Transmission of stony coral tissue loss disease (SCTLD) in simulated ballast water confirms the potential for ship-born spread.

Stony coral tissue loss disease (SCTLD) remains an unprecedented epizootic disease, representing a substantial threat to the persistence and health of coral reef ecosystems in the Tropical Western Atlantic since its first observation near Miami, Florida in 2014. In addition to transport between adjacent reefs indicative of waterborne pathogen(s) dispersing on ocean currents, it has spread throughout the Caribbean to geographically- and oceanographically-isolated reefs, in a manner suggestive of ship and ballast water transmission. Here we evaluate the potential for waterborne transmission of SCTLD including via simulated ballast water, and test the efficacy of commonly-used UV radiation treatment of ballast water. Two species of reef-building corals (Orbicella faveolata and Pseudodiploria strigosa) were subjected to (1) disease-exposed or UV-treated disease-exposed water, and (2) a ballast hold time series of disease-exposed water in two carefully-controlled experiments to evaluate transmission. Our experiments demonstrated transmission of SCTLD through water, rather than direct contact between diseased and healthy corals. While UV treatment of disease-exposed water led to a 50% reduction in the number of corals exhibiting disease signs in both species, the statistical risk of transmission and volume of water needed to elicit SCTLD lesions remained similar to untreated disease-exposed water. The ballast hold time (24 h vs. 120 h) did not have a significant effect on the onset of visible disease signs for either species, though there appeared to be some evidence of a concentration effect for P. strigosa as lesions were only observed after the 120 h ballast hold time. Results from both experiments suggest that the SCTLD pathogens can persist in both untreated and UV-treated ballast water and remain pathogenic. Ballast water may indeed pose a threat to the continued spread and persistence of SCTLD, warranting further investigation of additional ballast water treatments and pathogen detection methods.

Chronic traumatic encephalopathy: Diagnostic updates and advances.

Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease that occurs secondary to repetitive mild traumatic brain injury. Current clinical diagnosis relies on symptomatology and structural imaging findings which often vary widely among those with the disease. The gold standard of diagnosis is post-mortem pathological examination. In this review article, we provide a brief introduction to CTE, current diagnostic workup and the promising research on imaging and fluid biomarker diagnostic techniques. For imaging, we discuss quantitative structural analyses, DTI, fMRI, MRS, SWI and PET CT. For fluid biomarkers, we discuss p-tau, TREM2, CCL11, NfL and GFAP.

Patterns of Apoptosis and Autophagy Activation After Hydroxyurea Exposure in the Rat Cerebellar External Granular Layer: an Immunoperoxidase and Ultrastructural Analysis.

The time courses of apoptosis and autophagy activation were investigated in neuroblasts of the cerebellar external granular layer (EGL) following the treatment with a single dose (2 mg/g) of hydroxyurea (HU), a cytotoxic agent. The rats were examined at postnatal day 9 and sacrificed at appropriate times ranging from 10 to 60 h after drug administration. We used the Feulgen method, the TUNEL assay, immunohistochemistry for active caspase-3, and LC3B and p62/SQSTM1 immunoperoxidase procedures. The resulting data indicated that the administration of HU leads to the activation of apoptotic cellular events that began to increase 10 h after HU exposure, peaked at 30 h, and decrease thereafter. It also showed that apoptosis was followed by autophagy activation. Interestingly, LC3B and p62/SQSTM1-stained cells, as well as mitotic cells, started to appear 20 h after the HU injection and their counts increased until 40 h. Afterwards, the values remained stable. The current results highlight an important role of the apoptotic and autophagic processes in the EGL after HU administration. Moreover, they provide a clue for studying the mechanism of chemoresistance triggered by proliferating cells exposed to anticancer agents.

Prevalencia de alteraciones posturales de la columna vertebral, asociada al carente habito deportivo en jóvenes de 17 a 22 años de edad de abril-junio del 2017 / PREVALENCE OF POSTURAL ALTERATIONS OF THE SPINAL COLUMN, ASSOCIATED WITH THE LACK OF SPORT HABIT, IN YOUNG PEOPLE FROM 17 TO 22 YEARS OLD, 2017 / PREVALENCE OF POSTURAL ALTERATIONS OF THE SPINAL COLUMN, ASSOCIATED WITH THE LACK OF SPORT HABIT, IN YOUNG PEOPLE FROM 17 TO 22 YEARS OLD, 2017

Las modificaciones patológicas que afectan la postura son cada vez más frecuentes. Estudios recientes en América Latina, demuestran que las alterciones de la columna vertebral ha experimentado un incremento en la población infantil. Pese a que en nuestro país los estudios al respecto son escasos, existe una publicación en la Revista Ciencia, Tecnologia e Innovación la cual indica que 34 % de los joves sobrellevan una alteración en la columna vertebral. Las alteraciones de postura se van presentando a lo largo de la vida, afectando tanto a personas adultas y ancianas como a jóvenes en edad de desarrollo, que experimentan significativas adaptaciones para lacancear las nuevas proporciones de la musculatura profunda del rquis, favorecerán en un futuro a la aparición de problemas de espalda

In situ and in vitro impacts of the Deepwater Horizon oil spill on Vibrio parahaemolyticus.

Most established virulence genes in Vibrio parahaemolyticus (Vp), e.g., thermostable direct hemolysin (tdh), tdh-related hemolysin (trh), and type three secretion system 2 (TTSS2), are on the chromosome 2 pathogenicity island, which also possesses numerous uncharacterized genes. We hypothesized the 2010 Deepwater Horizon (DH) oil spill would cause an increase in populations of Vibrio parahaemolyticus carrying environmental adaptation genes. Vp isolated pre- and post-spill were analyzed for TTSS2 genes, and impacts of DH oil on Vp were examined in vitro. There was no change in TTSS2 in situ, but tdh and V. vulnificus levels were higher post-spill. In vitro exposure of water samples to DH oil produced no changes in Vp densities. Two years post-spill, total Vp remained low; tdh and trh increased. These results indicate the effects of the DH oil spill on potentially pathogenic Vp subpopulations were complex and difficult to discern from other concurrent anthropogenic and natural events.

Principal component and cluster analysis of morphological variables reveals multiple discrete sub-phenotypes in weaver mouse mutants.

The present study evaluates the usefulness of the principal component analysis-based cluster analysis in the categorization of several sub-phenotypes in the weaver mutant by using several morphological parameters from the cerebellar cortex of control, heterozygous (+/wv) and homozygous (wv/wv) weaver mice. The quantified parameters were length of the cerebellar cortex, area of the external granular layer, area of the molecular layer, number of the external granular layer cells (EGL), and number of Purkinje cells (PCs). The analysis indicated that at postnatal day 8, the genotype +/wv presented three sub-phenotypes tagged as +/wv (0), +/wv (1) and +/wv (2), whereas two sub-phenotypes designated as wv (0)/wv (1) and wv (0)/wv (2) were identified in the genotype wv/wv. The number of PCs for the genotype +/wv and the number of EGL cells for the genotype wv/wv were the variables that discriminated the best among sub-phenotypes. Each one of the sub-phenotypes showed specific abnormalities in the cytoarchitecture of the cerebellar cortex as well as in the foliar pattern. In particular, the wv (0)/wv (1) and wv (0)/wv (2) sub-phenotypes had the most altered cytoarchitectonics, followed by the +/wv (2) sub-phenotype and then by the +/wv (1) one. The sub-phenotype +/wv (0) was the less affected one. Apart from reporting for the first time the coexistence of several sub-phenotypes in the weaver mutant, our approach provides a new statistical tool that can be used to assess cerebellar morphology.

Ecology of Vibrio parahaemolyticus and Vibrio vulnificus in the coastal and estuarine waters of Louisiana, Maryland, Mississippi, and Washington (United States).

Vibrio parahaemolyticus and Vibrio vulnificus, which are native to estuaries globally, are agents of seafood-borne or wound infections, both potentially fatal. Like all vibrios autochthonous to coastal regions, their abundance varies with changes in environmental parameters. Sea surface temperature (SST), sea surface height (SSH), and chlorophyll have been shown to be predictors of zooplankton and thus factors linked to vibrio populations. The contribution of salinity, conductivity, turbidity, and dissolved organic carbon to the incidence and distribution of Vibrio spp. has also been reported. Here, a multicoastal, 21-month study was conducted to determine relationships between environmental parameters and V. parahaemolyticus and V. vulnificus populations in water, oysters, and sediment in three coastal areas of the United States. Because ecologically unique sites were included in the study, it was possible to analyze individual parameters over wide ranges. Molecular methods were used to detect genes for thermolabile hemolysin (tlh), thermostable direct hemolysin (tdh), and tdh-related hemolysin (trh) as indicators of V. parahaemolyticus and the hemolysin gene vvhA for V. vulnificus. SST and suspended particulate matter were found to be strong predictors of total and potentially pathogenic V. parahaemolyticus and V. vulnificus. Other predictors included chlorophyll a, salinity, and dissolved organic carbon. For the ecologically unique sites included in the study, SST was confirmed as an effective predictor of annual variation in vibrio abundance, with other parameters explaining a portion of the variation not attributable to SST.

Nontraumatic splenic pseudocyst. Case report.

BACKGROUND: Splenic cysts are uncommon and are classified as true cysts (with epithelial lining) and false cysts or pseudocysts. Splenic pseudocysts usually have a posttraumatic origin and are secondary to hematoma or to splenic infarction. At times there is no prior evidence of trauma, and the cyst may be secondary to a primary cyst with degeneration/atrophy of the epithelial lining. CLINICAL CASE: We present the case of a 50-year-old female with negative history of abdominal trauma. Clinically, the patient reported discomfort and pain in the left upper abdomen. Physical examination revealed a palpable and painful mass. reoperative ultrasonography and computerized tomography showed a large cyst in the spleen. Laparotomy and total splenectomy was performed. The cyst measured 9.5 × 9.0 cm. Histologically, the wall was composed of thick fibrous tissue, calcifications and no epithelial lining. CONCLUSIONS: "Nontraumatic" splenic pseudocyst is rare and may be secondary to a primary cyst with degenerative/atrophic changes in the epithelium. Clinically it is nonspecific, and symptoms are related to the mass effect of the cyst. Recommended treatment, according to the size of the cyst and its anatomic relation with the vasculature, is surgical with partial or complete splenectomy.

Regional differences in the vulnerability of substantia nigra dopaminergic neurons in weaver mice.

Vulnerability of midbrain dopaminergic (DA) neurons in the weaver mouse was studied at postnatal (P) days 8 and 90, in chosen coronal levels throughout the anteroposterior (AP) extent of the substantia nigra pars compacta (SNc). Wild-type (+/+) and homozygous weaver (wv/wv) mice used were the offspring of pregnant dams injected in several cases with tritiated thymidine on embryonic days 11-15. DA neurons were identified for their tyrosine hydroxylase immunoreactivity. Data reveal that at P8, the frequency of both +/+ and wv/wv late-generated DA cells increases from rostral to caudal SNc. No apparent DA-cell loss was observed at P8 in the mutant genotype, irrespective of the AP level considered. However, throughout the AP, there was a significant reduction in the number of these neurons at any level in 90-day-old weavers. Comparison of P8 and P90 +/+ SNc suggests that cell death is not a major aspect in the developmental regulation of normal DA neurons, although numerical cell depletion in the postnatal development of weaver SNc probably results from the amplification of a basal cell-death process, which affected all the coronal levels studied.