropylene) and mineral (aluminum oxide) surfaces were subsequently carried out to further interrogate the surface activity resultant from soy hydrolysis. It was found that during adsorption the hydrolysates tended to form less surface aggregates and adsorbed at faster rates compared with unmodified SP. Overall, the benefits derived from the application of SP hydrolysates are highlighted.

The gastroprotective effects of Eugenia dysenterica (Myrtaceae) leaf extract: the possible role of condensed tannins.

We applied a taxonomic approach to select the Eugenia dysenterica (Myrtaceae) leaf extract, known in Brazil as "cagaita," and evaluated its gastroprotective effect. The ability of the extract or carbenoxolone to protect the gastric mucosa from ethanol/HCl-induced lesions was evaluated in mice. The contributions of nitric oxide (NO), endogenous sulfhydryl (SH) groups and alterations in HCl production to the extract's gastroprotective effect were investigated. We also determined the antioxidant activity of the extract and the possible contribution of tannins to the cytoprotective effect. The extract and carbenoxolone protected the gastric mucosa from ethanol/HCl-induced ulcers, and the former also decreased HCl production. The blockage of SH groups but not the inhibition of NO synthesis abolished the gastroprotective action of the extract. Tannins are present in the extract, which was analyzed by matrix assisted laser desorption/ionization (MALDI); the tannins identified by fragmentation pattern (MS/MS) were condensed type-B, coupled up to eleven flavan-3-ol units and were predominantly procyanidin and prodelphinidin units. Partial removal of tannins from the extract abolished the cytoprotective actions of the extract. The extract exhibits free-radical-scavenging activity in vitro, and the extract/FeCl3 sequence stained gastric surface epithelial cells dark-gray. Therefore, E. dysenterica leaf extract has gastroprotective effects that appear to be linked to the inhibition of HCl production, the antioxidant activity and the endogenous SH-containing compounds. These pleiotropic actions appear to be dependent on the condensed tannins contained in the extract, which bind to mucins in the gastric mucosa forming a protective coating against damaging agents. Our study highlights the biopharmaceutical potential of E. dysenterica.

A novel abdominal aortic aneurysm model produced by periarterial application of hydrochloric acid.

Previous abdominal aortic aneurysm (AAA) animal modeling methodologies were either expensive or complicated. Here, we developed a novel AAA model which was simple to set up and generated minimal calcification. Twenty-four rats were divided randomly into four groups. Groups 1, 2 and 3 underwent surgery in which 15% hydrochloric acid (HCl) was applied periarterially to the abdominal aorta for 5 min, followed by sacrifice 1 week (group 1), 2 weeks (group 2), and 4 weeks (group 3) after surgery. The maximum aortic diameter (MAD) was measured at surgery and before animal sacrifice. Rats in group 4 were sham-treated. The MADs in group 1, 2 and 3 showed significant dilation compared with group 4, with a mean dilation rate of 33.8% in the first week after surgery. Histopathological examination revealed infiltration of macrophages into the adventitia, obvious apoptosis of smooth muscle cells, and rupture and collapse of the elastic fibers. Furthermore, no calcification was observed in the dilated aorta. The mRNA expression levels of inflammatory factors were at least two-fold higher in group 1 than in group 4, indicating significant inflammatory response in the progression of AAA information. In conclusion, periarterial application of 15% HCl is a convenient and reliable model to create an abdominal aortic aneurysm in rats, and the potential development mechanism may be related to the proinflammatory effects of HCl.

Growth hormone-releasing hormone antagonists protect against hydrochloric acid-induced endothelial injury in vitro.

Growth hormone-releasing hormone (GHRH) regulates the synthesis of growth hormone from the anterior pituitary gland, and it is involved in inflammatory responses. On the other hand, GHRH antagonists (GHRHAnt) exhibit the opposite effects, resulting in endothelial barrier enhancement. Exposure to hydrochloric acid (HCL) is associated with acute and chronic lung injury. In this study, we investigate the effects of GHRHAnt in HCL-induced endothelial barrier dysfunction, utilizing commercially available bovine pulmonary artery endothelial cells (BPAEC). Cell viability was measured by utilizing 3-(4,5-dimethylthiazol2-yl)- 2,5-diphenyltetrazolium bromide (MTT) assay. Moreover, fluorescein isothiocyanate (FITC)-dextran was used to assess barrier function. Our observations suggest that GHRHAnt exert protective effects against HCL-induced endothelial breakdown, since those peptides counteract HCL-triggered paracellular hyperpermeability. Based on those findings, we propose that GHRHAnt represent a new therapeutic approach towards HCL-induced endothelial injury.

Gabapentin alleviated the cough hypersensitivity and neurogenic inflammation in a guinea pig model with repeated intra-esophageal acid perfusion.

OBJECTIVE: The anti-tussive effect of gabapentin and its underlying neuromodulatory mechanism were investigated via a modified guinea pig model of gastroesophageal reflux-related cough (GERC). METHODS: Intra-esophageal perfusion with hydrochloric acid (HCl) was performed every other day 12 times to establish the GERC model. High-dose gabapentin (48 mg/kg), low-dose gabapentin (8 mg/kg), or saline was orally administered for 2 weeks after modeling. Cough sensitivity, airway inflammation, lung and esophagus histology, levels of substance P (SP), and neurokinin-1 (NK1)-receptors were monitored. RESULTS: Repeated intra-esophageal acid perfusion aggravated the cough sensitivity in guinea pigs in a time-dependent manner. The number of cough events was significantly increased after 12 times HCl perfusion, and the hypersensitivity period was maintained for 2 weeks. The SP levels in BALF, trachea, lung, distal esophagus, and vagal ganglia were increased in guinea pigs receiving HCl perfusion. The intensity of cough hypersensitivity in the GERC model was significantly correlated with increased SP expression in the airways. Both high and low doses of gabapentin administration could reduce cough hypersensitivity exposed to HCl perfusion, attenuate airway inflammatory damage, and inhibit neurogenic inflammation by reducing SP expression from the airway and vagal ganglia. CONCLUSIONS: Gabapentin can desensitize the cough sensitivity in the GERC model of guinea pig. The anti-tussive effect is associated with the alleviated peripheral neurogenic inflammation as reflected in the decreased level of SP.

Endothelial connexin43 mediates acid-induced increases in pulmonary microvascular permeability.

Acid aspiration, a common cause of acute lung injury, leads to alveolar edema. Increase in lung vascular permeability underlies this pathology. To define mechanisms, isolated rat lungs were perfused with autologous blood. Hydrochloric acid and rhodamine-dextran 70 kDa (RDx70) were coinstilled into an alveolus by micropuncture. RDx70 fluorescence was used to establish the spatial distribution of acid. Subsequently, FITC-dextran 20 kDa (FDx20) was infused into microvessels for 60 min followed by a 10-min HEPES-buffered saline wash. During the infusion, FITC fluorescence changes were recorded to quantify the ratio of peak to postwash fluorescence. The ratio, termed normalized fluorescence, was low for acid compared with buffer instillation both in microvessels abutting acid-treated alveoli and those located more than 700 µm away. In contrast, the normalized fluorescence was similar to buffer controls when a higher molecular weight tracer (FITC-dextran 70 kDa) was infused instead of FDx20, suggesting that normalized FDx20 fluorescence faithfully represented microvascular permeability. Inhibiting endothelial connexin43 (Cx43) gap junction communication with Gap27 blunted the acid-induced reduction in normalized fluorescence, although scrambled Gap27 did not have any effect. The blunting was evident not only in microvessels away from the site of injury, but also in those abutting directly injured alveoli. Thus the new fluorescence-based method reveals that acid increases microvascular permeability both at acid-instilled and away sites. Inhibiting endothelial Cx43 blocked the permeability increase even at the direct injury sites. These data indicate for the first time that Cx43-dependent mechanisms mediate acid-induced increases in microvascular permeability. Cx43 may be a therapeutic target in acid injury.

Simulated gastrointestinal digestion of Pru ar 3 apricot allergen: assessment of allergen resistance and characterization of the peptides by ultra-performance liquid chromatography/electrospray ionisation mass spectrometry.

RATIONALE: Non-specific lipid transfer proteins (ns-LTPs) are major food allergens of the Rosaceae family. The severity of allergic reactions often relates to resistance of the allergen to digestion. Thus, it is important to evaluate the digestibility of these proteins and characterise the peptides generated in the gastrointestinal tract. METHODS: Simulated gastrointestinal digestion of purified allergen Pru ar 3 was performed using pepsin for the gastric phase in aqueous HCl at pH = 2 and chymotrypsin and trypsin for the intestinal phase in aqueous NH(4)HCO(3) at pH = 7.8. The peptide mixture obtained was analysed by ultra-performance liquid chromatography/electrospray ionisation mass spectrometry (UPLC/ESI-MS). Peptide sequences were identified by comparing their molecular mass to that obtained by in silico digestion, and were confirmed by the ions obtained by in-source fragmentation. Semi-quantification was performed for the intact protein by comparison with internal standards. RESULTS: The resistance to gastrointestinal digestion of Pru ar 3 allergen was evaluated to be 9%. This value is consistent with that found for grape LTP, but much lower than the resistance found for peach LTP (35%). All the peptides generated were identified by ESI-MS on the basis of their molecular mass and from the ions generated from in-source fragmentation. Apart from low molecular mass peptides, five high molecular mass peptides (4500-7000 Da) containing disulphide bridges were identified. ESI-MS of the intact protein indicated a less compact folded structure when compared to that of the homologous peach LTP. CONCLUSIONS: An extensive characterisation of the peptides generated from the gastrointestinal digestion of Pru ar 3 allergen was performed here for the first time via UPLC/ESI-MS analysis. The digestibility of the allergen was evaluated and compared with that of other LTPs, demonstrating that only a small amount of undigested protein remains, and that specific proteolytic action involves immunodominant epitopes. These data might explain the lower allergenicity of apricot LTP compared to peach LTP, despite their high sequence homology.

Comparison of sulfuric and hydrochloric acids as catalysts in hydrolysis of Kappaphycus alvarezii (cottonii).

In this study, hydrolysis of marine algal biomass Kappaphhycus alvarezii using two different acid catalysts was examined with the goal of identifying optimal reaction conditions for the formation of sugars and by-products. K. alvarezii were hydrolyzed by autoclave using sulfuric acid or hydrochloric acid as catalyst with different acid concentrations (0.1-1.0 M), substrate concentrations (1.0-13.5%), hydrolysis time (10-90 min) and hydrolysis temperatures (100-130 (°)C). A difference in galactose, glucose, reducing sugar and total sugar content was observed under the different hydrolysis conditions. Different by-product compounds such as 5-hydroxymethylfurfural and levulinic acid were also observed under the different reaction conditions. The optimal conditions for hydrolysis were achieved at a sulfuric acid concentration, temperature and reaction time of 0.2 M, 130 °C and 15 min, respectively. These results may provide useful information for the development of more efficient systems for biofuel production from marine biomass.

[Study on germination characteristic of seed of Dendranthema indicum].

OBJECTIVE: To find out the optimum condition for the germination of seed of Dendranthema indicum by studying the effects of pretreatment,phytohormone and temperature on it, and offer the basis for its standardized culture. METHODS: The seed purity, weight per 1000 seeds, seed moisture content and seed viability were determined. The germination of D. indicum seed was tested under following conditions: pretreatment (acid, base, warm water, boiling water), phytohormone (IBA, 6-BA, NAA) and treatments under different temperature (10, 20, 25, 30 degrees C). RESULTS: The seed purity was 99.4%; The weight per 1000 seeds was 0.2941 g; The seed moisture content was 4.39%; The seed viability was 85.3%; The tests of pretreatment couldnt increase the germination of D. indicum seed; Phytohormone had limited effect on the germination of the seed; Temperature condition showed significant effects on the germination. CONCLUSION: The optimum condition for the germination of the seed of D. indicum is 25 degrees C on filter paper.

Role of Rac1 in regulation of NOX5-S function in Barrett's esophageal adenocarcinoma cells.

We have shown that a novel NADPH oxidase isoform, NOX5-S, is the major isoform of NADPH oxidases in an esophageal adenocarcinoma (EA) cell line, FLO, and is overexpressed in Barrett's mucosa with high-grade dysplasia. NOX5-S is responsible for acid-induced reactive oxygen species production. In this study, we found that mRNA levels of NOX5-S were significantly higher in FLO EA cells than in the normal human esophageal squamous cell line HET-1A or in a Barrett cell line, BAR-T. The mRNA levels of NOX5-S were also significantly increased in EA tissues. The data suggest that NOX5-S may be important in the development of EA. Mechanisms of functional regulation of NOX5-S are not fully understood. We show that small G protein Rac1 was present in HET-1A cells, BAR-T cells, and EA cell lines FLO and OE33. Rac1 protein levels were significantly higher in FLO and OE33 cells than in HET-1A or BAR-T cells. Knockdown of Rac1 with Rac1 small interfering RNA significantly decreased acid-induced increase in H(2)O(2) production in FLO EA cells. Overexpression of constitutively active Rac1 significantly increased H(2)O(2) production, an increase that was blocked by knockdown of NOX5-S. By immunofluorescence staining and immunoprecipitation, we found that NOX5-S was present in the cytosol of FLO EA cells and colocalized with Rac1 and SERCA1/2 Ca(2+)-ATPase which is located in the endoplasmic reticulum membrane. We conclude that Rac1 may be important in activation of NOX5-S in FLO EA cells.

BMP depletion occurs during prolonged acid demineralization of bone: characterization and implications for graft preparation.

Demineralization of allograft bone increases the bioavailability of matrix-associated bone morphogenetic proteins (BMPs), rendering these grafts osteoinductive. While osteoinductivity is related to BMP content, little is known about how the demineralization protocol, in particular, extended demineralization times, affects graft BMP levels. We characterized the BMP-7 content of <710 µm bovine bone powder demineralized under various conditions. Using 1 g of bone per 50 ml of 0.125 N, 0.25 N, or 0.5 N HCl, demineralization was performed at room temperature for 5 min to 24 h. Minimum residual calcium levels were obtained within 90 min and were <1 wt % using the 0.25 N and 0.5 N baths and 17 wt % using the 0.125 N bath. Measured peak BMP-7 levels were also obtained within 90 min and were 161-165 ng g(-1) using the 0.25 N and 0.5 N baths and 55.2 ng g(-1) using the 0.125 N bath. This compares to 5.1 ng g(-1) for undemineralized bone. Further acid bath exposure to 24 h resulted in BMP-7 decline to about 50% of the peak value, which was significant. The BMP-7 half-life was estimated to be 26 h. It is likely that the decline was due to diffusion of BMP-7 from the bone matrix into the acid. These results suggest the importance of not over demineralizing bone grafts and should stimulate further research that can be incorporated into the processing methodology followed by tissue banks.

[Clinical and functional disorders of the stomach-in patients with psoriasis in the presence of chronic opisthorchiasis].

OBJECTIVE: to study the clinical and functional status of the stompach in patients with psoriasis in the presence of chronic opisthorchiasis (CO). Subjects and methods. Ninety patients with psoriasis concurrent with CO (a study group (Group 1)), 70 with psoriasis (a comparison group (Group 2)), 70 with CO (Group 3), and 30 healthy individuals were examined. All the patients underwent fractional gastric secretory studies and esophagogastroduodenoscopy (EGDS). RESULTS: The study group showed a reduction in stimulated hydrochloric acid output (4.25+/-0.38 mmol/hour), which was significantly less than that in Groups 2 and 3 and healthy individuals [5.87+/-0.51 (p<0.001); 6.86+/-0.59 (p<0.05), and 10.73+/-0.84 mmnol/hour (p<0.001), respectively]. In the study group, stimulated pepsin output (4.87+/-0.49 mmol/hour) was also significantly less than that in the other groups. Reduced basal hydrochloric acid output was found in 65.5% of the study group patients, whose number was significantly larger than that in the comparison group [44.3% (p<0.05)] and its stimulated output was less in 80 and 62.9% in the study and comparison groups, respectively (p < 0.05). A reduction in pepsin output in the basal secretion phase was revealed in 57.8 and 37.1% of the patients in the study and comparison groups, respectively (p<0.05) while that in the stimulated phase was in 63.3 and 34.3% (p<0.001). Thus, gastric secretory function in psoriatic patients is characterized by reduced hydrochloric acid and pepsin outputs and it is more impaired in patients with mixed pathology, which necessitates anthelmintic therapy in this category of patients.