I guess because I run a highly ranked blog (that does not specialize in cars...) Ford decided I would be a good person to test drive a Lincoln MKS for a week. To give them credit they did not ask me to write about it, nor did they ask me about my cars or opinions about cars in general.
I've been avoiding writing about my experience because... well I knew it would be a long post and include more than a cursory review of the car.
The car they gave me was LOADED. The base price was $37,665, but the one I got was $45,255. It had all the optional equipment... The ultimate package (nav, double sunroof, etc...etc..etc...oh and THX audio).
But first of course you need my history... because without it the review would not be much use to anyone.
My first car was a Chrysler 1985 LeBaron GTS (Turbo). It was loaded for its day which meant that the Turbo was just OK and it had an onboard computer that kept track of all the stats of my gas and mileage etc... it was cool for 1985. It was a nice red color and I have to say that one thing that Chrysler knows how to do is paint a car - it looked new until the day I sold it. Now back to reality - the paint job was the best part of the car by leaps and bounds. Every part of the Chrysler broke in the 4-5 years I owned it - multiple times. I'm not exaggerating... every part. The automatic window track would break every week on both sides. I had them fixed over 10 times and eventually gave up and never opened them. The radio had to be replaced several times. The AC stopped working just in time for the windows to break in the up position. The steering had a problem multiple times. Even the open and close containers to hold my stuff would break. I had my radiator re-dipped twice because of leaks (which didn't seem to help). Then one day I was driving down the street and the bolt that held the drivers seat broke and I found myself in the back seat trying to stop the car without killing myself. To say that EVERY part broke on this car is a gross under-exaggeration. I cannot remember every single thing but if you name a part on the car it had problems. Oh, and it burned oil so I had to constantly re-fill it. Yes it was under warranty... but it spent a HUGE amount of time at the dealers and they were totally unable to fix anything permanently. Not to mention they were rude and just plain didn't care. I had one episode where the engine was sputtering constantly and dying at lights and I took it in and they could not re-produce the problem. After taking it in for the third time I left it running and got the manager outside (while the car was running) and we yelled at each other about it until of course the car decided to make my point for me. The final straw was the grey smoke that filled a courtyard from the tailpipe. It was out of warranty and that point and I took it to a service station who couldn’t tell me why it happened but it had stopped...so I took it as quickly as I could and traded it in to Ford for a new Ford Probe.
Before I get to the Probe let me just say that my 5 year experience with Chrysler was so terrible that I will NEVER buy a Chrysler again. If they offered me one for free I'd take it and sell it. The horrible car plus the completely bad customer experience was such that they lost me for life. I don't care if they are someday ranked number one (unlikely considering the recent bankruptcy) I will never buy one again.
I got the Ford Probe because I was still a student and had only so much money - but I wanted something sportier than the LeBaron. My experience with the Ford Probe was not as bad as with Chrysler. It didn't break all the time - but when it did I do have to say that I had a similar customer experience - they just sucked and didn't care. The dealerships were filthy and old and the people there were glassy eyed and just went about their day. The Probe was an OK car for about 4 years and then things started to break that were expensive and it started making noises that Ford couldn’t fix (buzzing, vibrating... basically the car was made out of plastic molding). I can't recall if I was engaged or married at the time but we decided to upgrade to a foreign car at this point.
I sold the Probe and moved up to my first foreign car - the Lexus ES300. Yes it was the low end model - but it was fantastic. The only fault we found in our entire time with the car was the two tone color on the outside (grey on the bottom white everywhere else... yuck). The car never had any major problems and spent little time at the shop. When we did go to the dealer we were treated like gold. They took us into a nice room and asked us what was wrong and made sure they had it completely correct. Then before giving the car back the service manager would drive it and make sure the problem was solved. The dealership was clean and comfortable and everyone there couldn't have been more helpful. It was like I had entered paradise after being stuck on an island called American cars for my entire life. (and they washed it every time)
Eventually we added our second car and it was the Lexus RX300 (which was my car - my wife kept the ES300). I LOVED it and Lexus continued with their great service and the car never had a problem.
Of course as you can expect after my experiences with cars at this point THERE WAS NO WAY IN HELL I WAS EVERY GOING TO BUY AN AMERICAN CAR AGAIN IN MY LIFE.
Well, then something happened that made me give up my beloved Lexus RX300... children were born - twins. So suddenly I woke up one day to find baby seats in the back of my RX300... (seriously - I had no idea it was coming) and I found out it was no longer mine... my wife had taken it over.
This worked out OK though... because I was nearing 40 years old and there
was no way I was taking her two tone car after all this time... so I traded her
car in and bought the car I always wanted when I was a teenager... which by
luck had JUST come out... the Nissan350Z Roadster. I went there and
bought it the first week they were out - I think I got one of the first 200 in
Of course being a man I really had no idea of what it meant to have twins... no less a girl and a boy... it meant that when they reached 4-5 years old we needed two cars that could handle them... and my Z was a two seater that couldn't handle a child. This meant I had to sell my Z and get a sedan (gasp!).
Oh, and I forgot - my wife had traded the RX300 in fairly quickly to get a
Toyota Minivan, so we had the
Back to my problem. I had to pick a sedan that I wanted but I didn't want to spend a ton on one. I ended up doing a TON of research and found that I loved the look of the Nissan Altima (post 2007 model). There was a problem though - I wanted the car loaded - I wanted the 3.5 v6 engine that my Z had, the Nav , the Sports Package, and the sound system... basically every option that I could have. To get that new would have cost me about32k and I had sold the Z for about 23k. What was I to do? Well I did something brand new to me and looked for a USED Altima with those specs. It took me a long time looking through EBAY, Craigslist, AutoTrader and every other possible place. Oh and it had to be black...Now the problem is that 90% of all Altima's are 2.5 V4's. That left me with a VERY hard project to get ALL of the options plus BLACK and have the 3.5V6. Well I got lucky and found one in New Orleans with just 13,000 miles on it (2007) and owned by the son of an Acura dealer (so it was taken care of). I got it for about 23k and now have had it for two years and I LOVE it. It's not as fast as my Z of course because it weighs more and isn't made to be a sports car - but its close. It's all leather, NAV , Sports, Bose Stereo, etc... I was very happy needless to say. And I had the same good experience when I had to take it to the dealer (which was totally rare because the car had already been broken in). I have to say that I am completely satisfied with the Altima and it's sitting outside my window as we speak.
So out of nowhere I get this email offering to let me test drive either some
boxy new minivan or the high end Lincoln MKS... so I picked the
latter. My wife and I both made it our main car for the five days
they gave us. We put the booster seats in it and both drove it for the
entire 5 days. My wife’s first impression was that it drove like
butter. It was very smooth in turning and it took bumps and railroad
tracks like they weren't there. However after driving it for a few days
problems became apparent. The back window is very small - my wife says as
small as my350Z (very small). Further everything on the inside of the car
is thick - including seat belts which made it hard to view back and to the
side. The car was designed very poorly for viewing traffic.
Other thing was that when the car was turned off it didn’t require that it be
in park... which once let the car drift back until my wife realized what was
going on... another safety issue. The turning radius of the car was
horrible. But she did like the car. By chance both the Lincoln MKS
and my Altima were nearly clones as far as features went. Both were black
with the same exact features including NAV etc... so it was like comparing two
very similar cars. The difference was that the
My conclusion is that like my Chrysler the Lincoln threw in a bunch of WOW
features like THX, double sunroofs, a NAV system and then ignored what's most
important - the overall appearance of the car, the visibility when
driving, the comfort of the seats (I preferred my Altima seats), oh and by the
way - my Altima could fit three boosters in the back seat while the Lincoln
could only fit two. I found that my Altima was designed to death to work
for the customer from every angle - from my cup holders to everything else the
Altima rocks. The
We've been bailing out our American Car Companies every 10 years because
they simply don't get it. Here we are again with our car companies being
partially bailed out. Do you ever see Foreign car company needing money
from a government to exist? We need a huge overhaul of American Car
companies - fire the execs, hire some young people to do design and forget the
stupid branding - just make a good car. We can have
Until this happens and I see press about how great an American car is and how terrific the service is... I will remain one of those Americans who say "never again".
Good news! The inside of our noses where the Avian Flu would take hold are 32C, and in order for the Avian Flu to take hold our noses would have to be about the temperature of the gut of a bird - or 40C.
So unless there is a mutation - we are pretty much safe from the human to human spread of Avian Flu (or the start of a pandemic).
Want to know more? Here are some choice parts of the study I linked to above. Note that unless you're a scientist clicking on the link will give you a massive headache.
And before some of you nerdy hypersensitive dweebs cry fowl (get it, fowl?) that I copied directly from the study... This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. (Direct Link - http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000424)
Influenza type A viruses are endemic in aquatic birds but can cross the species barrier to infect the human respiratory tract. While transmission from birds to humans is rare, the introduction of novel avian influenza viruses into immunologically naïve human populations has significant pandemic potential. Avian influenza viruses are adapted for growth at 40°C, the temperature of the avian enteric tract. However, the human proximal airways, the likely site of initial inoculation by influenza viruses, are maintained at a cooler temperature (32°C), suggesting that zoonotic transmission may be limited by temperature differences between the two hosts. Using an in vitro model of human ciliated airway epithelium, we show that avian influenza viruses grow well at 37°C, a temperature reflective of distal airways, but are restricted for infection at 32°C. A panel of genetically manipulated human influenza viruses possessing avian or avian-like surface glycoproteins were also restricted at 32°C, but not 37°C, suggesting that avian virus glycoproteins are not adapted for efficient infection at the temperature of the proximal airways. Thus, avian influenza virus infection is restricted in the human proximal airways due to the cooler temperature of this region, thus limiting the likelihood of zoonotic and subsequent human-to-human transmission of these viruses.
Influenza viruses circulating in the human population are predominately type A and B, with type A being more common . All influenza type A viruses originate from aquatic birds and successful introduction of these avian viruses into the human population, by either direct adaptation or reassortment with already circulating human viruses, has led to influenza pandemics of historical significance (reviewed in –,). Still, documented evidence of transmission of avian influenza viruses directly from birds to humans is rare, partly because species barriers restrict avian influenza virus infection of the epithelial cells of the human respiratory tract, the primary site of influenza virus infection and spread.
Influenza A viruses possess a hemagglutinin (HA) attachment protein that binds sialic acid residues to facilitate infection of target epithelial cells. The HA of human influenza viruses preferentially binds to terminal sialic acid (SA) residues with α2,6 linkages, whereas avian influenza viruses preferentially bind to SA with α2,3 linkages –. The prevalence of α2,6 SA but paucity of α2,3 SA in the human respiratory tract has been considered to restrict infection by avian influenza viruses . Recent reports, however, have detected significant levels of α2,3 SA on human airway epithelium both in vitro and ex vivo, including in nasopharyngeal and tracheobronchial tissue –. This SA distribution also correlated with avian influenza virus infection in vitro and ex vivo and raised the possibility that avian viruses could infect the upper airways in vivo. Therefore, although it is universally accepted that human-to-human transmission of avian influenza viruses requires adaptation of HA to switch from α2,3 to α2,6 SA usage, the cumulative data published to date indicate that SA linkages and their respective distribution in the human airways are not the sole barrier to avian influenza virus infection –. Other host factors and viral genes are likely also important determinants of infectivity.
One such host factor that may limit zoonotic transmission is the difference in host temperatures between avian and human tissues that are susceptible to influenza virus infection. Avian influenza viruses are adapted for replication in the avian enteric tract at 40–41°C. While the surface temperatures of the human respiratory tract are variable, a temperature gradient clearly exists in which the surface temperature of the proximal large airways (i.e., nasal and tracheal) average 32+/−0.05°C while temperatures of the smaller, distal airways (i.e., bronchioles) are closer to that of the core body temperature, 37°C ,. While multiple transmission routes have been described for influenza viruses, the proximal airways likely represent a predominant site for human influenza virus inoculation as they provide a large exposed surface area of virus-susceptible epithelial cells . These cells are directly accessible by large droplet aerosols and by way of digital inoculation of the nasopharynx and conjunctival mucosa ,. Inefficient infection by avian influenza viruses, even in the presence of α2,3-linked SA, may be due to the cooler temperature of the proximal airways compared to that of the distal airways/lung regions where H5N1 avian influenza viruses appear to replicate efficiently .
Avian influenza viruses are attenuated at temperatures below 37°C and cold sensitivity of avian viral RNA replication in cell lines was linked to the presence of a glutamic acid at amino acid 627 in the avian virus polymerase subunit, PB2, instead of a lysine in the human virus PB2 . Lysine substitution at residue 627 of H5N1 viruses improved virus replication in mice . In addition to PB2, work utilizing human-avian reassortant viruses in MDCK cells provided initial evidence that avian glycoproteins, HA and neuraminidase (NA), may mediate temperature-dependent effects on viral growth . To our knowledge, other viral genes have not been well characterized, nor the HA and NA further evaluated, in their contribution to temperature sensitivity of avian influenza viruses.
To characterize the temperature dependency of avian vs. human influenza viruses in a relevant model of the target cell types of the human airways, we utilized an in vitro model of human ciliated airway epithelium (HAE). This model closely mimics the morphological and physiological features of the human airway epithelium in vivo and has been previously used to investigate infection by diverse respiratory viruses –. In humans, ciliated airway epithelium is present throughout the airways, extending from the nasal cavity and large proximal airways into the distal bronchiolar airway regions. Previously, we have shown that both human and avian influenza viruses replicate well in HAE and that human and avian influenza virus cell tropism correlates with the respective distribution of the specific sialic acid linkages . However, these previous studies were conducted at 37°C, reflecting conditions encountered in the distal airways . Others have also utilized these airway cell systems to characterize influenza virus replication of wild-type and recombinant viruses at 35°C ,,. In the present study, we utilize the HAE model, in combination with influenza virus reverse genetics, to investigate the influence of temperature on human and avian influenza virus infection, replication and spread. We demonstrate that, compared to human influenza viruses, avian influenza viruses are severely restricted for infection of human airway epithelium at the temperature of the human proximal airways. Then, using different strategies to ‘avianize’ human influenza viruses, we show that the temperature restriction of avian viruses is closely associated with the avian HA and NA glycoproteins.