Physicochemical and Microbiological Quality of Dietetic Functional Mixed Cerrado Fruit Jam during Storage.

The objective of the research was to evaluate changes of dietetic functional mixed cerrado fruit jam (marolo, sweet passion fruit, and soursop) processed in a vacuum pot and stored for 180 days in BODs at 25°C and 35°C. The parameters evaluated were pH, soluble solids (SS), titratable acidity (TA), total sugars (TS), total carotenoids (TC), total phenolics (TP), vitamin C, antioxidant activity (DPPH), and microbiological analysis. There was a significant effect of storage time on pH, SS, TA, TC, TS, and TP. Vitamin C and DPPH showed an effect for the temperature x storage time interaction. Statistical models are not adjusted for pH and SS, presenting an average of 4.15 and 61%, respectively. Carotenoids decreased up to105 days; total sugars increased up to 105 days. The TP, vitamin C, and DPPH, at the temperatures evaluated, showed a decrease up to 105 days. Yeasts and filamentous fungi were not detected.

Application of mesocellular siliceous foams (MCF) for surface-assisted laser desorption ionization mass spectrometry (SALDI-MS) Analysis of fingermarks.

Recent advances in nanotechnology applied in forensic sciences have contributed to consider new approaches including chemical evaluation of latent fingermarks. Significant improvement to the detection of small organic molecules has been reached with matrix-free methods associated to laser desorption/ionization mass spectrometry. The present study investigated the application of mesocellular siliceous foam (MCF) as an ionizing agent for laser desorption/ionization (LDI-MS) analysis of fingermarks as a proof of concept research. Fingermarks from three different donors were deposited directly onto a MALDI target plate and α-CHCA matrix solution, MCF ethanolic suspension or MCF/magnetic powder mixture were used for treatment. Microscopy characterization of MCF support showed particles with irregular morphology and variable sizes, and a unordered porous surface with pores diameter ranging from about 10 to 20 nm. Results showed less intense peaks in the spectra produced by the MCF support (control). Analysis of fingermarks showed ions related to endogenous and exogenous molecular components, including possible lipids from human sebum and quaternary ammonium cations commonly present in cosmetics. Promising and reproducible results were obtained for the fingermarks dusted with the MCF/magnetic powder mixture. Considering the forensic applications of nanomaterials for the analysis of small molecules in biological samples by matrix-free LDI techniques, the advantages of silica based materials should be further investigated.

Toxicity and physicochemical parameters of composts including distinct residues from agribusiness and slaughterhouse sludge.

Composting is useful for treatment of residues from agribusiness, but the potential toxicity of the final compost should be evaluated before its agricultural destination. The objective of this study was to evaluate the physicochemical characteristics and the toxicity of agribusiness residues using onion seeds as bioindicators. All tested treatments were composed by sludge from a swine slaughterhouse and sawdust. Besides the control, which included no additional materials, the other treatments included aviary bedding, rice husk and residue from tobacco industries as structuring materials. After 120 days of composting, for all treatments, the temperature inside the composting piles approached the environmental temperature, the physicochemical parameters indicated that the composts were stabilized and, except for the treatment including tobacco residues, that could be used for agriculture without impairing plant germination. Although the treatments including tobacco residues and rice husk showed evidence of cytotoxicity and genotoxicity at the beginning of the composting period, that was not observed for the treatment including aviary bedding. Such potential toxicity was not observed at the end of composting for any of the tested treatments.

The anti-IRBP IgG1 and IgG2a response does not correlate with susceptibility to experimental autoimmune uveitis.

Susceptibility to experimental autoimmune uveitis (EAU) in inbred mice has been associated with a dominant Th1 response. Elevated anti-inter-photoreceptor retinoid-binding protein (anti-IRBP) IgG2a/IgG1 antibody ratios have been implicated as candidate markers to predict disease severity. In the present study, both the anti-IRBP antibody isotype and severity of EAU phenotypes were examined in 4 non-isogenic genetically selected mouse lines to determine if they can be used as general markers of disease. Mice between 8 and 12 weeks old selected for high (H(III)) or low (L(III)) antibody response and for maximum (AIR(MAX)) or minimum (AIR(MIN)) acute inflammatory reaction (AIR) were immunized with IRBP. Each experiment was performed with at least 5 mice per group. EAU was evaluated by histopathology 21 days after immunization and the minimal criterion was inflammatory cell infiltration of the ciliary body, choroid and retina. Serum IgG1- and IgG2a-specific antibodies were determined by ELISA. EAU was graded by histological examination of the enucleated eyes. The incidence of EAU was lower in AIR(MIN) mice whereas in the other strains approximately 40% of the animals developed the disease. Low responder animals did not produce anti-IRBP IgG2a antibodies or interferon-gamma. No correlation was observed between susceptibility to EAU and anti-IRBP isotype profiles. Susceptibility to EAU is related to the intrinsic capacity to mount higher inflammatory reactions and increased production of anti-IRBP IgG2a isotype is not necessarily a marker of this immunologic profile.

Trypanosoma cruzi-infected cardiomyocytes produce chemokines and cytokines that trigger potent nitric oxide-dependent trypanocidal activity.

BACKGROUND: The pathogenesis of myocarditis that occurs in Trypanosoma cruzi-infected mice is still poorly understood. Therefore, it is important to know the mediators that trigger leukocyte migration to the heart as well as the cellular source of these possible mediators. In this study, we investigated (1) NO synthase (NOS) induction, (2) NO synthesis, (3) trypanocidal activity, and (4) chemokine and cytokine mRNA expression by isolated cardiomyocytes infected with T cruzi. METHODS AND RESULTS: Mouse cardiomyocytes were isolated, infected with T cruzi, and evaluated for induction of inducible NOS (iNOS), nitrite production, trypanocidal activity, and cytokine and chemokine mRNA expression. We found that T cruzi-infected murine embryonic cardiomyocytes produced nitrite and expressed mRNAs for the chemokines chemokine growth-related oncogene, monokine induced by interferon-gamma, macrophage inflammatory protein-2, interferon-gamma-inducible protein, RANTES, and monocyte chemotactic protein, for iNOS, and for the cytokines tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta. Separate addition of IL-1beta, interferon-gamma, TNF-alpha or monocyte chemotactic protein, macrophage inflammatory protein-2, and interferon-gamma-inducible protein, to cultured cardiomyocytes resulted in NO production but low trypanocidal activity. However, simultaneous addition of IL-1beta, interferon-gamma, and TNF-alpha or the chemokines to cultures resulted in the induction of iNOS, high levels of nitrite, and a marked trypanocidal activity. The iNOS/L-arginine pathway mediated the latter activity, inasmuch as it was inhibited by treatment with N:(G)-monomethyl-L-arginine. CONCLUSIONS: These results indicate that iNOS activation and the proinflammatory cytokines and chemokines produced by cardiomyocytes are likely to control parasite growth and cell influx, thus contributing to the pathogenesis of chagasic cardiomyopathy seen in T cruzi-infected mice.

The adjuvant effect of jacalin on the mouse humoral immune response to trinitrophenyl and Trypanosoma cruzi.

We have evaluated the adjuvant action of jacalin, a lectin obtained from seeds of Artocarpus integrifolia, on humoral immune response against the trinitrophenyl (TNP) hapten when conjugated to it and to Trypanosoma cruzi. The protective effect of parasite-specific antibodies generated in mice immunized with epimastigote forms of T. cruzi plus jacalin was also evaluated by determining the parasitemia levels of animals after infection with 1000 trypomastigote forms. Immunization of mice with trinitrophenylated jacalin (TNP-JAC) in saline resulted in an antibody response to the TNP hapten that was eight and 16 times higher than that found in mice immunized with TNP-human gamma globulin (TNP-HGG) or TNP-bovine serum albumin (TNP-BSA), respectively. In addition, immunization with either a lysate or viable epimastigote forms of T. cruzi in the presence of jacalin resulted in a marked increase in the levels of anti-T. cruzi antibodies. The protective action of antibodies against acute infection by T. cruzi was evident when mice were immunized with 1.0 x 10(5) epimastigotes plus jacalin. These animals had a significantly lower parasitemia than those immunized with epimastigotes alone. In contrast, mice immunized with 1.0 x 10(6) epimastigotes developed very low levels of parasitemia, regardless of the presence of jacalin. These data suggest that jacalin is a potent adjuvant in the humoral response to TNP and T. cruzi, and that the protective action of the T. cruzi-specific antibodies depends on the number of parasites used in the immunization protocol.

Nitric oxide-induced apoptotic cell death in the acute phase of Trypanosoma cruzi infection in mice.

Production of gamma-interferon (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) in Trypanosoma cruzi-infected mice results in the activation of inducible nitric oxide synthase (iNOS) and in elevated nitric oxide (NO) synthesis, which is important for the macrophage trypanocidal activity. However, NO has been shown to be involved in suppression of host immunity. In the present investigation, we studied the role of NO in inducing apoptosis in cells from BALB/c mice acutely infected by T. cruzi. Splenocytes from infected mice had a reduced cell viability and elevated levels of spontaneous apoptosis after 48 h in culture. Inhibition of NO production by the addition of the L-arginine analog NG-monomethyl-L-arginine (L-NMMA), or of monoclonal antibodies (mAbs) to IFN-gamma or TNF-alpha spleen cells, partially restored cell viability and caused a decrease in the levels of apoptosis in splenocytes from infected animals. Spleen cells from T. cruzi-infected mice had an apoptosis-specific pattern of internucleosomal DNA fragmentation which was most marked at the ninth day after infection when the plasma NO levels and parasitemia were increased. Treatment of infected mice with L-NMMA, anti-TNF-alpha, or anti-IFN-gamma mAbs caused reduction of both NO production and the amount of apoptotic cells, suggesting that NO plays a direct role in the induction of apoptosis in vivo. Taken together, these data support the hypothesis that, as well as modulating immunosuppression, NO produced by IFN-gamma and TNF-alpha activated macrophages plays a role in apoptosis induction during the acute phase of experimental T. cruzi infection.

Detection of DNA in the plasma of septic patients.

Small amounts of plasma-free DNA have been observed both in healthy individuals and in patients with various diseases such as systemic lupus erythematosus, rheumatoid arthritis, viral hepatitis, and cancer. This communication demonstrates that septic patients also release DNA in plasma. After DNA extraction from plasma, exon 1 of the K-ras gene was amplified by PCR and products were analyzed by dot-blot hybridization. Plasmas from polytraumatic patients and control healthy individuals were used for comparisons with septic patients. Our results show that septic patients present DNA in their plasma. As far as we know, this is the first evidence of circulating DNA in septic patients.

Free DNA induces modification on the protein synthesis profile of human peripheral blood mononuclear cells of healthy donors.

Understanding how free DNA might act as a signal between cells is important for knowing how DNA orchestrates immune responses and for optimizing the therapeutic of cancer, infection and immunologic diseases. This communication demonstrates that DNAs from different origins (bacteria, T. cruzi, HeLa cells) and synthetic oligonucleotide containing an unmethylated CpG motif are capable of inducing alterations in the protein profile of normal human leukocytes. As far as we know there have been no similar studies regarding the comparative effects of different free DNAs on early protein synthesis of human peripheral blood mononuclear cells.

Expression of heat shock protein 70 in leukocytes of patients with sepsis.

The heat shock proteins are known to protect cells against diverse injuries such as cytotoxicity by TNFalpha acting mainly as chaperones for denatured proteins. Lipopolysaccharide stimulates the production and the release of numerous endogenous mediators of sepsis: tumor necrosis factor alpha, interleukin-1, and interleukin-6 that induce fever production. Moreover, temperature at 40 degrees C is sufficient to induce heat shock and attenuate both TNFalpha and IL-1 expression. We demonstrate a distinct profile in gene expression of HSP 70 family in leukocytes obtained from different phases of septic patients. Our findings strongly suggest that HSP 70 may play a role in the outcome of septic shock patients.

The role of IL-12 in experimental Trypanosoma cruzi infection.

Host resistance to Trypanosoma cruzi infection is dependent on both natural and acquired immune responses. During the early acute phase of infection in mice, natural killer (NK) cell-derived IFN-gamma is involved in controlling intracellular parasite replication, mainly through the induction of nitric oxide biosynthesis by activated macrophages. We have shown that IL-12, a powerful inducer of IFN-gamma production by NK cells, is synthesized soon after trypomastigote-macrophage interaction. The role of IL-12 in the control of T. cruzi infection in vivo was determined by treating infected mice with anti-IL-12 monoclonal antibody (mAb) and analyzing both parasitemia and mortality during the acute phase of infection. The anti-IL-12 mAb-treated mice had higher levels of parasitemia and mortality compared to control mice. Also, treatment of infected mice with mAb specific for IFN-gamma or TNF-alpha inhibited the protective effect of exogenous IL-12. On the other hand, TGF-beta and IL-10 produced by infected macrophages inhibited the induction and effects of IL-12. Therefore, while IL-12, TNF-alpha and IFN-gamma correlate with resistance to T. cruzi infection, TGF-beta and IL-10 promote susceptibility. These results provide support for a role of innate immunity in the control of T. cruzi infection. In addition to its protective role, IL-12 may also be involved in the modulation of T. cruzi-induced myocarditis, since treatment of infected mice with IL-12 or anti-IL-12 mAb leads to an enhanced or decreased inflammatory infiltrate in the heart, respectively. Understanding the role of the cytokines produced during the acute phase of T. cruzi infection and their involvement in protection and pathogenesis would be essential to devise new vaccines or therapies.

Induction of cell-mediated immunity during early stages of infection with intracellular protozoa.

Toxoplasma gondii and Trypanosoma cruzi are intracellular parasites which, as part of their life cycle, induce a potent cell-mediated immunity (CMI) maintained by Th1 lymphocytes and IFN-gamma. In both cases, induction of a strong CMI is thought to protect the host against rapid parasite multiplication and consequent pathology and lethality during the acute phase of infection. However, the parasitic infection is not eliminated by the immune system and the vertebrate host serve as a parasite reservoir. In contrast, Leishmania sp, which is a slow growing parasite, appears to evade induction of CMI during early stages of infection as a strategy for surviving in a hostile environment (i.e., inside the macrophages which are their obligatory niche in the vertebrate host). Recent reports show that the initiation of IL-12 synthesis by macrophages during these parasitic infections is a key event in regulating CMI and disease outcome. The studies reviewed here indicate that activation/inhibition of distinct signaling pathways and certain macrophage functions by intracellular protozoa are important events in inducing/modulating the immune response of their vertebrate hosts, allowing parasite and host survival and therefore maintaining parasite life cycles.

A morphometric study of maternal smoking on apoptosis in the syncytiotrophoblast.

OBJECTIVES: To study syncytiotrophoblast apoptosis in the placenta of smoking and non-smoking pregnant women. METHODS: Twelve neonates, pregnancies and placentas were available for study. Eight mothers smoked during pregnancy and the remaining four were non-smokers used as control subjects. The main outcome measure was the apoptotic syncytiotrophoblast index for each group. Apoptosis was detected by immunohistochemistry using the TUNEL method and quantitatively measured using a Merz grid. The apoptotic syncytiotrophoblast index was calculated as the ratio of mean apoptotic labeling to percent terminal villus area using high-power field microscopy. RESULTS: Significant differences in apoptotic syncytiotrophoblast index were observed between the control group (15.06+/-3.72) and the smoker group (1.66+/-1.74) (P < 0.0001, Mann-Whitney test), but no differences were detected in clinical or morphometric data between groups. CONCLUSIONS: The human placental syncytiotrophoblast undergoes apoptosis and this process is associated with inhibition of apoptosis by the smoking habit. The same way as the presence of trophoblast apoptosis is associated with modifications of the maternal-fetal exchange, the inhibitory effect of the smoking habit on syncytiotrophoblast could be responsible for the poor prognosis of pregnancy in the presence of maternal smoking.

Estabilidade da caranha em diferentes períodos de armazenamento / Stabilityof the caranhain differentstorage periods

O objetivo deste estudo foi verificar a influência do tempo de armazenamento na qualidade microbiológica, físico-química e sensorial do pescado caranha (Piaractusmesopotamicus). Os pescados foram estocados em gelo durante zero, sete, 14, 21 e 28 dias e submetidos às contagens de micro-organismos mesófilos, psicrotróficos, coliformes a 35ºC e 45ºC, Salmonella sp. e estafilococos coagulase positiva. Foram realizadas análises de temperatura, pH, acidez, bases voláteis, proteínas, lipídeos, cinzas, umidade, prova de cocção, bem como análise sensorial. As contagens de mesófilos, psicrotróficos, coliformes a 35ºC e 45ºC aumentaram com o tempo de armazenamento. A presença de Salmonella sp. não foi constatada, enquanto a contagem de estafilococos coagulase positiva foi de <10 (est) UFC/g em todos os períodos de estocagem. Observou-se, ainda, que o tempo de armazenamento apresentou influência em todas as variáveis físico-químicas, exceto para temperatura. Na análise sensorial, foi constatado um aumento linear do índice de qualidade (IQ) ao longo do armazenamento, e a rejeição ocorreu aos 14 dias.(AU)

The objective of this study was to verify the influence of storage time on the microbiological, physical-chemical, and sensorial quality of the fish (Piaractusmesopotamicus). The fish were stored on ice for 0, 7, 14, 21, and 28 days and submitted to counts of mesophilic, psychrotrophic, coliform microorganisms at 35ºC and 45ºC, Salmonella sp. and coagulase positive staphylococci. Analyzes of temperature, pH, acidity, volatile bases, proteins, lipids, ashes, humidity, cooking test, as well as sensorial analysis were performed. Counts of mesophiles, psychrotrophic, coliforms at 35°C and 45°C increased with storage time. The presence of Salmonella sp. was not observed, whereas the coagulase positive Staphylococcus count was <10 (est) CFU/g in all storage periods. It was also observed that the storage time had influence on all physical-chemical variables, except for temperature. In the sensorial analysis, a linear increase of the quality index (IQ) was verified throughout the storage and the rejection occurred at 14 days.(AU)

Utilização de técnicas de manejo comportamental e neuropsicológicas para intervenção dos transtornos de aprendizagem / Behavioral management and neuropsychological techniques for learning disabilies intervention

O diagnóstico de dislexia do desenvolvimento é um fator de risco para as dificuldades de aprendizagem da matemática e exige programas de intervenção específicos e alicerçados no perfil cognitivo desse grupo clínico. Além dos déficits cognitivos, esses indivíduos também apresentam prejuízos emocionais e sociais. O objetivo do estudo foi avaliar a eficácia de um programa de intervenção da matemática, focado na habilidade de transcodificação numérica. Técnicas de manejo comportamental foram associadas ao treino cognitivo para lidar com os prejuízos emocionais. A intervenção foi realizada em três pacientes com diagnóstico de dislexia e sintomas de baixa autoeficácia, desmotivação e ansiedade de desempenho. Os pacientes participaram de sessões individuais, sendo que o programa foi estruturado em 12 sessões de 60 minutos cada. Para avaliação da eficácia do programa utilizou-se um delineamento de pré e pós-teste. Os resultados demonstraram que todos os pacientes obtiveram ganhos tanto quantitativos, quanto qualitativos. Entretanto, nem todas as habilidades treinadas obtiveram uma melhora significativa, atribui-se esse desfecho a diferenças no perfil cognitivo e emocional dos pacientes...

The diagnosis of developmental dyslexia is a risk factor to mathematical learning difficulties and requires specific intervention programs grounded in the cognitive profile of this clinical group. Besides the cognitive deficits, these individuals have emotional and social impairment. The aim of the study was to evaluate the effectiveness of a math intervention program focused on numerical transcoding ability. Behavioral management techniques were used to deal with the emotional disregulation, during the cognitive intervention. The intervention was performed with three patients diagnosed with dyslexia and symptoms of low self-efficacy, demotivation and performance anxiety. Patients participated in individual sessions of the program which was structured in 12 sessions of 60 minutes each. In order to evaluate the effectiveness of the program, it was used pretest and posttest design. The results demonstrated that all patients had both quantitative and qualitative gain. However, some abilities did not show significative improvement. This scenario is related to pacients differences in cognitive and emotional profile

Early use of terlipressin in catecholamine-resistant shock improves cerebral perfusion pressure in severe traumatic brain injury.

BACKGROUND: Maintaining adequate cerebral perfusion pressure is an essential aspect in the treatment of severe acute brain injury. To accomplish this therapeutic goal vasopressors are usually required. Vasopressin is an important endogenous stress hormone and the infusion of low-dose vasopressin and terlipressin has been used to reverse severe hypotension. CASE REPORT: A 14-year-old male patient was admitted to the emergency room after a motorcycle accident. The patient had suffered severe traumatic brain injury, the Glasgow coma score (GCS) was four and there were signs of aspiration of gastric contents. Systemic inflammatory response syndrome and shock refractory to fluid management, norepinephrine and steroid replacement ensued. A terlipressin infusion, as a bolus dose of 1 mg, is associated with the ability to improve cerebral perfusion pressure with concomitant reduction of 80% of norepinephrine doses. DISCUSSION: The present report illustrates the potential benefits of terlipressin in refractory shock in a patient with severe traumatic brain injury. An increase in cerebral perfusion pressure (CPP) and a huge decrease in the dose of norepinephrine were observed. In the setting of severe brain injury associated with refractory hypotension, terlipressin may improve mean arterial pressure and cerebral perfusion pressure. CONCLUSION: In the setting of severe brain injury associated with refractory hypotension, terlipressin may have a role as a rescue therapy.

Gamma interferon modulates CD95 (Fas) and CD95 ligand (Fas-L) expression and nitric oxide-induced apoptosis during the acute phase of Trypanosoma cruzi infection: a possible role in immune response control.

We have previously shown that splenocytes from mice acutely infected with Trypanosoma cruzi exhibit high levels of nitric oxide (NO)-mediated apoptosis. In the present study, we used the gamma interferon (IFN-gamma)-knockout (IFN-gamma(-/-)) mice to investigate the role of IFN-gamma in modulating apoptosis induction and host protection during T. cruzi infection in mice. IFN-gamma(-/-) mice were highly susceptible to infection and exhibited significant reduction of NO production and apoptosis levels in splenocytes but normal lymphoproliferative response compared to the infected wild-type (WT) mice. Furthermore, IFN-gamma modulates an enhancement of Fas and Fas-L expression after infection, since the infected IFN-gamma(-/-) mice showed significantly lower levels of Fas and Fas-L expression. The addition of recombinant murine IFN-gamma to spleen cells cultures from infected IFN-gamma(-/-) mice increased apoptosis levels, Fas expression, and NO production. In the presence of IFN-gamma and absence of NO, although Fas expression was maintained, apoptosis levels were significantly reduced but still higher than those found in splenocytes from uninfected mice, suggesting that Fas-Fas-L interaction could also play a role in apoptosis induction in T. cruzi-infected mice. Moreover, in vivo, the treatment of infected WT mice with the inducible nitric oxide synthase inhibitor aminoguanidine also led to decreased NO and apoptosis levels but not Fas expression, suggesting that IFN-gamma modulates apoptosis induction by two independent and distinct mechanisms: induction of NO production and of Fas and Fas-L expression. We suggest that besides being of crucial importance in mediating resistance to experimental T. cruzi infection, IFN-gamma could participate in the immune response control through apoptosis modulation.

Interleukin-12 mediates resistance to Trypanosoma cruzi in mice and is produced by murine macrophages in response to live trypomastigotes.

Host resistance to infection by Trypanosoma cruzi is dependent on both natural and acquired immune responses. During the first week of infection in mice, NK cell-derived gamma interferon (IFN-gamma) is involved in controlling intracellular parasite replication, mainly through the induction of NO biosynthesis by activated macrophages. Interleukin-12 (IL-12) has been shown to be a powerful cytokine in inducing IFN-gamma synthesis by NK cells, as well as in mediating resistance to different intracellular protozoa. We have therefore studied the ability of T. cruzi to elicit IL-12 synthesis by macrophages and the role of this cytokine in controlling parasite replication during acute infection in mice. Our results show that macrophages cultured in the presence of live trypomastigote forms (but not epimastigotes) release IL-12 that can induce IFN-gamma production by normal spleen cells. IL-12 was detected in as little as 12 h after the addition of the trypomastigotes, and the level of IL-12 peaked at 48 h after the initial macrophage-parasite incubation. The addition of anti-IL-12 monoclonal antibody to macrophage-trypomastigote supernatants dose-dependently inhibited IFN-gamma production by naive splenocytes. Finally, the in vivo role of IL-12 in resistance to infection by T. cruzi was analyzed. Mice treated with anti-IL-12 monoclonal antibody had significantly increased parasitemia and mortality in comparison with those of control infected mice treated with control antibody. Together, these results suggest that macrophage-derived IL-12 plays a major role in controlling the parasitemia in T. cruzi-infected mice and that the animal's resistance during the acute phase of infection may, at least in part, be a consequence of postinfection levels of IL-12.