text:
Editor's Note: This article was originally published in the February 1995 issue of Scientific American. We are reposting it this week because Robert Tijan has just been named president of the Howard Hughes Medical Institute.
Asthma, cancer, heart disease, immune disorders and viral infections are seemingly disparate conditions. Yet they turn out to share a surprising feature. All arise to a great extent from overproduction or underproduction of one or more proteins, the molecules that carry out most reactions in the body. This realization has recently lent new urgency to research aimed at understanding, and ultimately manipulating, the fascinating biochemical machinery that regulates an essential step in protein synthesis: the transcription of genes. For a protein to be generated, the gene that specifies its composition must be transcribed, or copied, from DNA into strands of messenger RNA, which later serve as the templates from which the protein is manufactured.
Even before therapy became a goal, transcription had long captivated scientists for another reason: knowledge of how this process is regulated promises to clarify some central mysteries of life. Each cell in the body contains the same genome, the complement of some 150,000 genes that form the blueprint for a human being. How is it that the original cell of an organism— the fertilized egg—gives rise to a myriad of cell types, each using somewhat different subsets of those genes to produce different mixtures of proteins? And how do the cells of a fully formed body maintain themselves, increasing and decreasing the amounts of proteins they manufacture in response to their own needs and those of the larger organism?
To answer these questions and design drugs able to modulate transcription, investigators need to know something about the makeup of the apparatus that controls reading of the genetic code in human cells. After some 25 years of exploration, the overall structure of that apparatus is becoming clear. Work in my laboratory at the University of California at Berkeley and at other institutions has revealed that one part of the apparatus—the engine driving transcription of most, if not all, human genes— consists of some 50 distinct proteins. These proteins must assemble into a tight complex on DNA before a special enzyme, RNA polymerase, can begin to copy DNA into messenger RNA. The putative constituents have now been combined in the test tube to yield a fully operational transcription engine. Still other proteins essentially plug into receptive sockets on the engine and, in so doing, "program" it, telling it which genes should be transcribed and how quickly. Critical details of these interactions are emerging as well.
Clues from Bacteria
When my colleagues and I at Berkeley began focusing on human genes in the late 1970s, little was known about the transcription machinery in our cells. But studies begun early in that decade had provided a fairly clear picture of transcription in prokaryotes— bacteria and other primitive single-celled organisms that lack a defined nucleus. That work eventually lent insight into human and other eukaryotic (nucleated) cells and helped to define features of transcription that hold true for virtually all organisms. The bacterial research showed that genes are essentially divided into two functionally distinct regions. The coding region specifies the sequence of amino acids that must be linked together to make a particular protein. This sequence is spelled out by the nucleotides (the building blocks of DNA) in one strand of the DNA double helix; the nucleotides are distinguished from one another by the nitrogen-rich base they carry —adenine (A), thymine (T), cytosine (C) or guanine (G). The other region of a gene has regulatory duties. It controls the rate at which RNA polymerase transcribes the coding region of a gene into messenger RNA.
In bacteria, as in most prokaryotes, the regulatory region, called the promoter, resides within a stretch of nucleotides located a short distance—often as few as 10 nucleotides—in front of (upstream from) the start of the coding region. For transcription to proceed accurately and efficiently, RNA polymerase must attach to the promoter. Once it is so positioned, it slides over to the start of the coding region and rides along the DNA, like a train on a track, constructing an RNA replica of the coding sequence. Except in very long genes, the number of RNA molecules made at any moment depends mainly on the rate at which molecules of RNA polymerase attach to the promoter and initiate transcription.
Interestingly, RNA polymerase is a rather promiscuous molecule, unable to distinguish between the promoter and other DNA sequences. To direct the enzyme to promoters of specific genes, bacteria produce a variety of proteins, known as sigma factors, that bind to RNA polymerase. The resulting complexes are able to recognize and attach to selected nucleotide sequences in promoters. In this way, sigma factors program RNA polymerase to bypass all nonpromoter sequences and to linger only at designated promoters.
Considering the importance of sigma factors to the differential activation of genes in bacteria, my colleagues and I began our inquiry into the human transcription apparatus by searching for sigmalike molecules in human cells. But we had underestimated the complexity of the machinery that had evolved to retrieve genetic information from our elaborate genome. It soon became apparent that human sigma factors might not exist or might not take the same form as they do in bacteria.
Surprising Complexity
If there were no simple sigma factors in eukaryotes, how did such cells ensure that RNA polymerase transcribed the right genes at the right time and at the right rate? We began to see glimmerings of an answer once the unusual design of eukaryotic genes was delineated.
By 1983 investigators had established that three kinds of genetic elements, consisting of discrete sequences of nucleotides, control the ability of RNA polymerase to initiate transcription in all eukaryotes—from the single-celled yeast to complex multicellular organisms. One of these elements, generally located close to the coding region, had been found to function much like a bacterial promoter. Called a core promoter, it is the site from which the polymerase begins its journey along the coding region. Many genes in a cell have similar core promoters.
Walter Schaffner of the University of Zurich and Steven Lanier McKnight of the Carnegie Institution of Washington, among others, had additionally identi fied an unusual set of regulatory elements called enhancers, which facilitate transcription. These sequences can be located thousands of nucleotides upstream or downstream from the core promoter—that is, incredibly far from it. And subsequent studies had uncovered the existence of silencers, which help to inhibit transcription and, again, can be located a long distance from the core promoter.
In a somewhat imperfect analogy, if the core promoter were the ignition switch of a car engine, enhancers would act as the accelerator, and silencers as the brakes. Eukaryotic genes can include several enhancers and silencers, and two genes may contain some identical enhancer or silencer elements, but no two genes are precisely alike in the combination of enhancers and silencers they carry. This arrangement enables cells to control transcription of every gene individually.
Discovery of these elements led to two related—and, at the time, highly surprising—conclusions. It was evident that enhancers and silencers could not control the activity of RNA polymerase by themselves. Presumably they served as docking sites for a large family of proteins. The proteins that bound to enhancers and silencers—now called activators and repressors—then carried stimulatory or repressive messages directly or indirectly to RNA polymerase (that is, pressed on the accelerator or on the brakes). It also seemed likely that the rate at which a gene was transcribed would be dictated by the combined activity of all the proteins—or transcription factors—bound to its various regulatory elements.
A Human Factor Is Discovered
Nevertheless, we were hard-pressed to explain how proteins that bound to DNA sequences far from the core promoter of a gene could influence transcription of that gene. As is true of other laboratories, we began attacking this puzzle by trying to isolate human transcription factors, none of which had yet been found (with the exception of RNA polymerase itself). We assumed that once we had pure copies of the factors we would be able to gain more insight into exactly how they function.
Because many proteins that bind to DNA play no role in reading genes, we could not find transcription factors efficiently by screening nuclear proteins solely according to their ability to associate with DNA. My group therefore adopted a more discriminating strategy, looking for proteins that in a test-tube reaction both combined with DNA and stimulated transcription.
In 1982 William S. Dynan, a postdoctoral fellow in my laboratory, determined that some protein in a mixture of nuclear proteins fit all the requirements of a transcription factor. It bound to a regulatory element common to a select set of genes—an enhancer sequence known as the GC box (because of its abundance of G and C nucleotides). More important, when added to a preparation of nuclear proteins that included RNA polymerase, the substance markedly increased the transcription only of genes carrying the GC box. Thus, we had identified the first human transcription factor able to recognize a specific regulatory sequence. We called it speci- ficity protein 1 (Sp1).
We immediately set out to purify the molecule. One daunting aspect of this work was the fact that transcription factors tend to appear only in minuscule quantities in cells. Typically, less than a thousandth of a percent of the total protein content of a human cell consists of any particular factor. In 1985 James T. Kadonaga in my laboratory found a way to overcome this substantial technical barrier—and in the process introduced a powerful new tool that has since been used to purify countless transcription factors and other scarce DNA binding proteins.
Because Sp1 selectively recognized the GC box, Kadonaga synthesized DNA molecules composed entirely of that box and chemically anchored them to solid beads. Then he passed a complex mixture of human nuclear proteins over the DNA, predicting that only Sp1 would stick to it. True to plan, when he separated the bound proteins from the synthetic DNA, he had pure Sp1.
From studies carried out by Mark Ptashne and his colleagues at Harvard University, we knew that bacterial transcription regulators are modular proteins, in which separate regions perform distinct tasks. Once we learned the sequence of amino acids in Sp1, we therefore looked for evidence of distinct modules and noted at least two interesting ones.
One end of the molecule contained a region that obviously folded up into three "zinc fingers." Zinc-finger structures, in which parts of a protein fold around a zinc atom, are now known to act as the "hooks" that attach many activator proteins to DNA. But at the time Sp1 was only the second protein found to use them. Aaron Klug and his colleagues at the Medical Research Council in England had discovered zinc fingers, in a frog transcription factor, just a short time before [see "Zinc Fingers," by Daniela Rhodes and Aaron Klug; SCIENTIFIC AMERICAN, February 1993].
The other end of Sp1 contained a domain consisting of two discrete segments filled with a preponderance of the amino acid glutamine. We strongly suspected that this region played an important role during transcription because of a striking finding. In test-tube experiments, mutant Sp1 molecules lacking the domain could bind to DNA perfectly well, but they failed to stimulate gene transcription. This outcome indicated that Sp1 did not affect transcription solely by combining with DNA; it worked by using its glutamine-rich segment—now known as an activation domain—to interact with some other part of the transcription machinery. The question was, which part?
In 1988 when we began searching for the target of Sp1, we had some idea of where it lay. Our guess was based on an emerging understanding of the so-called basal transcription complex, one part of which seemed to be a likely target.
Closing in on a Target
In the mid-1980s Robert G. Roeder and his colleagues at the Rockefeller University had shown that RNA polymerase cannot transcribe eukaryotic genes unless several other transcription factors—now called basal factors—also collect on the core promoter. And over the course of the 1980s, Roeder's laboratory and others had identified at least six of those essential factors, called A, B, D, E, F and H.
In a test tube, this assembly of factors enabled RNA polymerase to transcribe a bound gene at a basal—low and invariant —rate, but it could not by itself modulate that rate. It was as if someone had constructed and switched on the engine of a car but had lost use of the steering wheel, the accelerator and the brakes. For instance, when my group mixed the components of the complex (including RNA polymerase) with a gene containing a GC box, we obtained a low, unchanging level of transcription. We saw a marked increase in transcription only when we incorporated Sp1 into the mixture.
By the late 1980s it was apparent that human cells harbor at least two separate classes of transcription factors. Basal factors are required for initiation of transcription in all genes; other proteins —activators and repressors—dictate the rate at which the basal complex initiates transcription. Different genes are controlled by distinct combinations of activators and repressors. We now suspect that in the body the basal complex arises spontaneously only rarely; most of the time, cells depend on activators to initiate its construction.
These various discoveries suggested that the glutamine-rich domain of Sp1 enhanced transcription by contacting a basal factor. More specifically, we suspected that Sp1 latched on to factor D, and facilitated its attachment to the promoter. We focused on this subunit because Phillip A. Sharp and Stephen Buratowski of the Massachusetts Institute of Technology had shown that it can land on the core promoter before all other basal factors and can facilitate assembly of the complete basal engine. In fact, factor D is the only basal component able to recognize DNA. It binds selectively to a sequence called the TATA box, found in the core promoters of many eukaryotic genes.
To pursue our hypothesis, we needed to know more about the composition of factor D, which we assumed was a solitary protein. Other investigators also wanted to know its makeup, and so the race was on to attain pure copies. Isolation from human cells proved more challenging than anyone anticipated. Consequently, many groups eventually tried their luck with yeast cells. Finally, in 1989, several laboratories independently succeeded in isolating a yeast protein that displayed the expected properties of factor D. The protein, named TBP (for TATA binding protein), recognized and bound selectively to the TATA box and led to a low level of transcription when it was joined at the core promoter by RNA polymerase and other constituents of the basal machinery.
Believing that the TBP protein was factor D itself, we undertook to test this idea in additional studies. Once we did that, we intended to determine exactly which regions of TBP were contacted by Sp1 and other regulators. Little did we know that we were about to be completely thwarted—and to make a critical discovery.
Unexpected Trouble
When B. Franklin Pugh in our laboratory replaced the impure preparations of factor D previously used in our test-tube reactions with purified molecules of TBP, he had no trouble replicating the earlier finding that such substitution in no way disrupted basal transcription. To our surprise and consternation, though, he found that Sp1 was no longer able to influence the basal machinery. We had to conclude that factor D and TBP were not, in fact, equivalent and that factor D actually consisted of TBP plus other subunits. (It is now known that many transcription factors consist of more than one protein.) Apparently, those subunits were not needed for operation of the basal machinery, but they were essential to regulation of that machinery by activators.
In other words, these additional components were not themselves activators, for they did not bind to specific sequences in DNA. Nor were they basal factors, because low, unregulated levels of transcription could be achieved without them. They seemed to constitute a third class of transcription factor, which we called coactivators. We further proposed that coactivators, not TBP, were the targets for the protein binding domains of activators. We envisioned that activators would bind to selected coactivators to speed up the rate at which the basal complex set molecules of RNA polymerase in motion.
We were attracted to this scenario because we had difficulty imagining how a single protein, TBP, would have enough binding sites to accommodate all the activators made by human cells. But if the coactivators that were tightly linked to TBP bore multiple binding domains, the coactivators could collectively provide the docking sites needed to relay messages from hundreds or thousands of activators to the transcription engine.
It was Pugh who originally proposed that coactivators might function as such adapter molecules. His data soon convinced me he was probably correct, but not everyone in our laboratory agreed. Indeed, our weekly meetings in early 1990 were often punctuated by heated discussions. Not surprisingly, when the coactivator concept was presented to other workers in the field, they, too, expressed considerable skepticism. This reaction to an unexpected and complicating result was probably justified at that stage, because our data were only suggestive, not conclusive. We had not yet isolated a single coactivator.
Coactivators: The Missing Links
To satisfy ourselves and the scientific community that we were correct, we had to devise an experimental procedure that would unambiguously establish whether coactivators existed and operated as the relays we envisioned. For approximately two years after Pugh formulated the coactivator hypothesis, we struggled to purify an intact and functional complex containing TBP and all the other associated constituents of factor D. I must admit to some dark moments when it seemed the rather unpopular coactivator hypothesis might be based on some error in our studies.
The breakthrough finally came in 1991, when Brian D. Dynlacht, Timothy Hoey, Naoko Tanese and Robert Weinzierl —graduate students and postdoctoral fellows in our laboratory—found an ingenious way to isolate pure copies of factor D. Subsequent biochemical analyses revealed that, aside from TBP, the complete unit included eight previously unknown proteins. Because we did not yet have proof that these proteins could function as coactivators, we referred to them more generically as TBP-associated factors, or TAFs.
We became convinced that TAFs do indeed convey molecular signals from activators to the basal transcription apparatus after we separated the bound proteins from TBP and completed several more experiments. For instance, we were able to show that mixing of the activator Sp1 with basal factors and RNA polymerase enhanced production of messenger RNA from a gene containing a GC box only when TAFs were added as well. Later, Jin-Long Chen, a graduate student, combined purified TBP and the eight isolated TAFs in a test tube along with a human gene and the rest of the basal transcription machinery. The various proteins assembled on the gene and proved able to respond to several different types of activator proteins. These activators, we later showed, produced their effects by coupling directly with selected TAFs. Together the coactivators in factor D do indeed constitute a kind of central processing unit that integrates the regulatory signals issued by DNA-bound activators.
A Universal Theme
The complexes formed by activators, coactivators and the basal machinery appear to be human equivalents of sigma factors; they, too, draw RNA polymerase to specific genes at specific rates. In a way, the complexes can be viewed as sigma factors that have been elaborated into many subunits. Gratifyingly, recent evidence from our group and others suggests we have uncovered a universal mode of gene regulation in eukaryotes. Those studies confirm that coactivators also exist in yeast and that factor D consists of multiple subunits in fungi as well as in humans.
As satisfying as these results are, they do not fully explain how binding of activators to enhancers and to coactivators influences the rate at which RNA polymerase transcribes genes in living cells. It may be that linkage of activators to enhancers causes DNA to bend in a way that brings the enhancers closer to one another and to the core promoter. This arrangement may help activators (alone or in concert with one another) to dock with coactivators and position factor D on the promoter. This step, in turn, would facilitate assembly of the complete basal complex. Formation of this complex may distort the underlying DNA in a way that enables RNA polymerase to begin its journey along the coding region.
Researchers know less about the functioning of repressors. Nevertheless, many of us think repressors may also bind to coactivators at times. This binding could inhibit transcription by preventing activators from attaching to their usual sites on coactivators. Other times repressors might bypass the basal machinery, blocking transcription by preventing activators from connecting with enhancers.
Although there are gaps in our knowledge, we can now begin to sketch out an explanation as to why different cells make different mixtures of proteins during embryonic development and in mature organisms. A gene will be transcribed at a measurable rate only if the various activators it needs are present and can successfully overcome the inhibitory effects of repressors. Cells vary in the proteins they make because they contain distinct batteries of activators and repressors. Of course, this scenario begs the question of how cells decide which transcription factors to produce in the first place, but progress is being made on that front as well.
Therapies of Tomorrow How might investigators use our newly acquired knowledge of gene regulation to develop drugs for combating life-threatening diseases involving excessive or inadequate transcription of a gene? In theory, blocking selected activators from attaching to enhancers or coactivators should depress unwanted transcription, and stabilizing the transcription machinery on a gene should counteract undesirably weak transcription.
Blockade could be achieved by fitting a molecular "plug" into an activator, thereby preventing its interaction with a coactivator, or by enticing an activator to attach to a decoy that resembles a coactivator. Stabilization of a complex might be achieved by deploying molecules that would strengthen the interaction between activators and DNA or between activators and coactivators. Such approaches are remote today, but it is exciting to consider a sampling of the applications that might eventually be possible.
Take, for example, the human immunode ficiency virus (HIV), which causes AIDS. To reproduce itself in human cells, HIV needs the viral transcription factor TAT to enhance transcription of HIV genes. If TAT could be inhibited by some agent that recognized TAT but ignored human transcription factors, replication of the virus might be halted without affecting production of proteins needed by the patient.
Conversely, treatment of some disorders —for instance, hypercholesterolemia —might involve enhancing the transcription of selected genes. Hypercholesterolemia increases a person's risk for heart disease. Cholesterol accumulates to destructive levels in the blood when low-density lipoprotein (LDL), otherwise known as the bad cholesterol, is not removed efficiently. In theory, the disease could be corrected by turning up transcription of the gene for the LDL receptor in liver cells. This receptor helps to clear LDL from the blood. This idea may soon be testable, because studies by Michael S. Brown and Joseph L. Goldstein of the University of Texas Health Science Center at Dallas are teasing apart the specific molecular constituents of the apparatus that regulates transcription of the receptor gene.
Until recently, no one put much effort into screening small molecules, natural products or other compounds for their ability to modulate transcription. Even so, a number of drugs already on the market have been found by chance to work by altering the activity of transcription factors. One of these, RU 486 (the French "abortion" pill), represses the function of particular steroid receptors, a class of activators that direct embryonic development. Similarly, the immunosuppressants cyclosporine and FK506 suppress transcription of a gene whose protein product is needed by certain cells of the immune system. These drugs act indirectly, however. They activate an enzyme that impedes the functioning of a transcription factor for the gene.
As time goes by, the precise combination of transcription factors that regulate individual genes is sure to be identi fied. And drug developers will probably use this information to devise sophisticated compounds for fighting cancer, heart disease, immune disorders, viral infections, Alzheimer's disease and perhaps even the aging process. How well these agents will succeed is anybody's guess, but it is likely that therapies of the future will benefit in one way or another from basic research into transcription—research that began not out of a wish to design drugs but rather out of a simple desire to get to the heart of the molecular machinery that controls the activity of our genes.


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West 2009, Seattle!
Seattle Washington, October 16th - 18th 2009
The PostgreSQL Conference U.S. team is pleased to announce the successful end to West 2009. This year the premiere West coast PostgreSQL Conference left its roots at Portland State University and moved north to sunny Seattle, Washington.
Held at Seattle Central Community College from October 16th through 18th, the move to Seattle opened up a larger metropolitan area for continuing to expose databases users, developers and administrators to the World's Most Advanced Open Source Database. Following previously successful West coast conferences we hosted a series of 3-4 hour tutorials, 90 minute mini tutorials, and 45 minute talks.

subset: commoncrawl


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With a giant blower sitting atop your hot rod's engine, you're going to get more than your share of attention from enthusiasts and those who'd like to throw a huffer on top of their ride. But when it comes to superchargers, it might be easy for the average "Joe" to overlook what's feeding that big chunk of polished aluminum its requisite amount of fuel and air. We're talking about the guy that may want to take the plunge and cut a big hole in his hood, but more than likely doesn't know the ins and outs of how a blower works, let alone how the carburetors need to be set up. So this "Joe" character sends away for a fully polished 6/71 in hopes of pumping out mega horsepower.
He's told that he'll need a set of fuel meters made (or reworked) to work with a Roots-style blower. Being an intelligent person (obviously a SUPER CHEVY reader), he orders two Holley blower carbs. Sounds easy, but in reality there is much more to it than just bolting the four barrels on and hammering the go-pedal.
The real science is figuring out the correct combination of carb components (jet, accelerator pump, idle feed restricters, needle and seat size, air bleeds, emulsion main circuitry, venturri size, and so on) to get the desired results. This can be an overwhelming experience to say the least. That's just the start, now figure into your growing equation, blower specs, hp and torque, cylinder head flow capabilities, and so on.
Yeah, we know, it's hard enough to remember our own cell phone number without having to set up our own carbs, and this is why we contacted the gurus at The Carb Shop in Ontario, California, to help us understand just what is necessary when trying to build ultimate power from a blower motor. They were able to give us some insight to what makes a carburetor different when used on a supercharged engine.
The main idea here is to move a greater amount of fuel and air through the carburetor and still have a good deal of control over each. When the blower starts pulling on those carbs, it is going to use whatever the carbs give it. This is where the control factor is so important.
If you're planning to add a Roots-style supercharger (or even a centrifugal blow-through design), you need to learn about the specific requirements of the carb(s) you'll be using. Following are a few tips that O.J. of the Carb Shop taught us. Check it out and hold on when you mash that accelerator pedal.
Here are what jet extensions look like. These are simply used to make sure no matter where the fuel goes in the bowl, the jets will still be able to pick some up. Under severe acceleration the fuel obviously moves to the back of the bowl, thus they are only needed in the rear.
These holes are the emulsion circuit, or air bleeds. This is a very important adjustment because the air bleeds control how much air is mixed with fuel to emulsify or lighten the fuel to achieve the necessary air/fuel balance. The emulsion well holes also control how much and when the boost starts.
The Idle Fuel Restrictor controls the amount of fuel being delivered at idle. With a blower's needing more fuel, even at idle, this becomes a necessary adjustment. All of these changes are strictly done with a set amount depending on horsepower, size of blower, and carbs, in addition to about another half-dozen factors.
The Carb Shop builds its own annular boosters out of solid aluminum billet. The one on the left is the Super and the other is the Super Pro Billet Booster. These can be drilled to work with any application and have been used extremely well on the dyno and at the track. Since the booster controls the type of fuel spray, it can be necessary to alter them for any number of factors.
After the booster is pressed into its housing, it will need to be swedged back into the carb with this special tool.
With the boosters in place, both sides of the carb body are milled perfectly flat for a precise sealing surface. After this was done, the next step was to clean the edges of all holes with a countersink bit.
With all of the blower modifications complete, the carb can be reassembled. The Carb Shop installs only reusable gaskets. These carbs may need to be further adjusted internally to gain even more efficiency and power.
Here is The Carb Shop's finishing touch on a blower-ready carb. The next step will be to test it on the dyno and if everything is in order, ship to the waiting customer.


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Xorg configuration is now at https://wiki.gentoo.org/wiki/Xorg/Configuration
Moved bugzilla and nvidia stuff to wiki
Fix bug #427860 - Use /etc/portage for make.conf and make.profile. Old location (/etc) is still supported, this is a heads up (new default)
update firmware/graphics driver stuff, thanks to chithanh for the patch via bug #419487
Fix #379391 - Prefix bin files with "radeon/" as suggested by email@example.com
Bug #379391 - Remove Radeon HD 62°00/6300 as this is now part of the 6000 series
Fix bug #379391 - Update xorg-config to include firmware information on latest radeon stuff. Thanks to email@example.com for reporting/content
update Xorg guide for the HAL removal. this took many hours, spread out over many weeks. there may still be a few things to add, but this will do as a working basic installation/walkthrough. bug 349698.
additional env-update reminder after editing 90xsession, bug 351370
add firmware for RadeonHD 5000 and 6000 cards, bug 352030
update xorg-drivers example for the removal of xf86-video-radeonhd
Add multiple monitor info, bug 328001
rewrite X guide for KMS, open-source drivers, and whatnot. inspired by bug 328001.
fix commandline order, bug 321223
Fix estonian layout bzcat command, bug 321093
added the -retro option per bug 267769. also added a bit on installing twm and xterm only for testing purposes, since otherwise startx will just display a black screen. having a few open xterm windows makes it easier to verify that X is setup correctly.
Latest stable xinit (1.2 and up) no longer install TWM, xterm, or xclock, so don't mention assume they're present
Add information about (re)starting hald, per an email from Janne Mäntylä
more fixes from bug 297245
typo fix, bug 297245
The big Xorg HOWOTO rewrite. This should take into account all the xserver 1.5 and 1.6 changes. I emphasized HAL/evdev for device management and configuration. xorg.conf is really only used as a last resort for things like display resolution. bug 267769.
The first of many rewrites I'll be making to the guide to bring it up to stable xserver 1.6 standards. bug 229769
recommend xorg-server, not xorg-x11, as the more recent versions that will be stabilized bring in a spamload of international alphabets and fonts. totally useless for a working desktop.
add the xorg-server 1.5 migration guide to metadoc, in the desktop_install and upgrade categories. bug 265116. also added it to the 'additional resources' section of the xorg install guide, for good measure.
A little handholding for pebkac users; removed a paragraph just to be sure. bug 254186
Update the xorg guide. clean up video_cards and input_devices information at the beginning. remove references to X11R6. add online help links. some general cleanup toward the end of the doc.
Coding style
a few more non-content changes i missed. there are FAR too many smileys in this doc. i blame swift\!
buncha small coding style fixes and punctuation, spelling, and grammar fixes. no content change.
updated xorg guide for bug 182752
clarify status of the radeon driver
added bit about /dev/input/mice to the xorg guide, bug 167337
revert previous change
the great email@example.com email cleanup, part one
#139583, update for modular xorg (VIDEO_CARDS, INPUT_DEVICES)
#101912 - Minor content change, make clear that the mouse output isn't meaningful. Fixed license to 2.5 as well.
#101912 - Minor grammatical fixes, thanks to Erik Musick for reporting.
Changed link attribute to make it point to absolute path. Thanks to rane on #gentoo-doc.
Add in a small sentence about psaux
#89479 - Adding hint on textmode in case xorgcfg itself fails or X crashes
Updates for new mouse device file location
Add info on xorgcfg
#86654 - Explain startx better, keep session stuff in right sections, patch from firstname.lastname@example.com
No xfree86 anymore
#71714 - TWM isnt always loaded on Xorg -config ... Add an explanation paragraph telling the users not to worry
Command is X, not Xorg -- see output of Xorg :)
Xorg is now stable on all relevant architectures (requirement for 2004.2). Removing the masked-warning-stuff-thingie
Add note about possible masked xorg (for the time being, should be unmasked soon(ish))
Wrong XkbRules, noticed by far too many ppl resulting in bugreports; sorry about that folks!
Fixed typos -- No content change --
New document: Xorg configuration
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== Documentation ==
== Documentation ==
* [://.org////
== Release Notes ==
== Release Notes ==
Revision as of 17:58, 24 January 2012
This is a significant update to the clustering stack - both for high availability and load balancing.
- Name: LonHohberger
- email: firstname.lastname@example.com
- Name: FabioMassimoDiNitto
- email: email@example.com
Current status
- Targeted release: Fedora 30
- Last updated: 24 Jan 2012
- Percentage of completion: 70%
Detailed Description
Upstream has been developing the new version of the stack. The major features are:
- Improved quorum subsystem which is integrated in to the Corosync Cluster Engine (95% complete)
- A new command-line interface for administration of both the Corosync Cluster Engine and the Pacemaker Cluster Resource Manager (50% complete)
- Convergence on a single set of resource agents from the Linux clustering community
- Enhanced fencing support in the Pacemaker Cluster Resource Manager
- Separation of GFS2-specific utilities in to a separate project.
Note that this transition includes deprecations:
- CMAN will no longer provide quorum. Instead, this functionality is now part of Corosync
- Removal of the obsolete 'rgmanager' package. All users are advised to use Pacemaker for their failover needs.
Benefit to Fedora
The increased reliability and versatility of the cluster components included in Fedora 17 allow administrators to deploy Fedora in environments where greater availability and clustered file systems are required. Removal of rgmanager matches the capabilities offered by several other Linux distributions and allows the Fedora community to consort efforts on a single failover stack.
How To Test
User Experience
- corosync (2.0)
- pacemaker
- cluster-glue
- dlm (in review)
All packagers and upstreams have been informed upfront and worked together to achieve this goal.
Contingency Plan
None necessary
Release Notes
In addition to the cluster features present in Fedora 11, Fedora 12 includes the following enhancements:
- The update to version 1.0 (flatiron) of the Corosync Cluster Engine offers (on top of Fedora 11's features):
- Plugin ABI & API stability guarantees for the duration of Corosync 1.0's lifetime
- High performance, cluster-wide messaging
- Ultra-high performance IPC subsystem available to other components and developers
- Rolling upgrade compatibility with 0.80.z releases of OpenAIS
- The update to version 3.0 of the Linux-Cluster Project offers:
- Reduced code and operational complexity compared to version 2 leading to greater reliability
- Pluggable, simplified configuration management framework with plugins for XML and LDAP (experimental), including schemas for both classes
- Improved code quality due to stricter coding guidelines
- The inclusion of pacemaker 1.0 offers (note: packages awaiting reviews):
- Improved resource & failover management over rgmanager
- Resource-dependency model allows for flexible placement of cluster resources
- Can run rgmanager's resource agents with minimal changes, offering an upgrade path for users of rgmanager
- Fine-grained resource management: administrators may operate on one resource instead of operating at the resource group level
- Improved resource & failover management over rgmanager


text:
A. Ashley Tabaddor teaches Immigration Law and Practice. Professor Tabaddor was appointed as an immigration judge in November 2005.
Judge Tabaddor served as an assistant U.S. attorney for the Central District of California in Los Angeles from May 2002 to November 2005. Judge Tabaddor also served as an adjunct professor at the University of Southern California Law School. She served as a trial attorney with the Office of Immigration Litigation, Civil Division, Department of Justice, in Washington, D.C., from September 2000 to May 2002. During this period, Judge Tabaddor also served as an adjunct professor at the George Washington University Law School. She served in the Office of the Chief Immigration Judge in Falls Church, Virginia as an attorney advisor from July 1999 to September 2000, and as a judicial law clerk/attorney advisor from September 1997 to July 1999. Judge Tabaddor worked as a summer law intern in the immigration court in Los Angeles from June 1996 to August 1996. She is a member of the California Bar. She received a B.A. cum laude from the University of California, Los Angeles, and a J.D. from the University of California, Hastings College of the Law.
Judge Tabaddor is author of "Race Matters: Are Middle Easterners Really White?" which is a review of Whitewashed: America's Invisible Middle Eastern Minority, by John Tehranian, Levantine Cultural Center, February 20, 2010; and the opinion In re Perez-Cruz, No. A95 748 837 (Immigration Ct. L.A., Cal. Feb 9, 2009), appeal filed.


text:
Use the Store Finder to find a retailer near you that carries Dancing Deer goodies. Simply enter your zip code and click 'submit'. For general store locations in your state, select a state and city and click 'submit.'
Be sure to call before you shop to make sure your favorite store has the Dancing Deer products you're looking for… and if they don't, be sure to ask a store manager to order some for you!


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|Hey Mom! Learn more about the Gerber Life Insurance Grow-Up Plan!
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Blessed with children, Struggling for more Week of May 21st
This thread is for women that have children who are trying to have more and struggling with infertility (IF). You fall into the IF category if you have been trying for more than a year or if you have known fertility issues. Some have secondary IF and some have primary IF. Some of us are TTC naturally and some need treatments of some type. All are welcome!
We also have women who are praying to make it. Due to prior losses or IF they don't feel like they should join a due date board till after the first 12 weeks. We are truly happy to support you as you transition. Please just keep in mind that we are a group of woman struggling with IF and be sensitive to that as you post. If you put a pregnancy ticker or smiley in your signature, please turn off your signature when you post in this thread. Thank you!
Please note: When your information needs to be updated, please highlight the area that needs to be updated. This will make it easier for me to update you.
If you'd like to be added please post your info using the format below. Please note: I remove names if you are inactive for one month. This really helps keep the list more manageable, if you would like to be added back, just repost your info.
Women TTC:
Screen Name (Real Name): twinpossible (Anya)
Age: 27
Current Children and age: Gracie and Emma (identical twins 1 year old)
Lost Children and Dates: May 8th 2012 "baby bean" lost at 11 weeks
Diagnosis: "unexplained" 5 years of testing...no clear issues have shown up
Treatment and meds: Welcome Womb, we think that's how we conceived last time.
Next Appointment: no more doctors for us, they have found zip. We are totally natural now since nothing else helped.
Cycles TTC another: just miscarried so waiting another week or so before TTC.
Screen Name: Ms.Kaun (Real Name): Eryn
Age: 27
Current Children and age: 3 Living (ages 9, 8 and 6) 4 angels.
Diagnosis: None yet, suspected PCOS. Appointment with a reproductive specialist coming up.
Treatment and meds: Metformin
Next Appointment: June 7th
Cycles TTC another: 13 but I only ovulated for 3 cycles the entire time resulting in 2 early pregnancy losses.
Screen Name (Real Name): 3 Ladybugs (Jennifer)
Age: 35
Current Children and age: 3 lost children (2006), 1 living son - 3.5 years old
Diagnosis: Unexplained infertility to start with, now in menopause due to chemo, also had pelvic radiation that complicates things a bit.
Treatment and meds: Have 5 frozen embryos (my last 5 bits of hope), meds are yet to be determined, will start a prenatal in the next couple of days, on fermented cod liver oil
Next Appointment: 5/16 to do a lining check, will see my oncologist on 7/18, need to schedule a port cath flush for the end of the month.
Cycles TTC another: Got cleared to do my FET back in 11/10 pending oncologist telling my RE I didn't have cancer... turns out I did. So have been waiting since then to get to this point. So honestly, no cycles TTC right now, but 2 years 4 months in the making!
Screen Name (Real Name): doodle19 (Shaye)
Age: 26
Current Children and age: Chloe, 4 years old Ella 13months
Lost Children and Dates: 09/2009 02/2012
Diagnosis: tube obstruction, left tube 100% blocked, right tube also has blocking(not 100%) but barely functioning.
Treatment and meds: Suggested IVF, but we are trying for a yr on our own first.
Next Appointment: 4/17/12
Cycles TTC another: 7months
Screen Name (Real Name): jacquelinemarie82 (Jacqueline)
Age: 30
Current Children and age: Jasmine, 2 years old (2/10/2010)
Lost Children and Dates: N/A
Diagnosis: male infertility
Treatment and meds: Currently on birth control for IVF in July.
Next Appointment: IVF tentatively scheduled for July. NTNP till then so I can get a break from the stress.
Cycles TTC another:
Screen Name (Real Name): ChihuahuaMama13 (Samantha)
Age: 26 (DF 27)
Current Children and age: Gabriel, 14 months (01/10/11)
Lost Children and Dates: N/A
Diagnosis: PCOS
Treatment and meds: Just started Metformin in late Fabruary 2012.
Next Appointment: N/A
Cycles TTC another: 9 months (6 cycles)
Screen Name (Real Name): Edensmomma (Jena)
Age (DH): 35 (ME) 26
Diagnosis:None yet
Treatment and meds: Nothing this cycle, as I was getting my hormone levels tested. Previously I was on Maca, soy isoflavones, fertilaid with no luck for 6 cycles. I'm thinking of trying another round of Soy Isoflavones next cycle.
Current Children and age: Girl 4 yo, Girl 2 yo
Lost Children and dates: M/C at 15 weeks on 10/23/11, baby born at home and requiring emergency D&C to stop hemorrhaging.
Next appointment: 4/11/12 to discuss fertility/clomid and test results from labs.
Cycles TTC:6
Screen Name (Real Name): Holly dolly (Holly)
Age: 31 (DH 32)
Current Children and age: ds1 Isaac 3/07 ds2 Carson 3/10
Lost Children and Dates: none
Diagnosis: We were NTNP for 4 years, was diagnosed with borderline PCOS (I have everything but the cysts) and anovulatory cycles. Found out I was pg with Isaac...no medical intervention...I ovulated around CD22. Started TTC when he was a year old. After almost 18 mos of trying started on Clomid. No response at CD14 u/s. I kind of gave up. A friend announced she was pg a few months later and I took a test so I could start provera. Got a positive. Dr figured I ovulated around CD 30. We've been NTNP since the end of October when I went off bc. I have cycled once (with the help of Provera).
Next Appointment: none planned at this point
Cycles TTC another: Technically on my second cycle...but 5 mos total
Screen Name (Real Name): Naturally Pampered (Amanda)
Age: 25 (DH 25)
Current Children and age: one DS age 4, 3/08/2008
Lost Children and Dates: 3/28/2005 & 10/30/2011
Diagnosis: Haven't had any testing
Treatment and meds: N/A
Next Appointment: N/A
Cycles TTC another: Implanon Out May 2011, BFP September 2011, M/C October 2011, Actively trying with no luck since loss.
Screen Name (Real Name): yellowitchgrl (Sarah)
Age: 30 (husband 34)
Current Children and age: Andrew-7, Luke-4
Lost Children and Dates: Zach (15w, 7/09), Toby (12w, 12/09), Simon (14w, 6/11)
Diagnosis: I'm perfectly healthy, so are the babies (except they're dead)
Treatment and meds: Praying and some extra folic acid (my idea, not docs)
Next Appointment: Not bothering.
Cycles TTC another: Not trying, but not preventing either
Screen Name (Real Name): ingrid5699 (Ingrid)
Age (DH): 41 (ME) 37
Current Children and age: Patrick, 5 years, Aurelia 3 years
Lost Children and dates: triplets Nov. 2004, baby B May 2006, latest little angel 2'12
Diagnosis: Me: endometriosis and immunological issues, DH: male factor
Treatment and Meds: fresh IVF #9 ahead, too many meds to list
Next appointment: May 16th for baseline u/s, start stims May 19th, retrieval the last week in May
Cycles TTC another: never prevented, 3 FET failures, 1 fresh cycle failure, one m/c this time around
Screen Name (Real Name): finleyjudemommy (Susan)
Age (DH): 47 (ME) 36
Current Children and age: B/G twins 6 and YDD 4
Lost Children and dates: M/C March 04, M/C June 09, Chemical Feb 10 and stillborn October 10
Next appointment: Need to get my thryoid under control before I can move on...hopeful that will be soon. Hopefully will be able to start Lupron as soon as next cycle starts.
Cycles TTC another: Entirely too many to count
Screen Name (Real Name): lalakiwi7 (Liesl - pronounced leesal)
Age (SO): 26 and hubby is 26, Happily married for 6 yrs. Together for 11.
Current Children and age: Noah is our oldest, not bio but almost adopted foster son (who is Ethiopian). Frances is our first born and only bio baby, she is two.
Lost child: early losses 7/2011 & 11/2007
Diagnosis: unexplained secondary IF assumed antibodies/issues from delivery complications to DD pregnancy.
Treatment and meds: baby asa, decadron, vitamins, and progesterone after O
Next Appointment: Jan for follie scan and first attempt at IUI with femera and trigger
Cycles TTC another: almost 2 yrs or more than 30 cycles
Screen Name (Real Name): love4leon (Rebecca)
Age: 37 (DH 38)
Current Children and age: Winnie 5 years
Diagnosis: Endometriosis (Me) DH diagnosed with Low sperm count, low motility, and liquidation. 5/11 diagnosed with testicular cancer. Finished chemo August 2011
Treatment and meds: IUI done 1/2/2011, 2/5/2011, 3/2011, 4/2011 Clomid days 5-9, trigger shot and IUI on 2/14/2012
Next Appointment: April 5th
Cycles TTC another: 25 cycles, but well over 2 years (took a break during cancer treatments
Screen Name (Real Name): carlaross (Carla)
Age: 36, DH 39
Current children and ages: Zach 17, Jarrod 16, Griffin 2 (12-28-09)
Diagnosis: DH had vasectomy '99 (previous marriage), reversal 3/09. Immediately (9 days after surgery) and had my LO 12-28-09. Never used birth control, began TTC another immediately after 1st PPAF, 8/10. After 15 cycles, we began a fertility workup and were devastated to find out he has complete scarring of the reversal site and a zero sperm count.
Cycles TTC another: since Aug 2010
Next appointment: January 9 (with my ob/gyn to begin my fertility workup and discuss options)
Screen Name (Real Name): slimy72 (Laurel)
Age: 28 Dh 30
Current Children and age: DS 3yo
Lost Children and Dates: 2003, 2004, 2005, 2006, 2011
Diagnosis: Endometriosis, do not ovulate regularly. Dh- MS, Celiacs, Ulcerative colitis, low count, poor morphology and motility, but that is suspected due to current medications, will be re-evaluated once off them.
Treatment and meds: Clomid, provera, prometrium, baby aspirin and a host of supplements and vitamins. Laprascope '09, lupron shots '09
Next Appointment: simmering for now, waiting for dh to be off meds before we schedule anything.
Cycles TTC another: 4 1/2 yrs for DS, 2 1/2 yrs so far for #2.
Screen name (Real Name): Melmonkey (Mel)
Age: me - 34, hubby - 35
Children and ages: girl almost 18 months
Losses: none
Diagnosis: unexplained
Treatment: Clomid 50mg cd 3-7
Next Appt: don't have one, hopefully in the next few months we'll be doing OB/Gyn appts again!
Cycles TTC another: AF showed Dec 2010....we have not prevented since then....
Screen Name (Real Name): sdavis514 (Sarah)
Age: 31 (DH 32)
Current Children and age: one DS age 4 1/2
Lost Children and Dates: none
Diagnosis: We were NTNP for 4 years, diagnosed with PCOS in 2003 and put on clomid from 9/04-1/05, no results, took break and became pregnant with DS with no intervention in Aug 2006. Recent blood work suggested no insulin resistance. Clomid again 9/11-1/12. BFNs IUI cycle in April - BFN
Treatment and meds: Clomid 100 mg cd 3-9, ovidrel trigger shot and progesterone suppositories
Next Appointment: Call when AF shows and start clomid, u/s cd 12 to check follicle sizes
Cycles TTC another: NTNP for 4 years, Actively TTC since Jan 11
Screen Name (Real Name): JCPACandMommy (Carissa)
Age: 31 (DH 35)
Current Children and age: one DS age3.5
Lost Children and Dates: none
Diagnosis: PCOS as of Jan '12 but I am ovulating
Treatment and meds: Femara 5mg once daily CD4-8,Metfomin 500mg 2x dialy, Prenatal Daily, B6 50mg Daily, MACA Root Powder Daily
Next Appointment: HSG March 8th then US on March 14
Cycles TTC another: Mirena Out April 5, 2011 was NTNP till Aug, then active TTC since then with No luck we are on Cycle #8
Women Pregnant and praying to make it. If you need to be added to this list please give your EDD and the date you will be 12 weeks. Thank you! To find out how many weeks you are use this link.
Screen Name (Real Name): Psylion (Alanna)
Age (DH): 37 (ME) 38
Diagnosis:high FSH and DOR
Treatment and meds: this will be our third injectables cycle with iui, the first two were with letrozole and menopur and this one is just menopur and metformin
Current Children and age: Sequoia is 4 1/2
Lost Children and dates: early MC 2/12
Next appointment: ?
Cycles TTC another: we only prevented a few months since DD was born
12 weeks: May 30, 2012[/COLOR]
Screen Name (Real Name): GracieMak'sMama (Sara)
Age: 22 (DH 23)
Current Children and age: one DD age 2(almost)
Diagnosis: Unexplained Infertility
Treatment and meds: Natural diet
Cycles TTC another: Almost a full year.
EDD: Oct 9th
12 weeks: 3/26
Lurkers/Waiting to TTC/Graduates/Cheerleaders
Screen Name (Real Name): amyltc (Amy)
Age: 28 my Dh is 32
Current Children and age: DD1 Allie, age 6, DD2 Hannah age 3
Lost Children and dates: none
Diagnosis: Endometriosis, surgery to remove 9/14/10, tipped uterus, mostly unexplained infertility, subclinical hypothyroidism Meds: Femara days 2-7, 150 iu Bravelle days 7,9,11, HCG trigger,levothyroxin (thyroid)
Next appointment: IUI April 18th
Cycles TTC another: 21 cycles of active TTC, no BC since our 3 yo was born.
Screen name (Real Name): Fleece Be With You (Jessica)
Age: 24
Children and ages: Hunter, born 9-18-09
Losses: none
Diagnosis: Celiac disease (unconfirmed, but a safe assumption at this point)
Treatment: Very limited version of GAPS diet, digestive enzymes, vitamin supplements
Next Appt: Seeing my chiropractor next week to look into my cortisol/adrenal issues.
Cycles TTC another: We haven't been preventing since Hunter was born.
Screen Name (Real Name): Harmony96 (Andrea)
Age: 33 (DH 31)
Current Children and age: DD (5), DS (29m)
Lost Children and Dates: ^i^ DS 11/27/11-12/24/11
Diagnosis: No official diagnosis, but currently having short luteal phases (6-7 days). Probably is just what my body "does" for its first few postpartum cycles.
Treatment and meds: Prenatal, folic acid, iron, several other supplements. Also trying to eat right and exercise (and hopefully lose about 15 pounds, but none of that has happened yet).
Next Appointment: N/A
Cycles TTC another: Lost baby was a c-section, had VBAC consult in March '12 and was told we could go ahead and try again if we felt ready.
Screen Name (Real Name): Hannah Elise (errr.. Hannah... hehe)
Age: 23, and dh is 22
Diagnosis: non-celiac gluten intolerant, malabsorption of nutrients
Treatment and meds: Gluten-free diet. Supplementing with Metagest (stomach acids and enzymes to improve proper digestion), aloe vera gel, and probiotics. Current Children and age: Asher (aka "Wee Goon"), 12.5 months
Cycles: 12/4/11, 1/12/12, 2/11/12, 3/20/12
Screen Name (Real Name): Vegan Princess (Cindy)
Age (SO):32
Current Children and age: Child 1: 2.5 yrs
Lost Children and dates: Chemical pregnancy (11/10), miscarriage at 9.5 weeks (5/11), possible chemical pregnancy (9/11)
Diagnosis: Diminished ovarian reserve for me. Moderate or severe male factor (depending on who you ask) for DH
Treatment and Meds:Beginning 2nd IUI cycle w/5mg femara, ovidrel trigger and prometrium. Will do this cycle and one more IUI and then meet with doctor to discuss IVF or using donor egg. - Moved to IVF
Next appointment: Follicle scan on 9/ 29. IUI on 10/1 or thereabouts. Will meet with RE to discuss game plan again in November.
Cycles TTC another: Had IUD removed 4/10 but really have been trying since 6/10.
Screen name (Real Name): heatherlovesCD's (Heather)
Age: me - 33, hubby - 38
Children and ages: boy 6, Twins girl/boy 4, Twins boy/boy 22 months.
Losses: March '07
Diagnosis: severe male factor infertility
Treatment: IVF/FET, 1 fresh IVF cycle = 1 boy. FET's = 1 early m/c, 2 sets of twins, 1 BFN
Cycles TTC another: I don't keep track. We have been TTC since 11/10.
Due date: Oct 15th
Date I'll be 12wks: 4/2/12
Screen Name (Real Name): Sillyutalktome (Jeanette)
Age: 30 (DH 29)
Current Children and age: Dd - M - 6/08
Lost Children and Dates: Etopic 7/09 (8 weeks) Possible chemical 6/10
Diagnosis: tubal infertility & male factor
Treatment and meds:1st IVF 10/18/11 BFN, FET planned for January
Screen Name (Real Name): Wordmama (Lucy)
Lost children: 8 early miscarriages, Libi (8 week ectopic, March 2011)
Diagnosis: Damaged right tube for me, poor morphology for DH
Treatment and meds:Prayer, maca, zinc
Cycles TTC another: Over a year
EDD: June 18, 2012
Screen Name (Real Name): Dewberri (joy)
Lost Children and dates: Dec. 2010 (6 wks); June 2011 (Kayle(e), 11wks)
Diagnosis: ANA, nonspecific
Treatment: Aspirin daily, Progesterone till 10 weeks
EDD: June 14, 2012
Screen Name (Real Name):Liz*RN*BSN (Elizabeth)
Lost Children: 5 early m/c
Diagnosis: PCOS, Recurrent Miscarriage, Factor 5 Leiden Clotting Disorder
Treatment and meds: Lovenox, Baby Aspirin, Metformin, PNV, Endometrin TTC: Over 1 year
Screen Name (Real Name): Meldo (Melissa)
Losses: 1
Diagnosis: DH has low sperm count/motility. Both of our kids were IVF/ICSI babies.
Cycles TTC another: It's our 8th (and last) IVF cycle.
EDD: May 1, 2012
Registered Users
Re: Blessed with children, Struggling for more Week of May 21st
Susan- Does that mean you will still transfer the 3 today?
Creator Of The Pixie Skirtie<br>www.hyenacart.com/Melmonkeyszoo
Re: Blessed with children, Struggling for more Week of May 21st
AFM: We have been chick crazy here........
After a bumpy road of infertility, 6 years of procedures,CLAIRE IS 2!!!!!!! missing our angel(9/5/12)
BF for 18 months, BLW, AP,don't believe in any schedule and became a slave to my baby who is attached to my boob and am tickled pink to be that way. Yes, I shower daily!
Registered Users
Re: Blessed with children, Struggling for more Week of May 21st
awww cute! I want to do chickens with the kids, but the husband is saying "no they smell" and he's right, but still so cute
Praying Carissa!
Super excited for you Susan! Keep us posted.
AFM- going through and getting rid of baby stuff today. It's bitter sweet, but needed for my sanity.
Sarah. Christian. Married to Jonathan. Proud Mama of 6 boys! Andrew (10), Luke(7) and James (2). My babies born into heaven : Zach, Toby and Simon WAHM behind Sarah's Stitches HyenaCart and Etsy, 10% off with the code: DSE10 Facebook Wetbags, Snack Sacks, Fleece Soakers, Dresses, Naked Time Mats, Dresses, Wipes, Affordable Weighted Blankets and more! Check out my novels!! Ask for other places to buy.
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Transferring today! I'm not taking the chance that they don't make it. Plus, I would be a raving loony until Wednesday and NOBODY wants that!
Susan, laundry doing , dish doing SAHM to twins F&J , A , 1 year old M, 3 early M/C's and Baby Jack born sleeping 10/22/10
Registered Users
Re: Blessed with children, Struggling for more Week of May 21st
Good luck today Susan!!
Melissa - Thanks for sharing the photo! I will have to show DS later as he loves birds. Mama has a bird phobia though so we can't have any chickens or anything, much to DS disappointment.
Sarah - I am sorry your having to do that! I need to go through my baby things today but for a different reason. A friend wants to borrow something that I have. I hope it is easier on you then you fear today.
Jennifer (39) - Wife since 12/2003 with 5 children - 3 waiting for me in heaven , and 2 delighting me everyday ! Lymphoma survivor and mother to baby born post pelvic radiation!
Registered Users
Re: Blessed with children, Struggling for more Week of May 21st
I'm honestly relieved. I've been begging my husband to let me get rid of them for about 6 months now. He's been holding out, but I hate holding onto this stuff which is useless clutter at this moment. It might be useful later, but for right now I want it gone from my life. I can buy more stuff later if it ever happens.
Before my first miscarriage I was at babies r us and almost bought a few things for the baby, but I held back and I'm so glad I did. Well right before my second miscarriage I bought a doppler to listen to the heart beat to feel better. It came the day after I lost him. With my third I got to 14 weeks and thought "okay, I'm going to buy some maternity shirts" and he died a few days later (which I knew from the doppler bought for the previous baby). Me and having these "things" around to remind me- it just sucks. I want them out of here. I might chuck the doppler too. I lovingly refer to my maternity clothes as my death shrouds.
I dislike clutter, and I very much dislike holding on to useless stuff, and all these things that remind me of what isn't and the 3 little guys who didn't wear these clothes even though they should have... it's going to be a relief to get them gone.
Sarah. Christian. Married to Jonathan. Proud Mama of 6 boys! Andrew (10), Luke(7) and James (2). My babies born into heaven : Zach, Toby and Simon WAHM behind Sarah's Stitches HyenaCart and Etsy, 10% off with the code: DSE10 Facebook Wetbags, Snack Sacks, Fleece Soakers, Dresses, Naked Time Mats, Dresses, Wipes, Affordable Weighted Blankets and more! Check out my novels!! Ask for other places to buy.
Registered Users
Re: Blessed with children, Struggling for more Week of May 21st
hand spinning, soap making, sheep raising wife to my hardworking and FT WOHM to my 'lil & 6 angels in heaven & our rainbow baby that joined us safely this summer!
ISO: Formula Checks- if you have some you won't use we would love to have them!
NB Diapers for sale: http://www.diaperswappers.com/forum/....php?t=1594851
Registered Users
Join Date: Apr 2011
Location: Junction City, KS
Posts: 1,853
Re: Blessed with children, Struggling for more Week of May 21st
Melissa Cute baby chick!!! I bet your LO love to watch them!
Susan FX for a GREAT transfer GL mama I'm for you!
AFM Im out this month it is deffinitly AF here cuz I'm still bleeding not really heavy but bleeding I'm hopeful this month we will be doing Femara, Trigger Inj. and IUI....FX for this month being the month since it is month #11
and for everyone!
Carissa~ Married to my Bestfriend and Soulmate Scott and Mommy to Aiden (04/10/08) TTC #2 after the loss of Blighted Ovum and Ectopic on Rt Ovary(10/25/12) and Blighted Ovum (07/28/13)
planning to and #2
Expecting our RAINBOW July 16, 2014!
My Ovulation Chart
Registered Users
Re: Blessed with children, Struggling for more Week of May 21st
Mel, thanks for the cute pic!
Sarah, I agree that getting rid of stuff will help you emotionally. I got rid of all my grey maternity shirts just because I wore a bunch of grey and felt like I was in prison so next pregnancy, no gray. Whatever helps you feel better, you should do.
Susan, looking forward to updates! How did you feel after the egg retrieval? Do you mind to give me a little rundown of what they do, how you felt, etc?
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14 7/8" X 11" 18lb 1/2" Blue Bar Hi-Lite Continuous Computer Paper - 3000/Case (1 Ply)
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Friday, August 13, 2010
Kansas City Family History Expo-A Blast!
I can't believe it has been nearly two weeks since the awesome Family History Expo in Kansas City and they are already gearing up for the next one in Salt Lake City! Son, Jason , accompanied me to KC and attended the Expo with me. (I actually "invited him" to be my chauffeur). He was in for a surprise when he arrived at the Family History Expo as he expected a small conference and a few meetings! As usual, Holly and her group put on an exceptional Expo and we both had a wonderful time there. The class offerings were excellent and Jason who is a History major was more than pleased with what he learned. We also met some really great new friends from the world of genealogy, one of whom was Thomas MacEntee of Genea-Bloggers fame.
Thomas hosted several lectures which centered around the use of social networking sites to aid the genealogist. I attended his fine presentation on Facebook and went away with several new things to try out and some great tips on how to properly use Facebook: making it work for us as genealogists and how to "safely" set up a new account. I use Facebook daily but gleaned many tips for its productive use that I had never considered before. Thomas also presented a class on Social Networking: "New Horizons For Genealogists" and another on Twitter: It's Not Just "What I Had For Breakfast" Anymore. It was great to finally meet Mr. MacEntee! He welcomed us warmly to the Bloggers of Honor area and even passed out some of his famous badge ribbons to add to our name badges. Along with his Genea-Bloggers ribbon, I now proudly sport one that names me as QUEEN. (You Go Genealogy Girl #1 has one from the Loveland Co., Expo that says she is a DIVA...) Surely the Queen must rule!!!
Everyone there was super nice but Thomas made my son and I feel welcome right away! Thanks to him for adding to our fun Expo experience.
Thomas MacEntee also has a new book out this week called "Approaching the Lectern: How To Become A Genealogy Speaker". It is available as an e-book, epub for the Kindle, and in printed form. For a nice review of his book, click here to see the article by Susan Peterson on her Long Lost Relatives blog. For more information you can check out either of Thomas MacEntee's sites: Destination: Austin Family or The Connected Genealogist. I have the printed form on order and am anxious to see it. I know it will have great information to aid us with our genealogy presentations!
Tomorrow I will share some other personalities from the Expo...
You Go Genealogy Girl #2, Cheri
2 comments:
Thanks so much for your kind words and the mention of my new book. I see you have placed the print version on order at Lulu. I am awaiting my "proof" copy and then I can "approve" the print version for order.
We're glad to hear that your son had fun at the Expo. Genealogy is addictive that way. Thank you for being such a great Blogger of Honor and showing your readers how fun attending an Expo can be.ReplyDelete
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Eloquent justifications for what is, ultimately, a description of plausibility.
Saturday, March 06, 2010
McGrath, Godfrey and "Assuming" Historicity.
I'll state for the record that I am not persuaded by the mythicist position, and think E P Sanders is probably the greatest living NT scholar. So I have some sympathy with McGrath.
I appreciate James' point (and even more with Steph's in the comments, I have always thought "assumption" such a terrible term here, though it's often used. . .just because people don't outline a full explanation doesn't mean they've "assumed" it). But there is a counterpoint to be scored here as well.
What other characters do we attempt to reconstruct in any detail based solely on texts? Especially texts that are all written "in-group," none of which are autobiographical?
Neil and I would probably disagree on what standard of evidence is required before we move forward, but I would concede (in the spirit of the 1913 Schweitzer he's been citing lately) that we can only move forward provisionally, recognizing the limits of our conjecture.
Even if we agreed there was an historical Romulus, for example, if you started telling me a specific act he did in the founding of Rome, with details about his consciousness while he did it, I'd laugh in your face. It seems preposterous everywhere but here. And even if we let you get away with it, your statement would be a lot more provisional. If someone replied that they doubt Romulus even existed, you would doubtlessly allow for the possibility, and acknowledge that your later conjectures were based on an earlier conjecture: That Romulus was real.
When we deal strictly with textual evidence elsewhere, we recognize the limits of our conjectures. But here we have none (still germane to my post Why Bother?). Not only do we not have to be provisional, we can suggest that all the gospels fundamentally misunderstood Jesus' message, and we know even better than they do what it was. While many critics would disagree with those sorts of efforts, we don't deprive them of dialogue, while virtually anywhere else we wouldn't deem to treat such speculation with a grain of seriousness.
As I pointed out before, we have no rules.
So, to get back to the point, Neil's probably wrong. Or at least should be more provisional in his comments. Sanders' may have assumed historicity. He may not have. He doesn't tell us, so we don't know. Some academics probably do. Some probably don't. But without an explanation we can't be sure what they've done, and can't be sure they've "assumed" anything. Simple decorum and charitability demands that we give them the benefit of the doubt.
But James is wrong too. What we do with texts is a lot different here than everywhere else. Not because we treat them differently--it's often suggested that the biblical historian is engaging in some new species of history. We can flatly reject that. We figure ways to find authentic information from texts the same way any other branch of history does. Sometimes with the same criteria.
But what we don't do is see the limits. We don't recognize the provisional nature. And (as I've said again and again lately), we build on people who also didn't see the provisional nature. The last guy's speculation becomes my fact in a sense we really don't see outside of this branch of historical inquiry.
It's not that we don't see any limits at all, of course, just that the ones we push are too far removed from what our evidence can really state to be of much use. But we still have an outer boundary, beyond which we pay proponents the most serious of insults: We deprive them of a dialogue partner.
Robert Eisenman flatly rejected hard science. Hard science he requested. Now there's an analogue to creationism. But he got dialogue partners. Baigent and Leigh, Barbara Thiering, hell, even Dan Brown. Truly ridiculous, crackpot ideas. That got dialogue partners.
Are we really going to suggest that an Earl Doherty or a Robert Price is so over the edge that even these crackpots are more deserving of engagement than they are? Because if we are, we're wrong. And wholly unjustified.
Here's the simple reality: Earl Doherty does very little that a Crossan or a Meier doesn't do. He uses the same criteria. He just attaches different (entirely subjective, the same as everyone else') weight to them. And by tweaking the weight--this criteria has more force than this one--he uses established methods to drive ineluctably to a given conclusion. That is how history is done, biblical or otherwise. And if it's okay for a Crossan or a Meier (as examples who rely heavily on methodological criteria for authenticity), the it's okay for Earl too.
19 comments:
- Steven Carr said...
'We figure ways to find authentic information from texts the same way any other branch of history does.'
So what can we conclude from the fact that the Gospel of John has no mention of any baptism by John the Baptist of Jesus?
Can we conclude , that the baptism must have happened, citing as evidence the fact that there is no baptism in the Gospel of John?
'Earl Doherty does very little that a Crossan or a Meier doesn't do.'
Meier reads the Gospel of John, sees that there is no baptism, and concludes that a baptism must have happened - that the church was 'stuck' with the fact that a baptism happened.
Would a Doherty ever do that?
- Rick Sumner said...
You don't learn, do you Steven? Polemic, quote mining, non sequiturs
Really. You're not helping your plight.
- Steven Carr said...
So no attempt at an argument or refuting my claims.
Just abuse of the post by somebody unable to show what was wrong with it.
I quoted your post, to engage in dialogue, and was met with abuse and no attempt at an argument....
Would a Doherty produce the howlers that Sanders produce in Jesus and Judaism?
Of course not.
We figure ways to find authentic information from texts the same way any other branch of history does
So what do mainstream Biblical historians extract from Paul's claim in Romans 10, that Jews could hardly be expected to believe until a preacher had been sent to them, and Christians had indeed been sent to preach about Jesus?
Should we conclude that Jews had never heard of Jesus, if not for Christians preaching about him?
You can search commentaries high and low and this will not even be discussed, let alone refuted.
Because mainstream commentators assume that Jews had heard of Jesus, before Christians started preaching about him.
They just assume the basics of the Gospel story, which is why they approach texts such as Romans 10 in the way that they do.
- Steven Carr said...
'quote mining'....
Another term for 'You skewered the pretensions of Biblical scholars by quoting them.
So I am not going to refute it, just hurl abuse at it by likening it to creationist quote mining.
But no matter what you call my quotes of Meier, that is what he wrote, and the plain fact is that he thinks the baptism is historical, partly because it was 'erased' from John's Gospel.
Yes, things are historical IF they are not mentioned in a text....
- Rick Sumner said...
You didn't quote mine Meier, Steven, you quote mined me.
No Steven, no attempt. Because they're irrelevant. You're just too obtuse to realize that.
You can reply to this question if you want, but I'm not much interested in any response since I already know the answer:
Have you ever, in your life, convinced anyone of anything with the nonsensical polemic you pollute blog comments with? Since it isn't effective, why bother?
You are the quintessential reason mythicism is dismissed so easily. A guy with an axe to grind and no critical insight.
- Steven Carr said...
Still no arguments.
Still pure abuse.
And Meier's words remain written on the page,regardless of how much you hate me for publicising the arguments used by top Biblical scholars.
He thinks things happened if there is a text with no record of them - if they were 'erased' from the text.
Would Doherty agrue like that?
- Stephen C. Carlson said...
Rick, if you're right, this would indicate(in Bayesian terms) that different people have different prior probabilities of historicity.
- James F. McGrath said...
Contrary to Steven's claim, Doherty's work does seem to me to be full of "howlers" - special pleading for interpretations of straightforward language in non-straightforward ways, false dichotomies, posited background conceptualities that have no basis in any sources from the time, and so on.
I don't think we should give them less attention that Barbara Thiering. I think we should give them all equally little attention, except inasmuch as we atempt to show with as much patience as we can muster why such views are not taken seriously by people with genuine expertise in the relevant fields.
Treatments of Jewish and Christian history seem to be particularly prone to extremes of historicity and dismissiveness. I explored another example not that long ago, namely the Acts of Thomas, where the work is essentially a novel which probably reflects almost nothing historical in terms of any specific story about Thomas, and yet also seems to have been based on at least some slender genuine knowledge about a trip by Thomas to India, since it gets right not only the name of a king, but also his brother. While scholars of early Christianity in recent years have been largely dismissive, scholars of Indian history enthusiastically point to the Acts of Thomas as providing one of the few instances of independent confirmation in what is otherwise a much less well-attested era in the history of South Asia.
And that's what I object to the most about mythicism. I think Godfrey's quote makes it clear that ahistoricity is being presupposed (since the presumption is that nothing in a text can make historicity more likely, and in some cases such as that of Jesus, texts are all we have). And yet the irony is that those who painstakingly look at the evidence, make a case for historicity or ahistoricity, however subjective and however far from certainty, are accused of "presuming historicity." And the irony is that mythicism is popular among people who consider themselves "freethinkers" and yet seem unable to see that they are not applying critical thinking evenly to their own views and assumptions in the way they do to those with whom they disagree.
- Steven Carr said...
So not even an attempt by James McGrath to defend Meier's claim that the baptism by John the Baptist was an event that the church was 'stuck' with, because it was 'erased' from John's Gospel.
In other words, it happened because it is not in one of the Gospels...
Instead we get wild allegations by McGrath, with no specifics whatever.
And once again,McGrath refuses to touch Romans 10, that I mentioned, where Paul makes it clear that Jews had never heard of Jesus, apart from Christians preaching about him.
- Rick Sumner said...
Hi James,
James wrote. . .Contrary to Steven's claim, Doherty's work does seem to me to be full of "howlers" - special pleading for interpretations of straightforward language in non-straightforward ways, false dichotomies, posited background conceptualities that have no basis in any sources from the time, and so on.
Doherty's hypothesis has some problems, for sure. And he has a horrible habit of relying on rhetoric to make his points, to overstate his evidence, and to treat his sources as though they are actively engaging the debate with him. He has an interesting theory, and is an absolutely horrible advocate of it. He needs a Huxley, so to speak.
And indeed some things seem almost comical (Justin and Tatian's proposed interchange is just absurd, for example), and he'd probably be better off to simply acknowledge a problem than to press it. But part of that problem owes to having to cover such a massive amount of material--the type range a genuinely different paradigm brings rather than just a new idea. Could his hypothesis be adapted to remove such things? I don't know. But I don't think we should decline to investigate it simply because it has difficulties.
Other things are simply fallacious, and he has a particular knack for relying on authority when he's arguing for something new. Certainly there are significant problems with his entire package. But how many discussions of Christian origins can truly claim to be free of any such difficulties? More importantly, how many can claim to have always been free of them? We can hardly claim Doherty's hypothesis hasn't withstood serious inquiry: It hasn't had any serious inquiry.
If one goes way back into the annals of the Crosstalk list, Stevan Davies once opined that Doherty offered something fundamentally new in a sense that nobody else he'd encountered had. That he had learned more from alternately engaging and endorsing facets of Doherty's hypothesis than anyone else'. Doherty challenges how we think in a sense that no one else I've read does.
As far as interpretations of straightforward language in non-straightforward ways, I just read 250 pages on a three word phrase (in translation, at least). Carr's Angels and Principalites. Tens of thousands of words on it.
I'm not aware of any area of NT studies that don't take non-straightforward readings of straightforward material. If that's your reason for rejecting him, it's very, very weak.
- Rick Sumner said...
James wrote. . .And that's what I object to the most about mythicism. I think Godfrey's quote makes it clear that ahistoricity is being presupposed (since the presumption is that nothing in a text can make historicity more likely, and in some cases such as that of Jesus, texts are all we have).
I think everyone approaches the texts with assumptions. Mythicist and historicist alike approach the texts with an idea of what they intend to find, and that idea colors how they view the material.
But Price is right: Dissimilarity alone can be employed to reject every single verse in the NT, if put in the right hands. Whether we use it to do that or not depends on what our predilections are, a sword that cuts both ways.
James wrote. . .And yet the irony is that those who painstakingly look at the evidence, make a case for historicity or ahistoricity, however subjective and however far from certainty, are accused of "presuming historicity."
To a large degree I agree with this, though it's another sword that cuts both ways. It's always phrased so that one's side is doing history, but the other isn't. And I think that's wrong. Once we move beyond the overly popular crap the mythicist is doing history, and they're especially doing biblical history. It's being played by the same rules the historicist uses, so it's not really sporting to tell them they can't have their ball on our field.
How do you intend to actually know if the mythicist position is as horrible as you assume it is if you don't engage the material? If you don't put forth your challenges and assess the responses? How do you know it can't be modified in the face of new questions when you don't bother asking them, and instead just call them creationists?
That a Thiering or an Eisenman is wrong is self-evident. The case is not so prima facie strong against an Earl Doherty. Even if we reject him, he deserves to be taken seriously, and the lack of fair and balanced engagement (rather than a string of thinly veiled insults) is to the historicist's discredit.
I noted at the outset that I ultimately reject Doherty. But I know why I do, I've engaged the material, I've given him his airtime, I've heard him out. And ultimately I found the theory wanting. But I know why I do.
At this point you can't make the same claim. So is any claim at all really justified?
- Rick Sumner said...
Hi Stephen,
I think there's some real hope with Bayesian probabilities in the study of history. Real hope. It's just going to take a better thinker than me to work out the nuances.
- Vinny said...
Thanks for that post.
- James F. McGrath said...
Rick, it may just be that everything I think about mythicism is colored by Steven Carr's failure to acknowledge that Jude's failure to mention Lee Harvey Oswald refutes that the Maitreya was his brother...
Having said that, I have read Doherty (even though I've been accused of not doing so). I just said it had been a while and I needed to refresh my memory. But I think I remember enough (and have confirmed from online sources) to say that Doherty's attempts to force events into "the sub-lunar realm" and treat phrases such as "according to the flesh" in such a context is not merely unpersuasive, but has no foundation or justification in any relevant sources. So I'm all for reading before rejecting. But we have, and then we did, and yet we keep hearing from mythicists that we ought to have found this stuff persuasive.
- Rick Sumner said...
I couldn't agree more in the case of people like Carr. There used to a be a Ted Hoffman kicking around who was just as bad. It's perhaps just bad luck for Doherty that most of his most vociferous supporters are even poorer debaters than he is. As I noted above, he desperately needs a Huxley. Unfortunately evolution was a slam dunk in the sense that no discussion--mythicist or otherwise--of Christian origins can be. So even a Huxley can't make a case without a receptive audience, and there doesn't seem to be one anywhere. And that, again, is to the shame of the historicist. Even if he's wrong, he does deserve to be taken seriously. It isn't some laughable "Jesus-is-based-on-Mithras-because-I-read-it-online" hypothesis.
Kata sarka provides a nice example of where Doherty hasn't really gotten a fair hearing actually. Because the discussion has largely focussed on whether or not he quote mined Barrett. Which he did.
The case he makes in his first book is horrible. It begins with an abuse of Barrett, and ends with the observation that it could be "quite useful."
I'm not sure that Doherty's reading of "according to the flesh" (which Carr, in customary fashion, very poorly explains) is that big of a stretch though. His appeal to Barrett is fallacious, of course. First of all he's quote mined him, second of all he's relied on an equivocation that only works in English.
But the term is used for Jesus, and Jesus alone in, for example, Ignatius To the Smyrneans and Acts. Why? It seems obvious to me that it serves as a qualifier, a way to get around the virgin birth. That Jesus enjoys legitimate sonship through Joseph, despite the lack of actual parentage.
It functions as a sort of idiom here, and it's really not that big a step to Doherty's interpretation. It's an argument he (unfortunately) missed, though I haven't read the new book yet so it may have been corrected.
It's a small enough step that if he's right everywhere else, or even most other places, his proposed reading almost has to become the default. We can't hang historicity on Rom.1:3. Or if we do, we at the very least can only do so provisionally. Which is how I think most of our conclusions should be framed, and I would hope that if we did so our conclusions would, in general, become less strained. We'd have less drum majorettes.
But in the end, for the record, I reject Doherty's reading. But I don't see it as a refutation of his thesis.
The sub-lunar realm is a little iffier. He seems to have abused his sources there. I'm not sure if a stronger case can be made or not.
- Rick Sumner said...
I thought I'd included this above. I'd intended to, at any rate.
James wrote. . .Having said that, I have read Doherty (even though I've been accused of not doing so).
In that case I extend my apologies. I'd misunderstood the situation, and was uncharitable my own self.
- James F. McGrath said...
No problem, Rick. It has been said a lot lately. And if there is a problem that confronts both mythicists and mainstream scholarship alike, it is that we all have a tendency, if we hear something enough, to think it must be true! :)
- Steven Carr said...
Rick, it may just be that everything I think about mythicism is colored by Steven Carr's failure to acknowledge that Jude's failure to mention Lee Harvey Oswald refutes that the Maitreya was his brother.
I see McGrath is now resorting to lies about what I write, as he cannot refute my arguments.
As McGrath well knows, the Maitreya does not exist, despite the fact that pictures of him have been posted on the Internet.
We can apply standards of mainstream Biblical scholarship to the case of the Maitreya, and see that they crash and burn there too, just as badly as they have crashed and burned for the past 100 years when scholars have applied the same standards to the historical Jesus.
Standards which include claiming that something happened because one text does not mention it (!)
It takes a lot more than claims that the Lord had a brother to show that there was a Jesus, especially when major church histories have no record of this person being a brother of Jesus.
McGrath is in an industry which has failed its customers for the past 100 years.
This is not surprising as all mainstream Biblical historians do not have a methodology which works.
Without tools, they are groping in the dark.
- James F. McGrath said...
Obviously someone who cannot recognize satire in their own time is going to have a tough time working out genres in ancient literature.
Why it has any bearing in Steven's mind on the question of the historical Jesus that some people didn't mention some things is beyond me. In the case of Jesus' brothers, we know that later Christians sometimes tried to turn brothers into cousins in order to maintain Mary's perpetual virginity. And that of course is helpful to historians, since it situated the sources that refer to Jesus' brother(s) without embarrassment in an earlier period.


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