- - in order to strengthen the self, and to learn its authentic interests. we experience such augmentations as pleasure, which may be why aesthetic values have always been deprecated by social moralists, from plato through our current campus puritans. the pleasures of reading indeed are selfish rather than social. you cannot directly improve anyone else ' s life by reading better or more deeply. i remain skeptical of the traditional social hope that care for others may be stimulated by the growth of individual imagination, and i am wary of any arguments whatsoever that connect the pleasures of solitary reading to the public good. the sorrow of professional reading is that you recapture only rarely the pleasure of reading you knew in youth, when books were a hazlittian gusto. the way we read now partly depends upon our distance, inner or outer, from the universities, where reading is scarcely taught as a pleasure, in any of the deeper senses of the aesthetics of pleasure. opening yourself to a direct confrontation with shakespeare at his strongest, as in king lear, is never an easy pleasure, whether in youth or in age, and yet not to read king lear fully ( which means without ideological expectations ) is to be cognitively as well as aesthetically defrauded. a childhood largely spent watching television yields to an adolescence with a computer, and the university receives a student unlikely to welcome the suggestion that we must endure our going hence even as our going hither : ripeness is all. reading falls apart, and much of the self scatters with it. all this is past lamenting, and will not be remedied by any vows or programs. what is to be done can only be performed by some version of elitism, and that is now unacceptable, for reasons both good and bad. there are still solitary readers, young and old, everywhere, even in the universities. if there is a function of criticism at the present time, it must be to address itself to the solitary reader, who reads for herself, and not for the interests that supposedly transcend the self. copyright © 2000 by harold bloom. all rights reserved. reproduced by permission of the publisher, simon & schuster.


sri lanka : year in review 2011article free pass in 2011 sri lanka continued to recover from its 26 - year civil war, which had ended in 2009. pres. mahinda rajapakse enjoyed great popularity among the majority sinhalese community for having defeated the tamil tigers ( liberation tigers of tamil eelam ; ltte ). as expected, the united people ’ s freedom alliance, led by rajapakse, dominated local government elections held in march and july. predominantly tamil areas formerly held by the ltte in the north and east of the country voted for the tamil national alliance. during 2011 the president moved to consolidate political power ( much of it held by members of his family ) in the executive branch of government while placing limits on media freedom, the role of civil society in sri lankan politics, and the expression of antigovernment dissent. in august it was announced that emergency regulations in place for nearly three decades were being lifted, but this still left many powers in government hands and failed to allay fears of repression among some sri lankans. international attention was directed throughout the year toward alleged violations of human rights in sri lanka. a highly critical report submitted to the un human rights council in september charged that both the ltte and government forces deliberately targeted civilians during the civil war. the government refused to permit an international investigation into human rights violations in sri lanka, and in october it announced the creation of a national action plan designed to protect and promote human rights and support reconciliation between the communities. former general sarath fonseka, who had commanded the sri lankan army in its victory over the tamil tigers and later had become a political rival of rajapakse, was sentenced to three years in prison for allegedly stating that the sri lankan government had committed war crimes during the civil war. fonseka was already serving a 30 - month jail term after having been convicted of corruption in military procurements. he denied both charges, claiming that they were politically motivated to keep him out of politics. economic growth in sri lanka, which had continued throughout the war period, slowed in 2009 because of the global recession but then accelerated rapidly. gdp was expected to rise by at least 8 % in 2011, despite floods in january that displaced more than a million people and damaged rice and other crops. major economic issues included continued poverty, employment creation and skill provision, the reconstruction of war - damaged areas, a large deficit in the government budget, and persistent inflation. nevertheless, an imf mission to sri lanka in august – september pronounced macroeconomic


emmanuel, count de las casesarticle free pass emmanuel, count de las cases, in full emmanuel - augustin - dieudonne - joseph, count de las cases ( born june 21, 1766, languedoc, france — died may 15, 1842, passy ), french historian best known as the recorder of napoleon ’ s last conversations on st. helena, the publication of which contributed greatly to the napoleonic legend in europe. an officer of the royal navy, las cases in 1790 emigrated from france to england, where he wrote and published his atlas historique... ( 1802 ), a work that attracted napoleon ’ s attention. consequently, on his return to france ( 1809 ) with other royalists rallying to napoleon, las cases was given a minor position on the council of state and created count in 1810. after napoleon ’ s defeat ( 1814 ), he returned to england but joined napoleon during the hundred days ( 1815 ), following him into exile at st. helena. for 18 months he recorded his conversations with napoleon on his principles of warfare, his identification of the french revolution with the empire, his political philosophy, and his sentiments on religion and philosophy. a letter of complaint about napoleon ’ s treatment led to las cases ’ deportation and to the seizure of his manuscript by the british government. forbidden to enter england, he traveled in germany and belgium until he was allowed to return to france after the death of napoleon in 1822. recovering his manuscript, he published his memorial de sainte - helene ( 1823 ), which at once became extremely popular. a deputy for saint - denis ( 1831 – 34 ; 1835 – 39 ), he sat with the extreme left, opposing the rule of louis - philippe. las cases ’ memorial de sainte - helene was the first defense of napoleon after his defeat. although prejudiced in napoleon ’ s favour, the identification of the idea of the revolution with napoleon furthered a union of liberals with bonapartists, thus contributing to the rise of napoleon iii. what made you want to look up " emmanuel, count de las cases "? please share what surprised you most...


dragonflies ( order odonata ) are divided into two distinct sub - orders, the zygoptera or damselflies and the anisoptera or dragonflies. you can find a description of these sub - orders on the " damselflies " and " dragonflies " pages. each species that has been recorded in great britain and ireland is described and illustrated on a separate page. the list below is your key to accessing these descriptions. click on a species name to see the species description. there you will find photographs, and written description, details of habitat, distribution and status and notes about similar species. please note that this site is not meant to be a substitute for a good field guide when trying to identify species. there are several good identification guides available, see the booklist for details. david goddard ( with help from tim beynon ) has put together a guide for assistance with pronunciation of latin names. the full checklist the full list of uk species is presented here ( with english and latin names ). you can use this list to navigate to a particular species detail page. species with a management fact file are indicated by [ mff ]. you can use this indication to navigate directly to their management fact file. click on images to enlarge.


not one, not two, but three female addax calves have been born at brookfield zoo within the last two months, and one more is expected by the end of the summer. the most recent was born this past saturday, july 9. the other two were born on may 30 and june 1. all are doing well and can be seen with their mothers — martha, sara, and mali — on exhibit in their outdoor habitat on the north side of the zoo. the three births are a welcomed addition to the north american zoo population because the species is critically endangered in its native africa. brookfield zoo has exhibited addax since 1935 and in 1941 was the first zoo in north america to have an addax birth. since the arrival of the first breeding pair, there have been 140 addax births at brookfield zoo. “ we are thrilled about the addax births at brookfield zoo and being able to share the significance and importance of these new additions with our guests, ” said amy roberts, curator of mammals for the chicago zoological society. “ what is really exciting is that there is the possibility that one of the calves or their descendants may one day be introduced to the wild as part of a collaborative program. ” the pairing of the three new moms with winston, who is the sire of all three calves, was based on a recommendation by the association of zoo and aquariums ’ addax species survival plan ( ssp ). the chicago zoological society, which manages the zoo, has been an active participant in the addax ssp since its inception in 1989. an ssp is a cooperative population management and conservation program for the species in north american zoos. the program manages the breeding of addax in zoos to maintain a healthy, self - sustaining population that is both genetically diverse and demographically stable. currently, there are 159 addax in 18 accredited north american zoos. once widespread across north africa, the addax has been largely driven to extinction in the wild by over - hunting since the mid - 1800s as well as civil unrest. additionally, although highly adapted to hyper - arid conditions, addax are nonetheless impacted by long periods of severe drought. the current addax population is restricted to a narrow band of desert between eastern niger and western chad. researchers estimate there to be less than 300 individuals remaining in the wild, with the last major population of around 200 in the tin toumma desert of eastern niger. however, there is hope for the species thanks to an international collaborative effort involving zoos in north america and europe,


than 300 individuals remaining in the wild, with the last major population of around 200 in the tin toumma desert of eastern niger. however, there is hope for the species thanks to an international collaborative effort involving zoos in north america and europe, the tunisian government, and the convention on migratory species. brookfield zoo is one of more than 40 zoos worldwide that has provided support for the reintroduction of zoo - born addax into fenced reserves in tunisia. current efforts are focusing on securing the remaining wild populations in niger and chad, increasing scientific management of captive populations in africa and elsewhere, and reintroducing individual animals to suitable, secure, and protected areas in former range states. addax have some of the most impressive horns of all antelope, which is one of the main reasons they have been over - hunted. in older individuals, they can spiral almost three turns and extend nearly three feet. they are one of a group of species called “ horse - like antelope, ” which are unusual in that the females have horns as long as those of the males. the species lives in one of the most inhospitable habitats in the world, and they are the most desert - adapted antelope. their feet are extra - large and spread out, perfect for staying on top of loose sand. their legs are shorter than most antelope, giving them a low center of gravity and keeping them steady — even when the sand shifts under foot. they get nearly all the moisture they need from the sap of vegetation and from dew, going almost their entire lives without drinking water at all. when vegetation is not available, they can live off the water stored in their body fat. they are nomadic, with no fixed territory, following the rains that produce the plants on which they depend. they have a relatively heavy body with a sandy - white coat in the summer that turns grayish - brown in the winter. white markings can be found on their legs and belly, with a black tuft of hair on their forehead, under the horns.


buildings don ’ t work they way they used to. 1 folks are always saying stuff like this. but let me make the case regarding just one factor and you decide. there are other factors of course, but i want to focus on only one for the moment. this one over - arching factor is the amount of energy exchange across the building enclosure. i think that higher levels of thermal resistance and reduced heat gain across building enclosures has forever changed the performance of buildings — and not necessarily in a good way. and things are going to get worse before they get better. sound familiar? the lens i am going to use to look at this factor is moisture. why? it is one of the principal damage functions acting on materials along with heat and ultra - violet radiation. 2 i think moisture is the key to understanding the performance of buildings in general — and in this particular case — in specific. the consequence of this reduced energy exchange is beginning to be seen all over the place : mold, part load humidity problems, rot, and corrosion. highly insulated building enclosures with reduced heat gain have low drying potentials and increased interior moisture loads. when they get wet they don ’ t dry. stuff is beginning to stink, rot, break and annoy. there are two things to look at here. levels of insulation and airtight assemblies and heat gain through glazing, roof assemblies and interior loads. adding insulation and providing airtight assemblies reduces energy flow. that is a good thing right? well, no — not always. less energy flow from the inside to the outside the colder things on the outside of the building get in the winter. the colder these things, the wetter these things get and the wetter they stay. this is not good. less energy flow from the outside to the inside in the summer and the less heat that is generated inside in the summer the less the air - conditioning system runs. this is a good thing right? well, no — not always. we create something called “ the part load humidity problem. ” higher levels of thermal resistance how do we dry wet wood? we kiln dry it. we heat the wood so that the water in the wood is warmer than its surroundings. we add energy to the water and it evaporates. there is a huge exchange of energy. when we put warm wet coffee beans in a room with very cold surfaces we call it freeze - drying. the moisture leaves the coffee beans and accumulates on the cold surfaces. there is a huge exchange of energy. the greater the


exchange of energy. when we put warm wet coffee beans in a room with very cold surfaces we call it freeze - drying. the moisture leaves the coffee beans and accumulates on the cold surfaces. there is a huge exchange of energy. the greater the rate of energy exchange the greater the rate of moisture movement. drying cannot happen with out an exchange of energy. when my mom and dad bought their first house in toronto, canada in 1957 there was no insulation in the walls and the house was leaky to air — it had a high air change driven by a traditional chimney. we lived in a 1, 200 square foot house and in january, when the outside temperature dropped to 0 degrees f., momma cranked up the 300, 000 btu oil furnace to maintain an interior temperature of 70 degrees f. the energy flow across the building enclosure was enormous, but oil was cheap, and we were comfortable and happy. the energy flow was so enormous the building enclosure was simultaneously kiln dried and freeze - dried. in fact, the drying potential was so high, we were uncomfortably dry. as a result poppa insisted that the furnace have a new fangled gadget attached to it — called a humidifier. how things have changed. well what changed? we ’ ve begun to insulate — and insulate exceptionally well — and we ’ re getting the assemblies “ tighter ” to air change and convection. that results in two things — less energy exchange therefore less drying potential — and things on the exterior side of the enclosure are colder in the winter. things being colder on the outside lead to something most folks don ’ t consider. many building materials are hygroscopic ( figure 1 ). this means they absorb moisture based on relative humidity. even more strangely, they don ’ t care about vapor pressure except if it affects relative humidity. this is a big deal. in fact it is a huge deal. figure 1 : sorption curve for common building materials — note that moisture content goes up as relative humidity goes up. there is no temperature dependence or vapor pressure dependence except where temperature affects relative humidity or where vapor pressure affects relative humidity. quick, snap quiz, psychrometric chart stuff …. as the temperature drops, and vapor pressure is kept constant, what happens to the relative humidity? buzz / clang / bell. yes, folks, you are correct, the relative humidity goes up. the implications are staggering. just making things on the outside of your building cold, hygroscopic things, makes them wetter


humidity? buzz / clang / bell. yes, folks, you are correct, the relative humidity goes up. the implications are staggering. just making things on the outside of your building cold, hygroscopic things, makes them wetter. period, end of story. but, but, the moisture content of the outside air in the wintertime is low. yes, grasshopper, it is, but its ’ relative humidity is high. the amount of moisture in the absolute sense is low, but in the relative sense it is high. and hygroscopic materials don ’ t care about the absolute sense ; they only care about the relative sense. why? second law stuff — isn ’ t it always? check out photograph 1. nice, normal, everyday type of house in cleveland, oh. twenty years old, no insulation in the wall cavities, built in 1965 ( yes, the photograph was taken in 1985 — we did have camera ’ s back then... ). the house was perfectly happy at this point for twenty years. then the homeowner decides to do something crazy, he decides to insulate the exterior walls to save energy and has the cavities blown with dry cellulose. what a dumb idea in 1985 eh? but, never the less, it was a beautiful job, no voids, yes it can be done, and yes it was done. no voids, no convection ( photograph 2 — notice how young this engineer once was ). next thing you know, the paint falls off, and the siding gets smelly, moldy and begins to decay ( photograph 3 ). huh? the insulation did this? yup. the drying potential is reduced due to the addition of the insulation so that the moisture entering the cladding assembly from the exterior due to rain and capillarity does not evaporate and this is further exacerbated by the colder siding having a higher local relative humidity and thus a higher equilibrium moisture content due to the sorption properties of wood. bummer. how to fix this? easy, wedges were used to create a gap at the overlaps of the siding reducing capillary uptake at the laps and increasing evaporation despite the cladding being colder ( photograph 4 ). this early lesson in sorption and drying potentials taught this engineer to drain and back - ventilate claddings – especially those on highly insulated assemblies ( photograph 5 ). photograph 1 : the “ typical house ” —


4 ). this early lesson in sorption and drying potentials taught this engineer to drain and back - ventilate claddings – especially those on highly insulated assemblies ( photograph 5 ). photograph 1 : the “ typical house ” — built in 1965 in cleveland, oh with no cavity insulation in the exterior wood frame walls. no problems for twenty years. insulation added to exterior walls in 1985 and within one year the paint begins to fail. photograph 2 : retrofit cellulose cavity insulation — dry blown cellulose packed into exterior wood frame walls. injected from the exterior at top of cavity. this author, very young at the time, amazed at how well the insulation worked. cavities were dry when opened. photograph 3 : wet cladding — problems with mold and decay were worse on north and east elevations. problems with peeling paint were worse on west and south elevations. solar radiation cycled the cladding moisture content more on the west and south elevations stressing the paint. uv cross - linked the paint making it less flexible. less flexibility, more movement on the south and the west led to the peeling paint. less energy on the north and the east led to the mold and the decay. photograph 4 : wedgie — so simple and so obvious. after the problem is understood. wedges created gaps that reduced capillary uptake of surface water, promoted drainage and back ventilation. photograph 5 : drainage and ventilation matt behind cladding — this is easy for new construction and re - cladding. existing buildings are going to be a problem. don ’ t say you weren ’ t warned. let ’ s extend this discussion to cavity insulation in general. the same thing happens to the cavity side of sheathing when we insulate cavities. it gets worse when the cavities also have no air flow or convection. 3 sheathings get colder. if the sheathing is hygroscopic, its equilibrium moisture content also goes up. why take the risk? insulate on the exterior of the sheathing. this makes the problem go away. the risk is so high in cold climates that folks are no longer insulating the cavities in steel stud walls in places like ottawa and montreal — all of the insulation goes on the outside. this is why insulating sheathing is pretty much the name of the game for highly insulated wall assemblies — or at a minimum claddings should be back ventilated and back - drained — or better, do both. this is easy for new construction


why insulating sheathing is pretty much the name of the game for highly insulated wall assemblies — or at a minimum claddings should be back ventilated and back - drained — or better, do both. this is easy for new construction. the problem is what to do with the existing building stock? what are we going to do if oil ever goes above $ 100 / barrel? dumb comment. yes, but now we have a real problem. folks cannot just go and blow / spray / fill cavities with a bunch of insulation without appreciating the consequences. this is not just a cold climate problem. it is a problem everywhere. in fact it gets worse when we go far south. read on mcduff … reduced heat gain i am going to let you in on a little secret that us mechanical engineers don ’ t often share with the rest of the world — air conditioning systems only dehumidify when they run. yup, when they don ’ t run, they don ’ t dehumidify. if there is no load, there is no dehumidification. 4 well, just make them run longer. how? they still make the air cold no matter how you run them. that is good if you need cold air. but what if you don ’ t need cold air? what if you only need dry air? well, you still have to make the air cold to get it to drop its water, and when you are done you still have cold air. so now what? well, you have to heat it back up if you want to use it. this is sometimes called cooling with re - heat. there are other tricks we can do — read on — but at the end of the day we have to add energy back to the air that we cooled. there is no other practical way to do it. it gets worse when we over - ventilate with humid air — especially when it is cloudy and not so hot. now all you are doing is bringing in moisture. but you are doing it when there is not much of a load — not much of a “ sensible load ” ( heat gain across the enclosure and heat gain from lights and appliances and people — the load you can “ sense ” ) to run the air conditioning system. this moisture that you are bringing in with the ventilation air is also a “ load ” — but it is a different kind of load that we have pretty much been ignoring up till now and getting away with it. the operative phrase to note is


system. this moisture that you are bringing in with the ventilation air is also a “ load ” — but it is a different kind of load that we have pretty much been ignoring up till now and getting away with it. the operative phrase to note is : “ getting away with it. ” mechanical engineers like me call this the “ hidden load ” or the “ latent load ” ( as in “ latent defect ” or “ hidden defect ” ) and our heads explode when we try to explain this problem to the indoor air crazies who think that only dilution is the solution to indoor pollution. i mean how can too much outside air be bad? 5 arrargah … to take the water out of the air you need to use energy. to make the air comfortable / useful the air can ’ t be too cold after you have taken the water out of it. typically heat ( energy ) has to be added back to the air. traditionally this heat ( energy ) was available through lousy glazing systems, too much glass, black roofs with no insulation, poorly insulated walls, energy inefficient lights, and crappy appliances. well, this traditional “ re - heat ” due to inefficiency and poor practice is disappearing. now we are stuck. if we don ’ t warm up the air after we dry it we are going to get into trouble. we haven ’ t been, and we are getting into trouble. the buildings are now getting too cold or too humid or worse, both. ah, this is easy you say. just make the air conditioning systems smaller — “ right size ” them. don ’ t make me scream. i am getting tired of being told by energy weenies that my equipment is too big. 6 i still have to satisfy the “ full load ” requirement. if you make the equipment too small it doesn ’ t satisfy the cooling requirements under full load. let the people be uncomfortable you say. people should suffer you say ; we have had it too good you say. yeah, sure, another greenie weenie value judgment that also makes me scream. i don ’ t think we should suffer. i like it being good. i don ’ t have a problem with using energy. i have a problem with wasting energy. until now we have gotten pretty good at dealing with this part - load problem with face - bypass, run - around coils, hot gas bypass and heat pipes but we have reached our limits. building enclosures have gotten so good, gla


. until now we have gotten pretty good at dealing with this part - load problem with face - bypass, run - around coils, hot gas bypass and heat pipes but we have reached our limits. building enclosures have gotten so good, glazing systems so good, interior load management so good, that we can ’ t use the same equipment to handle the “ sensible load ” and the “ latent load. ” did i mention just how good the glazing systems have become? did i mention the low shgc thing? we used to just install air conditioners and only cared about making it cold inside. we used one piece of equipment to handle the sensible and latent load. the reason this worked is that the latent load was small compared to the sensible load. not any more. the sensible load has gotten smaller big time. and, much to my chagrin, the latent load has gone up due to over ventilation. the old systems can ’ t handle the new sensible to latent ratios. we have to separate the two loads. we need separate systems for the sensible load and the latent load. this is a big deal and it results from the low heat gain in the modern enclosure. in other words energy conservation and good construction practice is biting us on the butt. we sometimes refer to this second separate latent load control system as supplemental dehumidification — and we need it when we have a low heat gain enclosure and efficient lighting and appliances. others call it “ preconditioning ” of outside air since the largest component of the latent load is the ventilation air or the outside air. whatever you call it, we need this second system. we don ’ t often get it and it hurts us. but, but these systems use energy. yes, as the saying goes — there is no thermodynamic free lunch. you need to use energy to make air cold and you need to use energy to make air dry. we have been very good at making air cold. we now have to get good at making air dry. think of it this way. for every 100 units of energy you save on the efficiency and on the cooling side, you are going to have to give back about 20 units of energy to be dry. you are still 80 units ahead. problem is, if you are greedy and want the entire 100 units your building fails and your occupants get very uncomfortable and probably very annoyed. it is pretty amazing to me but the hotel industry figured this out first. they pretty much had


80 units ahead. problem is, if you are greedy and want the entire 100 units your building fails and your occupants get very uncomfortable and probably very annoyed. it is pretty amazing to me but the hotel industry figured this out first. they pretty much had the problem first, so it stands to reason that they would also figure it out first. think about the typical hotel room. the drapes are pretty much closed all the time, the room is empty during the day, and you know the unit has been sized for the full load, with the drapes open, and the room full, and everything on and you know that someone in some bureaucracy somewhere wants way too much outside air. most of the time your latent load dwarfs your sensible load. so what do you do? you reduce the amount of outside air by installing timers on the exhaust fans and you pretty much ignore the faceless bureaucrat. then you only run the through - wall unit to control the temperature ( i. e. make it the “ sensible ” system ) and install a dehumidifier in each unit control the humidity ( the “ latent ” system ) ( photograph 6 ). a pretty primitive but effective “ fix. ” in new design we just “ hide ” the dehumidifier better — or better still make it part of the ventilation system. photograph 6 : hotel room fix — the through - wall unit controls the temperature ( the “ sensible ” system ). the dehumidifier controls the humidity ( the “ latent ” system ). guess where this technology is now making an impact — condos and apartments. small houses are next. we are already separating the latent from the sensible on most commercial design — after all it is the sensible thing to do. north versus south so how come it is worse in the south than the north? besides the south loosing the civil war? in the north, it still gets cold and the outside cold air is pretty dry — and walls tend to dry to the outside in the north - so the size of the moisture drying “ sink ” so to speak — has not changed. but in the south, walls also dry to the inside — and if the inside is humid because of the part load problem — the walls stay wetter because the moisture drying “ sink ” is smaller. additionally, in the south the moisture drive from the exterior into the wall is greater while at the same time the moisture drive from the wall into the interior is smaller as compared to the corresponding drives in opposite directions in the


drying “ sink ” is smaller. additionally, in the south the moisture drive from the exterior into the wall is greater while at the same time the moisture drive from the wall into the interior is smaller as compared to the corresponding drives in opposite directions in the north. let me translate. it is easier to get wet from the outside in the south than it is from the inside in them north. it is also easier to dry to the outside in the north than it is to dry to the inside in the south. with less energy available, it gets worse in the south faster than in the north. good air conditioning design leads to dry interiors and dry interiors allow walls to dry to the inside. part load humidity problems lead to wetter walls. higher levels of thermal insulation and lower heat gain lead to part load humidity problems. not good. ok, everybody relax. we want and we need much higher levels of thermal control ( air tight, insulated assemblies ) everywhere. we just have to be smart about it. we want and we need ultra efficient glazing, lights, appliances, and reflective surfaces everywhere. we just have to be smart about it. and we want and we need the right amount of outside air whenever we need it. we just have to be smart about it. this is neither expensive nor difficult, just different. we have to modify our building enclosure and mechanical system paradigms. get used to it or be steamrolled by the change. insulate on the outside. back ventilate and drain your cladding. separate your sensible load from you latent load. don ’ t over ventilate. existing buildings are going to be a bear. and have a nice day. yes, i know, pretty arrogant for a relative youngster to say. i am in my 50 ’ s, but when you get to this age you spend as much time looking back as you do looking forward. my mentors tell me that it helps with perspective. it has been said that in order to understand the future you have to understand the past. i am not so ambitious. i am only thinking of today. i think in order to understand the present you have to understand the past … someone once said that 80 percent of all building related durability problems are due to three principal damage functions ( water, heat and uv radiation ) with 80 percent of the 80 percent being water. i don ’ t know who said this. can someone help me out? i might have just made it up, but i have been saying it so long


functions ( water, heat and uv radiation ) with 80 percent of the 80 percent being water. i don ’ t know who said this. can someone help me out? i might have just made it up, but i have been saying it so long i no longer remember if i did or not. aren ’ t footnotes great … air flow — air change and convection — increases energy exchange therefore increases drying potential. my canadian friends heads are now going to explode because they have been taught that air leakage leads to “ wetting ” from interior sources. yes, in extreme climates with high interior moisture loads. think humidified buildings in canada. not everywhere else. come visit the united states, the dollar exchange now works for you and air leakage improves drying potentials. sensible load. i know you knew that i knew this, but some of the email i have been getting from you folks has been quite picky, which is good, but i want to head off the obvious emails, so continue to be picky, but not on this … some folks don ’ t seem to care about the energy thing either. i mean health is paramount and we should always err on the side of caution. how can we argue against health? easy, when the “ healthy ” measures are “ unhealthy. ” over - ventilation can be unhealthy — and energy wasteful. read on. this is leading to interesting discussions in the standard 62 committees. apparently the standard 62 committees are not about energy. apparently energy security is not a 62 problem nor is climate change nor are operating costs. apparently, it is some other committee ’ s problem. how about the energy committee ( standard 90. 1 )? except that the energy committee does not want to touch ventilation. cowards. my insider ’ s perspective ( on 62. 2 at least ) is that there is a lot of mileage to be made by scaring people about under ventilation, and folks are rising to the occasion. unfortunately, over ventilation in hot humid climates and in mixed humid climates has led to more indoor air problems due to mold resulting from part load issues than under ventilation anywhere else — in my not so humble opinion. and speaking of health and under ventilation where are all the dead bodies? where is the causal link between health and specific levels of specific indoor contaminants? in my not so humble opinion all of the rates have been just wild assed guesses without a sound epidemiological basis. but the resulting mold from over ventilation is real and demons


the immune system because the human body provides an ideal environment for many microbes, they try to pass your skin barrier and enter. your immune system is a bodywide network of cells, tissues, and organs that has evolved to defend you against such " foreign " invasions. the proper targets of your immune system are infectious organisms - - bacteria such as these streptococci ; fungi ( this one happens to be candida, the cause of yeast infections ) ; parasites, including these worm - like microbes that cause malaria ; and viruses such as this sars virus. markers of self at the heart of the immune response is the ability to distinguish between " self " and " non - self. " every cell in your body carries the same set of distinctive surface proteins that distinguish you as " self. " normally your immune cells do not attack your own body tissues, which all carry the same pattern of self - markers ; rather, your immune system coexists peaceably with your other body cells in a state known as self - tolerance. this set of unique markers on human cells is called the major histocompatibility complex ( mhc ). there are two classes : mhc class i proteins, which are on all cells, and mhc class ii proteins, which are only on certain specialized cells. markers of non - self any non - self substance capable of triggering an immune response is known as an antigen. an antigen can be a whole non - self cell, a bacterium, a virus, an mhc marker protein or even a portion of a protein from a foreign organism. the distinctive markers on antigens that trigger an immune response are called epitopes. when tissues or cells from another individual enter your body carrying such antigenic non - self epitopes, your immune cells react. this explains why transplanted tissues may be rejected as foreign and why antibodies will bind to them. markers of self : major histocompatibility complex your immune cells recognize major histocompatibility complex proteins ( mhc ) when they distinguish between self and non - self. an mhc protein serves as a recognizable scaffold that presents pieces ( peptides ) of a foreign protein ( antigenic ) to immune cells. an empty " foreign " mhc scaffold itself can act as an antigen when donor organs or cells are introduced into a patient ' s body. these mhc self - marker scaffolds are also known as a patient ' s " tissue type " or as human leukocyte antigens ( h


as an antigen when donor organs or cells are introduced into a patient ' s body. these mhc self - marker scaffolds are also known as a patient ' s " tissue type " or as human leukocyte antigens ( hla ) when a patient ' s white blood cells are being characterized. for example, when the immune system of a patient receiving a kidney transplant detects a non - self " tissue type, " the patient ' s body may rally its own immune cells to attack. every cell in your body is covered with these mhc self - marker proteins, and - - except for identical twins - - individuals carry different sets. mhc marker proteins are as distinct as blood types and come in two categories - - mhc class i : humans bear 6 markers out of 200 possible variations ; and mhc class ii : humans display 8 out of about 230 possibilities. organs of the immune system the organs of your immune system are positioned throughout your body. they are called lymphoid organs because they are home to lymphocytes - - the white blood cells that are key operatives of the immune system. within these organs, the lymphocytes grow, develop, and are deployed. bone marrow, the soft tissue in the hollow center of bones, is the ultimate source of all blood cells, including the immune cells. the thymus is an organ that lies behind the breastbone ; lymphocytes known as t lymphocytes, or just t cells, mature there. the spleen is a flattened organ at the upper left of the abdomen. like the lymph nodes, the spleen contains specialized compartments where immune cells gather and confront antigens. in addition to these organs, clumps of lymphoid tissue are found in many parts of the body, especially in the linings of the digestive tract and the airways and lungs - - gateways to the body. these tissues include the tonsils, adenoids, and appendix. the organs of your immune system are connected with one another and with other organs of the body by a network of lymphatic vessels. lymphocytes can travel throughout the body using the blood vessels. the cells can also travel through a system of lymphatic vessels that closely parallels the body ' s veins and arteries. cells and fluids are exchanged between blood and lymphatic vessels, enabling the lymphatic system to monitor the body for invading microbes. the lymphatic vessels carry lymph, a


the body ' s veins and arteries. cells and fluids are exchanged between blood and lymphatic vessels, enabling the lymphatic system to monitor the body for invading microbes. the lymphatic vessels carry lymph, a clear fluid that bathes the body ' s tissues. small, bean - shaped lymph nodes sit along the lymphatic vessels, with clusters in the neck, armpits, abdomen, and groin. each lymph node contains specialized compartments where immune cells congregate and encounter antigens. immune cells and foreign particles enter the lymph nodes via incoming lymphatic vessels or the lymph nodes ' tiny blood vessels. all lymphocytes exit lymph nodes through outgoing lymphatic vessels. once in the bloodstream, they are transported to tissues throughout the body. they patrol everywhere for foreign antigens, then gradually drift back into the lymphatic system to begin the cycle all over again. cells of the immune system cells destined to become immune cells, like all blood cells, arise in your body ' s bone marrow from stem cells. some develop into myeloid progenitor cells while others become lymphoid progenitor cells. the myeloid progenitors develop into the cells that respond early and nonspecifically to infection. neutrophils engulf bacteria upon contact and send out warning signals. monocytes turn into macrophages in body tissues and gobble up foreign invaders. granule - containing cells such as eosinophils attack parasites, while basophils release granules containing histamine and other allergy - related molecules. lymphoid precursors develop into the small white blood cells called lymphocytes. lymphocytes respond later in infection. they mount a more specifically tailored attack after antigen - presenting cells such as dendritic cells ( or macrophages ) display their catch in the form of antigen fragments. the b cell turns into a plasma cell that produces and releases into the bloodstream thousands of specific antibodies. the t cells coordinate the entire immune response and eliminate the viruses hiding in infected cells. b cells work chiefly by secreting soluble substances known as antibodies. they mill around a lymph node, waiting for a macrophage to bring an antigen or for an invader such as a bacteria to arrive. when an antigen - specific antibody on a b cell matches up with an antigen, a remarkable transformation occurs. the antigen binds


effective in killing bacteria. scientists long wondered how all the genetic information needed to make millions of different antibodies could fit in a limited number of genes. the answer is that antibody genes are spliced together from widely scattered bits of dna located in two different chromosomes. each antibody molecule is made up of two separate chains, a heavy chain and a light chain. the heavy chain is where the binding of antigens occurs, so much genetic variation is involved in its assembly. for example, to form a heavy chain, 1 of 400 possible variable gene segments ( v ) combines with 1 out of 15 diversity segments ( d ) and 1 out of 4 joining ( j ) segments. this makes 24, 000 possible combinations for the dna encoding the heavy chain alone. as this part of the gene assembles, it joins the variable coding segments with those for the constant - c segments of the heavy - chain molecule. t cells contribute to your immune defenses in two major ways. some help regulate the complex workings of the overall immune response, while others are cytotoxic and directly contact infected cells and destroy them. chief among the regulatory t cells are helper t cells. they are needed to activate many immune cells, including b cells and other t cells. cytotoxic t cells ( sometimes called killer t cells ) help rid your body of cells that have been infected by viruses as well as cells that have been transformed by cancer but have not yet adapted to evade the immune detection system. they are also responsible for the rejection of tissue and organ grafts. cytokines are diverse and potent chemical messengers secreted by the cells of your immune system. they are the chief communication signals of your t cells. cytokines include interleukins, growth factors, and interferons. lymphocytes, including both t cells and b cells, secrete cytokines called lymphokines, while the cytokines of monocytes and macrophages are dubbed monokines. many of these cytokines are also known as interleukins because they serve as a messenger between white cells, or leukocytes. interferons are naturally occurring cytokines that may boost the immune system ' s ability to recognize cancer as a foreign invader. binding to specific receptors on target cells, cytokines recruit many other cells and substances to the field of action. cytokines encourage cell growth, promote cell activation, direct cellular traffic, and destroy target cells - - including cancer cells. when cytokines attract specific


on target cells, cytokines recruit many other cells and substances to the field of action. cytokines encourage cell growth, promote cell activation, direct cellular traffic, and destroy target cells - - including cancer cells. when cytokines attract specific cell types to an area, they are called chemokines. these are released at the site of injury or infection and call other immune cells to the region to help repair damage and defend against infection. killer cells : cytotoxic ts and nks at least two types of lymphocytes are killer cells - - cytotoxic t cells and natural killer cells. both types contain granules filled with potent chemicals. both types kill on contact. they bind their targets, aim their weapons, and deliver bursts of lethal chemicals. to attack, cytotoxic t cells need to recognize a specific antigen bound to self - mhc markers, whereas natural killer ( nk ) cells will recognize and attack cells lacking these. this gives nk cells the potential to attack many types of foreign cells. phagocytes and their relatives some immune cells have more than one name. for example, the name " phagocytes " is given to the large immune cells that can engulf and digest foreign invaders, and the name " granulocytes " refers to immune cells that carry granules laden with killer chemicals. phagocytes include monocytes, which circulate in the blood ; macrophages, which are found in tissues throughout the body ; dendritic cells, which are more stationary, monitoring their environment from one spot such as the skin ; and neutrophils, cells that circulate in the blood but move into tissues when they are needed. macrophages are versatile cells ; besides acting as phagocytic scavengers, they secrete a wide variety of signaling cytokines ( called monokines ) that are vital to the immune response. neutrophils are both phagocytes and granulocytes : they contain granules filled with potent chemicals. these chemicals, in addition to destroying microorganisms, play a key role in acute inflammatory reactions. other types of granulocytes are eosinophils and basophils, which degranulate by spraying their chemicals onto harmful cells or microbes. the mast cell is a twin of the basophil, except it is not a blood cell. rather, it is responsible for allergy symptoms in the lungs, skin, and linings of the


spraying their chemicals onto harmful cells or microbes. the mast cell is a twin of the basophil, except it is not a blood cell. rather, it is responsible for allergy symptoms in the lungs, skin, and linings of the nose and intestinal tract. a related structure, the blood platelet, is a cell fragment. platelets, too, contain granules. they promote blood clotting and wound repair, and activate some immune defenses. phagocytes in the body if foreign invaders succeed in getting past your skin barriers and manage to reach body tissues, they are usually recognized, ingested, and killed by phagocytes strategically positioned throughout the body. macrophages and neutrophils are the main phagocytes involved, with macrophages as the first line of defense. monocytes stop circulating in the blood and mature into specialized macrophages that migrate into the tissues of the body and prepare for invasion. large numbers of mature macrophages reside in connective tissue, along the digestive tract, in the lungs, in the spleen, and even along certain blood vessels in the liver, where they are known as kupffer cells. neutrophils are short - lived immune cells that remain circulating in the blood. when tissue - based macrophages encounter an invader, neutrophils soon reinforce their immune response by coming to the site of infection in large numbers. the complement system consists of a series of about 25 proteins that work to " complement " the work of antibodies in destroying bacteria. complement also helps rid the body of antigen - antibody complexes. complement proteins are the culprits that cause blood vessels to become dilated and leaky, causing redness and swelling during an inflammatory response. complement proteins circulate in the blood in an inactive form. the so - called " complement cascade " is set off when the first complement molecule, c1, encounters antibody bound to antigen in an antigen - antibody complex. each of the complement proteins performs its specialized job, acting, in turn, on the molecule next in line. the end product is a cylinder that punctures the cell membrane and, by allowing fluids and molecules to flow in and out, dooms the target cell. mounting an immune response microbes attempting to get into your body must first get past your skin and mucous membranes, which not only pose a physical barrier but are rich in scavenger cells and iga antibodies. next, they must elude a series of nonspec


presenting cells enable specific receptors on helper t cells to bind the antigen and confirm ( via cd4 protein ) that an invasion has occurred. after binding, a resting helper t cell quickly becomes an activated helper t. it assumes command of the immune response, giving orders to increase the number of specific antibody - producing plasma cells and the cytotoxic killer cells needed to quell the attack. activation of t cells : cytotoxic killer t cells only recognize antigen in the grasp of class i mhc markers. here a resting cytotoxic t cell recognizes virus fragments, which are displayed by a macrophage in combination with a class i mhc marker. a receptor on a circulating, resting cytotoxic t cell ( and cd8 protein ) recognizes the antigen - protein complex and binds to it. the binding process and an activated helper t cell activate the cytotoxic t cell. because the surfaces of other infected cells bear the same virus fragments in combination with class i mhc markers, the activated cytotoxic t cells can quickly recognize, attack, and destroy the diseased cell. regulatory t cells your immune system also has a braking mechanism, a checkpoint to prevent immune responses to self. without this checkpoint, autoimmune disease could flourish. an additional type of immune cells - - regulatory t cells - - are these critical braking agents. researchers don ' t yet know exactly how regulatory t cells operate. some think these t cells recognize and compete for the same antigens as those that activate helper and cytotoxic t cells, but that regulatory t cells zero in on a different epitope. another possibility is that cytotoxic or helper t cells only multiply when regulatory t cells are absent. regulatory t cells have become important to researchers who are trying to increase the efficacy of vaccines for cancer and aids. in addition to increasing the antigenicity of the immunizing element, a better understanding of regulatory t cells will permit scientists to reduce the immune system ' s brake activity, which often limits the effectiveness of vaccines. immunity : active and passive whenever t cells and b cells are activated, some become " memory " cells. the next time that an individual encounters that same antigen, the immune system is primed to destroy it quickly. this is active immunity because the body ' s immune system prepares itself for future challenges. long - term active immunity can be naturally acquired by infection or artificially acquired by vaccines made from infectious agents that


the immune system is primed to destroy it quickly. this is active immunity because the body ' s immune system prepares itself for future challenges. long - term active immunity can be naturally acquired by infection or artificially acquired by vaccines made from infectious agents that have been inactivated or, more commonly, from minute portions of the microbe. short - term passive immunity can be transferred artificially from one individual to another via antibody - rich serum ; similarly, a mother enables an infant to naturally acquire protection while growing within her by donating her antibodies and certain immune cells. this is passive immunity because the infant who is protected does not produce antibodies, but borrows them. disorders of the immune system : allergy when your immune system malfunctions, it can unleash a torrent of disorders and diseases. one of the most familiar is allergy. allergies such as hay fever and hives are related to the antibody known as ige. the first time an allergy - prone person is exposed to an allergen - - for instance, grass pollen - - the individual ' s b cells make large amounts of grass pollen ige antibody. these ige molecules attach to granule - containing cells known as mast cells, which are plentiful in the lungs, skin, tongue, and linings of the nose and gastrointestinal tract. the next time that person encounters grass pollen, the ige - primed mast cell releases powerful chemicals that cause the wheezing, sneezing, and other symptoms of allergy. disorders of the immune system : autoimmune disease sometimes the immune system ' s recognition apparatus breaks down, and the body begins to manufacture antibodies and t cells directed against the body ' s own cells and organs. such cells and autoantibodies, as they are known, contribute to many diseases. for instance, t cells that attack pancreas cells contribute to diabetes, while an autoantibody known as rheumatoid factor is common in persons with rheumatoid arthritis. disorders of the immune system : immune complex disease immune complexes are clusters of interlocking antigens and antibodies. normally they are rapidly removed from the bloodstream. in some circumstances, however, they continue to circulate, and eventually they become trapped in, and damage, the tissues of the kidneys, as seen here, or the lungs, skin, joints, or blood vessels. disorders of the immune system : aids when the immune system is lacking one or more of its components


they become trapped in, and damage, the tissues of the kidneys, as seen here, or the lungs, skin, joints, or blood vessels. disorders of the immune system : aids when the immune system is lacking one or more of its components, the result is an immunodeficiency disorder. these disorders can be inherited, acquired through infection, or produced as an inadvertent side effect of drugs such as those used to treat cancer or transplant patients. aids is an immunodeficiency disorder caused by a virus that destroys helper t cells. the virus copies itself incessantly and invades helper t cells and macrophages, the very cells needed to organize an immune defense. the aids virus splices its dna into the dna of the cell it infects ; the cell is thereafter directed to churn out new viruses. human tissue typing for transplants although mhc proteins are required for t cell responses against foreign invaders, they can pose difficulty during transplantation. every cell in the body is covered with mhc self - markers, and each person bears a slightly unique set. if a t lymphocyte recognizes a non - self mhc scaffold, it will rally immune cells to destroy the cell that bears it. for successful organ or blood stem cell transplantations, doctors must pair organ recipients with donors whose mhc sets match as closely as possible. otherwise, the recipient ' s t cells will likely attack the transplant, leading to graft rejection. to find good matches, tissue typing is usually done on white blood cells, or leukocytes. in this case, the mhc - self - markers are called human leukocyte antigens, or hla. each cell has a double set of six major hla markers, hla - a, b, and c, and three types of hla - d. since each of these antigens exists, in different individuals, in as many as 20 varieties, the number of possible hla types is about 10, 000. the genes that encode the hla antigens are located on chromosome 6. a child in the womb carries foreign antigens from the father as well as immunologically compatible self - antigens from the mother. one might expect this condition to trigger a graft rejection, but it does not because the uterus is an " immunologically privileged " site where immune responses are somehow subdued. immunity and cancer when normal cells turn into cancer cells, some of the antigens on their


to trigger a graft rejection, but it does not because the uterus is an " immunologically privileged " site where immune responses are somehow subdued. immunity and cancer when normal cells turn into cancer cells, some of the antigens on their surface change. these cells, like many body cells, constantly shed bits of protein from their surface into the circulatory system. often, tumor antigens are among the shed proteins. these shed antigens prompt action from immune defenders, including cytotoxic t cells, natural killer cells, and macrophages. according to one theory, patrolling cells of the immune system provide continuous bodywide surveillance, catching and eliminating cells that undergo malignant transformation. tumors develop when this immune surveillance breaks down or is overwhelmed. a new approach to cancer therapy uses antibodies that have been specially made to recognize specific cancers. when coupled with natural toxins, drugs, or radioactive substances, the antibodies seek out their target cancer cells and deliver their lethal load. alternatively, toxins can be linked to a lymphokine and routed to cells equipped with receptors for the lymphokine. dendritic cells that attack cancer another approach to cancer therapy takes advantage of the normal role of the dendritic cell as an immune educator. dendritic cells grab antigens from viruses, bacteria, or other organisms and wave them at t cells to recruit their help in an initial t cell immune response. this works well against foreign cells that enter the body, but cancer cells often evade the self / non - self detection system. by modifying dendritic cells, researchers are able to trigger a special kind of autoimmune response that includes a t cell attack of the cancer cells. because a cancer antigen alone is not enough to rally the immune troops, scientists first fuse a cytokine to a tumor antigen with the hope that this will send a strong antigenic signal. next, they grow a patient ' s dendritic cells in the incubator and let them take up this fused cytokine - tumor antigen. this enables the dendritic cells to mature and eventually display the same tumor antigens as appear on the patient ' s cancer cells. when these special mature dendritic cells are given back to the patient, they wave their newly acquired tumor antigens at the patient ' s immune system, and those t cells that can respond mount an attack on the patient ' s cancer cells. the immune system and the nervous system biological links between the immune system and the central nervous system exist


newly acquired tumor antigens at the patient ' s immune system, and those t cells that can respond mount an attack on the patient ' s cancer cells. the immune system and the nervous system biological links between the immune system and the central nervous system exist at several levels. hormones and other chemicals such as neuropeptides, which convey messages among nerve cells, have been found also to " speak " to cells of the immune system - - and some immune cells even manufacture typical neuropeptides. in addition, networks of nerve fibers have been found to connect directly to the lymphoid organs. the picture that is emerging is of closely interlocked systems facilitating a two - way flow of information. immune cells, it has been suggested, may function in a sensory capacity, detecting the arrival of foreign invaders and relaying chemical signals to alert the brain. the brain, for its part, may send signals that guide the traffic of cells through the lymphoid organs. a hybridoma is a hybrid cell produced by injecting a specific antigen into a mouse, collecting an antibody - producing cell from the mouse ' s spleen, and fusing it with a long - lived cancerous immune cell called a myeloma cell. individual hybridoma cells are cloned and tested to find those that produce the desired antibody. their many identical daughter clones will secrete, over a long period of time, millions of identical copies of made - to - order " monoclonal " antibodies. thanks to hybridoma technology, scientists are now able to make large quantities of specific antibodies. genetic engineering allows scientists to pluck genes - - segments of dna - - from one type of organism and to combine them with genes of a second organism. in this way, relatively simple organisms such as bacteria or yeast can be induced to make quantities of human proteins, including interferons and interleukins. they can also manufacture proteins from infectious agents, such as the hepatitis virus or the aids virus, for use in vaccines. the scid - hu mouse the scid mouse, which lacks a functioning immune system of its own, is helpless to fight infection or reject transplanted tissue. by transplanting immature human immune tissues and / or immune cells into these mice, scientists have created an in vivo model that promises to be of immense value in advancing our understanding of the immune system.


online courseschallenging behaviour > continence promotion > coshh > classroom coursesmodule 1 - classroom courses > module 2 - classroom courses > module 3 - classroom courses > medication, infection and role of care worker - nocn level 2 ( module 2 ) - ( £120 per person ) medication, infection and role of care worker - nocn level 2 ( module 2 ) national qualification in supporting people with a learning disability. this is an induction course for those wishing to get a national qualification in supporting people with a learning disability. it is suitable for those working with vulnerable adults and children. - role of a care worker module ' s record of competence • legislations governing the prescribing, dispensing, administering, storage and disposal of medication. • medication policy • classifications of medication • types of medication • different routes / methods of administering medication. • safe practice of medication. • checking, recording & keeping receipts of medication. • medication administration record sheet • noting and reporting changes to individuals. • adverse reactions to medication. • checking of contra / indications whilst giving individual homely remedies. • importance of medication audits • safe disposal of medication. • supporting individuals who are self administering medication. role of a care worker. • roles & responsibilities - care activities • relevant policies and procedures • code of practice • working in partnership with others. • worker relationship / maintaining professional boundaries. • recording individual care plans. food safety and infection control. • legislations governing infection control • effective hand washing & hygiene • use of protective clothing. • cleaning of spillages. • safe handling of specimens • safe disposal of clinical waste. • safe storage of food. • washing of infected laundry, equipments & instruments. • notifiable diseases - e. g. mrsa, tuberculosis, scabies, head lice etc. written description and case study please choose a centre / date : | sorry, no dates available at the moment. |


locust care sheet locust are probably the largest type of insect that you will use as livefood. adults measure up to 8cm and are a yellow colour with darker brown / purple patches. they are popular for their large gut content which means they are highly nutritious feeders but are somewhat expensive compared to other foptions. the locust is a fascinating insect. they are quite pleasant to have around and will not try to bite like a cricket would. locust are often portrayed as a swarm insect that destroys crops and eats everything in their path. in fact, they are lower down the pecking order than crickets so the two should never be mixed, unless the aim is to feed the crickets. however, they do eat a lot and grow fairly quickly. only adult locust have wings that are able to give them flight. all locust have wings but only at the 5th and final moult a locust develops flying wings and are capable of flight over short distances. locust have amazing claws they can hold onto and climb just about anything including glass. they tend to hang upside down while shedding so their good grip comes is readily employed. housing and heating housing locust is just like housing crickets, you will want to put them in the biggest tub you can find ( of course glass is fine ), as long as it is sufficiently deep to deter any would - be escapees. ventilation is important to locust so make sure the lid is perforated with holes, you can do this with a drill or a soldering iron. as locust prefer to perch a substrate really is not necessary, so a simple stack of egg crates does the trick and also provides hiding places. for water, provide a dish of damp kitchen roll, this prevents drowning and is easily changed when it gets dirty. when it comes to cleaning time after a week or two, there are several options. you are probably best lifting out the hides slowly and transferring them to another tub while working around the rest of the locust while cleaning the tub. shake the locust off the egg crates and throw them away, swap them with clean ones and you have a nice clean tub of locust. alternatively you can use all the locust then throw the whole lot away before purchasing a fresh batch. as for temperature, locusts like a temperature of 25 - 33a°c ( 77 - 91. 4a°f ) and a dry atmosphere which will prevent fungal infections. feeding locust feeding is very similar to crickets. they need


batch. as for temperature, locusts like a temperature of 25 - 33a°c ( 77 - 91. 4a°f ) and a dry atmosphere which will prevent fungal infections. feeding locust feeding is very similar to crickets. they need to be provided with a good supply of dry foods, " bug grub " is an insect feeder that has a mixture of ingredients designed to be fed to insects so that they have a good gut content and provide ample nutrients to your pets. alternative foods can be used such as bran, weetabix, digestives and bread. fruits such as grapes, apples or vegetables such as potatoes, tomatoes and cabbage provide extra vitamins and moisture. if moist foods are available on a regular basis then a water dish is not really needed. breeding locust temperature and humidity are important in breeding. eggs are laid in a 4 inch deep dish filled with silver or sharp sand so prepare a tub as such. the sand should be kept moist but not too wet so it looks soggy. the female locust will position herself over the sand dish and push her down and deposit up to 200 eggs. hoppers will emerge after 10 - 12 days. the hoppers will go through 5 instar molting before becoming adult locust.


drive by a local wetland on an early spring evening, and if you ' re lucky you ' ll hear a harbinger of the changing season - the clear chirping chorus of tiny frogs known as spring peepers, classified by biologists as pseudacris crucifer. few themes in literature are more alluring than the lost world. places such as atlantis, shangri - la, conan doyle ' s " lost world ", and now the bestselling " the lost city of z " conjure up images of strange landscapes, exotic civilizations and hidden treasures. ecologists study phenology, which is the orderly progression of seasonal events in nature, such as the springtime arrival of migrating birds, the first chorus of spring peepers in vernal pools, and the development of tree colors each autumn despite the fact 60 percent of us in dutchess county drink groundwater every day, and all of us eat food irrigated by ground water, very few people know where it comes from, where it goes, or that groundwater is full of life thankfully, the argument about the reality of global climate change seems finished. the majority of the public now joins the consensus of climate scientists, who have furnished compelling proof that the planet is warming and that humans are at least partly to blame. what if our children could recognize the birds, plants and insects in their backyards as well as they know the brands of shoes on their feet or the secret weapons they need to get to the next level in a video game? if you ever saw " star wars, " you ' ll remember the trash compactor scene : trying to escape from the imperials, luke and his friends duck into what turns out to be a trash compactor, where things go from bad to worse. new york state is taking an essential step to deal with invasive species, one of the most damaging and difficult environmental problems of our time, by proposing to limit the importation of ballast water into the state. dengue ( pronounced den - ghee ) fever is caused by a virus spread by mosquitoes. it was formerly called " break - bone fever " because it causes excruciating pain to the muscles and joints of its human victims. we tend to think of nature as having reliable patterns ; the leaves turn color each autumn, seasonal birds come and go. but there are also examples of sudden, unexpected changes in the environment around us. specific trails and roads on our 2, 000 acre research campus have been designated for public access, and our grounds provide visitors


in the interior of central africa the first catholic missions were established by cardinal lavigerie ' s white fathers in 1879. in uganda some progress was made under the not unfriendly local ruler, mtesa ; but his successor, mwanga, determined to root out christianity among his people, especially after a catholic subject, st. joseph mkasa, reproached him for his debauchery and for his massacre of the protestant missionary james hannington and his caravan. mwanga was addicted to unnatural vice and his anger against christianity, already kindled by ambitious officers who played on his fears, was kept alight by the refusal of christian boys in his service to minister to his wickedness. himself was the first victim : mwanga. seized on a trifling pretext and on november 15, 1885, had him beheaded. to the chieftain ' s astonishment the christians were not cowed by this sudden outrage, and in may of the following year the storm burst. when he called for a young ' page ' called mwafu, mwanga learned that he had been receiving religious instruction from another page, st. denis sebuggwawo ; denis was sent for, and the king thrust a spear through his throat. that night guards were posted round the royal residence to prevent anyone from escaping. charles lwanga, who had succeeded joseph mkasa in charge of the ' pages ', secretly baptized four of them who were catechumens ; among them st kizito, a boy of thirteen whom lwanga had repeatedly saved from the designs of the king. next morning the pages were all drawn up before mwanga, and christians were ordered to separate themselves from the rest : led by lwanga and kizito, the oldest and youngest, they did so — fifteen young men, all under twenty - five years of age. they were joined by two others already under arrest and by two soldiers. mwanga asked them if they intended to remain christians. " till death! " came the response. " then put them to death! " the appointed place of execution, namugongo, was thirty - seven miles away, and the convoy set out at once. three of the youths were killed on the road ; the others underwent a cruel imprisonment of seven days at namugongo while a huge pyre was prepared. then on ascension day, june 3, 1886, they were brought out, stripped of their clothing, bound, and each wrapped in a mat of reed : the living fagg


seven days at namugongo while a huge pyre was prepared. then on ascension day, june 3, 1886, they were brought out, stripped of their clothing, bound, and each wrapped in a mat of reed : the living faggots were laid on the pyre ( one boy, st mbaga, was first killed by a blow on the neck by order of his father who was the chief executioner ), and it was set alight. the persecution spread and protestants as well as catholics gave their lives rather than deny christ. a leader among the confessors was st matthias murumba, who was put to death with revolting cruelty ; he was a middle - aged man, assistant judge to the provincial chief, who first heard of jesus christ from protestant missionaries and later was baptized by father livinhac, w. f. another older victim, who was beheaded, was st andrew kagwa, chief of kigowa, who had been the instrument of his wife ' s conversion and had gathered a large body of catechumens round him. this andrew together with charles lwanga and matthias murumba and nineteen others ( seventeen of the total being young royal servants ) were solemnly beatified in 1920. they were canonized in 1964. when the white fathers were expelled from the country, the new christians carried on their work, translating and printing the catechism into their nativel language and giving secret instruction on the faith. without priests, liturgy, and sacraments their faith, intelligence, courage, and wisdom kept the catholic church alive and growing in uganda. when the white fathers returned after king mwanga ' s death, they found five hundred christians and one thousand catchumens waiting for them. join the new media evangelization. your tax - deductible gift allows catholic. net to build a culture of life in our nation and throughout the world. please help us promote the church ' s new evangelization by donating to catholic. net right now. god bless you for your generosity. | print article | | email friend | | palm download | | forums | | questions | | more in this channel | | up | write a comment on this article |


st. bernard of menthon born in 923, probably in the castle menthon near annecy, in savoy ; died at novara, 1008. he was descended from a rich, noble family and received a thorough education. he refused to enter an honorable marriage proposed by his father and decided to devote himself to the service of the church. placing himself under the direction of peter, archdeacon of aosta, under whose guidance he rapidly progressed, bernard was ordained priest and on account of his learning and virtue was made archdeacon of aosta ( 966 ), having charge of the government of the diocese under the bishop. seeing the ignorance and idolatry still prevailing among the people of the alps, he resolved to devote himself to their conversion. for forty two years he continued to preach the gospel to these people and carried the light of faith even into many cantons of lombardy, effecting numerous conversions and working many miracles. for another reason, however, bernard ' s name will forever be famous in history. since the most ancient times there was a path across the pennine alps leading from the valley of aosta to the swiss canton of valais, over what is now the pass of the great st. bernard. this pass is covered with perpetual snow from seven to eight feet deep, and drifts sometimes accumulate to the height of forty feet. though the pass was extremely dangerous, especially in the springtime on account of avalanches, yet it was often used by french and german pilgrims on their way to rome. for the convenience and protection of travelers st. bernard founded a monastery and hospice at the highest point of the pass, 8, 000 feet above sea - level, in the year 962. a few years later he established another hospice on the little st. bernard, a mountain of the graian alps, 7, 076 feet above sea - level. both were placed in charge of augustinian monks after pontifical approval had been obtained by him during a visit to rome. these hospices are renowned for the generous hospitality extended to all travelers over the great and little st. bernard, so called in honor of the founder of these charitable institutions. at all seasons of the year, but especially during heavy snow - storms, the heroic monks accompanied by their well - trained dogs, go out in search of victims who may have succumbed to the severity of the weather. they offer food, clothing, and shelter to the unfortunate travelers and take care of the dead. they depend on gifts and collections for sustenance. at present,


go out in search of victims who may have succumbed to the severity of the weather. they offer food, clothing, and shelter to the unfortunate travelers and take care of the dead. they depend on gifts and collections for sustenance. at present, the order consists of about forty members, the majority of whom live at the hospice while some have charge of neighboring parishes. the last act of st. bernard ' s life was the reconciliation of two noblemen whose strife threatened a fatal issue. he was interred in the cloister of st. lawrence. venerated as a saint from the twelfth century in many places of piedmont ( aosta, novara, brescia ), he was not canonized until 1681, by innocent xi. his feast is celebrated on the 15th of june. more catholic encyclopedia browse encyclopedia by alphabet the catholic encyclopedia is the most comprehensive resource on catholic teaching, history, and information ever gathered in all of human history. this easy - to - search online version was originally printed in fifteen hardcopy volumes. designed to present its readers with the full body of catholic teaching, the encyclopedia contains not only precise statements of what the church has defined, but also an impartial record of different views of acknowledged authority on all disputed questions, national, political or factional. in the determination of the truth the most recent and acknowledged scientific methods are employed, and the results of the latest research in theology, philosophy, history, apologetics, archaeology, and other sciences are given careful consideration. no one who is interested in human history, past and present, can ignore the catholic church, either as an institution which has been the central figure in the civilized world for nearly two thousand years, decisively affecting its destinies, religious, literary, scientific, social and political, or as an existing power whose influence and activity extend to every part of the globe. in the past century the church has grown both extensively and intensively among english - speaking peoples. their living interests demand that they should have the means of informing themselves about this vast institution, which, whether they are catholics or not, affects their fortunes and their destiny. browse the catholic encyclopedia by topic copyright © catholic encyclopedia. robert appleton company new york, ny. volume 1 : 1907 ; volume 2 : 1907 ; volume 3 : 1908 ; volume 4 : 1908 ; volume 5 : 1909 ; volume 6 : 1909 ; volume 7 : 1910 ; volume 8 : 1910 ; volume 9 : 1910 ; volume 10 : 1911 ; volume 11 : - 1911 ; volume 12 :