IN SITU MEASUREMENTS OF THE ACOUSTIC TARGET STRENGTH OF CAPE HORSE MACKEREL TRACHURUS TRACHURUS CAPENSIS OFF NAMIBIA

The acoustic target strength (TS) of Cape horse mackerel Trachurus trachurus capensis was measured in situ at 38 kHz during two surveys over the Namibian continental shelf in 1998 and 1999 using a SIMRAD EK500 echosounder/ES38D submersible split-beam transducer. Scattered aggregations of horse mackerel 100–200 m deep were ensonified. The transducer was lowered to a depth of 85–140 m in order to resolve single targets at short ranges (5–50 m). Individual fish were tracked using specially developed software. Samples of ensonified fish were obtained using pelagic and demersal trawls; the former was fitted with a codend Multisampler for depth-specific sampling. Recorded TS estimates were low, producing b20-values ranging from -77.5 to -74.9 dB (-76.0 dB &#177 1.3), considerably lower than published estimates for horse mackerel (-73.4 dB &#60 b20 &#60 -65.2 dB). An explanation for the weak acoustic backscattering may be swimbladder compression. Surface-projected b20 values, which were computed using the depth of each target and the scattering area reduction rate previously found for herring (γ &#61 -0.29), corresponded to -72.6 dB. This value is close to the TS constant of -72 dB currently applied for horse mackerel in Namibian and Angolan waters.Afr. J. mar. Sci. 25: 239–25

Comparison of horse mackerel length frequencies obtained from research vessels and commercial midwater trawlers: implications for biomass estimation

The validity of abundance estimates from hydroacoustic surveys relies, inter alia, on the ability of the fishing gear on the research vessel to sample non-selectively. This study compares the length frequencies of Cape horse mackerel Trachurus trachurus capensis taken in Namibian waters by the R.V. Welwitchia and commercial midwater trawlers. Results indicate that the length distributions of catches taken by the Welwitchia were significantly different from those from commercial trawlers, with a greater proportion of fish >25 cm being sampled by the latter. Also, the biomass estimated per length-class from hydroacoustic surveys over the period 1994–2000 was compared with those from annual landings of the commercial fishery. The length distribution of horse mackerel in purseseine catches compares favourably with those from the research vessel. However, comparisons with the midwater trawl catches indicated that the length frequencies obtained from research vessels during the years 1994–1997 underestimated the number of large fish in the population and biased the biomass in those years. From 1998 to 2000 the bias was negligible. The magnitude of the error varied between years, but it remained fairly low. To compensate for this bias, length distribution data from midwater trawlers should be integrated into the acoustic biomass calculation procedure. Keywords: acoustic estimates, avoidance, horse mackerel, length frequencies, trawl catchesAfrican Journal of Marine Science 2001, 23: 265–27

Imagerie Des Retars Psychomoteurs De L’enfant A Lome

Objective: To determine by radiology the different etiologies of psychomotor delays (PMD) in Lomé (Togo). Material and Method: Retrospective study of 12 months in the radiology department of CAMPUS Teaching Hospital, concerned images of CT and MRI scans of children 0-16 years of age with PMD. Results: The mean age was 4.4 years +/- 4.35. The result was pathological in 69.63% of the cases.Cerebral atrophy was the most frequent lesion (40.50%), followed by hydrocephalus (23.14%). The congenital stenosis of the Sylvius aqueduct was the most frequent malformation (37.93%). Triventricular hydrocephalus accounted for 45.61% of hydrocephalus. The most common tumor lesions were choroid plexus carcinoma and craniopharyngioma (28.57% each). Meningo-encephalitis accounted for half of infectious cases. Conclusion: PMD is most often the consequence of several cerebral pathologies. The most frequent of which is cerebral atrophy

Cathepsin B-associated Activation of Amyloidogenic Pathway in Murine Mucopolysaccharidosis Type I Brain Cortex

Mucopolysaccharidosis type I (MPS I) is caused by genetic deficiency of alpha-l-iduronidase and impairment of lysosomal catabolism of heparan sulfate and dermatan sulfate. In the brain, these substrates accumulate in the lysosomes of neurons and glial cells, leading to neuroinflammation and neurodegeneration. Their storage also affects lysosomal homeostasis-inducing activity of several lysosomal proteases including cathepsin B (CATB). In the central nervous system, increased CATB activity has been associated with the deposition of amyloid plaques due to an alternative pro-amyloidogenic processing of the amyloid precursor protein (APP), suggesting a potential role of this enzyme in the neuropathology of MPS I. In this study, we report elevated levels of protein expression and activity of CATB in cortex tissues of 6-month-old MPS I (Idua -/- mice. Besides, increased CATB leakage from lysosomes to the cytoplasm of Idua -/- cortical pyramidal neurons was indicative of damaged lysosomal membranes. The increased CATB activity coincided with an elevated level of the 16-kDa C-terminal APP fragment, which together with unchanged levels of beta-secretase 1 was suggestive for the role of this enzyme in the amyloidogenic APP processing. Neuronal accumulation of Thioflavin-S-positive misfolded protein aggregates and drastically increased levels of neuroinflammatory glial fibrillary acidic protein (GFAP)-positive astrocytes and CD11b-positive activated microglia were observed in Idua -/- cortex by confocal fluorescent microscopy. Together, our results point to the existence of a novel CATB-associated alternative amyloidogenic pathway in MPS I brain induced by lysosomal storage and potentially leading to neurodegeneration

Sleep deprivation increases oleoylethanolamide in human cerebrospinal fluid

This study investigated the role of two fatty acid ethanolamides, the endogenous cannabinoid anandamide and its structural analog oleoylethanolamide in sleep deprivation of human volunteers. Serum and cerebrospinal fluid (CSF) samples were obtained from 20 healthy volunteers before and after a night of sleep deprivation with an interval of about 12 months. We found increased levels of oleoylethanolamide in CSF (P = 0.011) but not in serum (P = 0.068) after 24 h of sleep deprivation. Oleoylethanolamide is an endogenous lipid messenger that is released after neural injury and activates peroxisome proliferator-activated receptor-α (PPAR-α) with nanomolar potency. Exogenous PPAR-α agonists, such as hypolipidemic fibrates and oleoylethanolamide, exert both neuroprotective and neurotrophic effects. Thus, our results suggest that oleoylethanolamide release may represent an endogenous neuroprotective signal during sleep deprivation

Diagnosing mucopolysaccharidosis IVA

Mucopolysaccharidosis IVA (MPS IVA; Morquio A syndrome) is an autosomal recessive lysosomal storage disorder resulting from a deficiency of N-acetylgalactosamine-6-sulfate sulfatase (GALNS) activity. Diagnosis can be challenging and requires agreement of clinical, radiographic, and laboratory findings. A group of biochemical genetics laboratory directors and clinicians involved in the diagnosis of MPS IVA, convened by BioMarin Pharmaceutical Inc., met to develop recommendations for diagnosis. The following conclusions were reached. Due to the wide variation and subtleties of radiographic findings, imaging of multiple body regions is recommended. Urinary glycosaminoglycan analysis is particularly problematic for MPS IVA and it is strongly recommended to proceed to enzyme activity testing even if urine appears normal when there is clinical suspicion of MPS IVA. Enzyme activity testing of GALNS is essential in diagnosing MPS IVA. Additional analyses to confirm sample integrity and rule out MPS IVB, multiple sulfatase deficiency, and mucolipidoses types II/III are critical as part of enzyme activity testing. Leukocytes or cultured dermal fibroblasts are strongly recommended for enzyme activity testing to confirm screening results. Molecular testing may also be used to confirm the diagnosis in many patients. However, two known or probable causative mutations may not be identified in all cases of MPS IVA. A diagnostic testing algorithm is presented which attempts to streamline this complex testing process