Brucella melitensis biotype 1 outbreak in goats in northern KwaZulu-Natal

Brucella melitensis biotype 1 was confirmed in indigenous, outbred goats in three northern districts of the KwaZulu-Natal province following the diagnosis of human Malta fever in the same area. Six foci of infection were found during an extensive serological survey involving 6 266 goats carried out in most of the districts of the KwaZulu-Natal province. The prevalence in the positive herds varied between 17% and 100%. The diagnosis was confirmed by culturing milk samples from serologically positive animals. Infected goats were found in only three districts (Ubombo, lngwavuma and Pongola) and all infected herds fell within a 50-km radius.The articles have been scanned in colour with a HP Scanjet 5590; 600dpi. Adobe Acrobat X Pro was used to OCR the text and also for the merging and conversion to the final presentation PDF-format.mn201

The ^4He trimer as an Efimov system

We review the results obtained in the last four decades which demonstrate the Efimov nature of the $^4$He three-atomic system.Comment: Review article for a special issue of the Few-Body Systems journal devoted to Efimov physic

Rabies in southern Africa

The first confirmed outbreak of rabies in Africa, believed to have followed the importation of an infected dog from England in 1892, occurred in the eastern Cape Province of South Africa, and was brought under control in 1894. An unconfirmed epidemic of rabies in dogs occurred in western Zambia in 1901. By the following year the disease had apparently spread along a major trade route, to cause an outbreak in Zimbabwe which engulfed most of the country before being eradicated in 1913. The existence of endemic rabies of viverrids (mongooses and genets) was confirmed in South Africa in 1928, and since then the viverrid disease has continued to occur widely on the interior plateau of the country with spill-over of infection to cattle and a variety of other animals. From about 1947 onwards, an invasive form of dog rabies spread from southern Zambia and/or Angola into Namibia, across northern and eastern Botswana into Zimbabwe and the northern Transvaal by 1950, entered Mozambique in 1952, and spread from there to Swaziland in 1954. Dog rabies extended from southern Mozambique into Natal in 1961 to cause a major epidemic which was brought under control in 1968. The disease re-entered northern Natal from Mozambique in 1976 and since then dog rabies has proved difficult to control in the peri-urban settlements of Natal-KwaZulu. The disease spread from Natal to Lesotho in 1982, and into the Transkei region of the eastern Cape Province in 1987, to reach the Ciskei by 1990. The spread of the disease in dogs was followed by the emergence of rabies of jackals and cattle in central Namibia, northern Botswana, Zimbabwe and the northern Transvaal. A unique outbreak of rabies in kudu antelope occurred in central Namibia from 1977 to 1985, apparently involving oral spread of infection between individuals. A few cases of rabies in the bat-eared fox were recognized each year in Namibia from 1967 onwards, and from the 1970s the occurrence of the disease in the fox has emerged as a distinct problem in the northern Cape Province and spread to the west coast. The rabies-related viruses, Lagos bat, Mokola and Duvenhage, associated with bats, shrews and rodents in Africa, are known to have caused isolated cases of disease in South Africa, and on one occasion a small outbreak involving six cats and a dog in Bulawayo, Zimbabwe. However, the results of monoclonal antibody tests on numerous specimens indicate that the rabies-related viruses are not a major cause of disease in southern Africa.The articles have been scanned in colour with a HP Scanjet 5590; 600dpi. Adobe Acrobat XI Pro was used to OCR the text and also for the merging and conversion to the final presentation PDF-format.mn2014mn201

Structure and chromosomal location of the bovine gene for the heart muscle isoform of cytochrome c oxidase subunit VIII

We have isolated the bovine COX8H gene for the heart/muscle isoform of cytochrome c oxidase (COX) subunit VIII from a library of bovine genomic DNA cloned into lambda EMBL3. Primer extension assays on bovine heart mRNA mapped the 5′ ends of COX8H transcripts to a CA dinucleotide 62-bp upstream from the ATG codon. The gene thus spans 1565-bp and comprises two exons and one large intron of 1227 bp. Exon 1 encodes the 5′ untranslated region, a 24-amino acid presequence, and the first 13 amino acids of the mature COX VIII-H protein. Exon 2 encodes the remainder of the cDNA: amino acids 14 to 46 plus the 66-bp 3′ untranslated region. The exon-intron boundaries matched the consensus splice junction sequences. Two protein polymorphisms were seen: an Ala/Val polymorphism at position-6 in the presequence and the previously noted Lys/Arg polymorphism at residue 7 of the mature protein. A Taq I polymorphism occurs in the intron. The COX8H gene was mapped by bovine x rodent somatic cell hybrid mapping panels to bovine (BTA) Chromosome (Chr) 25 with 100% concordancy. BTA25 is conserved relative to the long arm of human (HSA) Chr 11, which contains COX8, the gene for the single human COX VIII subunit that is homologous to the liver isoform.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47018/1/335_2004_Article_BF00303255.pd

Intermittent but Not Continuous Static Stretching Improves Subsequent Vertical Jump Performance in Flexibility-Trained Athletes

Bogdanis, GC, Donti, O, Tsolakis, C, Smilios, I, and Bishop, DJ. Intermittent but not continuous static stretching improves subsequent vertical jump performance in flexibility-trained athletes. J Strength Cond Res 33(1): 203-210, 2019 - This study examined changes in countermovement jump (CMJ) height after an intermittent or a continuous static stretching protocol of equal total duration. Sixteen male, elite-level gymnasts performed 90 seconds of intermittent (3 × 30 seconds with 30 seconds rest) or continuous stretching (90 seconds) of the quadriceps muscle. A single-leg stretching and jumping design was used, with the contralateral limb serving as a control. The same individuals performed both conditions with alternate legs in a randomized, counterbalanced order. One-leg CMJ height was measured for the stretched and the control leg after warm-up, immediately after stretching, and at regular intervals for 10 minutes after stretching. Range of motion (ROM) of the hip and knee joints was measured before, after, and 10 minutes poststretching. Compared with the control leg, intermittent stretching increased CMJ height by 8.1 ± 2.0%, 4 minutes into recovery (2.2 ± 2.0 cm, 95% confidence interval [CI]: 1.0-3.4 cm, p = 0.001), whereas continuous stretching decreased CMJ height by 17.5 ± 3.3% immediately after (-2.9 ± 1.7 cm, 95% CI: -2.0 to -3.7 cm, p = 0.001) and by 12.0 ± 2.7% 1 minute after stretching (-2.2 ± 2.1 cm, 95% CI: -1.2 to -3.2 cm, p = 0.001). The increases in hip (2.9 and 3.6°, p = 0.001. d = 2.4) and knee joint ROM (5.1 and 6.1°, p = 0.001. d = 0.85) after the intermittent and continuous stretching protocols were not different. The opposite effects of intermittent vs. continuous stretching on subsequent CMJ performance suggests that stretching mode is an important variable when examining the acute effects of static stretching on performance in flexibility-trained athletes. © 2018 National Strength and Conditioning Association