C-reactive protein,platelets, and patent ductus arteriosus

The association between inflammation, platelets, and patent ductus arteriosus (PDA) has not been studied so far. The purpose of this study was to evaluate whether C-reactive protein (CRP) is related to low platelet count and PDA. This was a retrospective study of 88 infants with a birth weight ≤1500 g and a gestational age ≤30 weeks. Platelet count, CRP, and an echocardiogram were assessed in all infants. The subjects were matched by sex, gestational age, and birth weight. Differences were compared using the χ², t-test, or Mann–Whitney U-test, as appropriate. Significant variables were entered into a logistic regression model. The association between CRP and platelets was evaluated by correlation and regression analysis. Platelet count (167 000 vs. 213 000 µl^?1, p = 0.015) was lower and the CRP (0.45 vs. 0.20 mg/dl, p = 0.002) was higher, and the platelet count correlated inversely with CRP (r = ?0.145, p = 0.049) in the infants with vs. without PDA. Only CRP was independently associated with PDA in a logistic regression model (OR 64.1, 95% confidence interval 1.4–2941, p = 0.033).     

Quantification of hormonal changes by effects of hippotherapy in the autistic population

Zootherapy, more specifically in its equine form, has proliferated recently as a therapeutic activity and is one of the most common applications in the stimulation of autistic individuals. At the same time, the influence of certain hormones was recently revealed in the behavior of autistic spectrum disorders. We propose to objectify the influence of analyzing equestrian therapies through laboratory methods and non-invasive techniques (salivary samples), in the hormone levels of cortisol and progesterone, thus indirectly those of oxytocin, before and after hippotherapy sessions for people with Autism Spectrum Disorder (ASD). The main results indicated that equine therapy decreased (p ?? 0.05) the levels of salivary Cortisol in the rest of the sessions (before Hippotherapy 33.11 ± 0.96 ng/mL vs. after Hippotherapy 2.23 ± 0.75 ng/mL). And also the levels of salivary progesterone in the first session (before Hippotherapy 28.63 ± 12.81 ng/mL vs. after Hippotherapy 51.59 ± 33.11 ng/mL) and in the rest of the sessions (before hippotherapy 21.58 ± 12 pg/mL vs. after Hippotherapy 26.03 ± 11.98 pg/mL) which was always on the rise. These effective results were corroborated with the Cortisol/Progesterone Balance which reduced after equine therapy in the first session (before Hippotherapy 99.87 vs. after Hippotherapy 76.24) and the other sessions (before Hippotherapy 181.31 vs. after Hippotherapy 110.48). In conclusion, the Hippotherapy sessions for the population with ASD generated leads to an improvement in social attitudes, and it is confirmed with the effective modulation of the implicating hormones.     

Association analysis of genotypic frequencies of matrilin-1 gene in patients with osteoarthritis

OBJECTIVE: It has been suggested that genotypic variation in the gene which encodes the matrilin-1 (MATN-1) protein may be involved in the development of hip osteoarthritis (OA). We compared genotype frequencies of the MATN-1 gene (1p35) in patients with OA and controls to determine if there is any association between the MATN-1 genotype and OA. METHODS: 73 OA patients and 53 controls from a rheumatology ambulatory center and a university hospital were studied. They were unrelated subjects. Controls were free of clinical OA. OA was defined according to the American College of Rheumatology criteria. The MATN-1 microsatellite in the 3'untranslated region was amplified by PCR. The size of the amplification products was determined by capilar electrophoresis in a DNA Genetic Analizer Genotypic distribution was compared by the chi2 test. RESULTS: We identified 4 alleles according to their basepair (bp) length: A1 = 110 bp; A2 = 108 bp; A3 = 106 bp and A6 = 104 pb. Six genotypes were found, with an observed heterozygosity of 0.48. The most frequent genotype in OA and controls was A1/A1 (43.8% and 43.4%, respectively). No significant difference in genotype distribution was found between OA - even when discriminating by the affected joint - and controls. CONCLUSION: We did not find any difference in the MATN-1 genotype distribution in OA patients and controls. To our knowledge, this would be the first time a MATN-1 allele of 104 bp (A6) has been identified These results do not support a role of the MATN-1 genotypes in the occurrence of clinical OA.     

The presence of periodontopathogens associated with the tumour necrosis factor-alpha expression in patients with different periodontal status

The purpose of this study was to investigate the relationship between P gingivalis, T forsythia, T denticola, P intermedia, and A. actinomycetemcomitans in the sulci or pockets of patients with gingivitis (G), mild chronic periodontitis (MiCP), moderate chronic periodontitis (MoCP) and severe periodontitis (SP), and the expression of TNF-alpha in gingival tissue associated with clinical parameters. Six patients with G, 7 with MiCP, 23 with MoCP and 7 with SP were recruited. Pathogens obtained from the sulci or pockets were identified by PCR, and expression of TNF-alpha from gingival tissue was analysed Probing depth (PD), clinical attachment level (CAL) and loss of bone were recorded. P gingivalis was detected at the following rates: 16.6% in subjects with G 57.1% in MiCP 57.8 % in MoCP and 58.1% in SP (p < 0.05). P intermedia was not identified in subjects with G A. actinomycetemcomitans was only identified in subjects with MoCP (31.5%) and SP (42.8%). T denticola and T forsythia were identified in all subject groups. Bacterial combinations were identified as follows: P denticola + P intermedia and PR intermedia + T forsythia were associated (p = 0.04, p = 0.02) with the presence of TNF-alpha mRNA in 20% and 25% of subjects, respectively. P gingivalis + A. Actinomycetemcomitans andA. actinomycetemcomitans + T forsythia were associated with severe PD and CAL, respectively. The association between the presence of P intermedia and expression levels of TNF-alpha was significant (p = 0.05). These results indicate that the proportion of patients with P gingivalis increases with the progression of disease. We observed that the presence of P intermedia may trigger the expression of TNF-alpha and cause a worsening of the patient's clinical status.     

Association of ACE genotype and predominantly diastolic hypertension: a preliminary study.

BACKGROUND: The insertion/deletion (I/D) angiotensin-converting enzyme (ACE) polymorphism has been established as a cardiovascular risk factor in some populations, but the association with essential hypertension is controversial. Predominantly diastolic hypertension (PDH), or narrow pulse pressure hypertension, has been shown to have increased peripheral resistance. Because a DD genotype has been associated with higher plasma ACE levels and angiotensin II activity, we genotyped PDH patients for ACE I/D polymorphism. METHODS: Ninety-three patients with systolic blood pressure (BP)<140 mmHg systolic and diastolic BP>90 mmHg, or BP>140/90 mmHg with a pulse pressure<45 mmHg, were defined as PDH. The II, ID and DD genotype variants of ACE were characterised by the triple primer nested-PCR method. Results were compared to 75 normotensive control individuals. Statistical significance was assessed by the Chi square test. RESULTS: The genotype distribution among PDH patients was II=20 (21.5%), ID=34 (36.5%), DD=39 (42%), while the distribution among normotensive controls was II=16 (21.4%), ID=42 (56%), DD=17 (22.6%). The difference in genotype distribution between PDH patients and controls was significant (p<0.02). ACE allele frequencies in PDH patients and controls were D=0.60, I=0.40 and D=0.51, I=0.49, respectively, statistically non-significant (ns). CONCLUSION: These results suggest an association between ACE genotype DD and predominantly diastolic hypertension.     

Treatment with trkC agonist antibodies delays disease progression in neuromuscular degeneration (nmd) mice

Spinal muscular atrophy with respiratory distress type 1 (SMARD1) is a fatal autosomal recessive disorder seen in infants. It is characterized by lower motor neuron degeneration, progressive muscle paralysis and respiratory failure, for which no effective treatment exists. The phenotype of neuromuscular degeneration (nmd) mice closely resembles the human SMARD1. The identification of the mutated mouse gene in nmd mice, Ighmbp2, led to the discovery of mutations of the homologous gene in humans with SMARD1. We have studied the nmd mouse model with in vivo electrophysiological techniques and evaluated the efficacy of Mab2256, a monoclonal antibody with agonist effect on the tyrosine kinase receptor C, trkC, on disease progression in nmd mice. Treatment with Mab2256 resulted in a significant but transient improvement of muscle strength in nmd mice, as well as normalization of the neuromuscular depression during high-frequency nerve stimulation. These results suggest the potential of using monoclonal agonist antibodies for neurotrophin receptors in lower motor neuron diseases such as SMARD1.     

The effects of culture on WASI test performance in ethnically diverse individuals

The objective of this study was to examine differences between fluent English-speaking ethnically diverse (ED) individuals (from Hispanic, Asian, and Middle-Eastern descent) and monolingual English-speaking Anglo-Americans (MEAA) on the Wechsler Abbreviated Scale of Intelligence (WASI). A sample of 86 (50 ED and 36 MEAA) healthy individuals participated. The results revealed that the MEAA group outperformed the ED group on the verbal (i.e., Vocabulary and Similarities), but not the nonverbal (i.e., Block Design and Matrix Reasoning) subtests. Various cultural factors such as the level of acculturation and the degree to which the English language was used correlated with verbal skills. Number of years the education was obtained outide of the US was an important predictor of verbal and some nonverbal performance in the ED group. The findings from this study underscore the importance of taking cultural factors, particularly level of acculturation, into account when interpreting test scores of ED individuals.     

Activity of two different triazoles in a murine model of paracoccidioidomycosis.

A new orally absorbable triazole (Schering 39304) with a long serum half-life in man (60 hours), was tried in a murine model of progressive paracoccidioidomycosis and compared with itraconazole, another triazole which has proven effective in this mycosis. Only 15% of the infected, untreated mice survived while 53 to 75% of the animals receiving itraconazole survived. Mice treated with Schering 39304 exhibited higher (86-100%) survival rates. Statistically, the 5 mg/kg Sch 39304 was superior to the 50 mg/kg itraconazole dose. Lung cultures showed that 20 mg/kg/day of Sch achieved sterilization of the infectious foci. These results indicate that the new triazole will have a place in the treatment of paracoccidioidomycosis.     

Short‐term cytokine stimulation reveals regulatory T cells with down‐regulated Foxp3 expression in human peripheral blood

The identification of regulatory T cells (Treg cells) in human peripheral blood is an important tool in diagnosis, research, and therapeutic intervention. As compared to lymphoid tissues, the frequencies of circulating Treg cells identified as CD4⁺CD25⁺Foxp3⁺ are, however, low. We here show that many of these cells remain undetected due to transient down regulation of Foxp3, which rapidly decays in the absence of cytokine‐mediated STAT5 signals. Short‐term incubation of PBMCs or isolated CD4⁺ T cells, but not of lymph node cells, with IL‐2, ‐7, or ‐15 more than doubles the frequency of Foxp3⁺CD25⁺ among CD4⁺ T cells detectable by flow cytometry. This increase is not due to cell division but to upregulation of both proteins. At the same time, the uncovered Treg cells up‐regulate CD25 and down‐regulate CD127, making them accessible to viable cell sorting. “Latent” Treg cells have a demethylated FOXP3 TSDR sequence, are enriched in naïve, non‐cycling cells, and are functional. The confirmation of our findings in RA and SLE patients shows the feasibility of uncovering latent Treg cells for immune monitoring in clinical settings. Finally, our results suggest that unmasking of latent Treg cells contributes to the increase in circulating CD4⁺CD25⁺Foxp3⁺ cells reported in IL‐2 treated patients.