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C Rodrigues

Publications and source records attributed to C Rodrigues.

At least 37 records · Page 2Linked to original sources
PubMed2000

Fiber-rich diets alter rat intestinal leukocytes metabolism.

This study addressed the following question: What is the effect of fermentable and nonfermentable fiber-rich diets on intestinal immune cells' function and metabolism? For this purpose, weaning rats received, for 8 weeks, two types of fiber-enriched (30%) diets with different fermentable/nonfermentable fiber ratios, that is, oat bran (0.3) and wheat bran (0.14). The results of these two experimental groups were compared with those of the low-fiber control group having a 0.22 fermentable/nonfermentable fiber ratio. The total number and proportion of leukocytes in plasma, total number of cells in the lymphoid organs, lymphocyte proliferative activity and capacity of phagocytosis, hydrogen peroxide production, and adherence of macrophages were investigated. The activities of key enzymes of glycolysis and glutaminolysis, and of the Krebs cycle of lymphocytes from the mesenteric lymph nodes and macrophages from the intraperitoneal cavity were determined. The metabolic response of lymphocytes and macrophages from rats fed the three diets to Bacillus Calmette-Guérin-stimulus was also investigated. The number of lymphocytes in the mesenteric lymph nodes was lower in both fiber-rich diets than in the control but did not have any difference in the remaining lymphoid organs. Wheat bran caused a significant reduction in the phagocytosis capacity and adherence index of macrophages, whereas oat bran did not have a significant effect. The response of glucose and glutamine metabolism to Bacillus Calmette-Guérin-stimulus was not altered by the diets in lymphocytes, whereas in macrophages, the increase in glutaminase and hexokinase activities was abolished.

Journal Article↗
PubMed2000

Differential role of hippocampal cAMP-dependent protein kinase in short- and long-term memory.

One-trial step-down inhibitory (passive) avoidance training is followed by two peaks of cAMP-dependent protein kinase (PKA) activity in rat CA1: one immediately after training and the other 3 h later. The second peak relies on the first: Immediate posttraining infusion into CA1 of the inhibitor of the regulatory subunit of PKA, Rp-cAMPS, at a dose that reduces PKA activity during less than 90 min, cancelled both peaks. Long-term memory (LTM) of this task measured at 24 h depends on the two peaks: Rp-cAMPS given into CA1 0 or 175 min posttraining, but not between those times, blocked LTM. However, the effect of immediate posttraining Rp-cAMPS on LTM could not be reversed by the activator of the regulatory subunit of PKA, Sp-cAMPS, given at 180 min, which suggests that, for LTM, the first peak may be more important than the second. When given at 0, 22, 45, or 90, but not at 175 min from training, Rp-cAMPS blocked short-term memory (STM) measured at 90 or 180 min. This effect of immediate posttraining Rp-cAMPS infusion on STM but not that on LTM was readily reversed by Sp-cAMPS infused 22 min later. On its own, Sp-cAMPS had effects exactly opposite to those of the inhibitor. It enhanced LTM when given at 0 or 175 min from training, and it enhanced STM when given at 0, 22, 45, or 90 min from training. These findings show that STM and LTM formation require separate PKA-dependent processes in CA1. STM relies on the continued activity of the enzyme during the first 90 min. LTM relies on the two peaks of PKA activity that occur immediately and 180 min posttraining.

Animals↗
PubMed1999

Differential effects of post-training muscimol and AP5 infusions into different regions of the cingulate cortex on retention for inhibitory avoidance in rats.

Adult male Wistar rats were bilaterally implanted with indwelling cannulae in four different coordinates of the cingulate cortex: (1) the anterior cingulate (AC), (2) the rostral region of the posterior cingulate (RC), (3) the upper portion of the caudal region of the posterior cingulate (UC), and (4) the lower portion of the caudal region of the posterior cingulate (LC). After recovery, animals were trained in a step-down inhibitory avoidance task (3.0-s, 0.4-mA foot shock). Either immediately, or 90 or 180 min after training, animals received a 0.5-microl infusion of vehicle (phosphate buffer, pH 7.4), of muscimol (0.5 microg), or of AP5 (5.0 microg). Retention testing was carried out 24 h after training. Muscimol was amnestic when given into any of the three coordinates of the posterior cingulate cortex 90 min after training, and when given into LC immediately post-training. In addition, AP5 was amnestic when given into UC 90 min post-training, but not when given into any other region and/or at any other time. None of the treatments had any effect when given into AC. The results suggest that memory processing of the inhibitory avoidance task is regulated by the posterior but not by the anterior cingulate cortex, through muscimol-sensitive synapses, relatively late after training. AP5-sensitive synapses appear to play a very limited role in these processes, restricted to UC.

2-Amino-5-phosphonovalerate↗
PubMed1999

Autoimmune enteropathy with distinct mucosal features in T-cell activation deficiency: the contribution of T cells to the mucosal lesion.

BACKGROUND: Autoimmune enteropathy is normally characterised by crypt hyperplastic villous atrophy with enterocyte autoantibodies, activation of mucosal lymphocytes and increased epithelial HLA-DR. This case involved a severely affected Portuguese infant who was found to have lymphocyte activation deficiency and demonstrated correspondingly distinct mucosal features. METHODS: A female infant of nonconsanguineous parents was treated for vomiting and diarrhoea, first with milk exclusion and then with parenteral nutrition. Lymphocyte subsets and immunoglobulin concentrations were normal, but in vitro testing showed no activation in response to phytohaemagglutinin, Candida, or purified protein derivative, although the response to interleukin (IL)-2 was intact. Interleukin-2 deficiency was excluded. Analysis of jejunal biopsy specimens revealed only mild villous blunting with absent goblet cells, normal epithelial proliferation, and no crypt hyperplasia. The dense infiltrate of CD8+ and CD4+ T lymphocytes showed normal CD2 and CD3 expression but no activation or proliferation markers. HLA-DR was not increased on epithelium or lymphocytes. Thus, in addition to in vitro evidence for lymphocyte activation deficiency, the mucosal specimens showed no evidence of in situ T-cell activation. RESULTS: After development of overwhelming septicaemia, the patient died at 18 months, just before a planned bone marrow transplant. CONCLUSIONS: These findings confirm significant heterogeneity within autoimmune enteropathy. Formal immune function testing should be performed in all affected infants to identify T-cell activation deficiencies. The distinct mucosal findings suggest that activated T cells usually induce the crypt hyperplastic villous atrophy characteristic of classic autoimmune enteropathy.

Autoimmune Diseases↗
PubMed1999

Effects of post-training infusions of a mitogen-activated protein kinase kinase inhibitor into the hippocampus or entorhinal cortex on short- and long-term retention of inhibitory avoidance.

We recently demonstrated the time-dependent impairment of long-term retention of a step-down inhibitory avoidance task in rats induced by post-training infusion of the specific MAPKK (mitogen-activated protein kinase kinase) inhibitor PD 098059 into the hippocampus (HIP), amygdala (AMY), entorhinal cortex (EC) and posterior parietal cortex (PPC). Here we investigate the role of the MAPK cascade in the HIP and the EC on both short- and long-term retention of inhibitory avoidance in rats, using three different doses of the MAPKK inhibitor PD 098059. Adult male Wistar rats were trained and tested in inhibitory avoidance and given an infusion of PD 098059 (0.5, 5.0 or 50.0 microM) at 0, 30, 90, 120, 180, 270 or 360 min after training. A retention test session was carried out at 90, 180 or 270 min after training (short-term memory, STM) and/ or 24 h after training (long-term memory, LTM). When infused into the HIP at 0 min, but not at 30, 90, 120 or 180 min after training, PD 098059 impaired STM. Intrahippocampal PD 098059 impaired LTM when infused at 180 min, but not at 0, 30, 90, 120 or 270 min after training. When infused into the EC, PD 098059 enhanced STM when given at 0 min after training and had no effect when given at 30, 90, 120 or 180 min after training. In this structure, PD 098059 impaired LTM when given at 180 or 270 min, but not at 30, 90, 120 or 360 min after training. All effects were dose-dependent. These findings indicate that the MAPK cascade in the HIP and EC is differentially involved in short- and long-term retention of inhibitory avoidance in rats.

Animals↗
PubMed1999

17Beta-hydroxysteroid dehydrogenase-3 deficiency: diagnosis, phenotypic variability, population genetics, and worldwide distribution of ancient and de novo mutations.

17Beta-hydroxysteroid dehydrogenase-3 (17betaHSD3) deficiency is an autosomal recessive form of male pseudohermaphroditism caused by mutations in the HSD17B3 gene. In a nationwide study on male pseudohermaphroditism among all pediatric endocrinologists and clinical geneticists in The Netherlands, 18 17betaHSD3-deficient index cases were identified, 12 of whom initially had received the tentative diagnosis androgen insensitivity syndrome (AIS). The phenotypes and genotypes of these patients were studied. Endocrine diagnostic methods were evaluated in comparison to mutation analysis of the HSD17B3 gene. RT-PCR studies were performed on testicular ribonucleic acid of patients homozygous for two different splice site mutations. The minimal incidence of 17betaHSD3 deficiency in The Netherlands and the corresponding carrier frequency were calculated. Haplotype analysis of the chromosomal region of the HSD17B3 gene in Europeans, North Americans, Latin Americans, Australians, and Arabs was used to establish whether recurrent identical mutations were ancient or had repeatedly occurred de novo. In genotypically identical cases, phenotypic variation for external sexual development was observed. Gonadotropin-stimulated serum testosterone/androstenedione ratios in 17betaHSD3-deficient patients were discriminative in all cases and did not overlap with ratios in normal controls or with ratios in AIS patients. In all investigated patients both HSD17B3 alleles were mutated. The intronic mutations 325 + 4;A-->T and 655-1;G-->A disrupted normal splicing, but a small amount of wild-type messenger ribonucleic acid was still made in patients homozygous for 655-1;G-->A. The minimal incidence of 17betaHSD3 deficiency in The Netherlands was shown to be 1: 147,000, with a heterozygote frequency of 1:135. At least 4 mutations, 325 + 4;A-->T, N74T, 655-1;G-->A, and R80Q, found worldwide, appeared to be ancient and originating from genetic founders. Their dispersion could be reconstructed through historical analysis. The HSD17B3 gene mutations 326-1;G-->C and P282L were de novo mutations. 17betaHSD3 deficiency can be reliably diagnosed by endocrine evaluation and mutation analysis. Phenotypic variation can occur between families with the same homozygous mutations. The incidence of 17betaHSD3 deficiency is 0.65 times the incidence of AIS, which is thought to be the most frequent known cause of male pseudohermaphroditism without dysgenic gonads. A global inventory of affected cases demonstrated the ancient origin of at least four mutations. The mutational history of this genetic locus offers views into human diversity and disease, provided by national and international collaboration.

17-Hydroxysteroid Dehydrogenases↗
PubMed1999

Increased training prevents the impairing effect of intra-amygdala infusion of the non-NMDA receptor antagonist CNQX on inhibitory avoidance expression.

Intra-amygdala infusion of the non-N-methyl-D-aspartate (NMDA) receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) prior to testing impairs inhibitory avoidance retention test performance. Increased training attenuates the impairing effects of amygdala lesions and intra-amygdala infusions of CNQX. The objective of the present study was to determine the effects of additional training on the impairing effects of intra-amygdala CNQX on expression of the inhibitory avoidance task. Adult female Wistar rats bilaterally implanted with cannulae into the border between the central and the basolateral nuclei of the amygdala were submitted to a single session or to three training sessions (0.2 mA, 24-h interval between sessions) in a step-down inhibitory avoidance task. A retention test session was held 48 h after the last training. Ten minutes prior to the retention test session, the animals received a 0.5-microliter infusion of CNQX (0.5 microgram) or its vehicle (25% dimethylsulfoxide in saline). The CNQX infusion impaired, but did not block, retention test performance in animals submitted to a single training session. Additional training prevented the impairing effect of CNQX. The results suggest that amygdaloid non-NMDA receptors may not be critical for memory expression in animals given increased training.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1998

Giant cell tumor of the tendon sheath: a retrospective study of 28 cases.

BACKGROUND AND OBJECTIVES: Giant cell tumor of the tendon sheath (GCTTS) is a lesion of uncertain etiology. To better interpret pathogenesis and aid in the differentiation of GCTTS from other similar pathological processes we reviewed the literature and analyzed the available information. METHODS: We retrospectively studied clinicopathologic findings in 28 cases of GCTTS on the basis of anatomic location and histologic appearance of the lesion. RESULTS: The GCTTS could be divided into those involving the common digits (20 cases) and larger joint group (8 cases) based on anatomic location. Grossly the digit tumors were small, multiple, surrounded by a thin fibrous capsule, and had a variegated appearance, while the large joint tumors were relatively large and covered by one or more layers of synovium. Microscopically both groups consisted of a mixture of round to polygonal histiocytes, foam cells, hemosiderin laden macrophages, and multinucleated giant cells. The giant cells seemed more abundant in the digit tumors, while the pseudoglandular spaces lined by synovial cells were more striking in the large joint group. CONCLUSIONS: Local excision was the treatment of choice in the majority of the patients. Eight patients had local recurrence.

Adolescent↗
PubMed1998

Differential involvement of cortical receptor mechanisms in working, short-term and long-term memory.

Rats received, through bilaterally implanted indwelling cannulae, 0.5 microliter infusions of 6-cyano-7-nitroquinoxaline2,3-dione (CNQX) (0.5 microgram), D-2-amino-5-phophono pentanoic acid (AP5) (5.0 micrograms), muscimol (0.5 microgram), scopolamine (2.0 micrograms), SCH23390 (2.5 micrograms), saline or a vehicle into the CA1 region of the hippocampus, or into the antero-lateral prefrontal (PRE), posterior parietal (PP) and entorhinal cortex (EC). The infusions were given 6 min prior to one-trial step-down inhibitory avoidance training in order to measure their effect on working memory (WM), or immediately post-training in order to measure their effect on short-term (STM) and long-term memory (LTM), 1.5 and 24 h later, respectively. WM was inhibited by CNQX or muscimol given into any of the cortical areas, by SCH23390 given into CA1, PRE or PP, and by scopolamine given into PRE or EC. STM was unaffected by any of the treatments given into PRE, and was inhibited by CNQX or muscimol given into CA1, PP and EC and by scopolamine given into PP, and enhanced by SCH given into CA1. LTM was inhibited by CNQX, muscimol, scopolamine or SCH23390 given into PRE, by scopolamine given into PP, by SCH23390 given into the entorhinal cortex, and by AP5, CNQX, muscimol or scopolamine given into CA1. The results indicate a differential involvement of the various neurotransmitter systems in the three types of memory in the various brain areas, and a separation of the mechanisms and of the regions involved in each. In addition, some of the findings suggested links between WM and LTM processing in PRE, between WM and STM processing in EC and PP, and between all three types of memory in CA1.

Animals↗
PubMed1998

Interaction between midazolam-induced anterograde amnesia and memory enhancement by treatments given hours later in hippocampus, entorrhinal cortex or posterior parietal cortex.

Rats were bilaterally implanted with indwelling cannulae in the CA1 region of the dorsal hippocampus, the entorrhinal cortex or the posterior parietal cortex. After recovery from surgery, they were trained in a one-trial step-down inhibitory avoidance task using a 0.3 mA footshock. The animals received i.p. 15 min before training either saline (1 ml/kg) or midazolam (1 mg/kg). Three hours after training they received, through the cannulae, infusions of saline, norepinephrine (0.3 microg/side), SKF38393 (7.5 microg/side), or 8-Br-cAMP (1.25 microg/side) into the brain regions mentioned. Animals were tested for retention 24 h after the training session. Midazolam produced anterograde amnesia, and the post-training treatments (with the exception of SKF38393 given into the entorrhinal cortex) caused retrograde memory facilitation. The amnestic effect of midazolam and the facilitatory effect of the treatments given into the brain cancelled each other out. Therefore, the mechanisms triggered by midazolam can interact with others in areas involved in memory processing several hours after their onset.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1998

The impact of infection control on intensive care unit microbial isolates.

In todays world, good infection control practices in high pressure intensive care units is of vital importance. Endogenous infections from the patients own microbial flora now cause the majority of nosocomial infections as the exogenous infections are curtailed to a large extent with aggressive surveillance and prevention of infection. We analysed absolute numbers of microbial isolates as an indirect reflection of infection rate in the intensive care unit (ICU) for 6 months in 1992, 1994 and 1996. We demonstrated that inspite of the total admission to the ICU increasing, the impact of infection control is certainly felt with strict inforcement of protocols.

Cross Infection↗
PubMed1998

[Prepubertal testicular tumors].

Prepubertal testis tumours (T.T) are rare, with different characteristics and clinical course to adults and with a better prognosis. The authors report the experience of Maria Pia Hospital's over a 15 year period. There were 8 cases of T.T.: 3 Yolk sac tumours, 3 teratomas, 1 Leydig cell tumour and 1 epidermoide cyst. All patients are submitted to an inguinal orchiectomy. Follow-up ranged between six months and 14 years. There was no recurrence of the disease in seven patients are without disease recurrence. Mortality was nil.

Adolescent↗
PubMed1997

A simple technique to limit ICP catheter infection.

Infection of intracranial catheters is a common complication of ICP monitoring. The introduction of a simple technique of ensheathing the entire length of the external segment of the catheter in a sterile plastic sheath resulted in a decreased infection rate. In the study year, one of 78 patients developed catheter-induced meningitis, compared with seven of 64 patients in the year prior to the introduction of the protective plastic sheath. The use of a plastic sheath resulted in a low rate of infection.

Asepsis↗
PubMed1997

Late and prolonged post-training memory modulation in entorhinal and parietal cortex by drugs acting on the cAMP/protein kinase A signalling pathway.

Rats implanted bilaterally with cannulae in the entorhinal or posterior parietal cortex or in the amygdaloid nucleus were trained in one-trial step-down inhibitory (passive) avoidance using a 0.3 mA footshock. At 0, 3, 6 or 9 h after training, they received localized 0.5 microliter infusions into these areas of a vehicle, or of 8-Br-cAMP, forskolin (adenylyl cyclase activator), KT5720 (protein kinase A inhibitor), SKF38393 (dopamine D1 receptor agonist), SCH23390 (D1 antagonist), norepinephrine hydrochloride, timolol hydrochloride (beta blocker), 8-HO-DPAT (5-HT1A receptor agonist) or NAN-190 (5-HT1A antagonist) dissolved in 20% dimethylsulfoxide (DMSO) in saline (vehicle). Rats were tested for retention 24 h after training. 8-Br-cAMP, forskolin, SKF 38393 and norepinephrine caused memory facilitation and KT5720, SCH23390, timolol and 8-HO-DPAT caused retrograde amnesia when given into the entorhinal cortex 0, 3 or 6 h but not 9 h after training. When given into the posterior parietal cortex 0, 3 or 6 but not 9 h after training, KT5720 was amnestic. When given into this structure 3 or 6 h but not 0 or 9 h after training 8-Br-cAMP, forskolin and norepinephrine caused memory facilitation and KT5720, SCH23390 and timolol caused retrograde amnesia. All treatments given into the amygdala 0, 3 or 6 h after training were ineffective except for norepinephrine given at 0 h, which caused facilitation. The data point to a role of cAMP/protein kinase A-dependent mechanisms in memory formation in the entorhinal and parietal cortex, but not the amygdala, from 0 to 6 h after training, and to a strong modulation of these mechanisms by dopaminergic D1, beta-noradrenergic and 5-HT1A receptors. The lack of effect of NAN-190 but not 8-HO-DPAT in both cortical regions suggests that 5-HT1A receptors do not play a physiological role but can be activated pharmacologically. The fact that SCH23390 was amnestic but SKF38393 had no effect when given into the parietal cortex suggests that D1 receptors may play a maintenance rather than a stimulant role in this area.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗