Amblyomma ticks consumed by a giant cowbird, Molothrus oryzivorus.

The removal of ectoparasites is a common behavior found across animal taxa and is a determinant to avoid the negative effects of parasites' presence. Eventually, the elimination of ectoparasites is associated with mutualistic interactions. Cleaner birds remove ectoparasites, providing benefits to its mutualistic host by reducing parasite burden while they obtain a protein food source. Here we report some evidence that giant cowbirds (Molothrus oryzivorus) may have an important role as a cleaner bird. We found 74 adult ticks inside the ventriculus of one male giant cowbird. The ticks belonged to three different species: Amblyomma dubitatum, A. sculptum and A. triste. We found that the sex-ratio of the consumed adult ticks was not different from 1:1. Although additional data are necessary, the large number of ticks found suggests that the giant cowbird may have developed a mutualistic association with large, social mammals such as capybaras (Hydrochoerus hydrochaeris), since this animal is an important host species for the three tick species found in the present study.

Neuromuscular synapse degeneration without muscle function loss in the diaphragm of a murine model for Huntington's Disease.

Huntington's disease (HD) is an autosomal dominant neurodegenerative disease characterized by chorea, incoordination and psychiatric and behavioral symptoms. The leading cause of death in HD patients is aspiration pneumonia, associated with respiratory dysfunction, decreased respiratory muscle strength and dysphagia. Although most of the motor symptoms are derived from alterations in the central nervous system, some might be associated with changes in the components of motor units (MU). To explore this hypothesis, we evaluated morphofunctional aspects of the diaphragm muscle in a mouse model for HD (BACHD). We showed that the axons of the phrenic nerves were not affected in 12-months-old BACHD mice, but the axon terminals that form the neuromuscular junctions (NMJs) were more fragmented in these animals in comparison with the wild-type mice. In BACHD mice, the synaptic vesicles of the diaphragm NMJs presented a decreased exocytosis rate. Quantal content and quantal size were smaller and there was less synaptic depression whereas the estimated size of the readily releasable vesicle pool was not changed. At the ultrastructure level, the diaphragm NMJs of these mice presented fewer synaptic vesicles with flattened and oval shapes, which might be associated with the reduced expression of the vesicular acetylcholine transporter protein. Furthermore, mitochondria of the diaphragm muscle presented signs of degeneration in BACHD mice. Interestingly, despite all these cellular alterations, BACHD diaphragmatic function was not compromised, suggesting a higher resistance threshold of this muscle. A putative resistance mechanism may be protecting this vital muscle. Our data contribute to expanding the current understanding of the effects of mutated huntingtin in the neuromuscular synapse and the diaphragm muscle function.

Reduced expression of the vesicular acetylcholine transporter and neurotransmitter content affects synaptic vesicle distribution and shape in mouse neuromuscular junction.

In vertebrates, nerve muscle communication is mediated by the release of the neurotransmitter acetylcholine packed inside synaptic vesicles by a specific vesicular acetylcholine transporter (VAChT). Here we used a mouse model (VAChT KD(HOM)) with 70% reduction in the expression of VAChT to investigate the morphological and functional consequences of a decreased acetylcholine uptake and release in neuromuscular synapses. Upon hypertonic stimulation, VAChT KD(HOM) mice presented a reduction in the amplitude and frequency of miniature endplate potentials, FM 1-43 staining intensity, total number of synaptic vesicles and altered distribution of vesicles within the synaptic terminal. In contrast, under electrical stimulation or no stimulation, VAChT KD(HOM) neuromuscular junctions did not differ from WT on total number of vesicles but showed altered distribution. Additionally, motor nerve terminals in VAChT KD(HOM) exhibited small and flattened synaptic vesicles similar to that observed in WT mice treated with vesamicol that blocks acetylcholine uptake. Based on these results, we propose that decreased VAChT levels affect synaptic vesicle biogenesis and distribution whereas a lower ACh content affects vesicles shape.

Genetic analysis of PITX2 and FOXC1 in Rieger Syndrome patients from Brazil.

PURPOSE: Axenfeld-Rieger syndrome is a genetically heterogeneous, autosomal dominant disorder that is characterized by anterior segment defects, glaucoma, and extraocular anomalies. This study examined the two genes known to cause Rieger syndrome, PITX2 and FOXC1, for mutations in five Brazilian families with Axenfeld-Rieger syndrome. METHODS: Five families with a total of 23 persons affected by Axenfeld-Rieger syndrome were recruited for this study. A sequencing-based mutation screen was undertaken for the PITX2 and FOXC1 genes. Linkage analysis was used to study one large family for which no mutations were detected in the PITX2 or FOXC1 genes. RESULTS: Two of the five families harbored mutations in the PITX2 gene, but none of the families had a detectable FOXC1 mutation. Haplotypic analysis of three Rieger syndrome regions in a large family with Axenfeld-Rieger syndrome excluded linkage to the 4q25 (PITX2), 6p25 (FOXC1), and 13q14 (RIEG2) regions. CONCLUSIONS: It appears that the PITX2 gene is responsible for a significant portion of Axenfeld-Rieger syndrome in the Brazilian population. Furthermore, there is also evidence for the presence of genetic heterogeneity of the disorder within the Brazilian population. Finally, a large family with Axenfeld-Rieger syndrome has been identified that does not appear to harbor any of the three known loci. Axenfeld-Rieger syndrome gene segregation in this family likely represents a novel locus.

La oncocercosis en el Ecuador: III. Manifestaciones clínicas de la enfermedad en la Provincia de Esmeraldas

Notables variaciones en la frecuencia de las manifestaciones clínicas de la oncocercosis se observó en los focos endémicos de la enfermedad en la Provincia de Esmeraldas, Ecuador. En las áreas hipoendémicas, el 84.6% de los habitantes positivos para microfilarias, no presentaron manifestaciones clínicas de la enfermedad, mientras que en el área hiperendémica, las manifestaciones clínicas se presentaron en un 57.9% de los infectados. Queratitis ocular punctata, dermatitis macular papulosa de la piel y nódulos oncocercóticos subcutáneos, fueron las variantes clínicas principales y se presentaron con una frecuencia variable. Oncodermatitis de largo plazo e hipertrófica de la piel se observó raramente. Evidencia clínica de una invasión prolongada ocular y de la piel por las microfilarias se observó solamente en el área hiperendémica. De los habitantes positivos para microfilarias que tenían oncocercomas (26.1%), el 91.7% vivían en el área hiperendémica. Se encontraron 41.1% de los nódulos de la región de la cresta ilíaca. Las condiciones clínicas asociadas con una densidad alta de las microfilarias, por ejemplo, elefantiasis de las piernas y escrotal, linfoadenopatía, ingle colgante, hidrocele y hernia inguinal, se observó solamente en el área hiperendémica. Las características clínicas fueron muy similares a las que se observaron en Africa, pero la incidencia baja de las manifestaciones clínicas y la severidad de la enfermedad sugería una infestación reciente de la provincia