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.Yu, Haizhou2014-07-23The combination of nonsolvent-induced phase separation and the self-assembly of block copolymers can lead to asymmetric membranes with a thin highly ordered isoporous skin layer. The effective pore size of such membranes is usually larger than 15 nm. We reduced the pore size of these membranes by electroless gold deposition. We demonstrate that the pore sizes can be controlled precisely between 3 and 20 nm leading to a tunable sharp size discrimination in filtration processes. Besides fractionation of nanoparticles and biomaterials, controlled drug delivery is an attractive potential application.
© 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.Yu, Haizhou; Qiu, Xiaoyan; Nunes, Suzanapereira; Peinemann, Klaus-Viktor2014-01-01The combination of nonsolvent-induced phase separation and the self-assembly of block copolymers can lead to asymmetric membranes with a thin highly ordered isoporous skin layer.
The effective pore size of such membranes is usually larger than 15 nm. We reduced the pore size of these membranes by electroless gold deposition. We demonstrate that the pore sizes can be controlled precisely between 3 and 20 nm leading to a tunable sharp size discrimination in filtration processes. Besides fractionation of nanoparticles and biomaterials, controlled drug delivery is an attractive potential application. © 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.Yu, Haizhou; Qiu, Xiaoyan; Nunes, Suzana P; Peinemann, Klaus-Viktor2014-09-15The combination of nonsolvent-induced phase separation and the self-assembly of block copolymers can lead to asymmetric membranes with a thin highly ordered isoporous skin layer.
The effective pore size of such membranes is usually larger than 15 nm. We reduced the pore size of these membranes by electroless gold deposition. We demonstrate that the pore sizes can be controlled precisely between 3 and 20 nm leading to a tunable sharp size discrimination in filtration processes. Besides fractionation of nanoparticles and biomaterials, controlled drug delivery is an attractive potential application. © 2014 WILEY-VCH Verlag GmbH & Co.
KGaA, Weinheim.Cotta, R.M.; Roberty, N.C.1982-01-01The porosity - and temperature distribution in cylindrical fuels rods, were studied by numerical resolution of mass-and energy equation, as well as determining the evolution of the central void radii. The finite difference method with implicit formulation for heat conduction equation and explicit formulation for continuity equation, was used.
The Nichols model was used in the determination of the constitutive equation of the porous migration velocity. (E.G.) pt.Liu, Dali; Wang, Yun; Qiu, Lirong; Mao, Xinyue; Zhao, Weiqian2014-09-01A confocal pore size measurement based on super-resolution image restoration is proposed to obtain a fast and accurate measurement for submicrometer pore size of nuclear track-etched membranes (NTEMs). This method facilitates the online inspection of the pore size evolution during etching. Combining confocal microscopy with super-resolution image restoration significantly improves the lateral resolution of the NTEM image, yields a reasonable circle edge-setting criterion of 0.2408, and achieves precise pore edge detection. Theoretical analysis shows that the minimum measuring diameter can reach 0.19 μm, and the root mean square of the residuals is only 1.4 nm. Edge response simulation and experiment reveal that the edge response of the proposed method is better than 80 nm. The NTEM pore size measurement results obtained by the proposed method agree well with that obtained by scanning electron microscopy.Podgornik, Ales; Hamachi, Masataka; Isakari, Yu; Yoshimoto, Noriko; Yamamoto, Shuichi2017-11-01Effect of pore size on the performance of ion-exchange monolith tube chromatography of large biomolecules was investigated.
Radial flow 1 mL polymer based monolith tubes of different pore sizes (1.5, 2, and 6 μm) were tested with model samples such as 20 mer poly T-DNA, basic proteins, and acidic proteins (molecular weight 14 000-670 000). Pressure drop, pH transient, the number of binding site, dynamic binding capacity, and peak width were examined. Pressure drop-flow rate curves and dynamic binding capacity values were well correlated with the nominal pore size. While duration of the pH transient curves depends on the pore size, it was found that pH duration normalized on estimated surface area was constant, indicating that the ligand density is the same. This was also confirmed by the constant number of binding site values being independent of pore size. The peak width values were similar to those for axial flow monolith chromatography.
These results showed that it is easy to scale up axial flow monolith chromatography to radial flow monolith tube chromatography by choosing the right pore size in terms of the pressure drop and capacity. © 2017 WILEY-VCH Verlag GmbH & Co.
KGaA, Weinheim.Brassfield, H.C.; DeHollander, W.R.; Nivas, Y.1980-01-01A new method was developed for sintering ceramic uranium dioxide powders, in which ammonium oxalate is admixed with the powder prior to being pressed into a cylindrical green body, so that the end-point density of the final nuclear-reactor fuel product can be controlled. When the green body is heated, the ammonium oxalate decomposes and leaves discrete porosity in the sintered body, which corresponds to the ammonium oxalate regions in the green body. Thus the end-point density of the sintered body is a function of the amount of ammonium oxalate added. The final density of the sintered product is about 90-97% of the theoretical.
The addition of ammonium oxalate also allows control of the pore size and distribution throughout the fuel. The process leaves substantially no impurities in the sintered strucuture.
Bovine spongiform encephalopathy(BSE) was first recognized and defined as a pathological entity in the United Kingdom inNovember 1986 (Wells et al., 1996). Initial epidemiological investigations andexamination of archived brains indicated that the first cases occurred around April 1985.Subsequently, the largest freeborn epidemic of a transmissible spongiform encephalopathy(TSE) occurred which has had severe economic effects and has caused concern for publichealth.The initial clinical signs of thisfatal neurological disease are non-specific, typically involving behavioural changes. Asthe clinical phase progresses the disease is typified by alterations in mental state andof sensation and ataxia.
The majority of affected animals reach the advanced stages withintwo to three months from the onset, when slaughter on welfare grounds becomes necessary(Wilesmith et al., 1988).The disease affects adult animals,with a peak age at onset of four to five years of age. Both sexes and all breeds areequally susceptible.BSE can only be confirmedpost-mortem by pathological examination of brain tissue. Histological examination of thehind brain has been the primary method for the statutory diagnosis in the United Kingdom(Wells et al., 1989).
The histological changes are typical of the TSEs. Microscopiclesions in the central nervous system consist of bilaterally symmetrical, non inflammatoryvacuolation of neuronal perikarya and grey matter neuropil.BSE is transmissible by parenteralinoculation of inbred strains of mice (Fraser et al., 1988) and cattle (Dawson,Wells and Parker, 1990). In cattle the incubation period is approximately 18 months usingbrain homogenates from natural terminal cases.Epidemiological studies identifiedthe vehicle of infection to be meat and bone meal incorporated as a protein source inconcentrated feedstuffs (Wilesmith et al., 1988).
The most probable origin of B SEwas sheep scrapie. Most B SE cases forming the epidemic resulted from the recycling ofinfected cattle tissues, via meat and bone meal, within the cattle population (Wilesmith,Ryan and Atkinson, 199 1; Wilesmith and Wells, 199 1). A ban on the feeding of ruminantprotein to ruminants was introduced in July 1988 (HMSO, 1988b), shortly after the diseasewas made statutorily notifiable in June 1988. This feed ban was effective such that theincidence began to decline in 1993. However, it was not completely effective essentiallybecause of a problem of cross-contamination of cattle feedstuffs with ruminant protein,notably during its production (Wilesmith, 1996a; 1996b). Therefore the feeding ofmammalian protein to all farm animal species was prohibited in April 1996 (HMSO, 1996).The cross-contamination problem highlighted the low dose exposure phenomenon in theepidemiology of BSE. The low-dose exposure phenomenon had been recognized early in thecourse of the epidemic (Kimberlin and Wilesmith, 1994) and has subsequently been confirmedby studies of experimental oral exposure of cattle.
In these studies 1 g of brain, wetweight, from a terminal case resulted in disease with an incubation period within therange observed naturally (G.A.H. Wells and A.R. Austin, personal communication).The occurrence of BSE has had amajor impact on the trade in cattle, beef and bovine products from the United Kingdom.There have been consequences on a wide range of industries throughout the world, notablythe production of pharmaceutical products. It is likely that BSE has resulted in theoccurrence of feline spongiform encephalopathy (FSE) in domestic cats and cases ofspongiform encephalopathy in exotic species bred in zoological collections in the UnitedKingdom. More important has been the public health concern. In November 1989 the use ofcertain specified bovine offals (SB0s), which potentially contain relatively high titresof BSE infectivity, were banned for the use in human food. Subsequent studies of thepathogenesis of BSE have indicated that these were appropriate tissues to exclude.However, in March 1996 a new variant of the human TSE, Creutzfeldt-Jakob disease (CJD),was identified in the United Kingdom.
Strain typing studies in inbred strains of mice ofthis new form of CJD ( nvCJD) revealed similar patterns to those seen in BSE(Bruce et al., 1997). The identification of these patterns has raised questionsabout whether there will be a major epidemic of nvCJD (Cousens et al., 1997).However, the BSE epidemic in the United Kingdom has continued to decline. Although theremay be a slightly enhanced risk of infection for offspring of clinical cases, at leastwhile there was potential exposure from the feedborne source, there is no evidence for anatural transmission of BSE between cattle sufficient to prolong the epidemic, and it isclear that the incidence of B SE in the early part of the next millennium will be verylow.A number of TSEs had been identifiedand defined before the occurrence of BSE. They all share similar pathological andtherefore clinical features, but there are a number of differences between them. Thefollowing summarizes the essential features of these related diseases.ScrapieScrapie in sheep is the original TSEand has been an endemic disease of sheep in the United Kingdom for over 200 years. It hasbeen recorded in many other countries of the world, with Australia and New Zealand beingnotable exceptions. The disease also occurs in goats, but scrapie in this species has notbeen subject to the same degree of research.Scrapie in sheep has been the subject of researchboth as a natural disease and in laboratory studies using established inbred strains ofmice.
Laboratory studies provided the basis for the elucidation of the genetic risk factorin sheep scrapie. However, without the modem molecular genetic techniques, epidemiologicalstudies of natural sheep scrapie were difficult, as the confounding from this source couldnot be appropriately accounted for.
Therefore, although there were a relatively largenumber of studies of natural sheep scrapie in the 1950s and 1960s, their interpretation isdifficult (Hoinville, 1996). BSE was first recognized in the UnitedKingdom in 1986 as a result of the routine animal disease surveillance activities. Theinitial epidemiological studies and histological examination of archived bovine brainsindicated that the first cases occurred around 1985. The detection of BSE was probablyaided by the relatively high degree of active communication between animal keepers andveterinarians, who in turn seek help from the network of Veterinary Investigation Centres,whose staff may seek specialist advice from the Central Veterinary Laboratory. In amorepractical sense the disease was identified by its unusual clinical presentation, by thefact that one of the earliest affected herds was very large and multiple cases occurred,and by talk among herdowners about their 'unusual' animals, which stimulated theowners to seek veterinary attention (Wilesmith, 1996a). Although only a small number ofcases had been confirmed by histological examination by early 1987 (Wells et al., 1992),the epidemiological study primarily to investigate the potential aetiologies was startedin June 1987.The early studies relied on makingveterinarians involved in cattle medicine aware of the clinical signs and requesting theirvoluntary notification. Although the pathological features were reminiscent of scrapie,other potential aetiologies were not excluded.
Vehicles of a scrapie-like agent includedvaccines, hormones and other biological products, direct or indirect contact with sheepand a variety of free-living animals, imported cattle and semen and feedstuffs containinganimal-derived products. The other main potential aetiology was a toxic phenomenonresulting from the use of agricultural chemicals, such as herbicides and pesticides, andpharmaceutical products including organophosphorus preparations, synthetic pyrethroids andanthelmintics. A solely genetic origin was also investigated.All of the possible vehicles, exceptfeedstuffs, and the other actiologies, were eliminated by December 1987 following thecompletion of a case study of nearly 200 affected herds and cases of BSE (Wilesmith etal., 1988). With respect to feedstuffs, two possible vehicles of infection wereevident: meat and bone meal and tallow. The balance of evidence showed that meat and bonemeal was the primary vehicle and therefore responsible for most, if not all, cases.The suggestion that meat and bone meal wasthe primary vehicle was based initially on a consideration of the physicochemicalproperties of the scrapie agent which make it more likely to partition with the proteinfraction rather than the lipids of tallow. The geographical variation in incidence and thegeographical distribution and handling of tallow compared with meat and bone mealsupported the latter. In the early stages of the epidemic, although BSE occurredsimultaneously throughout the United Kingdom, the incidence was markedly greater in thesouth of England (see Figures 5 and 6).
Unlike meat and bone meal which, like proprietaryfeedstuffs, has a relatively local distribution, tallow is purchased and mixed by arelatively small number of companies which are much more distant and which distribute theproduct nationally. A similar incidence across the country would therefore have beenexpected if tallow was the primary vehicle of infection. The reasons for the north-southdifference in incidence were identified in a subsequent stage of the epidemiological studyand are described later.The feedborne hypothesis ingeneral was supported by particular features of the epidemic. The incidence of BSE isconsiderably greater in dairy herds than in beef suckler herds.
Commercial feedstuffscontaining meat and bone meal are less frequently used to feed beef stickler herds thanother animals. In addition, the risk of a herd experiencing a case of BSE increased withincreasing herd size. This was consistent with the fact that the larger the herd the morefeed is required and the greater the chances of buying an infected batch of feed.
In orderto investigate the meat and bone meal hypothesis more formally, a case-control study wasinitiated in early 1988 by recruiting unaffected herds for potential controls, before thehypothesis had become widely known. The final analysis of this study was completed in1991, allowing for the long incubation period, and the results provided supportingevidence that meat and bone meal was the source (Wilesmith, Ryan and Hueston, 1992).The initial findings wereconsidered sufficiently strong to make suspicion of the disease statutorily notifiable in June 1988 and ban the feeding of ruminant protein to all ruminants in July 1988(HMSO, 1988a; 1988b). Subsequently, a standard epidemiological questionnaire hasbeen completed for all suspect cases of B SE reported and the brain of every animalslaughtered has been examined histologically. These measures have resulted in a large andvaluable epidemiological database which has facilitated a detailed monitoring of theepidemic.The initial epidemiologicalstudies indicated clearly that BSE was a new disease and it had been identified veryshortly after its first occurrence. Some important questions were raised by these studies:When did exposure start? Which age groups of animals were at most risk from infection? Andhow did the cattle population of the United Kingdom become exposed to a scrapie-likeagent?The first two questionswere addressed by simulation studies (Wilesmith et al., 1988).
These provided someevidence that the majority of BSE cases observed resulted from infection in calf hood,suggesting an age-dependent susceptibility, and that effective exposure of the cattlepopulation commenced quite suddenly in 1981/82. The third question was addressed bydiscussions with representatives from the animal feedstuffs industry. The primary issue ofexposure was whether or not there had been an increase in the inclusion rate of meat andbone meal in cattle rations during the late 1970s and early 1980s. This proved not to bethe case as meat and bone meal had not recently been incorporated into proprietary cattlefeedstuffs.Attention therefore turnedto the processes used for the rendering of animal waste to produce meat and bone meal.
Twomajor changes in the industrial processes used in the United Kingdom were identified aspossibly significant. The first was a change from batch processing to continuousprocessing. The second was a reduction in the use of hydrocarbon solvents to maximize theextraction of tallow. Other considerations included the possible risks of rendering oftissues from other species, notably mink and whales.In order to obtain moredocumentary information, and therefore detailed aspects of these changes, a survey of allrendering plants in operation in the United Kingdom (excluding Northern Ireland) wasconducted in 1988 (Wilesmith, Ryan and Atkinson, 199 1). The moreappropriate data presentation is the epidemic curve of cases using the date of clinicalonset, rather than the date reported (Figure 3).Figure 3 indicates the peakof the epidemic in the early months of 1993.
If this peak monthly incidence had beenmaintained for 12 months, it would have represented an annual incidence of 1 percent ofadult animals. Subsequently the epidemic declined, as expected as a result of the ruminantfeed ban. A notable aspect of the epidemic, as indicated by the accumulated data, is thatin the absence of the feed ban the number of suspect cases reported per week could havereached 5 000 by the end of 1995. This incidence would have presented practicaldifficulties in the veterinary examination, in incinerating the carcasses or inmaintaining data entry, compounded by associated severe financial implications.In addition to the problemof not being able to provide a current epidemiological curve because a proportion ofsuspect cases being reported today will be attributed to a date of onset six monthspreviously, this presentation does not remove the potential observational bias. There isan observed seasonality in incidence, with an increase commencing in mid-August each year.This is coincident with the change in the degree and frequency of observation of cattlerelated to the seasonality of calving; in the important years of the epidemic, 70percentofcows calved in August, September and October.An important aspect of theepidemiology of B SE is that the majority of cases that have occurred result frominfection from the recycling of infected cattle tissues, via meat and bone meal.
This isof crucial importance for the risk assessment for the occurrence of BSE in any countrywhich has had BSE seeded into the cattle population as a result of the importation ofeither meat and bone meal or of cattle from the United Kingdom. The epidemiological originof BSE is relatively unimportant for countries that have imported either meat and bonemeal or live cattle from the United Kingdom. The important factor is the prevention ofexposure of the cattle population through potentially infected meat and bone meal.This can only be achieved by an effective ban on the exposure of cattle toruminant-derived protein.As is evident from thefindings in the United Kingdom and in Switzerland, this prevention of exposure cannot besolely dependent on the rendering processes in use. All means of preventing the exposureof infection of cattle have to be put in place.The age-specific incidencesof BSE (Table 1) have been a very important aspect of the descriptive epidemiology of BSEthroughout the epidemic.
In the very early stages of the epidemic and the epidemiologicalinvestigations the age-specific incidences were used to assess the results and fit of thesimulation studies with respect to the observed and predicted age-specific patterns ofdisease. The age-specific incidences of BSE have also been of importance in understandingthe dynamics of the epidemic as a whole.
The effects of recycling infected cattle tissuesare evident from these age-specific incidences. For example, the incidence inseven-year-old animals was greater in 1995 than in previous years and only showed adecrease in 1996. This can be explained by the fact that animals reaching seven years ofage in 1995 would not have been affected by the feed ban, reflecting the apparentage-dependent susceptibility. The first effects of the feed ban of July 1988becameapparent from the change in incidence in two-year-old animals in 1991 (Wilesmith and Ryan,1992) and subsequently in three-year-old animals in 1992 (Wilesmith and Ryan, 1993)beforethe decline in the national incidence in1993. The reduction in incidence in these twoyounger age groups did not affect the national incidence because the contribution ofclinical cases in the two- to three-year-old animals to the annual incidence was small.Because of the effects of recycling, the fact that most animals become infected in thefirst six months of life and the mean incubation period of 60 months, the incidence in theolder animals increased.
This more than counteracted any reduction in the incidence in theyounger age groups. It was therefore not until the feed ban affected the incidence inanimals four years old and greater that the epidemic declined. A study of the age-specificincidences highlights the difficulties of determining the effects of any control measureson a disease with a long incubation period when the risk of infection was increasingexponentially when the control measures were introduced.Table 1: Age-specificincidences of confirmed cases of BSE in adult animals in affected herds with home-bredcases, by year (percentage). YearWithin-herd incidence (%) a92.213.133.152.471.7a Percentage refers to animals that havecalved at least once.This means that the averagedose of infectivity was extremely low and the main effect of recycling was to increase thenumber of batches of meat and bone meal with the minimum 'threshold' amount ofinfectivity necessary to infect cattle, rather than the concentration of infectivitywithin batches. The details of this recycling are the subject of current modelling studiesas this phenomenon is clearly important to elucidating the epidemiology of.,CJD. Adult herd sizeNumber of herds at riskNumber of affected herdsCumulative incidence (%)1.81 1205.0299319.3816241.2182.5The finalherd aspect of the epidemiology of BSE is that of adult herd size.
Throughout the epidemicthe larger the adult herd, the greater it, risk of experiencing a clinical case. Table 4provides the cumulative incidence of home-bred cases by herd size from the beginning ofthe epidemic in 1986 to October 1997. This feature is consistent with the feedbornehypothesis. The larger the herd, the more feed is required and therefore the greater thechance of buying an affected batch. It also suggests that surveillance to detect theoccurrence of BSE would benefit from concentrating on large herds.A remarkable feature of thestart of the epidemic was the more or less simultaneous occurrence of BSE throughoutEngland, Scotland and Wales and associated islands (Figure 5).
This is consistent with awidespread common source of infection.However, there was a markedgeographic variation in incidence. In the early years of the epidemic the incidence ofBSE, as determined by the cumulative percentage of dairy herds with at least one case ofBSE in a home-bred animal,The reasons for thisvariation in incidence were essentially elucidated from the survey of rendering plants(Wilesmith, Ryan and Atkinson, 1991). These were threefold. First, the use of solventextraction in the production of meat and bone meal was confined to Scotland, where nearly80 percent of production was subject to this process. Second, in the past there were anumber of small rendering plants producing tallow and the fat-rich intermediate productgreaves. This was sold to the large rendering plants where it was totally reprocessed, andthe resulting meat and bone meal had been subject to a double heat treatment.
Theproportion of total production processed in this way in each geographical region was foundto be negatively correlated with the regional incidences of BSE. Third, there wasvariation among feedstuff producers in their use of meat and bone meal and geographicvariation in the market share that the producers had.
This variation was relative, as allfeedstuff producers had used meat and bone meal as an ingredient. This effect was and hasbeen most evident within the Channel Islands.Although proprietary cattlefeedstuffs have been purchased from mainland England, there has been a markedly greaterincidence on the island of Guernsey than on the island of Jersey. This was simply becausethe main producers of cattle feedstuffs imported into Guernsey used meat and bone mealmore frequently than the main producer of rations imported to Jersey. This fortuitousoccurrence was obviously a useful natural epidemiological experiment and assisted inestablishing the meat and bone meal hypothesis. In the United Kingdom (excluding NorthernIreland) the geographic variation in incidence has changed notably since the occurrence ofcases in animals born after the feed ban in July 1988. This is discussed in the followingsection.As indicated in earliersections the incidence of BSE began to decline as expected during 1993 However, in 1991 itbecame evident that the feed ban was possibly not totally effective, as cases began tooccur in animals born after the feed ban (BABs).These cases have attractedmuch attention and speculation about the natural transmission of BSE between cattle,either maternally or horizontally Therefore there has been considerable epidemiologicalresearch to determine the reasons for their occurrence. The distribution of these cases bytheir month and year of birth is given in Figure 7.A cohort study wasinitiated in 1989 to examine for maternal risk factors.
This was a long-term study andresults were not possible before the end of 1996. Maternal transmission of BSE on its owncould never sustain the disease in the cattle population of the United Kingdom. This issimply because the 'contact rate' will never exceed 1: 1, that is not everyinfected animal will produce a calf which reaches adulthood and in turn produces a calf(Wilesmith and Wells, 1991). However, studies to examine for maternal risk factors havebeen conducted as these are detectable earlier than any risks of horizontal transmission.They therefore potentially provide the means for determining whether or not BSE istransmissible other than by the feedborne route.When a sufficient number ofBAB cases had occurred in 1993 a case-control study was initiated to investigate amaternal risk factor and the possibility of horizontal transmission (Hoinville, Wilesmithand Richards, 1995).
The results of this study did not detect a maternal risk factor, inthat the offspring of animals that were subsequently affected with BSE were not foundsignificantly more often among the cases. There was a marginally statistically significantrisk for animals born up to three days after a subsequently affected animal calved, butthis was considered to be unlikely to indicate a causal association. Most important, theresult of this case-control study indicated that neither maternal nor horizontaltransmission could account for the majority of cases in animals born after the feed ban.During and subsequent tothe course of this study epidemiological analyses of the main database together within-depth studies of BAB cases have been conducted to quantify the effects of the feed banand to determine the reason for the occurrence of cases in such animals. The effect of thefeed ban has been examined by both modelling studies and the use of standardized morbidityratios. These rates have provided a relatively simple means of monitoring the effects ofthe epidemic (Hoinville, 1994).
This analysis allows for the fact that cases will accrueto any birth year cohort- the problem of right truncation (Figure 8).In this analysis the riskof developing BSE for an animal born in any month and year after the feed ban in July 1988was compared with the risk of disease for an animal born in the same month in the 12months (June 1987 to July 1988) before the ban, allowing both cohorts the same time todevelop disease. For example, in June 1996 the risk of disease occurring in animals bornin June 1990 could be determined using the data accumulated for this cohort and comparedwith data for cases accumulated by June 1994 among animals born in June 1988. Theunderlying assumption in this analysis is that there has been no change in the incubationperiod distribution in successive birth cohorts since 1988. No such change is apparent.The results are shown in Figure 8 and indicate that there was a more or less instant, butnot complete, effect for animals born in August 1988. This may have been unexpected, butcattle feedstuff producers had been forewarned of the introduction of the ban on thefeeding of ruminant-derived protein and would have therefore been able to conform with theban in a timely manner.
In subsequent birth cohorts the risk of developing disease hasdeclined. The risk of becoming infected for animals born in December 1990 was 10 percentof the risk for animals born in December 1987.
The risk did not decline significantly foranimals born in 1991, 1992 and 1993. Although the feed ban was effective it was notcompletely so - therefore additional studies were required.TABLE 5 The regionaldistribution of home-bred cases born in each 12-month (July to June) birth cohort (July1985 to June 1991). Cases of spongiformencephalopathy (SE) in domestic cats, various species of Felidae in zoos and exoticruminants have occurred concurrently with the BSE epidemic. Those occurring in the UnitedKingdom are summarized in Table 6.The cases in nyala andgemsbok are of some interest as they both occurred in the same zoological collection inthe south of England (Jeffrey and Wells, 1988; Wilesmith etaL, 1988). These animalswere infected as a result of the use of meat and bone meal in their concentrate rations(for a very short period), because of a shortage of soya as the protein source. Onenotable feature of the disease in these two species and the other exotic ungulates hasbeen the age at onset, which has been much younger than cattle with BSE.
The observedclinical duration of SE was much shorter on average than for BSE, but this may be due todifficulties in the observation of these animals.The cases of SE in thegreater kudu, Arabian oryx, eland, scimitar oryx and the bison were all likely to be aresult of infection from commercial feedstuffs containing meat and bone meal, and, in somecases, proprietary cattle rations. One of the causes in a greater kudu was the offspringof one of the affected kudu.
This was initially considered to be the possible caseof maternal transmission (Kirkwood et al., 1992). However, subsequentinvestigation revealed that this case was most likely to have become infected from cattlefeedstuffs.TABLE 6: Spongiformencephalopathies in domestic cats and exotic species in the United Kingdom (excludingNorthern Ireland). CountryNumber of casesIndigenous animalsImported animalsBelgium10Canada01Denmark01Falkland islands01France290Germany06Ireland24112Italy02Luxembourg10Netherlands20Oman02Portugal786Switzerland2640There hasbeen an estimation of the risk of BSE occurring in animals exported from the UnitedKingdom to European countries, which were members of the European Community in 1989(Schreuder et al., 1997). An important part of the estimation process was todetermine the potential exposure of the human populations in these countries to the BSEagent, in view of the occurrence of CJD. The results indicated that there may have been anincomplete ascertainment of cases of BSE in imported animals. This is probably inevitablegiven the non-specificity of the initial clinical signs (see Chapter 6) and the fact thatBSE occurs at a low within-herd incidence, frequently as single cases.
However, it isimportant to realize the magnitude of the risks of the introduction of infected cattle,because of the potential inclusion of their tissues in meat and bone meal within therecipient countries. Rendering systems that are capable of reducing the concentration ofthe BSE agent in the resultant meat and bone meal have been identified (Taylor, Woodgateand Atkinson, 1995), However, it is important to recognize that no study can identify arendering system (in terms of particle size, temperature and processing time) that cantotally inactivate the BSE, or other TSE, agent. Only reduction in the concentration ofthe agent can be identified by a study. Therefore countries that could have been'seeded' with the BSE agent, by the past importation of cattle or meat and bonemeal from the United Kingdom, should have all control in place measures (see Chapter 8),and not rely on an individual measure such as a suggested effective rendering system.Figure 3 (p. 12) indicatesthat the BSE epidemic in the United Kingdom is in rapid decline, with an approximate 40percent reduction each year.
If this continues, the incidence of BSE will be very low inthe early 2000s. It is impossible to predict the tail of the epidemic, and therefore theyear of the last case, because of the protracted incubation period. Long incubation periodcases could occur well into the future, as has been the case in the kudu epidemic in PapuaNew Guinea.In refining the predictionsof the future course of the BSE epidemic in the United Kingdom, much of theepidemiological research has been concentrated on determining whether or not there areother means of transmission of the BSE agent than by the feedborne source. As describedpreviously, the occurrence of cases in animals born after the feed ban could not beattributed, in the main, to horizontal or maternal transmission from the case-controlstudy (Hoinville, Wilesmith and Richards, 1995).
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My sister has a Heatrae Sadia megaflo hot water tank with two immersion heaters for her hot water. Heating is separate, by storage heaters (no gas supply to flats). She has had some problems, and an electrician has been called a couple of times. Last time, he told her how to reset the thermostat if it tripped. However, there are a couple of things I'd like advice on, please.From my reading so far, I think that the lower immersion heater is the overnight timed one, and the upper is the boost one - is this always the case?The thermostats are 'COTHERM type: TSE T115'. There is a little red plastic switch labelled SAFETY which the electrician told her to 'pop out'.
However, using a small screwdriver to press this switch does not release it out again. Should it, in fact, be pushed in?I ask both questions because I took the cover off the lower stat and the switch is level with the blue surround, whereas the top one (which the electrician adjusted last time) is depressed. However, the boost currently works and the main water heating does not.Finally, if this happens again, is it most likely to be a dodgy stat, or will the whole element need replacing?Sorry for the long post, thanks in advance for any advice. The only time a reset button should be used is when you have two forms of heating for example solid fuel. In a way you do have two forms of heating as you have two elements and since thermosyphon will cause water at top to also be heated from bottom element then top one can trip due to fault in bottom one. Since Megaflow is an un-vented system I would be worried about the trip and would want to replace the thermostat.The boost is always top and storage bottom again because of thermosyphon.Because the Megaflow is a special it may work at higher than boiling temperatures so thermostats need careful selection.
Not really done much work on them most around here seem to use Glenhill as unlike Megaflow they don't need annual inspections as not pressurised. I'm with Ericmark.
The only time I have seen a CoTherm trip in an all-electric Megaflo is when the owner drained down the system and left the elements powered upThe red button should be depressed to just below level with the blue housing.If you have a test meter, there are two test points on the stat (marked 1 and 2) you should get 230V between them with the power and the reset on and the thermostat turned up.You'll only be able to do this on the lower element during the off peak times.I'm not sure at what temp the safety trip on these goes off. I think the standard is 90ºC. Check the temperature setting on the stats and make sure its not set on maximum.PS Eric. From April 2004, new and replacement Immersion Heater Thermostats need to incorporate an overheat safety cut-out. They are fiited as standard to comply with regs.
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I would expect the lower thermostat to be set to a lower temperature than the upper one.When the cylinder is heated, there will be a temperatue gradient from hottest at the top of the cylinder, cooling towards the bottom. Hot water rises, just like hot air.If the lower thermostat is set too high, the thermosyphon could heat water at the top of the cylinder enough to trip the cutout in the upper heater before the water at the bottom of the cylinder gets hot enough to operate the lower heater's thermostat.You could try setting the lower 'stat temperature about 10 degrees lower than the operating temperature the upper cutout operates at, then 20 degrees etc. Until you find a point where the upper cutout doesn't trip.
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