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Background: Pogostemon heyneanus leaves infusions are relevant in ethnopharmacology for treating colds, coughs, headaches, and asthma. Purpose: The essential oil chemical composition of a Pogostemon heyneanus specimen was monthly monitored from October 2021 to July 2022 to evaluate the climatic influences on its yield and chemical composition and antinociceptive, andanti-inflammatory properties. Methods: The leaves, collected monthly over a 10-month period, were submitted to hydrodistillation. The oils obtained were analyzed by gas chromatography coupled to a mass spectrometer and gas chromatography coupled to flame ionization detector. The P. heyneanus essential oil (PhEO) was tested in vivo to evaluate its peripheral analgesic actions through the abdominal writhing test induced by acetic acid, and peripheral analgesia by tail immersion. Neurogenic and inflammatory pain were evaluated by formalin test, and acute oral toxicity of the oil was also verified. Results: PhEO presented 27 chemical constituents with the highest predominance of patchoulol (43.6%-76.9%), α-bulnesene (0.2%-12.7%), α-guaiene (0.4%-8.9%), seychellene (3.8%-5.1%) and pogostol (0.0%-8.2%). The climatic parameters insolation, humidity, rainfall, and temperature did not influence the essential oil yield or the main chemical constituents, except for pogostol, which presented a strong (r = 0.73) and statistically significant ( p < 0.05) correlation with temperature. PhEO did not display toxicity at the maximum 300 mg/kg dosage. The oil showed low peripheral and central analgesic action at 100 mg/kg, while in the neurogenic and inflammatory pain inhibition tests, no actions related to PhEO were observed. In the carrageenan-induced peritonitis test, PhEO did not reduce the migration of leukocytes to the peritoneal cavity compared to the control group. Conclusion: Pogostemon heyneanus is a resistant plant to seasonal influences and a source of patchoulol. Despite ethnopharmacological indications, no in-vivo biological activities such as neurogenic or inflammatory pain were identified in the present work. So, the low influence of the climatic parameters on chemical composition can infer that the low pharmacological activity is also not subject to climatic variations, that is, it does not change due to the climate., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Santos, Jerônimo, Ribeiro, Lopes, Leão Neto, da Silva, da Silva, Silva, da Silva, Freitas, Mourão, Setzer, Maia and Figueiredo.)

Objective: To assess the effect of atelectasis during mechanical ventilation on the periatelectatic and normal lung regions in a model of atelectasis in rats with acute lung injury induced by lipopolysaccharide., Methods: Twenty-four rats were randomized into the following four groups, each with 6 animals: the Saline-Control Group, Lipopolysaccharide Control Group, Saline-Atelectasis Group, and Lipopolysaccharide Atelectasis Group. Acute lung injury was induced by intraperitoneal injection of lipopolysaccharide. After 24 hours, atelectasis was induced by bronchial blocking. The animals underwent mechanical ventilation for two hours with protective parameters, and respiratory mechanics were monitored during this period. Thereafter, histologic analyses of two regions of interest, periatelectatic areas and the normally-aerated lung contralateral to the atelectatic areas, were performed., Results: The lung injury score was significantly higher in the Lipopolysaccharide Control Group (0.41 ± 0.13) than in the Saline Control Group (0.15 ± 0.51), p < 0.05. Periatelectatic regions showed higher lung injury scores than normally-aerated regions in both the Saline-Atelectasis (0.44 ± 0.06 x 0.27 ± 0.74 p < 0.05) and Lipopolysaccharide Atelectasis (0.56 ± 0.09 x 0.35 ± 0.04 p < 0.05) Groups. The lung injury score in the periatelectatic regions was higher in the Lipopolysaccharide Atelectasis Group (0.56 ± 0.09) than in the periatelectatic region of the Saline-Atelectasis Group (0.44 ± 0.06), p < 0.05., Conclusion: Atelectasis may cause injury to the surrounding tissue after a period of mechanical ventilation with protective parameters. Its effect was more significant in previously injured lungs.

Introduction: Lactation overnutrition is a programming agent of energy metabolism, and litter size reduction leads to the early development of obesity, which persists until adulthood. Liver metabolism is disrupted by obesity, and increased levels of circulating glucocorticoids are pointed as a possible mediator for the obesity development, since bilateral adrenalectomy (ADX) can reduce obesity in different models of obesity. Methods: This study aimed to evaluate the effects of glucocorticoids on metabolic changes and liver lipogenesis and insulin pathway induced by lactation overnutrition. For this, on the postnatal day 3 (PND), 3 pups (small litter-SL) or 10 pups (normal litter-NL) were kept with each dam. On PND 60, male Wistar rats underwent bilateral adrenalectomy (ADX) or fictitious surgery (sham), and half of ADX animals received corticosterone (CORT- 25 mg/L) diluted in the drinking fluid. On PND 74, the animals were euthanized by decapitation for trunk blood collection, and liver dissection and storage. Results and Discussion: SL rats presented increased corticosterone, free fatty acids, total and LDL-cholesterol plasma levels, without changes in triglycerides (TG) and HDL-cholesterol. The SL group also showed increased content of liver TG, and expression of fatty acid synthase (FASN), but decreased expression of PI3K p110 in the liver, compared to NL rats. In the SL group, the ADX decreased plasma levels of corticosterone, FFA, TG and HDL cholesterol, liver TG, and liver expression of FASN, and IRS2, compared to sham animals. In SL animals, CORT treatment increased plasma levels of TG and HDL cholesterol, liver TG, and expression of FASN, IRS1, and IRS2, compared with the ADX group. In summary, the ADX attenuated plasma and liver changes observed after lactation overnutrition, and CORT treatment could reverse most ADX-induced effects. Thus, increased circulating glucocorticoids are likely to play a pivotal role in liver and plasma impairments induced by lactation overnutrition in male rats., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 de Souza, Stopa, Martins, Wunderlich, Lopes, de Fatima Silva, Komino, Zaia, Zaia, Lima and Uchoa.)

Introduction: breast cancer is the cancer with the highest incidence in women in Brazil, representing 29.7% of all cancers. More than two thirds of women with breast cancer show expression for hormone receptors, and in these cases, hormone therapy with tamoxifen is indicated, which may represent a risk factor for the development of endometrial cancer (four-fold greater relative risk)., Objective: this study aimed to evaluate the association of tamoxifen and the development of endometrial disturbances and to assess possible other associated risk factors., Patients and Method: a total of 364 breast cancer patients were evaluated, 286 who used tamoxifen and 78 who did not use this hormone therapy. Results: patients who used tamoxifen had a mean follow-up time of 51.42 months similar to those without hormone therapy (p=0.081). A total of 21 (7.3%) women who used tamofixen and no cases among women without hormone therapy presented endometrial changes during follow-up (p=0.01). Despite information regarding obesity was available for only 270 women, obesity was also significantly associated with the development of endometrial changes (p=0.008)., Conclusion: furthermore, the association between tamofixen and endometrial changes remained significant (p=0.039) after adjusting for obesity.

Aims: Litter size reduction on the first days of life results in increased body weight and adiposity, with higher levels of circulating glucocorticoids. Obese rodents are more sensitive to the anabolic effects of glucocorticoids and less responsive to glucocorticoids feedback on hypothalamic-pituitary-adrenal (HPA) axis. This study aimed to evaluate effects of the treatment with corticosterone on metabolic responses and HPA axis in adult male rats reared in small litters., Main Methods: From postnatal day (PND) 60 to 88, adult male rats of normal (NL- 10 pups/dam) and small (SL- 3 pups/dam) litters received oral treatment with Corticosterone (CORT-15 mg/L) in the drinking water or no treatment, composing the four experimental groups (NL-water; NL-CORT; SL-water and SL-CORT), for the evaluation of energy homeostasis and HPA axis., Key Findings: Male rats of SL-water group presented on PND88: glucose intolerance, higher adiposity, plasma triglycerides, free fatty acids, total and low-density lipoprotein (LDL) cholesterol and corticosterone. SL-water animals showed increased mRNA of corticotrophin-releasing hormone (CRH) in the hypothalamic paraventricular nucleus (PVN) and proopiomelanocortin (POMC) in the pituitary, with decreased mRNA expression of PVN mineralocorticoid receptor. NL-CORT animals presented glucose intolerance, increased body weight, food intake, total and LDL cholesterol. Glucocorticoid treatment reduced corticosterone levels and adrenal cortex thickness in NL group, associated with increased mRNA of PVN CRH and pituitary POMC, without effects on SL animals., Significance: Lactation overnutrition promotes hyperreactivity of HPA axis and reduces the responsiveness to glucocorticoids effects on energy balance and negative feedback of HPA axis in adult male rats., (Copyright © 2022 Elsevier Inc. All rights reserved.)

This work evaluated the effects of neonatal overfeeding, induced by litter size reduction, on fertility and the noradrenaline-kisspeptin-gonadotrophin releasing hormone (GnRH) pathway in adult female rats. The litter size was adjusted to 3 pups with each mother in the small litters (SL) and 10 pups with each mother in the normal litters (NL). SL females exhibited metabolic changes associated with reproductive dysfunctions, shown by earlier vaginal opening and first estrus, later regular cyclicity onset, and lower and higher occurrences of estrus and diestrus phases, respectively, as well as reduced fertility, estradiol plasma levels, and mRNA expressions of tyrosine hydroxylase in the locus coeruleus, kisspeptin, and GnRH in the preoptic area in adult females in the afternoon of proestrus. These results suggest that neonatal overfeeding in female rats promotes reproductive dysfunctions in adulthood, such as lower estradiol plasma levels associated with impairments in fertility and noradrenaline-kisspeptin-GnRH pathway during positive feedback., (Copyright © 2020 Elsevier B.V. All rights reserved.)

This study aimed at comparatively evaluate, by visual method, the fluorescence intensity in vitro and in vivo of six resins composed of different classifications and viscosities compared to natural enamel. For the in vitro study, seventy specimens were prepared and for the in vivo study, a restoration was performed on the cervical portion of the buccal face of 6 anterior maxillary teeth, which under ultraviolet light were compared to the dental structure. The specimens and restorations were photographed only under the illumination of an ultraviolet lamp. The photographic record was performed, with standardized parameters for all photographs (ISO 100). After visual analysis of the images by three evaluators calibrated in the in vitro study and by ten evaluators calibrated in the in vivo study, numerical values were assigned to resins without fluorescence (zero), medium fluorescence (1) and high fluorescence (2). The evaluations were submitted to the Kruskal-Wallis and Dunn test, which among the limitations of this study and according to the employed methodology, it was found that there was no statistical difference in fluorescence intensity among the composite resins evaluated, since all types of resins achieved fluorescent metamerism with dental enamel., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

The effect of low-level laser therapy (LLLT) on an experimental model of ventilator-induced lung injury (VILI) was evaluated in this study. 24 adult Wistar rats were randomized into four groups: protective mechanical ventilation (PMV), PMV + laser, VILI and VILI + laser. The animals of the PMV and VILI groups were ventilated with tidal volumes of 6 and 35 ml kg-1, respectively, for 90 minutes. After the first 60 minutes of ventilation, the animals in the laser groups were irradiated (808 nm, 100 mW power density, 20 J cm-2 energy density, continuous emission mode, and exposure time of 5 s) and after 30 minutes of irradiation, the animals were euthanized. Lung samples were removed for morphological analysis, bronchoalveolar lavage (BAL) and real time quantitative polynucleotide chain reaction (RT-qPCR). The VILI group showed a greater acute lung injury (ALI) score with an increase in neutrophil infiltration, higher neutrophil count in the BAL fluid and greater cytokine mRNA expression compared to the PMV groups (p < 0.05). The VILI + laser group when compared to the VILI group showed a lower ALI score (0.35 ± 0.08 vs. 0.54 ± 0.13, p < 0.05), alveolar neutrophil infiltration (7.00 ± 5.73 vs. 21.50 ± 9.52, p < 0.05), total cell count (1.90 ± 0.71 vs. 4.09 ± 0.96 × 105, p < 0.05) and neutrophil count in the BAL fluid (0.60 ± 0.37 vs. 2.28 ± 0.48 × 105, p < 0.05). Moreover, LLLT induced a decrease in pro-inflammatory and an increase of anti-inflammatory mRNA levels compared to the VILI group (p < 0.05). In conclusion, LLLT was found to reduce the inflammatory response in an experimental model of VILI.

Although anthracycline (ANT)-based treatment strongly contributes to cancer survivorship, the use of these agents is limited by the risk of cardiotoxicity. For those patients who evolve to heart failure, myocardial regenerative approaches are of particular interest, and a growing body of preclinical studies has been investigating the use of cell therapy for ANT-induced cardiomyopathy (AIC). However, since animal models and modalities of cell therapy are highly heterogeneous between studies, the efficacy of cell therapy for AIC is not clear. Thus, we conducted a systematic review and meta-analysis of experimental studies reporting the use of cell therapy with mesenchymal stromal cells (MSC) or bone marrow mononuclear cells (BMMNC) in animal models of AIC with regard to global cardiac function. The Medline, EMBASE, and Web of Science databases were searched from inception to November 2019. Two reviewers independently extracted data on study quality and the results of left ventricular ejection fraction (LVEF) and fractional shortening (FS) obtained by echocardiography. The quality of outcomes was assessed using the Cochrane, Collaborative Approach to Meta-Analysis and Review of Animal Data from Experimental Studies (CAMARADES), and SYRCLE bias risk tools. Pooled random-effects modeling was used to calculate pooled mean differences (MD) and 95% confidence intervals (CIs). Twenty-two studies comprising 381 small animals (rabbits and rodents) were included. A pooled meta-analysis of all treatments showed that cell therapy increased LVEF by 9.87% (95% CI 7.25-12.50, P  < 0.00001) and FS by 7.80% (95% CI 5.68-9.92, P  < 0.00001) in small animals with AIC. Cell therapy with MSC/BMMNC is effective to mitigate the deleterious effects of ANT on cardiac function in preclinical models. Nevertheless, due to the small number of studies and considerable heterogeneity, future translational studies must be designed to diminish between-study discrepancies and increase similarity to the clinical landscape.

Overpopulation and environmental degradation due to inadequate resource-use are outcomes of human's ecosystem engineering that has profoundly modified the world's landscape. Despite the age-old concern that unchecked population and economic growth may be unsustainable, the prospect of societal collapse remains contentious today. Contrasting with the usual approach to modeling human-nature interactions, which are based on the Lotka-Volterra predator-prey model with humans as the predators and nature as the prey, here we address this issue using a discrete-time population dynamics model of ecosystem engineers. The growth of the population of engineers is modeled by the Beverton-Holt equation with a density-dependent carrying capacity that is proportional to the number of usable habitats. These habitats (e.g., farms) are the products of the work of the individuals on the virgin habitats (e.g., native forests), hence the denomination engineers of ecosystems to those agents. The human-made habitats decay into degraded habitats, which eventually regenerate into virgin habitats. For slow regeneration resources, we find that the dynamics is dominated by rounds of prosperity and collapse, in which the population reaches vanishing small densities. However, increase of the efficiency of the engineers to explore the resources eliminates the dangerous oscillatory patterns of feast and famine and leads to a stable equilibrium that balances population growth and resource availability. This finding supports the viewpoint of growth optimists that technological progress may avoid collapse.

Adolescence is a period of vulnerability to substance use disorders (SUDs). Epidemiological studies indicate that about 23% of Brazilian adolescents use drugs, with alcohol being the most widely consumed substance. The etiology of SUDs is complex, influenced by an interaction of genetic risk, individual development, environmental factors, context of use, and substance used. Clinicians should consider diagnostic criteria and be aware of behavioral changes that may indicate drug use and its consequences in various aspects of adolescent life. Identification and treatment of comorbid conditions is critical to the management of SUDs in this age group. Interventions should restrict access to drugs and facilitate prompt recognition of initial use, preventing progression to serious patterns of abuse or dependence. Intervention should be broad, including academic and occupational activities as well as social relationships and leisure, which are critical to the reestablishment of normal adolescent development.

Aims: The effects of several potassium (K(+)) channel blockers were studied to determine which K(+) channels are involved in peripheral antinociception induced by the cannabinoid receptor agonist, anandamide., Main Methods: Hyperalgesia was induced by subcutaneous injection of 250 μg carrageenan into the plantar surface of the hind paw of rats. The extent of hyperalgesia was measured using a paw pressure test 3 h following carrageenan injection. The weight in grams (g) that elicited a nociceptive response, paw flexion, during the paw pressure test was used as the nociceptive response threshold., Key Findings: Doses of 50, 75, and 100 ng of anandamide elicited a dose-dependent antinociceptive effect. Following a 100 ng dose of anandamide no antinociception was observed in the paw that was contralateral to the anandamide injection site, which shows that anandamide has a peripheral site of action. Pretreatment with 20, 40 and 80 μg AM251, a CB(1) receptor antagonist, caused a dose-dependent decrease in anandamide-induced antinociception, suggesting that the CB(1) receptor is directly involved in anandamide effect. Treatment with 40, 80 and 160 μg glibenclamide, an ATP-sensitive K(+) channel blocker, caused a dose-dependent reversal of anandamide-induced peripheral antinociception. Treatment with other K(+) channel antagonists, tetraethylammonium (30 μg), paxilline (10 μg) and dequalinium (50 μg), had no effect on the induction of peripheral antinociception by anandamide., Significance: This study provides evidence that the peripheral antinociceptive effect of the cannabinoid receptor agonist, anandamide, is primarily caused by activation of ATP-sensitive K(+) channels and does not involve other potassium channels., (Copyright © 2011. Published by Elsevier Inc.)

Background and Purpose: It has been demonstrated that cannabinoids evoke the release of endogenous opioids to produce antinociception; however, no information exists regarding the participation of cannabinoids in the antinociceptive mechanisms of opioids. The aim of the present study was to determine whether endocannabinoids are involved in central antinociception induced by activation of mu-, delta- and kappa-opioid receptors., Experimental Approach: Nociceptive threshold to thermal stimulation was measured according to the tail-flick test in Swiss mice. Morphine (5 microg), SNC80 (4 microg), bremazocine (4 microg), AM251 (2 and 4 microg), AM630 (2 and 4 microg) and MAFP (0.1 and 0.4 microg) were administered by the intracerebroventricular route., Key Results: The CB(1)-selective cannabinoid receptor antagonist AM251 completely reversed the central antinociception induced by morphine in a dose-dependent manner. In contrast, the CB(2)-selective cannabinoid receptor antagonist AM630 did not antagonize this effect. Additionally, the administration of the anandamide amidase inhibitor, MAFP, significantly enhanced the antinociception induced by morphine. In contrast, the antinociceptive effects of delta- and kappa-opioid receptor agonists were not affected by the cannabinoid antagonists. The antagonists alone caused no hyperalgesic or antinociceptive effects., Conclusions and Implications: The results provide evidence for the involvement of cannabinoid CB(1) receptors in the central antinociception induced by activation of mu-opioid receptors by the agonist morphine. The release of endocannabinoids appears not to be involved in central antinociception induced by activation of kappa- and delta-opioid receptors.

Aims: In this study, we investigated whether the opioid system and the nitric oxide pathway were involved in the peripheral antinociception induced by a cannabinoid receptor agonist anandamide., Main Methods: Hyperalgesia was induced by a subcutaneous injection of carrageenan (250 microg) into the plantar surface of the rat's hindpaw and measured by the paw pressure test 3h after injection. The weight in grams (g) required to elicit a nociceptive response, paw flexion, was determined as the nociceptive threshold., Key Findings: Anandamide elicited a dose-dependent (50, 75, and 100 ng per paw) antinociceptive effect. The highest dose of anandamide did not produce antihyperalgesia in the contralateral paw, indicating a peripheral site of action. The CB(1) receptor antagonist AM251 (20, 40, 80 and 160mug per paw) antagonized peripheral antihyperalgesia induced by anandamide (100 ng), in a dose-dependent manner, suggesting CB(1) receptor activation. Anandamide-induced peripheral antihyperalgesia was reverted by blockers of the l-arginine/NO/cGMP pathway N(G)-nitro-l-arginine (NOARG; 24, 36 and 48 microg per paw) and 1H-[1,2,4] Oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 25, 50 and 100 microg per paw), in a dose-dependent manner. Furthermore, opioid receptor antagonist naloxone (12.5, 25 and 50 microg per paw) antagonized the peripheral antihyperalgesia induced by anandamide., Significance: This study provides evidence that the peripheral antinociceptive effect of the cannabinoid receptor agonist anandamide may result from l-arginine/NO/cGMP pathway activation and that the opioid system is also involved.

We investigated the effect of chloride and potassium channel blockers on the antinociception induced by GABA(C) receptor agonist CACA (cis-4-aminocrotonic acid) using the paw pressure test, in which pain sensitivity was increased by an intraplantar injection (2 microg) of prostaglandin E(2) (PGE(2)). CACA administered locally into the right hindpaw (25, 50 and 100 microg/paw) elicited a dose-dependent antinociceptive effect which was demonstrated to be local, since only higher doses produced an effect when injected in the contralateral paw. The GABA(C) receptor antagonist (1,2,5,6 tetrahydropyridin-4-yl) methylphosphinic acid (TPMPA; 5, 10 and 20 microg/paw) antagonized, in a dose-dependent manner, the peripheral antinociception induced by CACA (100 microg), suggesting a specific effect. This effect was reversed by the chloride channel coupled receptor blocker picrotoxin (0.8 microg/paw). Glibenclamide (160 microg) and tolbutamide (320 microg), blockers of ATP-sensitive potassium channels, charybdotoxin (2 microg), a large-conductance potassium channel blocker, dequalinium (50 microg), a small-conductance potassium channel blocker, and cesium (500 microg), a non-specific potassium channel blocker did not modify the peripheral antinociception induced by CACA. This study provides evidence that activation of GABA(C) receptors in the periphery induces antinociception, that this effect results from the activation of chloride channel coupled GABA(C) receptors and that potassium channels appear not to be involved.

Although alternative splicing of many genes has been found associated with different stages of tumorigenesis and splicing variants have been characterized as tumor markers, it is still not known whether these examples are sporadic or whether there is a broader association between the two phenomena. In this report we evaluated, through a bioinformatics approach, the expression of splicing factors in both normal and tumor tissues. This was possible by integrating data produced by proteomics, serial analysis of gene expression (SAGE) and microarray experiments. We observed a significant shift in the expression of splicing factors in tumors in both SAGE and microarray data, resulting from a large amount of experiments. We discuss that this supports the notion of a broader association between alternative splicing and cell transformation, and that splicing factors may be involved in oncogenic pathways.

Prader-Willi syndrome (PWS) is a neurobehavioral disorder caused by deletions in the 15q11-q13 region, by maternal uniparental disomy of chromosome 15 or by imprinting defects. Structural rearrangements of chromosome 15 have been described in about 5% of the patients with typical or atypical PWS phenotype. An 8-year-old boy with a clinical diagnosis of PWS, severe neurodevelopmental delay, absence of speech and mental retardation was studied by cytogenetic and molecular techniques, and an unbalanced de novo karyotype 45,XY,der(4)t(4;15)(q35;q14),-15 was detected after GTG-banding. The patient was diagnosed by SNURF-SNRPN exon 1 methylation assay, and the extent of the deletions on chromosomes 4 and 15 was investigated by microsatellite analysis of markers located in 4qter and 15q13-q14 regions. The deletion of chromosome 4q was distal to D4S1652, and that of chromosome 15 was located between D15S1043 and D15S1010. Our patient's severely affected phenotype could be due to the extent of the deletion, larger than usually seen in PWS patients, although the unbalance of the derivative chromosome 4 cannot be ruled out as another possible cause. The breakpoint was located in the subtelomeric region, very close to the telomere, a region that has been described as having the lowest gene concentrations in the human genome.

The precise excision of introns from mRNAs is executed by the spliceosome, a cellular machinery composed by five small nuclear RNAs and hundreds of proteins. In the last few years, several groups have used proteomics and computational biology tools to characterize the components of the human spliceosome. These reports have identified basically all known splicing factors and several new proteins. The composition of the human spliceosome confirms the link between splicing and other steps in gene expression. Here we comment on these reports and discuss the perspectives for the coming years.

During the course of systemic inflammatory reactions and chronic venous congestion, the documented phenomenon of increased spleen size is respectively called reactional hyperplasia and congestive splenomegaly. In Chagas' disease, the inflammatory process observed in the heart of chronically infected patients can result in heart failure and ultimately in congestive failure. In order to evaluate the spleen response to both inflammatory and cardiac processes, in this retrospective study we compare the weight of spleens from normal and chagasic patients, with or without congestive failure. Information about patient age, sex, race and spleen weight was collected from autopsy reports. Eighty-eight selected cases were divided into four groups: 1) chagasic patients with congestive failure, 2) chagasic patients without congestive failure, 3) non-chagasic patients with congestive failure, 4) non-chagasic patients without congestive failure. The average age was 44.9 +/- 15.4 years, 53.4% were Caucasians and 70.5% were males, and no significant difference in these parameters was observed between the four groups. The spleen weight for the groups presenting congestive failure was 183.7 +/- 85.9 g for chagasic and 206.3 +/- 101.0 g for non-chagasic patients; for the groups without congestive failure the average spleen weight was 173.7 +/- 118.9 g for the chagasic and 117.2 +/- 52.0 g for non-chagasic patients. The spleen weight was significantly higher for the chagasic patients without congestive failure when compared to the non-chagasic group without congestive failure. These results suggest that the inflammatory component in Chagas' disease plays an important role in the increase of spleen weight together with hemodynamic alterations arising from congestive heart failure.

Nonselective beta-adrenergic blockers (propranolol and nadolol) are effective in preventing initial variceal hemorrhage, although their influence on improving survival is less dramatic. There is no role for either sclerotherapy or prophylactic portosystemic shunts for the prevention of initial variceal hemorrhage. Both endoscopic therapy (sclerotherapy, esophageal variceal ligation) and nonselective beta-adrenergic blockers are effective in reducing the risk of recurrent bleeding related to portal hypertension; however, there are significant numbers of failures with both approaches, and the effect on survival is less impressive. Randomized controlled trials evaluating each of these therapeutic options are reviewed in this article.