First experiences with a new infrared thermometry device in mammary gland diagnosis

A parasitology survey was conducted in five villages in North Sumatra, Indonesia. A total of 3,207 blood smears, 2,066 stool specimens and 969 sera were examined. Sixty (1.9%) inhabitants had malaria (Plasmodium vivax 41, P. falciparum 19), and 20 had Brugia malayi microfilaraemia. The most common intestinal helminths were Trichuris trichiura (87%), Ascaris lumbricoides (75%) and hookworm (58%). Other helminths found in low numbers were Enterobius vermicularis, Strongyloides stercoralis, Taenia sp., Fasciolid, Dicrocoeliid and Echinostoma sp. eggs. Entamoeba coli (25%) was the most common intestinal protozoa followed by Endolimax nana (8%), Entamoeba histolytica (7%), Giardia lamblia (6%), Iodamoeba bütschlii (5%), Entamoeba hartmanni (1%) and Chilomastix mesnili (1%). The amoeba prevalence rate was 31 per cent. Testing of sera for Entamoeba histolytica and Toxoplasma gondii antibodies by the indirect haemagglutination test demonstrated positive reactors in 13 per cent and nine per cent of the population respectively. The greatest number of seropositives for Toxoplasma gondii was at elevations of sea level to five meters and the lowest number at elevations of 5OO-1,000 meters.     

Effects of hydrotherapy on pressure ulcer healing

We have earlier reported a higher Fcgamma-receptor (FcgammaR)-mediated generation of reactive oxygen species, measured as luminol-enhanced chemiluminescence (CL) from peripheral neutrophils in adult periodontitis patients. The aims of this study were to confirm our previous results and to elucidate the mechanism of this phenomenon by measuring CL in parallel with the intracellular production of hydrogen peroxide, after stimulation with opsonized bacteria. To determine whether the higher CL was associated with altered responsiveness to priming, the cells were preincubated with tumor necrosis factor alpha (TNFalpha) and lipopolysaccharide (LPS). While CL was significantly higher in subjects with periodontitis, there was no difference in hydrogen peroxide production between the patients and the controls, indicating that the hyperreactivity is related to the generation of other oxygen species than H2O2 and/or to processes in the outer cell membrane. The responsiveness to priming with LPS on CL was slightly but not significantly higher in the periodontitis group, suggesting that priming could be of value for distinguishing subjects with periodontitis. When assaying intracellular production of H2O2, TNFalpha and LPS had both a priming and an activating effect. There were no significant differences between the two groups. In conclusion, this study shows a higher FcgammaR-mediated CL of peripheral neutrophils from adult patients with periodontitis, thus confirming our earlier results. The hyperreactivity seems to be related to the outer cell membrane or to oxygen species other than H2O2.     

Gastric mucosal EGF and PDGF receptor expression with ulcer healing by ebrotidine

OBJECTIVES: Epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) play important roles in the process of mucosal repair and restitution, and their biological effects are mediated by receptors located on the target cell surfaces. The purpose of this study was to assess the effect of the antiulcer agent, ebrotidine, on the expression of EGF and PDGF receptors with chronic ulcer healing. METHODS: Chronic gastric ulcers were developed in the rat by acetic acid technique. The animal were divided into two groups and were treated twice daily for 14 consecutive days, either with ebrotidine at 100 mg/kg, or placebo. At different stages of treatment, the animals were sacrificed and used for the isolation and quantification of gastric mucosal EGF and PDGF receptors. RESULTS: The binding assays revealed that ulcer healing was accompanied by an increase in mucosal expression of both types of receptors. A 1.7-1.8-fold increase in PDGF and EGF receptors occurred by the 4th day after the development of ulcer and reached a maximum of 3-fold increase by the 14th day, when the ulcer was essentially healed. Treatment with ebrotidine caused accelerated ulcer healing (7 days) which was accompanied by a significant enhancement in receptor expression. Compared to the controls, a 1.5-fold increase in EGF and 1.7-fold increase in PDGF receptor expression occurred by the 7th day of ebrotidine treatment, and a 1.4- to 1.5-fold increase was still observed at the 14th day of treatment. CONCLUSIONS: The results suggest that ebrotidine is capable of enhancement of gastric mucosal proliferative activities associated with ulcer healing through the stimulation of EGF and PDGF receptor expression.     

Mucosal adenosine deaminase activity and gastric ulcer healing

Adenosine deaminase activity was studied in gastric corpus mucosa close to an ulcer crater. It was found that 6 weeks of therapy with ranitidine was accompanied by a decrease in enzyme activity in the mucosa around healed ulcers and an increase around those which failed to heal. The different activities of adenosine deaminase in the vicinity of healed and unhealed ulcers may indicate its possible role in peptic ulcer healing.     

Zinc deficiency delays gastric ulcer healing in rats

Zinc is an important element in wound healing. Zinc compounds hasten the healing of gastric ulcers, by an unknown mechanism(s). We studied the effect of the induction of zinc deficiency on gastric ulcer healing. Rats were given a control or zinc-deficient diet for six weeks and then subjected to the induction of acetic acid-induced chronic gastric ulcers. Four days later, zinc-deficient rats were divided into two groups. In the first group, the zinc-deficient diet was continued. In the second group, the diet was changed to the control diet. Zinc-deficient rats had a mean serum zinc concentration approximately 70% of that in controls. Zinc deficiency did not affect the formation of gastric ulcers; however, it reduced cell proliferation by day 4 and delayed ulcer healing. Zinc supplementation brought zinc to control levels within a week, but failed to reverse the delay in ulcer healing. We conclude that zinc is crucial for healing of gastric ulcers, especially at the early stage.     

The impact of Helicobacter pylori eradication on peptic ulcer healing

OBJECTIVE: Current literature was reviewed analyzing the outcome of peptic ulcer healing in relation to the results of the posttherapeutic Helicobacter pylori (HP) status. METHODS: Literature was reviewed along with an analysis of 60 studies, comprising a total of 4329 patients. RESULTS: Successful Helicobacter pylori eradication was found to induce a better response in peptic ulcer healing, regardless of diagnosis: gastric ulcer 88% vs 73% (odds ratio [OR] 2.7, p < 0.01), duodenal ulcer 95% vs 76% (OR 5.6, p < 0.0001), and peptic ulcer 95% vs 76% (OR 6.6, p < 0.0001), for patients having their HP infection successfully cured versus those remaining HP-positive, respectively (Fisher's exact test). For all evaluated time points (< or = 6, 7-8, and 10-12 wk after beginning treatment), HP-negative patients had higher healing rates than HP-positive patients (95% vs 82%, 94% vs 69%, and 96% vs 78% with corresponding OR of 4.2, 6.5, and 7.4, all p < 0.0001, Fisher's exact test). The use of concomitant acid suppression therapy during initial HP eradication provided a benefit on peptic ulcer healing only for patients with persistent HP infection (improved healing rates of 78% vs 67%; otherwise rates were 94-96%). Likewise, prolonged acid inhibition in HP treatment failures after the initial HP treatment phase resulted in 7-20% improved healing rates, whereas patients becoming HP-negative did not profit. CONCLUSION: Successful HP eradication therapy accelerates peptic ulcer healing even without concomitant acid suppression.     

Does smoking influence the eradication of Helicobacter pylori and duodenal ulcer healing with different regimens?

To determine the effect of smoking on Helicobacter pylori eradication and ulcer healing, we investigated 232 patients with H. pylori-positive duodenal ulcer. Patients were given one of seven different treatment protocols and divided into three groups according to smoking habits. Group 1 (n = 128) consisted of non-smokers, group 2 (n = 65) of mild smokers (5-20 cigarettes/day) and group 3 (n = 39) of heavy smokers (> 20/day). The eradication of H. pylori and ulcer healing rate was controlled eight weeks later after ceasing the therapy. The overall eradication rate was 66% in all patients and 68%, 66%, 59% in each group, respectively. The eradication rates showed no statistical difference between groups. Complete ulcer healing was achieved in 84% of all patients and ulcer healing rate between groups did not show any significance (85%, 83% and 82% respectively). These results suggest that smoking status does not influence the eradication of H. pylori and duodenal ulcer healing rates at eight weeks in patients on different treatment schedules.     

Acid suppression with ranitidine plus oral triple therapy improves ulcer healing but not Helicobacter pylori eradication

BACKGROUND/AIMS: To evaluate whether the addition of 2 weeks of ranitidine to a 1-week oral triple therapy (OTT) regimen improved ulcer healing and H. pylori eradication. METHODOLOGY: Two hundred and eleven consecutive patients with an endoscopic diagnosis of active duodenal ulcer (DU) and a positive antrum biopsy for H. pylori were enrolled. Those attending the Hospital Vera Cruz (Group A, n=142) received a 14-day course of ranitidine (150 mg after breakfast and dinner) plus a 1-week OTT, consisting of bismuth subcitrate, (240 mg after the 3 meals), tetracycline (500 mg, 10 min before the three meals and at bedtime), and furazolidone (200 mg after breakfast and dinner). Patients from the Hospital das Clinicas (Group B, n=69) received the same OTT as Group A but without ranitidine. Patients underwent endoscopy again on average 40 days (range: 30-60 days) after completing therapy in order to assess ulcer healing and H. pylori status. RESULTS: Both schedules were equally efficient in eradicating H. pylori with 90% (128/142) eradication in group A, and 84% (58/69) in group B (p=0.2). In contrast, the addition of ranitidine to OTT improved ulcer healing when compared with OTT alone (96%, 137/142, vs. 70%, 48/69; p<0.001). CONCLUSIONS: Our results demonstrate that the association of acid suppression, obtained with 2 week ranitidine administration with OTT improved ulcer healing but did not enhance H. pylori eradication.     

Influence of Aloe vera on collagen turnover in healing of dermal wounds in rats

Treatment of full-thickness wounds with A. vera, on rats resulted in increased biosynthesis of collagen and its degradation. A corresponding increase in the urinary excretion of hydroxyproline was also observed. Elevated levels of lysyl oxidase also indicated increased crosslinking of newly synthesised collagen. The results suggest that A. vera influences the wound healing process by enhancing collagen turnover in the wound tissue.     

Platelet-derived growth factor reverses the effects induced by NSAIDs on ulcer healing

BACKGROUND: It is known that non-steroidal anti-inflammatory drug (NSAID) use delays the healing of peptic ulcers and that growth factors play an important role in the ulcer healing process. AIM: To evaluate the effect of platelet-derived growth factor (PDGF) in healing chronic gastric ulcers in rats treated with NSAIDs. METHODS: Chronic gastric ulcers were induced with acetic acid in male Wistar rats and then treated with either aspirin (100 mg/kg/day), indomethacin (2 mg/kg/day), PDGF-BB (0.1 nM/kg/day) or combinations. Gastric secretion and ulcer size, wound contraction, mucosal regeneration and cell proliferation were assessed in histological specimens. RESULTS: Both aspirin and indomethacin delayed the healing rate of gastric ulcers and reduced ulcer contraction, mucosal regeneration and cell proliferation. All these effects were completely reversed by oral treatment with PDGF-BB without affecting gastric acid secretion. CONCLUSION: Oral administration of PDGF accelerates ulcer healing and reverses the effects induced by NSAIDs on ulcer healing without affecting gastric secretion.     

Delayed healing of chronic gastric ulcer after Helicobacter pylori infection in mice

It has been suggested that there is a close relationship between Helicobacter pylori and the onset or recurrence of gastroduodenal disease. The aim of this study was to examine the effect of H. pylori on the healing of chronic gastric ulcers induced in mice. H. pylori administered to nude mice delayed the healing of experimental acetic acid-induced gastric ulcers. Histological examination showed the occurrence of high densities of H. pylori on the surface of epithelial cells and in the ulcerated area. Repeated administration of amoxicillin (10 mgkg(-1) daily for 5 days) eradicated H. pylori and increased the rate of healing of gastric ulcers in H. pylori-infected mice, but metronidazole, which also eradicated the organisms, did not significantly affect the rate of healing. In conclusion, H. pylori-infection delayed the healing of gastric ulcers induced by the serosal application of acetic acid in mice, possibly by aggravation or prolongation of the mucosal inflammation. Amoxicillin eradicated H. pylori and promoted gastric ulcer healing in mice infected with H. pylori.     

Helicobacter pylori eradication and ulcer healing with daily lansoprazole, plus 1 or 2 weeks co-therapy with amoxycillin and clarithromycin

BACKGROUND: Proton pump inhibitor based combination therapy is one standard strategy for Helicobacter pylori eradication. AIM: To compare the eradication and duodenal ulcer healing efficacy of two 2-week, single dose, lansoprazole based combination therapies. METHODS: Healthy adult patients with endoscopically confirmed, H. pylori associated duodenal ulcer disease (3 mm > ulcer < 20 mm) were eligible for the study. All patients received a 14 day course of lansoprazole 30 mg o.m., and were randomized to receive either 7 or 14 days of amoxycillin 1 g b.d. and clarithromycin 500 mg b.d. Patients were endoscoped at entry and 14-17 days later. Symptomatic, unhealed patients received a further 14 days of therapy with lansoprazole 30 mg o.m. Eradication was confirmed a minimum of 28 days after cessation of all therapy by urease reaction and histological assessment of gastric body and antral biopsies (three biopsies each site). RESULTS: Sixty-two patients were randomized to a treatment arm, of which 58 could be included in an intention-to-treat and key-point-available analysis. H. pylori eradication rates were identical, at 93% (95% CI: 73-98% (1 week), 78-99% (2 week)). In the combined group, all but 13 ulcers were healed at 2 weeks; six required further therapy because of symptoms, while six of the seven asymptomatic patients went on to heal. CONCLUSION: An eradication regimen, based on a 2-week course of single dose lansoprazole with 1 week of antibiotic co-therapy, is effective in eradicating H. pylori, while the 2 weeks of acid suppression is usually effective in duodenal ulcer healing.     

Rapid expression and specific localization of tenascin in gastric ulcer healing in rats

This study was done to investigate the gene expression and localization of tenascin in ulcerated gastric tissues during the healing process with Northern blot analysis and immunohistochemical technique. Gastric ulcers in rats were produced by acetic acid. Tenascin mRNA levels in the ulcerated tissue were significantly increased in a biphasic manner (12 h and day 5), preceding the increase in collagen type IV and laminin mRNA levels, and returned to control levels on day 11. In intact tissues, tenascin was mainly localized in the basement membrane above the proliferative zone, in contrast to the predominant localization of collagen type IV and laminin below the proliferative zone. On the ulcer margin from 12 h to day 5, tenascin was abundantly observed in the lamina propria around nonproliferating new epithelial cells, but collagen type IV and laminin were not seen in this lamina propria. On day 7, tenascin, expressed in the lamina propria, was replaced by collagen type IV and laminin. Thus, the rapid expression and unique localization of tenascin suggest the important role of tenascin in gastric ulcer healing.     

In vitro wound repair by human gastric fibroblasts: implications for ulcer healing

Fibroblasts modulate epithelial biological activities and play a key role in the ulcer healing process. There is no information regarding the biological response of human gastric fibroblasts to regulatory compounds. The aim of this study was to assess the effects of growth factors and prostaglandins on an in vitro model of human gastric fibroblast wound repair. Subconfluent fibroblast cultures were used to study proliferative responses, determined by [3H]thymidine incorporation into DNA. In vitro wound repair was determined in confluent fibroblast monolayers after mechanical denudation. The presence of putative growth factors secreted by fibroblasts was studied in conditioned medium by heparin-affinity chromatography and immunodetection with specific antibodies. Serum and platelet-derived growth factor (PDGF) -BB induced a dramatic increase in both gastric fibroblast proliferation and closure of wounded cell monolayers, whereas these activities were inhibited by both transforming growth factor (TGF) -beta1 and prostaglandin E1. Basal activities in unstimulated gastric fibroblasts were lower than those obtained in skin fibroblasts. Conditioned medium stimulated fibroblast proliferation and wound repair activity, which was inhibited by the addition of suramin, and was partially dependent on the presence of PDGF-like factor. PDGF is a major, autocrine promotor of human gastric fibroblast-dependent wound repair activities, which are inhibited by prostaglandins and TGF-beta. These findings might be important for future therapeutic ulcer healing approaches.     

Skin flap closure by dermal laser soldering: a wound healing model for sutureless hypospadias repair

OBJECTIVES: Laser tissue soldering (LTS) with the diode laser and human albumin-hyaluronate-indocyanine green solder is a safe and effective method of providing an immediate leak-free closure during hypospadias repair. In this report, we compare the physiology, histology, and immunohistochemistry of wound healing following LTS and suturing in a rat skin flap model. METHODS: A 4 x 5-cm skin flap was raised and bisected (4 cm) on the dorsum of 48 Sprague-Dawley rats. The central wound was either closed from a dermal approach by suturing or LTS or left open, and studied at 0, 3, 5, 7, 10, 14, and 21 days postoperatively. An intraoperative comparison was made between suturing and LTS with respect to operative time. Postoperatively, flaps were excised for tensiometric analysis, and sections were stained with hematoxylin-eosin to define wound architecture. Resting skin temperature, laser exposed temperature without solder, and maximum temperature with solder (one drop) were measured at the level of the deep dermis, superficial striated muscle layer, and within the solder. Mean peak temperatures were recorded during a 1-minute laser activation time. RESULTS: Mean continuous suturing time (4.9 +/- 1.1 minutes) was significantly (P < 0.001) faster than either LTS (7.7 +/- 0.77 minutes) or discontinuous suturing (8.2 +/- 0.62 minutes). Two seromas (sutured) and two instances of partial wound dehiscence (1 sutured, 1 LTS) were noted. Tensile strength was increased significantly (P < 0.001) for up to 5 days in the LTS group, but was equal to suturing at 7 and 10 days. Immediate tensile strength after LTS was equivalent to a 7-day healed wound. At 14 days, wounds initially left open and those closed by LTS were stronger than sutured wounds (P < 0.05). There was no evidence of thermal injury or foreign body reaction in the LTS group. Solder was incorporated within the dermis in all wounds at 21 days. Laser activation of solder resulted in significant increases in temperature at all three tissue levels: 65.0 +/- 5.2 and 69.9 +/- 6.8 degrees C in the deep and superficial skin (no significant difference between the two), and 101 +/- 15.6 degrees C within the solder (P < 0.001 versus superficial and deep skin). CONCLUSIONS: Our results indicate that sutureless dermal LTS of skin flaps provides increased tensile strength for up to 7 days, with relatively greater tensile strength provided within the first 3 days. Our laser technique does not appear to alter the normal wound healing process. Rather, solder-tissue interaction initially, and extracellular matrix infiltration of solder later, provide the basis for improved wound strength. For hypospadias repair using skin flaps, these wound attributes may permit sutureless surgery.     

Role of metalloproteinases in the development and healing of acetic acid-induced gastric ulcer in rats

The three main components involved in thrombosis and haemostasis are thrombin, platelets, and plasmin. Almost all inhibitors of thrombosis are focused either on the inhibition of thrombin or on the inhibition of platelets. We designed a construct using the fibrinolytic activity of staphylokinase, fused via a cleavable linker to an antithrombotic peptide of 29 amino acids. The peptide was designed to include three inhibitory regions: (1) the Arg-Gly-Asp (RGD) amino acid sequence to prevent fibrinogen binding to platelets; (2) a part of fibrinopeptide A, an inhibitor of thrombin; and (3) the tail of hirudin, a potent direct antithrombin. The amino acid sequence of the 29 amino acid peptide was reverse translated, and the gene was chemically synthesised and cloned into an expression vector as a 3' fusion to the staphylokinase gene. Gene expression was induced in E. coli Top 10 cells and the fusion protein, designated PLATSAK, was purified using metal affinity chromatography. The purified fusion protein significantly lengthened the activated partial thromboplastin time and thrombin time and inhibited the amidolytic activity of thrombin. The fibrinolytic activity was almost equal to that of recombinant staphylokinase as measured with a thrombelastograph. Platelet aggregation was not markedly inhibited by PLATSAK, probably due to the unfavourable three dimensional structure, with the Arg-Gly-Asp sequence buried inside. Our results confirm that it is feasible to design and produce a hybrid multifunctional protein that targets various components of the haemostatic process.     

A method of evaluating drug efficacy by statistical analysis of healing speed of peptic ulcer

At present, the evaluation of anti-ulcer drugs is generally accomplished simply by calculating the cumulative healing rate at a certain point of time during treatment, which does not implicate any analysis of the healing speed of the ulcer. If the cumulative healing rate of an ulcer is expressed as a function of drug administration time, t, then it will be possible to calculate parameters concerning the healing speed of ulcers and thus evaluate drug efficacy as the time series analysis of the cumulative healing rate. A new method of evaluating anti-ulcer drugs by a statistical analysis of healing speed is proposed. A non-linear regression analysis was performed between two variables, t (time of drug administration: week) and y (non-healing rate: %), to obtain the exponential function y = Ae-kt. The theoretical values calculated from the exponential equation were in close proximity to the observed values. With this analysis, four parameters concerning the healing speed were defined, namely the healing rate constant, the initiation time of healing, the half-life of non-healing rate and the time necessary for 50% healing. With this method, the efficacy of drugs on peptic ulcer healing was dynamically analysed, the non-healing rate (y) being expressed as an exponential function of length of time (t) of treatment, thus obtaining digital parameters for healing speed.