text:
SB942 Enrolled                                LRB9002925LDdvA
AN ACT in relation  to  functions  of  State  government,
amending named Acts.
Section 5.   The  Court  of  Claims  Act  is  amended  by
changing  Sections  6,  8,  18,  21,  22-1,  24,  and 26-1 as
(705 ILCS 505/6) (from Ch. 37, par. 439.6)
Sec. 6. The court shall hold a  regular  session  at  the
Capital  of  the  State  beginning  on  the second Tuesday of
January, May and November, and such special sessions at  such
places  as it deems necessary to expedite the business of the
court.
Sec. 8. Court of Claims jurisdiction.   The  court  shall
have   exclusive  jurisdiction  to  hear  and  determine  the
following matters:
(a)  All claims against the State founded upon any law of
the  State  of  Illinois,  or  upon  any  regulation  adopted
thereunder by  an  executive  or  administrative  officer  or
agency;   provided,   however,   the  court  shall  not  have
jurisdiction (i) to hear  or  determine,  other  than  claims
arising  under  the Workers' Compensation Act or the Workers'
Occupational Diseases Act, or claims for  expenses  in  civil
litigation,  or  (ii)  to review administrative decisions for
which a statute provides that review shall be in the  circuit
or appellate court.
(b)  All  claims  against  the  State  founded  upon  any
contract entered into with the State of Illinois.
(c)  All  claims  against  the  State  for  time unjustly
served in prisons of this State where the persons  imprisoned
shall  receive  a  pardon from the governor stating that such
pardon is issued on the ground of innocence of the crime  for
which they were imprisoned; provided, the court shall make no
award in excess of the following amounts: for imprisonment of
5  years  or less, not more than $15,000; for imprisonment of
14 years or less but over 5 years, not more than $30,000; for
imprisonment of over 14 years, not  more  than  $35,000;  and
provided  further, the court shall fix attorney's fees not to
exceed 25%  of  the  award  granted.   On  December  31,  the
effective  date  of  this  amendatory  Act of 1996, the court
shall make  a  one-time  adjustment  in  the  maximum  awards
authorized by this subsection (c), to reflect the increase in
the  cost  of  living  from  the  year in which these maximum
awards were last adjusted until  1996,  but  with  no  annual
increment exceeding 5%.  Thereafter, the court shall annually
adjust  the  maximum awards authorized by this subsection (c)
to reflect the increase, if any, in the Consumer Price  Index
For  All  Urban  Consumers for the previous calendar year, as
determined by the United States Department of  Labor,  except
that  no  annual  increment  may  exceed  5%.   For  both the
one-time adjustment and the subsequent annual adjustments, if
the Consumer Price Index decreases during  a  calendar  year,
there  shall  be  no  adjustment for that calendar year.  The
changes made by Public Act 89-689 this amendatory Act of 1996
apply to all claims filed on or after  January  1,  1995  and
that  are  pending on December 31, the effective date of this
amendatory Act of 1996 and  all  claims  filed  on  or  after
December  31,  the  effective  date of this amendatory Act of
(d)  All claims against the State for  damages  in  cases
sounding in tort, if a like cause of action would lie against
a private person or corporation in a civil suit, and all like
claims   sounding   in   tort   against  the  Medical  Center
Commission, the  Board  of  Trustees  of  the  University  of
University,  or  the  Board  of  Trustees  of  the   Illinois
Mathematics  and Science Academy; provided, that an award for
damages in a case sounding in tort, other than certain  cases
involving  the operation of a State vehicle described in this
paragraph, shall not exceed the sum of $100,000 to or for the
benefit of any claimant.  The $100,000  limit  prescribed  by
this  Section  does  not  apply to an award of damages in any
case sounding in tort arising out of the operation by a State
employee of a vehicle owned,  leased  or  controlled  by  the
State.   The  defense  that  the  State or the Medical Center
Commission or the Board of  Trustees  of  the  University  of
Mathematics  and  Science  Academy  is  not  liable  for  the
negligence  of  its  officers,  agents,  and employees in the
course of their employment is not applicable to  the  hearing
and determination of such claims.
(e)  All  claims  for  recoupment  made  by  the State of
Illinois against any claimant.
(f)  All claims pursuant to the Law Enforcement Officers,
Civil Defense Workers, Civil Air Patrol Members,  Paramedics,
Firemen, Chaplains, and State Employees Compensation Act.
(g)  All  claims  filed  pursuant  to  the  Crime Victims
Compensation Act.
(h)  All  claims  pursuant  to  the   Illinois   National
Guardsman's Compensation Act.
(i)  All  claims  authorized by subsection (a) of Section
10-55 of the Illinois Administrative Procedure  Act  for  the
expenses  incurred  by  a  party  in  a contested case on the
administrative level.
(Source:  P.A.  88-45;  89-4,  eff.  1-1-96;   89-689,   eff.
12-31-96; revised 4-24-97.)
(705 ILCS 505/18) (from Ch. 37, par. 439.18)
Sec.  18.   The  court  shall  provide,  by rule, for the
maintenance of separate records of claims which arise  solely
due  to lapsed appropriations and for claims for which amount
of recovery sought is less than $5,000 $2,500. In  all  other
cases,  the  court  or Commissioner as the case may be, shall
file with its clerk a written opinion in each case upon final
disposition thereof.  All  opinions  shall  be  compiled  and
published annually by the clerk of the court.
Sec.  21.  The  court is authorized to impose, by uniform
rules, a fee of $15 for the filing of a petition in any  case
in  which  the  award  sought  is more than $50 and less than
$1,000 and $35 in any case  in  which  the  award  sought  is
$1,000  or  more;  and  to  charge  and collect for copies of
opinions or other documents filed in the Court of Claims such
fees as may be prescribed by the rules of the Court. All fees
and charges so collected shall be  forthwith  paid  into  the
State Treasury. In claims based upon lapsed appropriations or
lost  warrant  or  in  claims filed under the Law Enforcement
Officers, Civil Defense Workers, Civil  Air  Patrol  Members,
Paramedics,   Firemen,   Chaplains,   and   State   Employees
Compensation   Act,   the   Illinois   National   Guardsman's
Compensation Act, or the Crime Victims Compensation Act or in
claims filed by medical vendors for medical services rendered
by  the  claimant  to persons eligible for Medical Assistance
under programs administered by  the  Illinois  Department  of
Public Aid, no filing fee shall be required.
(705 ILCS 505/22-1) (from Ch. 37, par. 439.22-1)
Sec.  22-1.  Within  1  year  from  the date that such an
injury was received or such a cause of  action  accrued,  any
person  who  is  about to commence any action in the Court of
Claims against the State  of  Illinois,  the  Medical  Center
Commission,  the  Board  of  Trustees  of  the  University of
Illinois,  the  Board  of  Trustees  of   Southern   Illinois
University,   the   Board   of   Trustees  of  Chicago  State
University,  the  Board  of  Trustees  of  Eastern   Illinois
University,   the   Board  of  Trustees  of  Governors  State
University,  the  Board  of  Trustees   of   Illinois   State
University,  the  Board  of Trustees of Northeastern Illinois
University,  the  Board  of  Trustees  of  Western   Illinois
University,   or  the  Board  of  Trustees  of  the  Illinois
Mathematics and Science Academy, for damages  on  account  of
any  injury  to  his  person  shall file in the office of the
Attorney General and also in the office of the Clerk  of  the
Court  of  Claims, either by himself, his agent, or attorney,
giving the name of the person to whom the cause of action has
accrued, the name and residence of the  person  injured,  the
date  and  about  the  hour  of  the  accident,  the place or
location where the accident occurred, a brief description  of
how  the  accident  occurred, and the name and address of the
attending physician, if any, except as otherwise provided  by
the Crime Victims Compensation Act.
In actions for death by wrongful act, neglect or default,
the executor of the estate, or in the event there is no will,
the  administrator  or  other  personal representative of the
decedent, shall file within 1 year of the date  of  death  or
the  date  that  the  executor or administrator is qualified,
whichever occurs later, in the office of the Attorney General
and also in the office of the Clerk of the Court  of  Claims,
accrued,  the  name  and  last residence of the decedent, the
date  of  the  accident  causing  death,  the  date  of   the
decedent's  demise,  the place or location where the accident
causing the death occurred, the date and about  the  hour  of
the  accident,  a  brief  description  of  how  the  accident
occurred,  and  the  names  and  addresses  of  the attending
physician and treating hospital if any, except  as  otherwise
provided by the Crime Victims Compensation Act.
A claimant is not required to file the notice required by
this  Section  if he or she files his or her claim within one
year of its accrual.
Sec.  24.    From  funds  appropriated  by  the   General
Assembly  for  the  purposes  of  this  Section the Court may
direct immediate payment of:
(a)  All claims arising solely as a result of the lapsing
of an appropriation out of which the  obligation  could  have
been paid.
(b)  All claims pursuant to the "Law Enforcement Officers
and  Firemen  Compensation Act", approved September 30, 1969,
(c)  All  claims  pursuant  to  the  "Illinois   National
Guardsman's   and   Naval   Militiaman's  Compensation  Act",
approved August 12, 1971, as amended.
(d)  All  claims   pursuant   to   the   "Crime   Victims
Compensation Act", approved August 23, 1973, as amended.
(e)  All  other claims wherein the amount of the award of
the Court is less than $5,000 $2,500.
(705 ILCS 505/26-1) (from Ch. 37, par. 439.24-6.1)
Sec. 26-1.  Except  as  otherwise  provided  herein,  the
maximum   contingent   fee  to  be  charged  by  an  attorney
practicing before the Court shall not exceed  20  percent  of
the  amount  awarded,  which  is  in excess of the undisputed
amount of the claim, unless further fees shall be allowed  by
the  Court at a hearing fixing such fees.  In cases involving
lapsed appropriations or lost  warrants  where  there  is  no
dispute  as  to  the liability of the respondent, the fee, if
any, for services rendered is to be fixed by the Court  at  a
nominal amount.
Nothing  herein  applies  to  awards  made  under the Law
Enforcement Officers, Civil Defense Workers, Civil Air Patrol
Members, Paramedics  and  Firemen  Compensation  Act  or  the
Illinois   National   Guardsman's   and   Naval  Militiaman's
Compensation  Act  or  the   "Illinois   Uniform   Conviction
Information  Act",  enacted  by the 85th General Assembly, as
heretofore or hereafter amended.
(705 ILCS 505/20 rep.)
Section 10.  The  Court  of  Claims  Act  is  amended  by
repealing Section 20.
Section  15.   The  Crime  Victims  Compensation  Act  is
(740 ILCS 45/2) (from Ch. 70, par. 72)
Sec.  2.  Definitions.   As  used in this Act, unless the
context otherwise requires:
(a)  "Applicant"  means  any  person  who   applies   for
compensation under this Act or any person the Court of Claims
finds  is entitled to compensation, including the guardian of
a minor or of a person under legal  disability.  It  includes
any  person  who  was  a  dependent of a deceased victim of a
crime of violence for his support at the time of the death of
that victim.
(b)  "Court of Claims" means the Court of Claims  created
by the Court of Claims Act.
(c)  "Crime  of  violence" means and includes any offense
defined  in  Sections  9-1,  9-2,  9-3,  10-1,  10-2,  11-11,
11-19.2, 11-20.1, 12-1, 12-2,  12-3,  12-3.2,  12-4,  12-4.1,
12-4.2,  12-4.3,  12-5,  12-13, 12-14, 12-14.1, 12-15, 12-16,
12-30, 20-1 or 20-1.1 of  the  Criminal  Code  of  1961,  and
driving   under  the  influence  of  intoxicating  liquor  or
narcotic drugs as defined in Section 11-501 of  the  Illinois
Vehicle  Code,  and  if  none  of  the said offenses occurred
during a civil riot, insurrection or  rebellion.   "Crime  of
violence"  does  not  include  any  other offense or accident
involving a  motor  vehicle  except  those  vehicle  offenses
specifically  provided  for  in  this  paragraph.   "Crime of
violence" does  include  all  of  the  offenses  specifically
provided  for  in this paragraph that occur within this State
but are subject to federal jurisdiction and crimes  involving
terrorism as defined in 18 U.S.C. 2331.
(d)  "Victim"  means  (1)  a  person killed or injured in
this State as a result of a crime of violence perpetrated  or
attempted  against  him,  (2) the parent of a child killed or
injured in this State as a result  of  a  crime  of  violence
perpetrated  or  attempted  against  the  child, (3) a person
killed or injured in this State while attempting to assist  a
person  against whom a crime of violence is being perpetrated
or attempted, if that attempt of assistance would be expected
of a reasonable man under the  circumstances,  (4)  a  person
killed  or  injured  in  this  State  while  assisting  a law
enforcement official apprehend a person who has perpetrated a
crime of violence or prevent the  perpetration  of  any  such
crime  if  that  assistance  was  in  response to the express
request of the law enforcement  official,  (5)  a  child  who
personally witnessed a violent crime perpetrated or attempted
against  a  relative,  or  (6)  an Illinois resident who is a
victim of a "crime  of  violence"  as  defined  in  this  Act
except,  if  the  crime  occurred  outside  this  State,  the
resident  has  the same rights under this Act as if the crime
had occurred in this State upon a  showing  that  the  state,
territory,  country, or political subdivision of a country in
which the crime occurred does  not  have  a  compensation  of
victims  of  crimes  law  for which that Illinois resident is
eligible.
(e)  "Dependent" means a relative of  a  deceased  victim
who  was  wholly  or  partially  dependent  upon the victim's
income at the time of his death and shall include  the  child
of a victim born after his death.
(f)  "Relative"  means  a  spouse,  parent,  grandparent,
stepfather,    stepmother,    child,   grandchild,   brother,
brother-in-law, sister,  sister-in-law,  half  brother,  half
sister, spouse's parent, nephew, niece, uncle or aunt.
(g)  "Child"  means  an  unmarried son or daughter who is
under 18 years of age and includes a  stepchild,  an  adopted
child or an illegitimate child.
(h)  "Pecuniary  loss"  means,  in  the  case  of injury,
appropriate medical expenses and hospital expenses  including
expenses of a medical examination, medically required nursing
care  expenses,  appropriate  psychiatric care or psychiatric
counseling expenses, expenses for care  or  counseling  by  a
licensed  clinical  psychologist  or licensed clinical social
worker  and  expenses  for  treatment  by  Christian  Science
practitioners   and   nursing   care   appropriate   thereto;
prosthetic appliances, eyeglasses, and hearing aids necessary
or damaged as a result of  the  crime;  replacement  services
loss, to a maximum of $1000 per month; dependents replacement
services  loss,  to  a  maximum  of  $1000 per month; loss of
tuition paid to attend grammar school or high school when the
victim had been enrolled as a full-time student prior to  the
injury,  or  college  or  graduate school when the victim had
been enrolled as a full-time day or night  student  prior  to
the  injury  when  the  victim  becomes  unable  to  continue
attendance  at  school  as  a result of the crime of violence
perpetrated against him; loss of  earnings,  loss  of  future
earnings  because  of  disability  resulting from the injury,
and, in addition, in the case of death,  funeral  and  burial
expenses  to  a  maximum  of $3000 and loss of support of the
dependents of the victim. Loss of future  earnings  shall  be
reduced by any income from substitute work actually performed
by  the victim or by income he would have earned in available
appropriate substitute work he was capable of performing  but
unreasonably  failed to undertake.  Loss of earnings, loss of
future earnings and loss of support shall  be  determined  on
the  basis  of  the victim's average net monthly earnings for
the 6 months immediately preceding the date of the injury  or
on  $1000  per  month,  whichever  is less.  If a divorced or
legally separated applicant is claiming loss of support for a
minor child of the deceased, the amount of support  for  each
child  shall  be  based  either  on the amount of support the
minor child received pursuant  to  the  judgment  for  the  6
months  prior  to the date of the deceased victim's injury or
death, or, if the subject of pending litigation filed  by  or
on  behalf  of  the  divorced  or legally separated applicant
prior  to  the  injury  or  death,  on  the  result  of  that
litigation.   Pecuniary  loss  does  not  include  pain   and
suffering or property loss or damage.
(i)  "Replacement    services    loss"   means   expenses
reasonably  incurred  in  obtaining  ordinary  and  necessary
services in lieu of  those  the  permanently  injured  person
would  have performed, not for income, but for the benefit of
himself or  his  family,  if  he  had  not  been  permanently
injured.
(j)  "Dependents  replacement  services  loss" means loss
reasonably incurred by dependents after a victim's  death  in
obtaining  ordinary  and  necessary services in lieu of those
the victim would have performed,  not  for  income,  but  for
their benefit, if he had not been fatally injured.
(Source: P.A.  89-313,  eff.  1-1-96;  89-428, eff. 12-13-95;
89-462, eff. 5-29-96.)
Section 99.  Effective date.  This Act takes effect  upon


Lyons turns 30 on Feb. 21, and here's the exciting thing: the man has found a niche in the badlands neighborhood of big game pitching.
ST. LOUIS — Tyler Lyons made his first MLB debut on May 22, 2013 against the San Diego Padres, hurling seven dominant innings. These days, however, he's feeling pretty comfortable as a late inning bullpen weapon for the St. Louis Cardinals. Escaping the clutches of arbitration certainly leaves a confident feeling, but Lyons isn't changing his preparation.
"Arbitration doesn't change much, because I am not doing anything different this offseason, whether it's a relief role or not. I'm just getting ready to pitch."
Lyons hasn't dealt with any lingering injuries this offseason, something that has plagued the past couple breaks. Lower body struggles have been the Achilles heel of Lyons' success rate, largely pertaining to knee troubles. This winter has been about as smooth sailing as his 2017 season, which saw the Southpaw settle in a relief role.
In 50 appearances covering 54 innings, Lyons averaged 11.3 strikeouts per nine innings, something he credited to being more aggressive on the mound. Coming into the sixth, seventh, and eighth innings, Lyons was able to unleash more silver bullets that otherwise would have been saved in a start or longer appearance.
After three separate appearances where he pitched three innings or more, Lyons found himself pitching a single inning during August and September, which resulted in more strikeouts and less walks. When you only have 15-20 pitches to fire, a pitcher will let the hitter eat plenty during the action.
When asked about the vacant closer role and if President of Baseball Operations John Mozeliak leaning on internal options for the bullpen rehab excites him, Lyons doesn't waver in his initial stance of straight business. He's simply getting ready to pitch, doesn't pay attention to offseason drama, and can contribute in a number of ways. He's a baseball soldier in a matter of speaking.
While his role on the team has been defined, Lyons is suddenly learning the complexities of being a father. He became a father on Nov. 30 to a baby girl, and is a green belt in the diaper changing department, even though he fears what is ahead of him. "We are both just figuring it out," said Lyons.
Lyons turns 30 on Feb. 21, and here's the exciting thing: the man has found a niche in the badlands neighborhood of big game pitching. While he was a serviceable spot starter, Lyons has the chance to be a dynamic bullpen asset for a team currently looking for an arm to establish order in the late night game.
Lyons posted career best marks in ERA, FIP, WHIP, and K/9 innings last year, and more assurance in the late game arena will certainly result in an even more impressive 2018. After all, he is healthy and ready to roll in January.
Tyler Lyons broke in with the Cardinals as a starter, but he will make his mark in the game as a reliever. Closer? Only time will tell.


Dropping someone to the airport this weekend?
Cork Airport has introduced some new rules for motorists and passengers as they plan for a healthy eight per cent boost in traffic at Ireland's fastest growing transport hub.
The new Set Down Lane started operating at 9am this morning, Thursday, March 21st, with new charges in place for those who linger a little too long.
Our advice? Say your goodbyes at home, check in early and hit the duty free.


This ride has a little bit of everything. It's 3D and is a coaster at times.
The scenery from the inside of the bank to the under ground tunnels are spectacular. The ride is incredibly smooth and highly entertaining.in my opinion still inferior to the Forbidden J..ourney ride at Islands of Adventure but again what isn't.
This looks to be the most popular ride of the park. It is partly a roller-coaster, partly a dark ride with projections and special effects. The story is very nice and it a lot of fun. The 3D effect is very convincing and the short roller coaster sections are great. I think Harry Potter and the Forbi..dden Journey is a better more unique attraction, but this one is superb as well.
Gringotts awaits at the far end of Diagon Alley, a goblin-run bank that hides much more than treasures. This place is, as expected, wrapped in secrets, a thrilling and pulse-pounding adventure that will take you right into the heart of magic and face to face with Harry, Ron and Hermione. Simply irresistible!


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While a couple of betting sites arrangements supply obliging customer game plan, Legends gives steady course of action that is also pleasant and person. The site offers focal points for both new and dug in gamers and furthermore various headways at any kind of offered time. The most generally perceived challenge is that the site does not give an indistinguishable number of budgetary choices from some unique locales. Interlopes are a standout amongst the timeliest games betting districts. The site is made to be anything but difficult to utilize and give a key territory to putting wagers. The additional offers offered by the site are great and also expeditiously open to amateurs and instructed players.
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This is enlisted as Camera Raw and this is specifically for the editing of RAW images. This is a great tool for the professional photographer who doesn't want to convert his or her photographs to JPG or JPEG files and therefore it counts as a novelty inside Photoshop. Here is how to use it.
Keeping your photos in RAW and being able to edit them this way is a great deal. Photographers don't need to convert their images to JPEG for them to be editable anymore.
No matter how much you exercise on your image you can still revert them back to their original outlook.


Didsbury 1 Murcia 0We landed easily, fought our way through Passport Control and Baggage reclaim – a broken stroller souring the mood.
I find that however keen I am to stay on holiday that the first flat-vowelled Passport Officer and the first nasal "Yor-ite" remind me of how much I love this sceptred chunk of the North West: but not this time.
We arrived home slightly low, a great holiday shaded by its proximity to work, school, nursery and cold mornings. Except the Pearly Princess whose paleness had found the constant Spanish heat difficult and had made her quieter than usual. As we stepped into the damp mulch of British summertime she grew, her voice returned and as pulling into Didsbury she whooped and clapped – which perked us up.
Four hours later Didsbury Son fell quickly into a pain that needed a speedy drive (still in shorts and sunglasses) to Children's A&E. He is fine now, but needed an operation and is a bit sore.
My trepidation at coming home and the feeling of general malaise dispelled by the ease of getting from Didsbury to A&E in 15 minutes, the care he received from everyone and the quality of the drugs. Three of Manchester's longstanding cornerstones.
Drains the tan a bit too quickly, but did feel like another rite of passage all around.


Dahlia 'Cafe Au Lait' is a radiant variety with large flowers, up to 25cm across, in colours of gorgeous peachy cream shades. They create spectacular displays in the border and work especially well as a cut flower. 'Cafe Au Lait' is a much loved variety of Dahlia and is best planted alongside other plants with subtle coloured flowers. Its flowering period is long, from June through to the first frost, but remember to keep deadheading to encourage more blooms to flower.


text:
Q: Swift flood fill algorithm randomly stopping Here is the raw code but I will explain it roughly:
func processTile(_ tile: Tile) {
    // Add tile to pos list if valid, otherwise prune the
    branch
    if isBarrier(tile) || alreadyChecked(tile) {
        return
    } else {
        posList.append(tile.pos)
    }

    depth++ ; if depth > maxDepth { return }

    for neighborTile in neighbors(of: tilePos) {
        processTile(neighborTile)
    }
}

This is the main recursive function. Basically it checks if a tile is part of a room by being neither a barrier tile or already checked. If either one of those cases is true then the branch of the flood tree is pruned and ended. If the tile was valid and was added to the list then the depth is incremented with a check on it. Then the tile's neighbors are all checked with the same process.
For some reason the flood algorithm just stops randomly. I changed the code adding a print() in front of the returns to see why a branch just stops. This worked for all the correct pruning cases where it hits a barrier or already checked tile, but when it would just randomly stop and not check a tile it didn't even log anything.
The only thing I can think of is that Swift stops executing the functions after a certain level of recursion. If this is the case does anyone know what the maximum number of recursions is? And what a possible workaround would be. I'm thinking you would have to make a list of all the "edge" tiles of the flood, and a list of all the "interior" tiles of the flood. Then have a while loop running until there are no edge tiles which just expands the flood.

redpajama_set_name: RedPajamaStackExchange


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Thank you for visiting Mitchell Photography, a full-service professional photography business specializing in classic elegance with a modern edge.
We help you make the most of your moments with high-quality, fully-edited images of your engagement session or wedding, your maternity pictures of those ever precious baby's first year photos, those fleeting moments and milestones as babies grow into children, and the excited yet nervous age of high school senior graduation -- and those irreplaceable family keepsake heirloom photographs taken annually at holidays or on special occasions to document your family's growth.
We can photograph your session in our full-service professional photography studio on a variety of backdrops with props, or at an outdoor venue of your choice.
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Make the most of your moments with Mitchell Photography.
Congratulations on your recent engagement! You're on your way to announcing your special day, asking friends, family, and loved ones to save the date, and planning what will be one of the most amazing days of your lifetime. Check Mitchell Photography's galleries and info to find out if we're a good match to capture the story of your engagement and help prepare for your wedding photography. Remember, when the wedding day is over, the cake is eaten and the DJ goes home. The decorations are cleared away and all that's left are the photographs.
When your wedding day is over, one of the only things you'll have to commemorate the day, other than a brand new marriage and a delightful spouse, is your photographs. You have endless options for photographers, so it's important you do your homework, research photographers in your area, and choose the best photographer for you based not just on price, but also on quality. Your photographer doesn't just take random snaps of your special day, but uses art, science, and experience to capture the story of your special day and all of its intricate details.
Welcome to Mitchell Photography's Maternity Portraits. We're thankful you're considering Mitchell Photography to capture these precious maternity moments when your unborn baby is growing within. Please take a moment to check out our maternity gallery to make sure our style matches yours. Then, check out our maternity pricing page - including how you can get your maternity session for free! Then, check out the maternity blog where we post regular updates including tips and tricks on how to prepare for your session, what to expect, and more. Finally, subscribe to our newsletter to stay in-the-know about special events, sales, promotions, and other important updates.
Welcome to Mitchell Photography's Newborn Portraits. We're thankful you're considering Mitchell Photography to capture these precious first moments of your baby's life. Please take a moment to check out our newborn gallery to make sure our style matches yours. Then, check out our newborn pricing page - including how you can get your maternity session for free! Then, check out the newborn blog where we post regular updates including tips and tricks on how to prepare for your session, what to expect, and more. Finally, subscribe to our newsletter to stay in-the-know about special events, sales, promotions, and other important updates.
Congratulations on reaching your graduating year in high school! Whether you're just getting ready to start your senior year or you're just wrapping it up, it's an exhilarating time when you bridge the gap between childhood and adulthood. Now is your chance to shine, to be the superstar, and to announce that you have arrived on your own terms. Don't settle for any photographer, and don't get herded in with the masses for a rushed session just like everyone else's. At Mitchell Photography, we can custom-tailor a senior portrait session that's as unique as you are.
You may never have imagined your family would grow so quickly! It seems like only yesterday you were bottle-breaking and potty-training, and now you've got family members of all ages, in all grades, all over the place with personal agendas. But if you don't take the time to stop, to gather, to commemorate the growth, all you'll have left is a few smartphone snapshots of bygone childhoods. Celebrate your family's milestones by engaging in annual family portraits.


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9/11-Themed Bar Opens in Fort Worth, TX to Mixed Reviews
Lauren Moyer
Lauren Moyer Published: May 25, 2021
In Texas, there's just about a bar for every type of person. You have your local dive bars with live music, your over-the-top downtown city life bars where you're sure to catch a glimpse of Matthew McConaughey, and of course bars with some really big country dance floors. What they didn't have was a bar themed after one of the most tragic events in U.S. history — 9/11. That is ... until now.
I wish we could be exaggerating, but nope. It's very real and very open. It all started when a guy named Jesse Tyler passed by the bar asking himself, 'Huh, that couldn't be about what I think it's about, right?'. It meant exactly that. Tyler posted the photos of the bar to Twitter and the viral sensation took off from there.
Inside the bar are pictures of the Twin Towers on that fateful morning on September 11, 2001. As smoke can be seen billowing out of the buildings, the bar also has a list of posted times and what happened during those moments.
A sign posted inside one of the windows reads, "Bar9Eleven...more than a name ... more than a date ... a state of mind. Never forget, ever."
What did the owner have to say about it?
The bar's owner Brent Johnson spoke to Texas Monthly about the heat his business was getting on social media. Johnson said he believes that the name isn't in bad taste. He told the magazine that he saw a study one September that "80% of Americans" didn't know that the anniversary of the event was approaching.
"I don't want anyone who comes into my restaurant to forget that day," Johnson said, recalling the way it felt to watch the events unfold as he opened his first Tex Mex restaurant in 2001.
Johnson says Bar9Eleven opened sometime between 2012 and 2014.
The internet isn't all that happy ... or all that upset
So let's venture back to Twitter, where folks there aren't that happy with what Johnson had to say.
"So many questions. Does this place get a lot of business?" one Twitter user said. "Do they realize it's not paying tribute but exploiting the day? People, man."
Meanwhile, another Twitter user by the name of Michelle called the bar a "whole other dimension level of tacky."
Other users mocked the name claiming all sorts of conspiracy theories — ones I won't repeat here.
It won't be a bar I'll be visiting, but you can make that decision for yourself.
Remember that terrible mattress ad?
This isn't the first time a Texas business has caught hate surrounding 9/11. Back in 2016, a mattress store in San Antonio decided to run a Twin Tower sale where you could "get any mattress for a twin price!"
Yep. You can probably guess where this was headed.
The outrage came once the owner of Miracle Mattress seemed to push two employees into two stacks of twin mattresses as she screamed. She then ended the ad with "we'll never forget."
Source: 9/11-Themed Bar Opens in Fort Worth, TX to Mixed Reviews
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redpajama_set_name: RedPajamaCommonCrawl


A cookbook to provide a web server able to serve php pages with Apache and PHP fpm. It relies on apache2 cookbook and php-fpm. Those cookbooks are pinned on well known working minor version to prevent breaking changes. In addition (even if this is not a requirement), the cookbook will install php packages through PHP cookbook. Indeed most of the time you will need php::default in your role which will conflict with the php-fpm package if they are different. You can disable the installation of php packages with node['rackspace_apache_php']['php_packages_install']['enable'].
description "apache and php role"
You can change any of the apache2,php-fpm and php cookbook attributes to tune rackspace_apache_php configuration. ** However you should not change ** ['php-fpm']['package_name'],['php-fpm']['service_name'] or ['php']['packages'] (as they are part of this cookbook logic) without checking it works.
The goal of this library is to do the basic configuration to serve PHP pages through Apache. It will only configure apache2 and the default php handler, users are free to configure their vhost if they need anything more specific.
You will have to add your own Vhost to configure the handler, here is an example using a web_app resource and the apache_conf definition from the upstream apache2 cookbook to create a virtual host and the Apache configuration necessary to handle php requests (templates not provided). It also leverages the ['php-fpm']['pools'] attribute from the upstream php-fpm cookbook to create a custom defined php-fpm pool listening on a socket. Although not provided below, the templates for the apache_conf definition and the web_app resource should contain the necessary directives to pass requestes for php files to the php-fpm pool.


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Tag Archives: book reviews
Evolution goes viral! (And how real science works)
This is the fourth in a series of posts about a new book by Michael Behe, Darwin Devolves. Behe is a leading proponent of intelligent-design creationism (IDC), which asserts that known processes cannot adequately account for evolution and, therefore, some intelligent agent must be involved in the process. Behe is a professor of biochemistry, which gives him knowledge and credentials that most IDC advocates do not have. However, my posts explain why I think his logic is unsound and his evidence weak and biased.
In brief, Behe argues that random mutation and natural selection are almost entirely degradative forces that break or blunt the various functions encoded by genes, producing short-term advantages that are so pervasive that they prevent constructive adaptations, which he claims are very unlikely to emerge in the way that evolutionary biologists have proposed. Unlike young-Earth creationists, Behe accepts the descent of living species from common ancestors over billions of years. To reconcile these seemingly conflicting views, Behe invokes that an intelligent agent (presumably God, though IDC proponents avoid that word so that their ideas might appear to be scientific) has purposefully guided evolution over its long history by somehow inserting new genetic information into chosen lineages along the way. To make his strange argument, Behe works very, very hard to convince readers that standard evolutionary processes are (i) really, really good at degrading functions, and (ii) really, really bad at producing anything new.
In my first post, I explained that Behe's arguments confuse and conflate what is easy and commonplace over the short run (i.e., mutations that break or blunt functional genes) with the lasting impacts of less frequent but constructive adaptations (i.e., new functions and subsequent diversification) over the long haul of evolution. My second post examined a case involving polar bears, which Behe highlighted as a compelling example of degradative evolution, but where a careful review of the science suggests that gene function improved. Behe also highlighted results from my lab's long-term evolution experiment with bacteria, but in my third post I explained that he overstates his case by downplaying or dismissing evidence that runs counter to his argument.
In this post, I'll discuss an experiment that Behe ignores in Darwin Devolves. (Behe clearly knows the work, because he wrote about it on the Discovery Institute's anti-evolution blog. But as usual, he spun the story to obscure the problems for his arguments, all the while accusing the scientists who collect data to test hypotheses of spinning the story.) In fact, as I'll explain, the results also undermine the claims in Behe's two previous books, Darwin's Black Box and The Edge of Evolution, about the supposed shortcomings of evolution.
(Before presenting this experiment, I want to mention briefly two other papers that readers interested in what else Behe missed or downplayed might want to read. First, Rees Kassen posted a preprint of a paper on "Experimental evolution of innovation and novelty." He reviews empirical evidence and discusses conceptual issues bearing on the origin of new functional abilities observed in many experiments with bacteria and other microbes. Second, Chris Adami, Charles Ofria, Rob Pennock, and I published a paper over 15 years ago that demonstrated the logical fallacy of Behe's assertions about irreducible complexity. Behe mentions that paper derisively, without addressing its substance in Darwin Devolves, as follows: "A computer simulation of computer program development that ignores biology entirely." A more accurate statement would have been: "Computer programs can evolve by random mutation and natural selection the ability to perform complex functions that show the concept of irreducible complexity is total nonsense." The rest of this post is longer than I planned, because I want to provide background for readers who aren't microbiologists, and because—like so much of science—it's an interesting story with unexpected twists and turns along the way.)
IV. Phage lambda evolves a new capability without breaking anything
There are a lot of viruses in the world. Fortunately, most of them don't infect humans. Many of them infect bacteria, as it so happens. In fact, before antibiotics were used as therapeutic agents, there was hope that bacteriophages ("bacteria eaters"), or phages for short, would be useful in treating diseases. And now, with the evolution of pathogenic bacteria that are resistant to many or all available drugs, researchers are reconsidering the possibility of using phages to treat some infections.
My lab is best known for the long-term evolution experiment (LTEE) with E. coli bacteria. But over the years, my students have also performed other experiments with a variety of microbes, including some viruses that infect E. coli. One of those viruses is called lambda. For decades, lambda was probably the most intensively studied virus on the planet—just as E. coli was a model for understanding bacterial genetics and physiology, lambda became a model for understanding viral genetics and infection.
One reason lambda became a hit was because it has an interesting life cycle. After lambda enters a bacterial cell (and assuming the cell lacks some internal defenses), the virus can do one of two things. It can commandeer the host, hijacking the cellular machinery to produce a hundred or so progeny before bursting the host cell and releasing its "babies" to find new cells to infect. Alternatively, the virus's DNA may be integrated into the host's chromosome, hiding out and being replicated alongside the host's genes—though the virus may later exit the chromosome and reactivate its lethal program. (Pretty neat, and a bit scary, right?)
Well, as cool as that is, it's not what my student Justin Meyer (now on the faculty at UCSD) was studying. He was using a strain of lambda that can't integrate into the bacterial cell's chromosome—a successful infection takes only the first route, killing the cell in the course of making more viruses. Justin was studying this simpler virus because we were interested in whether the evolution of the bacterial hosts in response to the presence of lambda virus might depend on what food we gave the bacteria.
Let's back up and explain why that might matter. Viruses like lambda don't just glom onto any part of a bacterial cell; instead, they adsorb to specific receptors on the cell's surface, with a successful attachment triggering the injection of their DNA into the cell. Lambda recognizes a particular cell-surface protein called LamB. (Despite decades of study of the interaction between lambda and E. coli, including experiments that specifically sought to see whether mutants could exploit other receptors, no one had ever seen lambda use any other receptor.) Of course, E. coli doesn't make LamB for the sake of the virus. The LamB protein is one of several "porin" proteins that E. coli produces, and which serve as channels to allow molecules, like sugars, to cross the outer cell envelope. (Other proteins transport sugars across the inner cell membrane.) LamB, in particular, is a fairly large channel that allows the sugars maltose and maltotriose to enter the cell. Maltose and maltotriose are made of two and three linked glucose molecules, respectively. Glucose, being smaller, can readily enter a cell via smaller channels. When growing on glucose, E. coli cells don't bother to produce much LamB protein. However, when cells sense that maltose or maltotriose, but not glucose, is present they activate the gene that encodes LamB. In doing so, however, the cells become more vulnerable to lambda, because that protein serves not only to transport these larger sugars but also as the receptor for the virus.
Coming back to Justin Meyer's research, we wanted to see how different sugars affected the bacteria's evolutionary response to lambda. (Justin and I have a paper in press comparing outcomes across the glucose, maltose, and maltotriose environments.) We reasoned that, if the bacteria were fed glucose, they could damage or delete the lamB gene that encodes the LamB protein. If the bacteria mutated the LamB protein, then the virus might counter with a mutation that restored their affinity for the mutated protein; but if the bacteria deleted or otherwise destroyed the LamB protein, we reasoned the virus would go extinct.
However, the first experiment using only the glucose treatment played out differently than what we expected—that's science, and that's why you do experiments—and it set Justin's research off in a new direction. Instead of mutating the lamB gene, the bacteria evolved resistance to the virus by mutating another gene, called malT, that encodes a protein that activates the production of LamB. The viruses didn't go extinct, however, because there was some residual, low-level expression of the LamB protein. That was enough to keep the viruses going, which also meant they could keep evolving.
To make a long story short, after just 8 days, one of six lambda populations evolved the ability to infect malT-mutated cells by attaching to a different surface protein, one called OmpF (short for outer membrane protein F). This evolved lambda virus could now infect E. coli cells through the original receptor, LamB, or this new one, OmpF. It had gained a new functional capability.
To understand this change, Justin sequenced the genome of this virus. He found a total of 5 mutations compared to the lambda virus with which he had begun. All 5 mutations were in the same gene, one that encodes the J protein in the "tail" of the virus that interacts with the cell surface. He also sequenced the J gene for some other viruses isolated from the same population. He found one virus that had 4 of these 5 mutations, but which could not infect cells via the OmpF receptor. Did that mean that only one of the 5 mutations was necessary to evolve this new function?
As it turns out, the answer is no. To better understand what had happened, Justin scaled up his experiments and ran an additional 96 replicates with lambda, E. coli, and glucose. In 24 cases, the viruses evolved the new mode of infection within three weeks. Justin sequenced the J gene from the viruses able to target OmpF in those 24 cases, and in 24 other cases where the virus could still use only the LamB receptor. He found that all 24 with the new capability had at least 4 mutations; these included 2 changes that were identical in all 24 lines, a third that further mutated one of the same codons (sets of 3 DNA bases that specify a particular amino acid to be incorporated into a protein), and another mutation that was always within a span of 11 codons. All of these mutations cause amino-acid substitutions near the end of the J protein, which is known to interact with the LamB receptor. The J protein is over 1100 amino acids in length, and so this concentration and parallelism (repeatability across lineages) is striking and strongly implies that natural selection favored these mutations.
Remember, too, that nothing is broken. These viruses can now use both the original LamB receptor and the alternative OmpF receptor. (This fact was demonstrated by showing that the viruses can grow on two different constructed hosts genotypes, one completing lacking LamB and the other completely lacking OmpF.)
None of the 24 viruses that had not evolved the ability to use the OmpF receptor had all 4 of these mutations. However, three of them shared 3 of the 4 mutations with viruses that had acquired that new ability. And yet, none of those had any capacity to grow on cells that lacked the LamB receptor. In other words, the set of all 4 of these mutations was needed to produce this new ability—no subset could do the job. (We initially lacked one of the four possible viral genotypes having each subset of 3 mutations. Later work confirmed that all four mutations are required.)
At first glance, it seems like none of the viral lineages should have been able to acquire all 4 mutations, at least if you accept the flawed reasoning from Behe's previous book on The Edge of Evolution. If you need all 4 mutations for the new function, so the thinking goes, and if none of them provide any degree of that function, then you would need all 4 mutations to occur in one lineage by chance, which is extremely unlikely. (How unlikely is difficult to calculate precisely. To get some inkling, none of the 48 sequenced J genes—including both those that did and did not evolve the new capability—had even one synonymous mutation. Synonymous mutations don't change the amino-acid sequence of an encoded protein, and so they provide a benchmark for the accumulation of selectively neutral mutations.)
And yet, 24 of the 96 lineages did just that—they evolved the new ability, and in just a few weeks time. If you're into intelligent design, then I guess you'd have to conclude that some purposeful agent was pretty darn interested in helping the viruses vanquish the bacteria. If you're a scientist, though, you're trained to think more carefully and look for natural explanations—ones that you can actually test.
So how could 4 mutations arise so quickly in the same lineage? Natural selection. But wait, didn't Justin find that all 4 of those mutations were required for the virus to exploit the new OmpF receptor? Yes, he did.
Our hypothesis was that the mutations that set the stage for the virus to evolve the ability to target OmpF were beneficial because they improved lambda's ability to use its original LamB receptor. But wait, that's the receptor they've always used. Shouldn't they already be perfectly adapted to using that receptor? How can there be room for improvement?
If you've read my posts on polar bears and bacteria, you've probably got the idea. When the environment changes, all bets are off as to whether a function is optimally tuned to the new conditions. Lambda did not evolve in the same medium where Justin ran his experiments; and while lambda certainly encountered E. coli and the LamB receptor in its history, the cell surfaces the virus had to navigate in nature were more heterogeneous than what they encountered in the lab. In other words, there might well be scope for the viral J protein to become better at targeting the LamB receptor under the new conditions.
To an evolutionary biologist, this hypothesis is so obvious, and the data on the evolution of the J protein sequence so compelling, that it scarcely needs testing. Nonetheless, it's always good to check one's reasoning by collecting new data, and another talented student joined the project who did just that. Alita Burmeister (now a postdoc at Yale) competed lambda strains with some (but not all) of the mutations needed to use OmpF against a lambda strain that had none of those mutations. She studied six "intermediate" viruses, each of them isolated from an independent population that later evolved the ability to use OmpF.
Alita ran two sets of competitions between the evolved and ancestral viruses. In one set, the viruses fought over the ancestral bacterial strain; in the other set, they competed for a bacterial strain that had previously coevolved with lambda and become more resistant to infection. Four of the six evolved intermediate viruses outcompeted their ancestor for the naïve bacteria, and all six prevailed when competing for the tough-to-infect coevolved host cells. Alita ran additional experiments showing that the intermediates were better than the ancestral virus at adsorbing to bacterial cells—the precise molecular function that the J protein serves. These results clearly support the hypothesis that the first few mutations in the evolving virus populations improved their ability to infect cells via the LamB receptor.
Natural selection did its thing, in other words, discovering mutations that provided an advantage to the viruses. Some of the resulting viruses—those with certain combinations of three mutations—just happened to be poised in the space of possible genotypes such that a fourth mutation gave them the new capacity to use OmpF.
Now let's step back and think about what this case says about the validity of the arguments that Behe has made in his three books.
Anybody remember Behe's first book, Darwin's Black Box, published in 1996? There, Behe claimed evolution doesn't work because biological systems exhibit so-called "irreducible complexity," which he defined as "… a single system composed of several well-matched, interacting parts that contribute to the basic function, wherein the removal of any one of the parts causes the system to effectively cease functioning." Evolution can't explain these functions, according to Behe, because you need everything in place for the system to work. Strike one! Lambda's J protein required several well-matched, interacting amino acids to enable infection via the host's OmpF receptor. Removing any one of them leaves the virus unable to perform that function. (Alas, Behe's argument wasn't merely mistaken, it also wasn't new—since Darwin, and as explained in increasing detail by later biologists, we've known that new functions evolve by coopting and modifying genes, proteins, and other structures that previously served one function to perform a new function.)
The Edge of Evolution, Behe's second book, claimed that evolution has a hard time making multiple constructive changes, implying the odds are heavily stacked against this occurring. Strike two!! Lambda required four constructive changes to gain the ability to use OmpF, yet dozens of populations in tiny flasks managed to do this in just a few weeks. That's because the intermediate steps were strongly beneficial to the virus, so that each step along the way proceeded far faster than by random mutation alone.
Darwin Devolves says that adaptive evolution can occur, but that it does so overwhelmingly by breaking things. Strike three!!! The viruses that can enter the bacterial cells via the OmpF receptor are not broken. They are still able to infect via the LamB receptor and, in fact, they're better at doing so then their ancestors in the new environment. (In his blog post after our paper was published in Science, Behe used the same sleight of hand he used to downplay the evolution of the new ability to use citrate in one LTEE population. That is, Behe called lambda's new ability to infect via the OmpF receptor a modification of function, instead of a gain of function, based on his peculiar definition, whereby a gain of function is claimed to occur only if an entirely new gene "poofs" into existence. However, that's not the definition of gain-of-function that biologists use, which (as the term implies) means that a new function has arisen. That standard definition aligns with how evolution coopts existing genes, proteins, and other structures to perform new functions. Behe's peculiar definition is a blatant example of "moving the goalposts" to claim victory.)
As Nathan Lents, Joshua Swamidass, and I wrote in our book review, "Ultimately, Darwin Devolves fails to challenge modern evolutionary science because, once again, Behe does not fully engage with it. He misrepresents theory and avoids evidence that challenges him."
If you've followed the logic and evidence in the three systems I've written about—polar bears adapting to a new diet, bacteria fine-tuning and even evolving new functions as they adapt to laboratory conditions, and viruses evolving a new port of entry into their hosts—you'll understand why Behe's arguments against evolution aren't taken seriously by the vast majority of biologists. As for Behe's arguments for intelligent design, they rest on his incredulity about what evolution is able to achieve, and they make no testable predictions about how the designer intervenes in the evolutionary process.
[The images below show infection assays for 4 lambda genotypes on 2 E. coli strains. The dark circles are "plaques"—areas in a dense lawn of bacteria where the cells have been killed by the virus. The viruses (labeled at bottom) include the ancestral lambda virus and 3 evolved genotypes. One bacterial strain expresses the LamB receptor (top row), while the other lacks the gene that encodes LamB (bottom row). All 4 viruses can infect the cells that produce LamB, but only the "EvoC" virus is able to infect the cells without that receptor. Images from Meyer et al., 2012, Science paper.]
Tagged as Alita Burmeister, beneficial mutations, book reviews, Charles Ofria, Chris Adami, cooption, epistasis, evidence, experimental evolution, gain of function, genetics, intelligent design creationism, Joshua Swamidass, Justin Meyer, lambda, logic, Michael Behe, mutation, Nathan Lents, phage, receptors, Rees Kassen, Rob Pennock, science, science and religion, science communication, testable hypotheses, viruses
On damaged genes and polar bears
Michael Behe has a new book called Darwin Devolves, published by HarperOne. Nathan Lents, Joshua Swamidass, and I wrote a review of that book for the journal Science. (You can find an open-access version of our review here.) As our review says (in agreement with Behe), there are many examples of evolution in which genes and their functions have been degraded, sometimes yielding an advantage to the organism. Unfortunately, though, Behe largely ignores the ways that evolution generates new functions and thereby produces complexity. That's a severe problem because Behe uses the evidence for the ease of gene degradation to support his overarching implication that our current understanding of the mechanisms of evolution is inadequate and, consequently, the field of evolutionary biology has a "big problem" and is therefore in scientific trouble.
I hope to accomplish several things in a series of posts. (I initially planned to write three posts, but it will now be more than that, as I delve deeper into several issues.) In my first post, I explained why Behe's so-called "first rule of adaptive evolution" does not imply what he says it does about evolution writ large. In summarizing, I wrote that Behe is right that mutations that break or blunt a gene can be adaptive. And he's right that, when such mutations are adaptive, they are easy to come by. But Behe is wrong when he implies these facts present a problem, because his thesis confuses frequencies over the short run with lasting impacts over the long haul of evolution.
In this post, I take a closer look at Behe's "rule" and how one might decide whether or not a particular mutation is damaging to a particular gene in a particular context. I'll then describe and discuss the example that Behe chose to illustrate his argument at the outset of his book, calling attention to the fact that his inferences were indirect, and as a result a key conclusion was quite possibly wrong. [These issues came to my attention based on work by Nathan Lents, Art Hunt and Joshua Swamidass. They voiced concerns about this example on their own blogs, here and here. I've now done my own reading, and in this post I attempt to provide just a tiny bit of important technical background before addressing the main concern, as I see it.]
II-A. How does one know if a mutation has damaged a gene?
Behe's first rule of adaptive evolution says this: "Break or blunt any functional gene whose loss would increase the number of a species' offspring." Every biologist knows that many mutations break or reduce the functionality of genes and the products they encode. Every biologist also realizes that this can sometime increase an organism's fitness (i.e., its survival and reproductive success), in particular when two conditions are met. First, the function has to be one that is not—or rather, no longer—useful to the organism. For example, eyes are no longer useful to an organism whose ancestors lived above ground, but which itself now lives in perpetual darkness in a cave. Second, there must be a meaningful cost to the organism (again, in the currency of fitness) of having the functional form of the gene, and that cost must be reduced or eliminated for the mutated version of the gene. This second point means that mutations that break or blunt a particular gene—even one that is useless—are not necessarily advantageous; they might instead be selectively neutral, such as when an encoded protein is still expressed but, for example, has diminished activity on a substrate that isn't even present. Therefore, compelling evidence for a broken or blunted gene in a particular lineage suggests that the gene's function is under what evolutionary biologists call "relaxed" selection—relaxed because some capability that was useful during the history of a lineage is no longer important under the organisms' present circumstances. However, that does not mean that the loss or diminution of the capability necessarily provided any advantage; instead, the gene could have decayed by the random fixation of mutations that were entirely inconsequential for fitness.
Two very important issues center on (i) how an observer can tell whether a particular mutation breaks or blunts a gene; and (ii) how that observer can determine whether the resulting mutation is advantageous. In short, neither inference is ironclad without an in-depth case-by-case investigation, although there are shortcuts that biologists often take because they make sense and are often sound, provided one takes care to understand the potential limitations of the inference. To characterize the biochemical consequences of a mutation, for example, the gold standard would be to perform detailed analyses of the activities of proteins encoded by different forms (alleles) of the same gene. That's difficult, technical work.
But as I said, there are shortcuts that allow scientists to draw reasonable inferences in some cases. For example, a mutation that generates a premature stop codon (a so-called "nonsense" mutation) usually eliminates the encoded protein's function. However, there are exceptions, such as when the premature stop is very near the end of the gene. It's also possible that a truncated protein might even have some new activity and function, or that it might accumulate additional mutations that produce a new activity. That's unlikely in any one case, but a lot of unlikely things can happen over the vast scales of space and time over which evolution has operated. As the Nobel laureate François Jacob famously wrote years ago, "natural selection does not work as an engineer works. It works like a tinkerer—a tinkerer who does not know exactly what he is going to produce but uses whatever he finds around him whether it be pieces of string, fragments of wood, or old cardboards; in short, it works like a tinkerer who uses everything at his disposal to produce some kind of workable object."
At the other end of the spectrum with respect to inferred functionality, some mutations change the DNA sequence of a gene, but they have no affect on the resulting amino-acid sequence of a protein. That happens because the genetic code is redundant, with multiple codons for the same amino acid. Such mutations are called "synonymous" and they are generally presumed to be neutral precisely because they don't change a protein. Once again, however, there are some exceptions to this usually reliable inference; a synonymous mutation could affect, for example, the rate at which the protein is produced and even its propensity to fold into a specific conformation.
In the middle ground between these (usually) clear-cut extremes are the cases where a mutation produces an amino-acid substitution in the encoded protein. Does that mutation change the protein's activity? If it does, is it necessarily damaging to the protein and/or to the organism with that altered protein? Biochemical and structural studies of proteins have shed light on this issue by identifying so-called "active sites" of many proteins—positions in the structure of a protein molecule where it interacts with a substrate and facilitates a chemical reaction. Mutations in and around active sites are more likely to affect a protein's activity than ones that are far away. Also, even at the same site in a protein, different mutations are likely to have more pronounced affects on the protein's activity, depending on whether the substitution affects the charge and/or size of the amino acid at that site.
Computational biologists have developed tools that take into account these types of information, which can be used to draw tentative inferences or make predictions about the likely effect of a specific mutation. Not surprisingly, one application is for understanding possible health effects of genetic variation in humans. For example, are certain variants in some gene likely to affect an individual's susceptibility to cardiovascular disease?
One such tool is called PolyPhen-2. The website says: "PolyPhen-2 (Polymorphism Phenotyping v2) is a software tool which predicts possible impact of amino acid substitutions on the structure and function of a human proteins using straightforward physical and comparative considerations." In addition to using structural information described above, it also uses information on whether a given site is highly conserved (little or no variation) or quite variable across humans and related species for which we have information. Why does it use that information? In essence, the program assumes that evolution has optimized a given protein's activity for whatever it does in humans, related species, and our common ancestors. If a particular site in a protein varies a lot, according to that implicit assumption, the variants probably aren't harmful because, well, if they were, then those lineages would have died out. If a site is hardly variable at all, by contrast, it's presumably because mutants at those sites damaged the protein's important function and led to the demise of those unfortunate lineages.
All that makes a lot of good sense … provided the protein of interest is performing the same function, and with the same optimal activities, in everybody and every species used in the analysis. Let's look now at a specific case that Behe chose to highlight in his book.
II-B. The APOB gene in polar bears
Behe sets the stage for his rule—"break or blunt any functional gene whose loss would increase the number of a species' offspring"—by summarizing the results of a study by Shiping Liu and coauthors that compared the genomes of polar bears and brown bears. Their paper examined mutations that distinguish these two species. The authors identified a set of mutations that had accumulated along the branch leading to modern polar bears, and in a manner that was consistent with those changes having been beneficial to the polar bears. One of the mutated genes, which was discussed in some detail both by the paper's authors and by Behe, is called APOB. As Liu et al. wrote (p. 789), the APOB gene encodes ApoB, "the primary lipid-binding protein of chylomicrons and low-density lipoproteins (LDL) … LDL cholesterol is a major risk factor for heart disease and is also known as 'bad cholesterol.' ApoB enables the transport of fat molecules in blood plasma and lymph and acts as a ligand for LDL receptors, facilitating the movement of molecules such as cholesterol into cells … The extreme signal of APOB selection implies an important role for this protein in the physiological adaptations of the polar bear."
As part of their study, Liu et al. analyzed the polar-bear version of the APOB gene using the PolyPhen-2 computational tool described above. Roughly half the mutations in APOB were categorized by that program as "possibly damaging" or "probably damaging," and the rest were called "benign." Behe than concluded that some of the mutations had damaged the protein's function, and that these mutations were beneficial in the environment where the polar bear now lives. In other words, Behe took this output as strong support for his rule.
So what's the problem? The PolyPhen-2 program, as I explained, is designed to identify mutations that are likely to affect a protein's structure and therefore its function. It assumes such mutations damage (rather than improve) a protein's function because structurally similar mutations are rare in humans and other species used for comparison. It does so because it presumes that natural selection has optimized the protein to perform a specific function that is the same in all cases, so that changes must be either benign or damaging to the protein's function. In fact, the only possible categorical outputs of the program are benign, possibly damaging, and probably damaging. The program simply cannot detect or suggest that a protein might have some improved activity or altered function.
The authors of the paper recognized these limiting assumptions and their implications for the evolution of polar bears. In fact, they specifically interpreted the APOB mutations as follows (p. 789): "… we find nine fixed missense mutations in the polar bear … Five of the nine cluster within the N-terminal βα1 domain of the APOB gene, although the region comprises only 22% of the protein … This domain encodes the surface region and contains the majority of functional domains for lipid transport. We suggest that the shift to a diet consisting predominantly of fatty acids in polar bears induced adaptive changes in APOB, which enabled the species to cope with high fatty acid intake by contributing to the effective clearance of cholesterol from the blood." In a news piece about this research, one of the paper's authors, Rasmus Nielsen, said: "The APOB variant in polar bears must be to do with the transport and storage of cholesterol … Perhaps it makes the process more efficient." In other words, these mutations may not have damaged the protein at all, but quite possibly improved one of its activities, namely the clearance of cholesterol from the blood of a species that subsists on an extremely high-fat diet.
It appears Behe either overlooked or ignored the authors' interpretation. Determining whether those authors or Behe are right would require in-depth studies of the biochemical properties of the protein variants, their activities in the polar bear circulatory stream, and their consequences for survival and reproductive success on the bear's natural diet. That's a tall order, and we're unlikely to see such studies because of the technical and logistical challenges. The point is that many proteins, including ApoB, are complex entities that have multiple biochemical activities (ApoB binds multiple lipids), the level and importance of which may depend on both intrinsic (different tissues) and environmental (dietary) contexts. In this example, Behe seems to have been too eager and even determined to describe mutations as damaging a gene, even when the evidence suggests an alternative explanation.
[The picture below shows a polar bear feeding on a seal. It was posted on Wikipedia by AWeith, and it is shown here under the indicated Creative Commons license.]
Tagged as beneficial mutations, book reviews, comparative biology, genomics, Joshua Swamidass, Michael Behe, missense mutations, Nathan Lents, natural selection, polar bears, protein structure, Rasmus Nielsen, science, science and religion, science communication, sequence conservation, time
February 18, 2019 · 12:59 pm
Reply to Michael Behe's gentle comment
Michael Behe posted a kind, brief comment on my previous post. As I began to write my reply, I realized his comment and my reply would interest many readers, and hence this separate post.
Here is his comment, and my reply follows.
Good day, Mike (if I may): Thank you for your kind words. I do appreciate the fact that you remain upbeat about my lab's research, and much other work that you describe in your writings, even though I disagree with the "big picture" that you take from the evolution literature.
I find it interesting and personally enjoyable (despite some frustrations as well) that evolution remains such a "hot" topic. That's true scientifically, with many extraordinary discoveries in recent years—from fossils like Tiktaalik and Archaeopteryx [edit: this one was discovered long ago, but it's better understood now] to the DNA-based evidence that Denisovans and Neanderthals contributed to the genomes of many of us living today. It's also the case that evolution remains "hot" for many non-scientists, and that's wonderful. Whether for secular or religious reasons, we humans are deeply interested in where we came from and how we came about. In my own small way, I take pleasure in knowing that my lab's research helps people get a glimpse of how evolution works.
I'm concerned, though, when these scientific and religious perspectives get intertwined and confused, even when they concern those big, important questions that interest all of us. I get even more concerned when I see what I regard as non-scientific ideas (such as "intelligent agents" introducing "purposeful design" by unstated and untestable means) being used to undermine the admittedly imperfect (and always subject to revision) understanding of evolution that science provides to those who want to learn. And I am most disturbed when these confusions appear to be part of a deliberate "wedge" strategy with ulterior sociopolitical motives. People will undoubtedly have diverse views about whether scientific explanations are adequate and/or satisfying ways to understand the world, but I see danger in trying to undermine scientific methodology and reasoning to advance religious beliefs and political goals.
Tagged as book reviews, disagreement, education, evolution, fossils, genomics, Humanity, LTEE, Michael Behe, science, science and religion, wedge strategy
Michael Behe has a new book coming out this month called Darwin Devolves. Nathan Lents, Joshua Swamidass, and I wrote a review of that book for the journal Science. (You can also find an open-access copy of our review here.) It provides an overview of the problems we see with his thesis and interpretations. As our review states, Behe points to many examples of evolution in which genes and their functions have been degraded, but he largely ignores the ways that evolution generates new functions and thereby produces complexity. That's a severe problem because Behe uses the evidence for the ease of gene degradation to support his overarching implication that the current scientific understanding of the mechanisms of evolution is inadequate and, consequently, the field of evolutionary biology has a "big problem."
I won't attempt to summarize Behe's entire book nor our short review, as people can read those for themselves if they want. Instead, I hope to accomplish three things in this post and two more that will follow. In this first post, I explain why Behe's so-called "first rule of adaptive evolution" does not imply what he says it does about evolution writ large. In the second post, I'll discuss whether my long-term evolution experiment (the LTEE for short) does or doesn't provide strong support for Behe's position in that regard. In my third post, I'll explain why I think that Behe's positions, taken as a whole, are scientifically untenable.
I. Behe's "First Rule of Adaptive Evolution" Confounds Frequency and Importance
Behe's latest book is centered around what he calls "The First Rule of Adaptive Evolution: Break or blunt any gene whose loss would increase the number of offspring." As he wrote in an immediate, dismissive response to our review: "The rule summarizes the fact that the overwhelming tendency of random mutation is to degrade genes, and that very often is helpful. Thus natural selection itself acts as a powerful de-volutionary force, increasing helpful broken and degraded genes in the population."
Let's work through these two sentences, because they concisely express the thrust of Behe's book. The first sentence regarding "the tendency of random mutation" is not too bad, though it is overly strong. I would tone it down as follows: "The tendency of random mutation is to degrade genes, and that is sometimes helpful." My reasons for these subtle changes are that: (i) many mutations are selectively neutral or so weakly deleterious as to be effectively invisible to natural selection; (ii) while loss-of-function mutations are sometimes helpful to the organism, I wouldn't say that's "very often" the case (though it may be in some systems, as I'll discuss in part II); and (iii) even those degradative mutations that are not helpful on their own sometimes persist and occasionally serve as "stepping stones" on the path toward new functionality. This last scenario is unlikely in any particular instance, but given the prevalence of degrading mutations it may nonetheless be important in evolution. (This scenario does not fit neatly within the old-fashioned caricature of Darwinian evolution as only proceeding by strictly adaptive mutations, but it is certainly part of modern evolutionary theory.)
Behe's next sentence then asserts the power of the "de-evolutionary" process of gene degradation. This is an unjustifiable extrapolation, yet it is central to Behe's latest book. (It's not the sort of error I would expect from anyone who is deeply engaged in an earnest effort to understand evolutionary science and present it to the public.) Yes, natural selection sometimes increases the frequency of broken and degraded genes in populations. But when it comes to the power of natural selection, what is most frequent versus most important can be very different things. What is most important in evolution, and in many other contexts, depends on timescales and the cumulative magnitude of effects. As a familiar example, some rhinoviruses are the most frequent source of viral infections in our lives (hence the expression "common cold"), but infections by HIV or Ebola, while less common, are far more consequential.
Or consider an investor who bought stocks in 100 different companies 25 years ago, of which 80 have been losers. Ouch? Maybe not! A stock can't lose more than the price that was paid for it, and so 20 winners can overcome 80 losers. Imagine if that investor had picked Apple, for example. That single stock has increased in value by well over 100-fold in that time, more than offsetting even 80 total wipeouts all by itself. (In fact, research on the stock market has shown the vast majority of long-term gains result from a small minority of companies that, like Apple, eventually become big winners.)
In the same vein, even if many more mutations destroy functions than produce new functions, the latter category has been far more consequential in the history of life. That is because a new function may enable a lineage to colonize a new habitat or realm, setting off what evolutionary biologists call an "adaptive radiation" that massively increases not only the numbers of organisms but, over time, the diversity of species and even higher taxa. As one example, consider Tiktaalik or some relative thereof, in any case a transitional kind of fish whose descendants colonized land and eventually gave rise to all of the terrestrial vertebrates—amphibian, reptiles, birds, and mammals. That lineage left far more eventual descendants (including ourselves), and was far more consequential for the history of life on Earth, than 100 other lineages that might have gained a transient advantage by degrading some gene and its function before eventually petering out.
Asteroid impacts aren't common either, but the dinosaurs (among other groups) sure felt the impact of one at the end of the Cretaceous. (There remains some debate about the cause of that mass extinction event, but whatever the cause its consequences were huge.) Luckily for us, though, some early mammals survived. Evolution often leads to dead ends, sometimes as a consequence of exogenous events like asteroids, and other times because adaptations that are useful under a narrow set of conditions (such as those caused by mutations that break or degrade genes) prove vulnerable over time to even subtle changes in the environment. It has been estimated that more than 99% of all species that have ever existed are now extinct. Yet here we are, on a planet that is home to millions of diverse species whose genomes record the history of life.
Summing up, Behe is right that mutations that break or blunt a gene can be adaptive. And he's right that, when such mutations are adaptive, they are easy to come by. But Behe is wrong when he implies these facts present a problem for evolutionary biology, because his thesis confuses frequencies over the short run with lasting impacts over the long haul of evolution.
[The picture below shows the Tiktaalik fossil discovered by Neil Shubin and colleagues. It was posted on Wikipedia by Eduard Solà, and it is shown here under the indicated Creative Commons license.]
Tagged as adaptation, adaptive radiations, beneficial mutations, book reviews, Charles Darwin, evolution, extinction, Joshua Swamidass, logic, Michael Behe, mutation, Nathan Lents, natural selection, science, science and religion, short- and long-term effects, stock market, Tiktaalik


Josh Groban recently completed a lengthy tour, which took him across North America and Europe at the end of 2018.
Production support company Clair Global assisted on the tour, run by production manager Zito.
"When I spoke to Clair account manager Todd Johnson, he assigned the tour contract to Britannia Row Productions who, I know from my own experience, have a long and deep association with L-Acoustic systems. From the moment we loaded into rehearsals back in October it became obvious that, while the concern was warranted, the crew was all over it.
"I judge the quality of a crew by how little I have to interreact with them! A great team knows what needs to be done and enacts the right plan.


text:
Santa Monica Developer Offers 23 Properties for Sale
By Jorge Casuso
December 23, 2020 -- Santa Monica's biggest residential developer will put 23 proposed projects totaling some 2,100 residential units for sale next month, a source familiar with the offering confirmed Wednesday.
If WSC (formerly WS Communities) finds a buyer for the properties -- all but two of which are entitled -- it would likely be the city's largest real estate deal in modern times, the source said.
Three WSC Projects on 5th Street (Courtesy WSC)
WSC, which is headed by Scott Walter, has amassed a portfolio of closely knit properties, most of them Downtown, bought by prominent Westside developr Neil Shekhter over the past 10 years.
The company has been navigating Santa Monica's onerous planning pipeline to got the entitlements needed to build the housing developments.
"Most of the properties are shovel-ready and construction can be completed in about two years," the source said.
Most of the entitled properties -- which total 1,632 units in more than 1 million square feet of residential space -- are closely connected and some pair affordable housing developments offsite, making a portfolio offering more practical, the source said.
The bulk of the properties are between 5th Street and Lincoln Boulevard and Colorado Avenue and Wilshire Boulevard, based on the "Future Projects" list on WSC's website.
Six of the properties offered in the portfolio are market-rate single room occupancy (SRO) developments totaling 361 "micro-units" that must be at least 220 square feet excluding the closet and bathroom.
They received the go ahead in June 2019 under a settlement agreement between the City and WSC that requires 15 percent of the units be affordable to persons earning 80 percent of the median income ("Market Rate SROs Get Go-ahead Under Settlement Agreement," July 1, 2019).
The portfolio also includes a 183-unit project at 3030 Nebraska Avenue, a 140-unit complex at 601 Colorado Avenue, a 134-unit building at 1415 5th Street and 100-unit buildings at 1430 Lincoln Boulevard and 1543 7th Street.
A Walker & Dunlop team headed by Blake Rogers is handling the sale.
According to The Real Deal, an LA real estate news site, Rogers teased the sale on Tuesday morning.
"The Santa Monica Collection: A 2,113 Unit Generational Development Opportunity in Downtown Santa Monica," Rogers wrote.
A price has not been provided for the portfolio, which will be listed next month, according to The Real Deal.
The website notes that the portfolio "is set to hit the market at a time when L.A. County multifamily deals have plummeted."
Still, a deal would dwarf the 1999 sale of Santa Monica Shores, the 17-story, 532-unit rent-controlled complex facing the beach in Ocean Park.
That deal was considered perhaps the largest real estate transaction in Santa Monica history ("Ocean Park Beach Front Towers Sell for $95 million," May 15, 1999).
The announced sale comes one week after WSC and NMS filed a lawsuit in federal court challenging the City's new restrictions on residential leases ("Apartment Owners Sue City Over Leasing Requirements," December 16, 2020).
The plaintiffs -- which together own the 32 apartment buildings and proposed projects included in the lawsuit -- contend that the ordinance upends their business model.


Susan and I are excited to be leading the NC State Delegation to Hong Kong, China and South Korea. The connections we build abroad strengthen the NC State community and enhance our effectiveness as a university. The delegation plans to engage alumni, corporate leaders and university officials to develop partnerships that expand the impact of an NC State education. Global awareness, as incorporated in goal five of the strategic plan, reinforces the student and faculty experience we cultivate on campus — an experience enhanced by the importance of civic and global knowledge, real-world experience and multiple perspectives. With more than 32 partner institutions and 44 different Memorandums of Understanding, NC State's collaborative efforts in China and South Korea are imperative to meeting our strategic goals.
On this trip, we will meet with leaders of partner institutions and explore platforms for broadening engagement. Through more than 65 established programs in 10 Asian countries, our students and faculty engage in global experiences and partnerships that provide exchange, educational and research opportunities in a variety of disciplines from genomics and biotechnology to entrepreneurship and mechanical engineering design. But we must expand those connections to reflect the growing interests of a global society.
Additionally, we will meet with alumni, who are eager to reconnect with their alma mater, and industry leaders, who are interested in textiles and the global supply chain, a very pertinent connection for NC State. We also will visit global corporate leaders such as Samsung to build partnerships that bring international employment to our graduates. As a research-intensive, service-oriented institution of academic excellence, it is crucial we dedicate time and energy to cultivating these mutually beneficial global relationships — relationships that provide NC State students and faculty opportunities for success beyond campus coordinates.
NC State faculty engage with international students in the classroom and laboratory.
But the results are not limited to our presence on our sister continent to the east. At home, we benefit from the presence of international students on campus and currently have more than 700 from China alone. Many of these students are from universities we will visit. Like NC State, these universities are national leaders; and these collaborations utilize the strengths of NC State to foster economic development on a world-wide scale.
New forms and speeds of communication have brought us closer than ever to our neighbors overseas. We are linked economically in a way that requires a delicate balance to maintain the prosperity of all. But at the base of our connection lies our desire to create opportunity through innovation and education. The flow of knowledge and understanding between universities benefits all parties. So wish us bon voyage, Wolfpack, or more appropriately, 一路平安, as we embark on this important journey for NC State. As always, Susan and I are honored and excited to represent the Wolfpack family locally, nationally and internationally.


text:
Q: Protobuf-net serialization/deserialization I checked but seem to be unable to see how to directly serialize a class to a byte array and subsequently deserialize from a byte array using Marc Gravell's protobuf-net implementation.
Edit: I changed the question and provided code because the original question of how to serialize into byte[] without having to go through stream was admittedly trivial. My apologies.
Updated Question: Is there any way to not have to deal with generics and instead infer the type of the property "MessageBody" through reflection when it is passed through the constructor? I assume I cannot serialize object type, correct? The current solution looks very cumbersome in that I need to pass in the type of the MessageBody each time I instantiate a new Message. Is there a sleeker solution to this?
I came up with the following:
class Program
{
    static void Main(string[] args)
    {
        Message<string> msg = new Message<string>("Producer", "Consumer", "Test Message");

        byte[] byteArray = msg.Serialize();
        Message<string> message = Message<string>.Deserialize(byteArray);

        Console.WriteLine("Output");
        Console.WriteLine(message.From);
        Console.WriteLine(message.To);
        Console.WriteLine(message.MessageBody);

        Console.ReadLine();

    }
}

[ProtoContract]
public class Message<T>
{
    [ProtoMember(1)]
    public string From { get; private set; }
    [ProtoMember(2)]
    public string To { get; private set; }
    [ProtoMember(3)]
    public T MessageBody { get; private set; }

    public Message()
    {

    }

    public Message(string from, string to, T messageBody)
    {
        this.From = from;
        this.To = to;
        this.MessageBody = messageBody;
    }

    public byte[] Serialize()
    {
        byte[] msgOut;

        using (var stream = new MemoryStream())
        {
            Serializer.Serialize(stream, this);
            msgOut = stream.GetBuffer();
        }

        return msgOut;
    }

    public static Message<T> Deserialize(byte[] message)
    {
        Message<T> msgOut;

        using (var stream = new MemoryStream(message))
        {
            msgOut = Serializer.Deserialize<Message<T>>(stream);
        }

        return msgOut;
    }
}

What I like to get to is something such as:
Message newMsg = new Message("Producer", "Consumer", Foo);
byte[] byteArray = newMsg.Serialize();
and
Message msg  = Message.Deserialize(byteArray);
(where Deserialize is a static method and it always deserializes into an object of type Message and only needs to know what type to deserialize the message body into).

A: The code the OP posted wouldn't quite work for me, the following is a slight adaptation taking onboard a little more of Marc Gravell's suggestions. Inheriting from Message was needed to prevent "Cyclic inheritance is not allowed", and as noted in the code comments below GetBuffer wasn't working out either.
Hoping it helps someone else, took me a good few hours to get it all to work...

      [ProtoContract]
      public abstract class Message
      {
        public byte[] Serialize()
        {
          byte[] result;
          using (var stream = new MemoryStream())
          {
            Serializer.Serialize(stream, this);
            result = stream.ToArray(); //GetBuffer was giving me a Protobuf.ProtoException of "Invalid field in source data: 0" when deserializing
          }
          return result;
        }
      }

      [ProtoContract]
      public class Message : Message
      {
        [ProtoMember(1)]
        public string From { get; private set; }
        [ProtoMember(2)]
        public string To { get; private set; }
        [ProtoMember(3)]
        public T MessageBody { get; private set; }

        public Message()
        { }

        public Message(string from, string to, T messageBody)
        {
          this.From = from;
          this.To = to;
          this.MessageBody = messageBody;
        }

        public static Message Deserialize(byte[] message)
        {
          Message result;
          using (var stream = new MemoryStream(message))
          {
            result = Serializer.Deserialize>(stream);
          }
          return result;
        }
      }

A: there's a few different questions here, so I'll answer what I can see: if I've missed anything just let me know.
Firstly, as noted, a MemoryStream is the most common way of getting to a byte[]. This is consistent with most serializers - for example, XmlSerializer, BinaryFormatter and DataContractSerializer also don't have an "as a byte[] overload", but will accept MemoryStream.
Generics: you don't need to use generics; v1 has Serializer.NonGeneric, which wraps this away from you. In v2, the "core" is non-generic, and can be accessed via RuntimeTypeModel.Default; of course Serializer and Serializer.NonGeneric continue to work.
For the issue of having to include the type: yes, the protobuf spec assumes the receiver knows what type of data they are being given. A simple option here is to use a simple wrapper object as the "root" object, with multiple typed properties for the data (only one of which is non-null). Another option might spring from the inbuilt inheritance support via ProtoInclude (note: as an implementation detail, these two approaches are identical).
In your specific example, perhaps consider:
[ProtoContract]
[ProtoInclude(1, typeof(Message<Foo>))]
.... More as needed
[ProtoInclude(8, typeof(Message<Bar>))]
public abstract class Message
{   }
[ProtoContract]
public class Message<T> : Message
{
    ...
}

Then just serialize with <Message> - the API will create the right type automatically.
With recent builds, there is also a DynamicType option that includes type data for you, for example:
[ProtoContract]
public class MyRoot {
    [ProtoMember(1, DynamicType=true)]
    public object Value { get; set; }
}

This will work for any Value that holds a contract-type instance (but not for primitives, and ideally not involving inheritance).

A: I also found that if using a .PROTO file (.cs compiled/generated with Google.Protobuf and Google.Protobuf.Tools packages), you'll use the record.WriteTo function in the serializer in and the static Parser.ParseFrom function in your Deserializer.
using Confluent.Kafka;
using System;
using System.IO;
using CodedOutputStream = Google.Protobuf.CodedOutputStream;
using SerializationContext = Confluent.Kafka.SerializationContext;

public class KafkaSerializer: ISerializer<Message>
{
    public byte[] Serialize(Message record, SerializationContext context)
    {
        using (var stream = new MemoryStream())
        {
            using (var codedStream = new CodedOutputStream(stream))
            {
                record.WriteTo(codedStream);
                codedStream.Flush();
                return stream.ToArray();
            }
        }
    }
}

public class KafkaDeserializer : IDeserializer<Message>
{
    public Message Deserialize(ReadOnlySpan<byte> data, bool isNull, SerializationContext context)
    {
        var msg = Message.Parser.ParseFrom(data);
        return msg;
    }
}