Das M74-Syndrom des Ostseelachses (Salmo salar): Symptome, Verbreitung und Ursachen

An overview is presented on the M74-Syndrome of Baltic salmon which is known since 1974 and which, since 1992, has caused considerable losses of artificially produced yolk-sac larvae in Swedish and Finnish hatcheries responsible for compensatory salmon stocking programmes. The syndrome only affects offspring of wild salmon ascending the rivers for spawning and not offspring derived from salmon broodstocks permanently kept in hatcheries. The syndrome seems to be restricted to the Baltic Sea where it has been recorded in all of the remaining Swedish (except the west coast) and Finnish salmon rivers as well as in populations of Estonian rivers and the Russian River Neva. In Sweden and in Finland, the syndrome has been recorded in recent years in offspring of up to 80 % of female salmon used for spawning and resulted in a larval mortality of up to 90 %. A nutrition-associated thiamine (vitamin B1) deficiency is considered as primary cause. However, other environmental factors seem to be involved in addition. There is concern that the syndrome constitutes a major threat with respect to the survival of the few still naturally reproducing populations of Baltic salmon.

Improved utilization and increased availability of fishery products as an effective control of aggravated animal protein deficiency - induced malnutrition in Nigeria

The estimated potential of Nigerian fish resources is 1,830,994 tonnes(t) whereas the demand based on per capita consumption of 12.0kg and a population of 88.5 million is 1.085 million tonnes. Supply is presently less than 500,000 tons. The gap between demand and supply have to be met through improved utilization and increased availability of fish and fishery products. The role of fish in nutrition is recognized, since it supplies a good balance of protein, vitamins and minerals and a relatively low caloric content. This paper appraises the consumption and utilisation pattern of fish in Nigeria, the spoilage of fish and prevention of losses as a means of increasing the availability of fish for human consumption and consequent control of aggravated animal protein deficiency - induced malnutrition. The paper further highlights the point that without increased landings, increased supply of fish can be achieved through reduction of postharvest loss of what is presently caught. The use of newly designed smoke - drying equipment to achieve such goal is highlighted. The paper also emphasises the need to put into human food chain those non-conventional fishery resources and by-catch of shrimp and demersal trawl fishes by conversion into high value protein products like fish cakes, fish pies and salted dried cakes

HSPC117 deficiency in cloned embryos causes placental abnormality and fetal death

Somatic cell nuclear transfer (SCNT) has been successfully used in many species to produce live cloned offspring, albeit with low efficiency. The low frequency of successful development has usually been ascribed to incomplete or inappropriate reprogramming of the transferred nuclear genome. Elucidating the genetic differences between normal fertilized and cloned embryos is key to understand the low efficiency of SCNT. Here, we show that expression of HSPC117, which encodes a hypothetical protein of unknown function, was absent or very low in cloned mouse blastocysts. To investigate the role of HSPC117 in embryo development, we knocked-down this gene in normal fertilized embryos using RNA interference. We assessed the post-implantation survival of HSPC117 knock-down embryos at 3 stages: E9 (prior to placenta formation); E12 (after the placenta was fully functional) and E19 (post-natal). Our results show that, although siRNA-treated in vivo fertilized/produced (IVP) embryos could develop to the blastocyst stage and implanted without any difference from control embryos, the knock-down embryos showed substantial fetal death, accompanied by placental blood clotting, at E12. Furthermore, comparison of HSPC117 expression in placentas of nuclear transfer (NT), intracytoplasmic sperm injection (ICSI) and IVP embryos confirmed that HSPC117 deficiency correlates well with failures in embryo development: all NT embryos with a fetus, as well as IVP and ICSI embryos, had normal placental HSPC117 expression while those NT embryos showing reduced or no expression of HSPC117 failed to form a fetus. In conclusion, we show that HSPC117 is an important gene for post-implantation development of embryos, and that HSPC117 deficiency leads to fetal abnormalities after implantation, especially following placental formation. We suggest that defects in HSPC117 expression may be an important contributing factor to loss of cloned NT embryos in vivo. (C) 2010 Elsevier Inc. All rights reserved.

Primary antibody deficiency and diagnostic delay.

AIMS: To assess the occurrence of diagnostic delay in primary antibody deficiency in the period 1989-2002, since a similar study in 1989, and to assess the impact of UK national guidelines communicated in 1995. METHODS: A retrospective case note review was performed of 89 consecutive patients with antibody deficiency referred to a regional referral centre for clinical immunology in north west England and north Wales. The delay in diagnosis and the estimated resulting morbidity in terms of infections were assessed. RESULTS: Fifty six of the 89 patients experienced delay in diagnosis. The overall median delay was 2 years (mean, 4.4), resulting in substantial morbidity (equivalent to two major infections and one minor infection). This shows a moderate improvement since the previous study in 1989 and since the introduction of UK national guidelines in 1995. Respiratory infections are the most frequent presenting infections, and respiratory physicians the most common source of referral. CONCLUSIONS: There is still considerable delay in the diagnosis of primary antibody deficiency, but the data suggest an improvement in practice since the previous study in 1989 and the distribution of national guidelines in 1995.

Outer membrane proteins induced by iron deficiency in Anabaena sp PCC 7120

Iron deficiency can induce cyanobacteria to synthesize siderophore receptor proteins on the outer membrane to enhance the uptake of iron. In this study, an outer membrane of high purity was prepared from Anabaena sp. PCC 7120 based on aqueous polymer two-phase partitioning and discontinuous sucrose density ultra-centrifugation, and the induction of outer membrane proteins by iron deficiency was investigated using 2-D gel electrophoresis. At least. five outer membrane proteins were newly synthesized or significantly up-regulated in cells transferred to iron-deficient conditions, which were all identified to be siderophore receptor proteins according to MALDI-TOF-MS analyses. Bacterial luciferase reporter genes luxAB were employed to monitor the transcription of the encoding genes. The genes were induced by iron deficiency at the transcriptional level in different responsive modes. Luciferase activity expressed from an iron-regulated promoter may be used as a bioreporter for utilizable iron in natural water samples. (C) 2009 National Natural Science Foundation of China and Chinese Academy of Sciences. Published by Elsevier Limited and Science in China Press. All rights reserved.

Effects of thiamine on treatment performance of textile wastewater

Textile wastewater is commonly treated with activated sludge process technology. However, its treatment performance has not been demonstrated to be very effective. In this study, the effects of micronutrient thiamine on removal efficiencies of dissolved organic carbon (DOC) and chemical oxygen demand (COD) of textile wastewater in a batch test, together with its effect on the oxygen uptake rate (OUR) of activated sludge, were evaluated. Significant improvements were observed in the removal rates of DOC, COD and OUR with 121%, 156% and 121% of those of the control, respectively, when 0.5-2.0 mg/L thiamine was added to the wastewater treatment system. Thiamine could be probably used to improve the treatment performance of textile wastewater.