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The present study carried out assessments regarding thermal sensations under different weather conditions in three urban areas in Cuiabá, Brazil, a Tropical Savannah climate (Aw) region. Thermal acceptability by means of thermal sensation votes (TSV) was addressed based on the estimation of the Universal Thermal Climate Index (UTCI) values. Important issues related to clothing thermal insulation (Icl), the effect of gender on thermal sensation, and implications of artificial conditioning (AC) systems are also evaluated. Micrometeorological variables were determined and 685 questionnaires were applied to evaluate individual pedestrian thermal preferences. The Icl observed in the Tropical climate was lower than that intrinsically inputted by the UTCI for Temperate climates. The local thermal comfort zone ranged between 21.5 and 28.5 °C, with both thresholds higher than those observed in studies conducted in Subtropical, Mediterranean, and Continental Temperate climates while the local hot thermal sensation categories were displaced at least 3 °C above than those for the aforementioned climates. The effect of gender on thermal sensation indicated that females are more sensitive to cold stress conditions than males, requiring higher Icl for temperatures below 28 °C. The physiological adaptation by continuous exposure to AC systems reduced the neutral temperature between AC and non-artificial conditioning system users (NAC) by 0.8 °C, with more intense differences in hot TSV ranges. This study reveals differences between stated TSV classes derived for other climates and those resulting from TSV declared by Savannah local residents, indicating that local thermal sensation scale for UTCI in an important key for environment planning.

Background: A hyperbolic function as well as a linear relationship between power output and time to exhaustion (Tlim) has been consistently observed during dynamic non-resistive exercises. However, little is known about its concept to resistance exercises (RE), which could be defined as critical load (CL). This study aimed to verify the existence of CL during dynamic RE and to verify the number of workbouts necessary to determine the optimal modeling to achieve it., Methods: Fifteen healthy men (23±2.5 yrs) completed 1 repetition maximum test (1RM) on a leg press and 3 (60%, 75% and 90% of 1RM) or 4 (+ 30% of 1RM) workbouts protocols to obtain the CL by hyperbolic and linear regression models between Tlim and load performed. Blood lactate and leg fatigue were also measured., Results: CL was obtained during RE and 3 workbouts protocol estimate it at 53% while 4 tests at 38% of 1 RM. However, based on coefficients of determination, 3 protocols provided a better fit than the 4-parameter model, respectively (R2>0.95 vs. >0.77). Moreover, all intensities increased blood lactate and leg fatigue, however, when corrected by Tlim, were significantly lower at CL., Conclusions: It was possible to determinate CL during dynamic lower limbs RE and that 3 exhaustive workbouts can be used to better estimate the CL, constituting a new concept of determining this threshold during dynamic RE and reducing the physically demanding nature of the protocol. These findings may have important applications for functional performance evaluation and prescription of RE programs.

Male albino rats with diabetes induced by the administration of streptozotocin (STZ) (45 mg/kg, i.v.) were treated with oral administration of diphenyl diselenide (DPDS) pre-dissolved in soya bean oil. A significant reduction in blood glucose levels was observed in STZ-induced diabetic rats treated with DPDS compared with an untreated STZ diabetic group. The pharmacological effect of DPDS was accompanied by a marked reduction in the level of glycated proteins, and restoration of the observed decreased levels of vitamin C and reduced glutathione (GSH; in liver and kidney tissues) of STZ-treated rats. DPDS also caused a marked reduction in the high levels of thiobarbituric acid reactive substances (TBARS) observed in STZ-induced diabetic group. Finally, the inhibition of catalase, delta aminolevulinic acid dehydratase (eth-ALA-D) and isoforms of lactate dehydrogenase (LDH) accompanied by hyperglycemia were prevented by DPDS in all tissues examined. Hence, in comparison with our earlier report, the present findings suggests that, irrespective of the route of administration and the delivery vehicle, DPDS can be considered as an anti-diabetic agent due to its anti-hyperglycemic and antioxidant properties.

Diphenyl diselenide (PhSe)2, the parent compound of disubstituted diaryl diselenides, produces significant antidepressant-like effect when evaluated in the forced swimming test (FST) in rats. The goal of this study was to investigate the effects of diphenyl diselenide (PhSe)2, m-trifluoromethyl-diphenyl diselenide (F3CPhSe)2 and p-methoxy-diphenyl diselenide (CH3OPhSe)2 on [3H]-serotonin uptake in rat platelets and synaptosomes. At concentrations higher than 10 microM (PhSe)2, and (F3CPhSe)2 inhibited about 20% [3H]-serotonin uptake in platelets. (CH3OPhSe)2 inhibited [3H]-serotonin uptake in platelets at concentrations higher than 1 microM. Similarly, (PhSe)2, (F3CPhSe)2, and (CH3OPhSe)2 significantly inhibited [3H]-serotonin uptake (about 50%) in synaptosomes from rat brain at concentrations higher than 1 microM. The maximal inhibitory effects of (PhSe)2, (F3CPhSe)2, and (CH3OPhSe)2 on [3H]-serotonin uptake from rat synaptosomes were 65%, 96%, and 80%, respectively. In conclusion, our results demonstrate that disubstituted diaryl diselenides altered monoaminergic system by interacting with monoamine uptake.

The aim of the present study was to evaluate pharmacological and toxicological properties of (Z)-2-(methylthio)-1-(butyltelluro)-1-phenylethene 1a, (Z)-1-(4-methylphenylsulfonyl)-2-(phenyltelluro)-2-phenylethene 1b, (Z)-2-(butyltelluro)-1-(benzylthio)-1-heptene 1c and (Z)-2-(phenylthio)-1-(butyltelluro)-1-phenylethene 1d. In vitro, vinylic telluride derivatives 1a, 1d and 1c were more effective in reducing lipid peroxidation than compound 1b. The maximal inhibitory effect of vinylic telluride derivatives on lipid peroxidation was in the following order: 1a = 1d > 1c > 1b. Compound 1b was more potent in inhibiting delta-ALA-D activity (delta-aminolevulinate dehydratase) than compounds 1c and 1d. Based on the in vitro properties presented by compounds 1a (an antioxidant) and 1b (a pro-oxidant), toxicological parameters were assessed in vivo and ex vivo in rats. Calculated LD50 of compounds 1a and 1b, administered by oral route, were 20.5 and 1.44 micromol kg(-1), respectively. Compound 1b induced behavioral alterations in the open field test. Renal and spleenic delta-ALA-D activities were inhibited in rats treated orally with compound 1a. Compound 1b stimulated delta-ALA-D activity in liver and spleen of rats. Rats treated with compound 1b had increased hepatic, renal and spleenic lipid peroxidation. Renal and hepatic markers were not altered when compounds 1a and 1b were administered to rats at doses of around LD50, while compound 1a at high doses changed aspartate aminotransferase activity and urea levels. Based on in vitro results, this study demonstrated that compounds 1a and 1d are promising antioxidant compounds. Ex vivo data reinforce compound 1a as a promising drug for more detailed pharmacological studies.

The aim of this study was to investigate the effects caused by subchronic exposure to diphenyl diselenide in rats. Adult Wistar rats were exposed to diphenyl diselenide (5-300 micromol kg(-1), subcutaneously) once a day for 14 days. The subchronic administration of diphenyl diselenide at a dose of 300 micromol kg(-1) significantly increased aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities in plasma. Conversely, this exposure did not alter lactate dehydrogenase (LDH) activity, urea and creatinine levels in plasma. The activity of delta-aminolevulinate dehydratase (delta-ALA-D) from liver and kidney was inhibited by high dosages of diphenyl diselenide. Diphenyl diselenide did not alter renal Na(+)/K(+)ATPase. A decline in body weight gain was associated with a decrease in food consumption in rats treated with 100 or 300 micromol kg(-1) diphenyl diselenide. At these dosages (100 and 300 micromol kg(-1)), diphenyl diselenide did not cause histological alterations in the liver of rats. Taken together, these results demonstrated that subchronic exposure to diphenyl diselenide at high doses induced minor toxicological effects., (2008 John Wiley & Sons, Ltd)

In the present study, we investigated if thiol-reducing agents are capable of altering mercury (Hg2+), lead (Pb2+) and cadmium (Cd2+) effects on platelet glutamatergic system. Dimercaprol (BAL), a dithiol chelating agent therapeutically used for the treatment of heavy metals poisoning, was capable of protecting the [3H]-glutamate binding against the effects caused by Pb2+ and Hg2+. 2,3-Dimercaptopropane-1-sulfonic acid (DMPS), another dithiol-reducing chelating agent, was capable of protecting the effect caused by Cd2+, Pb2+ and Hg2+. The similar effect was observed with addition of dithiothreitol (DTT) on [3H]-glutamate binding in human platelets. Dithiol-reducing agents (BAL, DMPS and DTT) alone did not alter [3H]-glutamate binding. In contrast, reduced glutathione (GSH), a monothiol-reducing agent, caused a significant inhibition on [3H]-glutamate binding at all concentrations tested. GSH did not modify heavy metal effects on [3H]-glutamate binding in platelets. The findings of the present investigation indicate that dithiol-reducing agents are capable of altering Hg2+, Pb2+ and Cd2+ effects on platelet glutamatergic system. In vitro data on chelating-metal interactions provide only an estimated guide to the treatment of heavy metal poisoning. Consequently, more studies in intoxicated patients are necessary to determine the precise use of the peripheral models and chelating agents.

In the present study, we investigated potential toxic effects of diphenyl ditelluride, as measured by biochemical and hematological parameters. Rats were given a daily dose of 0.3 micromol/kg diphenyl ditelluride by subcutaneous route and sacrificed at different times (24 and 48 h). Hepatic and renal TBARS levels were changed by diphenyl ditelluride exposure at the dose 0.9 micromol/Kg in rats. Diphenyl ditelluride exposure demonstrated an increase in AST (aspartate aminotransferase), ALT (alanine aminotransferase) and LDH (lactate dehydrogenase) activities. Plasma creatinine and urea levels increase after diphenyl ditelluride exposure. Diphenyl ditelluride also produced a significant decrease in plasma triglyceride and cholesterol levels. In contrast, this compound, at all doses tested, induced a marked increase in total leukocyte counts. The present study suggests that diphenyl ditelluride induces hematological disorders and provides evidence for renal and hepatic toxicity in rats.

Research strategies have been developed to characterize parameters in peripheral tissues that might easily be measured in humans as surrogate markers of damage, dysfunction or interactions involving neural targets of toxicants. The similarities between platelet and neuron may even be clinically important, as a number of biochemical markers show parallel changes in the central nervous system (CNS) and platelets. The purpose of our research was to investigate the effect of Hg(2+), Pb(2+) and Cd(2+) on the [(3)H]-glutamate binding and [(3)H]-glutamate uptake in human platelets. The involvement of oxidative stress in the modulation of glutamatergic system induced by heavy metals was also investigated. The present study clearly demonstrates that Hg(2+), Cd(2+), and Pb(2+) inhibited [(3)H]-glutamate uptake in human platelets. Hg(2+) inhibited [(3)H]-glutamate binding, while Cd(2+) and Pb(2+) stimulated [(3)H]-glutamate binding in human platelets. Hg(2+), Cd(2+) and Pb(2+) increased lipid peroxidation levels and reactive oxygen species (ROS) measurement in platelets. The present limited results could suggest that glutamatergic system may be used as a potential biomarker for neurotoxic action of heavy metals in humans.

Organochalcogens are important intermediates and useful reagents in organic synthesis. Recent data from our laboratory demonstrated that bis and tris-selenide alkene derivatives are attractive synthetic targets because of their chemio-, regio- and stereo-selective reactions. Since the erythrocytic delta-aminolevulinate dehydratase (delta-ALA-D) activity could be an important indicator of toxicity, this report investigated bis and tris-selenide alkene derivatives effects on blood delta-ALA-D in vitro. To investigate the mechanisms by which these compounds inhibit human blood delta-ALA-D activity, a thiol reducing agent or zinc chloride were used. 1,2-Bis-selenide alkene derivatives 1a (R=4-MeOC(6)H(4)), 1b (R=4-ClC(6)H(4)) and 1c (R=2,4,6-Me(3)C(6)H(2)) did not inhibit human blood delta-ALA-D activity. 1,1,2-Tris-selenide alkene derivative 2a (R=C(6)H(5)) was the most potent delta-ALA-D inhibitor. Compounds 2b (R=4-MeOC(6)H(4)) and 2c (R=4-ClC(6)H(4)) displayed similar inhibitory potency towards delta-ALA-D activity. Dithiothreitol, a hydrophobic SH-reducing agent, was able to restore and to protect delta-ALA-D activity inhibited by tris-selenide alkene derivatives. Conversely, ZnCl(2) did not alter the enzyme inhibition induced by tris-selenide alkene derivatives. From these findings we suggest that 1,1,2-tris-selenide alkene derivatives inhibited delta-ALA-D activity by an interaction with essential sulfhydryl groups for the enzyme activity.

Objectives: This study analyzed the influence of type 2 diabetes mellitus and primary hypothyroidism on the activity of the delta-aminolevulinate dehydratase (delta-ALA-D) in human blood., Design and Methods: Delta-ALA-D enzyme activity was determined in normal (healthy) people (n=29), compensated (DMC, n=11) and non-compensated diabetic patients (NDMC, n=23), and in patients with compensated (CH, n=19) and non-compensated primary hypothyroidism (NCH, n=10). The determination of lead, copper, zinc and magnesium was performed by graphite furnace atomic absorption spectrometry., Results: This study shows that delta-ALA-D activity was decreased (P<0.05) in situations associated to hyperglycemia maintained for long periods (HbA1c high). Another finding of this study suggests that states of hypofunction of the thyroid gland, when non-compensated, increase the activity of delta-ALA-D (P<0.001). In addition, copper was elevated in HNC, zinc was diminished in DMC, HC and HNC, and magnesium was diminished in the HNC group., Conclusion: This result points out that there is a correlation among diabetes, hypothyroidism and delta-ALA-D activity.

The aim of the present study was to evaluate pharmacological and toxicological properties of 1-buthyltelurenyl-2-methylthioheptene (compound 1). In vitro, compound 1 at 1 microM was effective in reducing lipid peroxidation induced by Fe/EDTA. Compound 1 presented neither thiol peroxidase nor thiol oxidase activity and did not change delta-ALA-D (delta-aminolevulinate dehydratase) activity (10-400 microM). Calculated LD(50) of compound 1, administered by oral route, was 65.1 micromol/kg. Rats treated with compound 1 did not reveal any motor impairment in the open field. Hepatic, renal and cerebral lipid peroxidation in treated rats did not differ from those in control rats. Conversely, 0.5 micromol/kg of compound 1 decreased lipid peroxidation in spleen. Delta-ALA-D activity in liver and spleen was inhibited in rats treated with the higher dose of compound 1 but no significant differences were detected in renal delta-ALA-D activity. AST (aspartate aminotransferase) and ALT (alanine aminotransferase) activities as well as urea and creatinine levels were increased by high doses of compound 1 (50-75 micromol/kg). Compound 1 induced a significant decrease in plasma triglyceride levels but none of the doses tested changed the cholesterol level. This is a promising compound for more detailed pharmacological studies involving organotellurium compounds.

An efficient and simple synthetic protocol for the Biginelli reaction has been developed for the preparation of several new dihydropyrimidinones, under ultrasound irradiation in the presence of NH(4)Cl, in good yields and short reaction time. Some of the synthesized compounds were tested in vitro for their antioxidant activity. All of the selected compounds showed some antioxidant activity. Analogues compounds 3b and 4b exhibited a strong activity against lipid peroxidation induced by Fe + EDTA, while compounds 3b and 3d were the most potent in reducing ROS levels.

Glutamate is the most abundant excitatory neurotransmitter in the mammalian brain, and it is increasingly being implicated in the pathophysiology of mental illness. In fact, changes in glutamate neurotransmission seem to be involved in the etiology of schizophrenia, major depression and bipolar disorders. Furthermore, the alterations in platelet sensitivity in major depression are distinct from those of bipolar disorders. The aim of the present investigation was to determine whether patients with bipolar disorders exhibited differences in [(3)H]-glutamate uptake of platelets. [(3)H]-Glutamate uptake of platelets from controls (n=14), patients with bipolar disorders under lithium treatment (600-1800 mg/day for 6 months) (n=7) and patients with bipolar disorders with psychotic features (n=8) were carried out. Analysis of blood platelets from the three groups of subjects revealed significant differences in [(3)H]-glutamate uptake between the control and psychotic patients. The specific glutamate uptake for the control and psychotic groups was 20.5+/-8.4 and 37.5+/-18.1 pmol glutamate/mg protein/10 min, respectively (mean+/-SD). These results indicate that peripheral glutamate metabolism of platelets is modified in bipolar disorders and that more detailed studies must be carried out to determine whether these peripheral modifications correlate with central modifications in humans and in animal models of the disease.

Bis and tris-selenide alkene derivatives, a class of organoselenium compounds, were screened for antinociceptive and antioxidant activities. In vitro, bis-selenide alkene 1c (R=2,4,6-Me(3)C(6)H(2)), 1d (R=4-ClC(6)H(4)) and 1e (R=4-MeOC(6)H(4)) protected against lipid peroxidation about 50%, whereas 1b (R=C(6)H(5)) and 1a (R=C(4)H(9)) protected only 23%. Compound 1d presented lesser IC(50) against lipid peroxidation than other bis-selenide alkene compounds (1d>1e> or =1c>1a=1b). The maximal inhibitory effect of tris-selenide alkenes on lipid peroxidation was in the following order 2c>2a=2b. Compound 1e increased the rate of GSH, but not DTT, oxidation. Tris-selenide alkene 2c (R=4-MeOC(6)H(4)) demonstrated the higher rate of thiol oxidation, while 2a (R=C(6)H(5)) did not change DTT oxidation but oxidized GSH. Conversely, compound 2b (R=4-ClC(6)H(4)) did not change the rate of GSH oxidation, but oxidized DDT. Bis-selenide alkene derivatives 1c, 1d and 1e were the most promising compounds tested in vitro. In vivo, compounds 1c and 1d (5-50mg/kg, subcutaneously) produced significant inhibition of acetic acid- and capsaicin-induced pain. Compounds 1c and 1d increased the tail-flick response latency time. The antinociception effect of 1c and 1d was not abolished by naloxone (an antagonist of opioid receptor, 1mg/kg, subcutaneously), suggesting that the antinociceptive effect is not influenced by the opioidergic mechanism.

In the present study, we investigated the in vitro effect of diphenyl ditelluride, diphenyl diselenide and ebselen on Na(+), K(+)-ATPase activity of rat brain. The results demonstrated that all compounds significantly inhibited (in the muM range) Na(+), K(+)-ATPase activity. Diphenyl ditelluride, at low concentrations, provoked an increase in Na(+), K(+)-ATPase activity. Dithiothreitol (DTT), at 3mM, protected the inhibition caused by diphenyl ditelluride, diphenyl diselenide and ebselen in Na(+), K(+)-ATPase activity. Post-incubation of diphenyl diselenide-treated homogenate with DTT completely recovered enzyme activity. DTT was able to recover the enzyme inhibition induced by 20muM of diphenyl ditelluride, but was partially able to recover inhibition induced by high concentrations of organotellurium compound. Conversely, DTT did not recover ebselen-induced Na(+), K(+)-ATPase inhibition. The mechanism of inhibition by diphenyl diselenide, diphenyl ditelluride and ebselen in Na(+), K(+)-ATPase activity revealed: decreased maximal velocity and K(m). Cerebral Na(+), K(+)-ATPase is a potential molecular target for the toxic effect of organochalcogens and the inhibition may occur through a change in the crucial thiol groups of this enzyme.

The effect of diphenyl diselenide, (PhSe)2, administration on 2-nitropropane (2-NP)-induced hepatic damage was examined in male rats. Rats were pre-treated with a single dose of diphenyl diselenide (10, 50 or 100 micromol/kg). Afterward, they received only one dose of 2-NP (100 mg/kg body weight dissolved in olive oil). The parameters that indicate tissue damage such as plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), alpha-fetoprotein (AFP), creatinine and urea were determined. Since toxicity induced by 2-NP is related to oxidative stress, lipid peroxidation was also evaluated. Diphenyl diselenide (100 micromol/kg) significantly reduced plasma ALT, gamma-GGT, AFP levels when compared to 2-NP group. Treatment with diphenyl diselenide, at all doses, effectively protects the increase of lipid peroxidation when compared to 2-NP group. Histological examination revealed that 2-NP treatment causes a moderate swelling and degenerative alterations on hepatocytes and diphenyl diselenide (100 micromol/kg) protects against these alterations. Diphenyl diselenide (50 and 100 micromol/kg) significantly decreased the urea level. This study evidences the protective effect of diphenyl diselenide by 2-NP-induced acute hepatic damage.

Blood platelets have repeatedly been suggested as an excellent model for various aspects of the synaptic apparatus. Considering that organochalcogens affect some parameters of glutamatergic neurotransmission in rats, in the current study we evaluated the effect of diphenyl diselenide (PhSe)2, diphenyl ditelluride (PhTe)2, and Ebselen on glutamatergic neurotransmission in human platelets. (PhTe)2 and (PhSe)2 caused a significant inhibition, but Ebselen did not interfere in Na-independent glutamate binding. Dithiothreitol (DTT) did not completely prevent the [3H]glutamate binding inhibition caused by 100 microM (PhTe)2. (PhSe)2, (PhTe)2, and Ebselen (100 microM) significantly inhibited [3H]glutamate uptake, whereas organochalcogens at 1 and 10 microM had no significant effect on the [3H]glutamate uptake in human platelets. In this study, platelets were demonstrated to be a suitable model for neurotoxicological research, and, to the best of our knowledge, this is the first report documenting the toxic effects of organochalcogens in human platelets.

Organochalcogens are important intermediates and useful reagents in organic synthesis, which can increase human exposure risk to these chemicals in the workplace. As well, there are a number of reported cases of acute toxicity following organochalcogen ingestion of vitamins and dietary supplements. Since, the erythrocytic delta-ALA-D activity could be an important indicator of toxicity this report investigated the organochalcogens effects on blood delta-ALA-D in vitro. To investigate a possible involvement of cysteinyl groups in the inhibitory actions of diphenyl diselenide, diphenyl ditelluride and Ebselen (4-100 micro M), the effects of thiol reducing agents (0-3 mM) or zinc chloride (0-2 mM) were examined. Diphenyl ditelluride, diphenyl diselenide and Ebselen inhibited in a concentration-dependent manner delta-ALA-D activity from human erythrocytes. Ebselen was lesser delta-ALA-D inhibitor than (PhSe)(2) and (PhTe)(2), whereas the diorganoyldichalcogenides displayed similar inhibitory potency towards delta-ALA-D. Dithiothreitol, a hydrophobic SH-reducing agent, was able to reactivate and to protect inhibited delta-ALA-D. The pre-incubation of blood with the inhibitors changed considerably the reversing potency of thiols. From these findings we suggest that organochalcogens inactivate in vitro human erythrocyte delta-ALA-D by an interaction with the sulfhydryl group essential of the enzyme activity.

The occupational importance of tellurium and selenium is growing rapidly, but the biochemistry of exposure is poorly understood. Here we report the potential toxic effects of diphenyl diselenide (PhSe)(2), diphenyl ditelluride (PhTe)(2) and Ebselen in rats and mice. The results suggest that (PhTe)(2) is more toxic in rats than mice. (PhSe)(2), (PhTe)(2) and Ebselen are more toxic by intraperitoneal (i.p.) than subcutaneous (s.c.) route. Calculated LD(50) for (PhTe)(2), i.p., was 0.65 micromol/kg in rats and 150 micromol/kg in mice, and LD(50), s.c., was 0.9 micromol/kg in rats and >500 micromol/kg in mice. Calculated LD(50) for Ebselen, i.p., was 400 micromol/kg in rats and 340 micromol/kg in mice and LD(50), s.c., was >500 micromol/kg in both mice and rats. (PhTe)(2) at small doses increased 2-fold serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities in rats. LD(50) for all organochalcogens administrated in mice inhibited blood delta-ALA-D activity. The present study provides evidence for liver and renal toxicity of (PhTe)(2).

With the purpose of evaluating the response of sequential applications of Montenegro intradermoreaction (IDRM), we have repeated four times the test in the inhabitants of an endemic area for kala-azar, that resulted negative 3-4 years ago. Firstly, we have repeated three IDRM in those who remained negative, with a 60-day interval among them. In the second stage, we have performed a last reaction in all participants of the study. From the total of 49 individuals with prior negative IDRM, 19 (38.8%) have positivated the test in some of the times, 17 (34.7%) have given up the study and 13 (26.5%) remained with a negative result in all the applications. In the second stage, the repetition of IDRM has shown that from the 14 positive in some of the tests, 8 remained like this and 6 have become negative. Our results confirm the possibility of late hypersensitivity induction in some individuals as a consequence of IDRM application.

Growth hormone (GH) and glutamine (GLN) are considered bowel trophic factors and are used experimentally after bowel resection. Their clinical uses in short bowel syndrome (SBS) are still not standardized. It is of interest to verify metabolic, nutritional and side effects of the association of GH and GLN in SBS. Three patients, 39 (A), 33 (B), and 01 years old (C) underwent bowel resection with jejunum anastomosis 15 cm (A) and 60 cm (B) distant from the Treitz angle, and 40 cm (C) preserving the ileo cecal valve. GH Saizen (Serono-A), Genotropin (Pharmacia-B), and Norditropin (Novonordisk C) were administered in doses of 0.14 mg/kg/day. GLN (0.4 g/kg/day) was given orally for 10 days (A), 30 days (B) and 60 days to patient C (0.28 g/kg/day). Central TPN and adequate oral diet was administered according to the bowel adaptation phase. On the first day after beginning treatment patient A exhibited symptoms of hypoglycemia. There were no other side effects. After treatment, body weight was higher and analysis by bioelectrical impedance showed more lean mass and less fat mass compared to pre-treatment measurements. Nitrogen retention was progressively higher with treatment. Simultaneous treatment with GH and GLN does not cause significant side effects, and is associated with a favorable distribution of the body compartments and nitrogen retention in patients with the short bowel syndrome.

The central venous catheter is considered the lifeline of patients requiring long-term parenteral nutrition, and its infectious complications accordingly represent a frequent cause for hospitalization and morbidity. Modern catheters made of Silastic increase the duration and efficiency of venous access, but their substitution is also more complex and expensive. In a small series of patients undergoing home parenteral nutrition due to short bowel syndrome, and carrying. Silastic catheters, infection of the cannula was treated by administration of systemic as well as local antimicrobial agents. The septic process was resolved without the need of removing the catheters, and with excellent tolerance to the medications. It is concluded that in-situ sterilization of long-term catheters should be attempted in selected cases.