We had everyone over for dinner last night. We went to mass, then my Dad made dinner for all of us. We came back to our house. And we had lots and lots of fun!
I'm starting to think, family is not just the people who are related by blood. My sister doesn't talk to my Dad or me. And I've never gotten to see my baby brother. My mom is not really a mom. It's hard to talk about that. But she just chose to not be a part of our family.
My only real family is my Dad and my abuelitas. We all live together. And I really do LOVE it! We're very close. And we all get along really well.
But I think family is about more people that love you. Like my Nana and Nono. My Nana is a lot like a mom to me. She is always here for me when I need her. She told me to call her whenever I need or want to talk. We have lots of friends who are really close. They're my tios and tias. All of their kids are close to me too.
Family is about people that love you. No matter what, they are always there for you. I like that. I like the family that we have made. It feels nice to have so many people around me that really do love me. They don't expect me to lie for them, or to give them money. They just love me, and I love them. :) C
Wednesday, April 14, 2010
How I Write
I thought I'd share some of the things I keep in mind when writing my posts. These are lessons I've learned through trial and error in the 18 months I've been blogging, and that I wish I'd been told when I started out.
In no particular order:
In no particular order:- Write little and often. I find that I'm most productive at the beginning and the end of a session of writing: in the middle, it's easy to lose steam and spend a long time doing very little. So I now generally write in regular short bursts (20 minutes or so). Each post will take as many bursts as it needs to be finished, which is usually 2 or 3, but sometimes more.
- Keep it brief. Two short posts are better than one long one, because a lot of people (e.g. me) just don't read long posts. At the moment, I aim for about 500 words per post with a maximum limit of 1,000 words. If that's not enough space, I'll split the ideas over multiple posts. This is easier to read, and I find it makes it easier to write too, once you get into the swing of it. Some might worry that this makes it impossible to express complex ideas, but I really don't think it does. You just need to express them clearly.
- Think, then write. You should know what you're going to write about before you start typing: it's hard to write and think at the same time. This is easier said than done, and often you'll think of new ideas while writing, so it's not an absolute rule. But you should know the major points you'll be making before writing.
- Don't start at the beginning. Don't write the first sentence first, spending ages reworking it until it's perfect, and only then move on to the second sentence. Write the basic skeleton first, no matter how badly it reads, and then tidy it up afterwards. It's a lot easier to do the tidying up once you know how it all fits together.
- If in doubt, leave it out. Some people would disagree with this, and it's ultimately a matter of personal style, but this is my rule: if I'm not sure how confident I am in something, or if I'm not sure it's interesting enough to bother with, I won't post it. If I'm not sure a paragraph is a good addition to a post, I'll cut it.
How I Write
I thought I'd share some of the things I keep in mind when writing my posts. These are lessons I've learned through trial and error in the 18 months I've been blogging, and that I wish I'd been told when I started out.
In no particular order:
In no particular order:- Write little and often. I find that I'm most productive at the beginning and the end of a session of writing: in the middle, it's easy to lose steam and spend a long time doing very little. So I now generally write in regular short bursts (20 minutes or so). Each post will take as many bursts as it needs to be finished, which is usually 2 or 3, but sometimes more.
- Keep it brief. Two short posts are better than one long one, because a lot of people (e.g. me) just don't read long posts. At the moment, I aim for about 500 words per post with a maximum limit of 1,000 words. If that's not enough space, I'll split the ideas over multiple posts. This is easier to read, and I find it makes it easier to write too, once you get into the swing of it. Some might worry that this makes it impossible to express complex ideas, but I really don't think it does. You just need to express them clearly.
- Think, then write. You should know what you're going to write about before you start typing: it's hard to write and think at the same time. This is easier said than done, and often you'll think of new ideas while writing, so it's not an absolute rule. But you should know the major points you'll be making before writing.
- Don't start at the beginning. Don't write the first sentence first, spending ages reworking it until it's perfect, and only then move on to the second sentence. Write the basic skeleton first, no matter how badly it reads, and then tidy it up afterwards. It's a lot easier to do the tidying up once you know how it all fits together.
- If in doubt, leave it out. Some people would disagree with this, and it's ultimately a matter of personal style, but this is my rule: if I'm not sure how confident I am in something, or if I'm not sure it's interesting enough to bother with, I won't post it. If I'm not sure a paragraph is a good addition to a post, I'll cut it.
Itchy Rash Outerthigh
Catwoman's cat Luna is now serving five years. Tri-
peciosos This kitten blue eyes, live in Blanes, Gerona. Share your life with the dog and human Llanca love it.
 |
| Photos: Catwoman |
Congratulations Luna and family.
Tuesday, April 13, 2010
The Hunt for the Prozac Gene
One of the difficulties doctors face when prescribing antidepressants is that they're unpredictable.
One person might do well on a certain drug, but the next person might get no benefit from the exact same pills. Finding the right drug for each patient is often a matter of trying different ones until one works.
So a genetic test to work out whether a certain drug will help a particular person would be really useful. Not to mention really profitable for whoever patented it. Three recent papers, published in three major journals, all claim to have found genes that predict antidepressant response. Great! The problem is, they were different genes.
First up, American team Binder et al looked at about 200 variants in 10 genes involved in the corticosteroid stress response pathway. They found one, in a gene called CRHBP, that was significantly associated with poor response to the popular SSRI antidepressant citalopram (Celexa), using the large STAR*D project data set. But this was only true of African-Americans and Latinos, not whites.
Garriock et al used the exact same dataset, but they did a genome-wide association study (GWAS), which looks at variants across the whole genome, unlike Binder et al who focussed on a small number of specific candidate genes. Sadly no variants were statistically significantly correlated with response to citalopram, although in a GWAS, the threshold for genome-wide significance is very high due to multiple comparisons correction. Some were close to being significant, but they weren't obviously related to CRHBP, and most weren't anything to do with the brain.
Uher et al did another GWAS of response to escitalopram and nortriptyline in a different sample, the European GENDEP study. Escitalopram is extremely similar to citalopram, the drug in the STAR*D studies; nortriptyline however is very different. They found one genome-wide significant hit. A variant in a gene called UST was associated with response to nortriptyline, but not escitalopram. No variants were associated with response to escitalopram, although one in the gene IL11 was close. There were some other nearly-significant results, but they didn't overlap with either of the STAR*D studies.
Finally, one of the STAR*D studies found a variant significantly linked to tolerability (side effects) of citalopram. GENDEP didn't look at this.
The UST link to nortriptyline finding is the strongest thing here, but for citalopram / escitalopram, no consistent pharmacogenetic results emerged at all. What does this mean? Well, it's possible that there just aren't any genes for citalopram response, but that seems unlikely. Even if you believe that antidepressants only work as placebos, you'd expect there would be genes that alter placebo responses, or at the very least, that affect side-effects and hence the active placebo improvement.
The thing is that the "antidepressant response" in these studies isn't really that: it's a mix of many factors. We know that a lot of the improvement would have happened even with placebo pills, so much of it isn't a pharmacological effect. There are probably genes associated with placebo improvement, but they might not be the same ones that are associated with drug improvement and a gene might even have opposite effects that cancel out (better drug effect, worse placebo effect). Some of the recorded improvement won't even be real improvement at all, just people saying they feel better because they know they're expected to.
If I were looking for the genes for SSRI response, not that I plan to, here's what I'd do. To stack the odds in my favour, I'd forget people with an moderate or partial response, and focus on those who either do really well, or those who get no benefit at all, with a certain drug. I'd also want to exclude people who respond really well, but not due to the specific effects of the drug.
That would be hard but one angle would be to only include people whose improvement is specifically reversed by acute tryptophan depletion, which reduces serotonin levels thus counteracting SSRIs. This would be a hard study to do, though not impossible. (In fact there are dozens of patients on record who meet my criteria, and their blood samples are probably still sitting in freezers in labs around the world... maybe someone should dig them out).
Still, even if you did find some genes that way, would they be useful? We'd have had to go to such lengths to find them, that they're not going to help doctors decide what to do with the average patient who comes through the door with depression. That's true, but they might just help us to work out who will respond to SSRIs, as opposed to other drugs.
Binder EB, Owens MJ, Liu W, Deveau TC, Rush AJ, Trivedi MH, Fava M, Bradley B, Ressler KJ, & Nemeroff CB (2010). Association of polymorphisms in genes regulating the corticotropin-releasing factor system with antidepressant treatment response. Archives of general psychiatry, 67 (4), 369-79 PMID: 20368512
Uher, R., Perroud, N., Ng, M., Hauser, J., Henigsberg, N., Maier, W., Mors, O., Placentino, A., Rietschel, M., Souery, D., Zagar, T., Czerski, P., Jerman, B., Larsen, E., Schulze, T., Zobel, A., Cohen-Woods, S., Pirlo, K., Butler, A., Muglia, P., Barnes, M., Lathrop, M., Farmer, A., Breen, G., Aitchison, K., Craig, I., Lewis, C., & McGuffin, P. (2010). Genome-Wide Pharmacogenetics of Antidepressant Response in the GENDEP Project American Journal of Psychiatry DOI: 10.1176/appi.ajp.2009.09070932
Garriock, H., Kraft, J., Shyn, S., Peters, E., Yokoyama, J., Jenkins, G., Reinalda, M., Slager, S., McGrath, P., & Hamilton, S. (2010). A Genomewide Association Study of Citalopram Response in Major Depressive Disorder Biological Psychiatry, 67 (2), 133-138 DOI: 10.1016/j.biopsych.2009.08.029
One person might do well on a certain drug, but the next person might get no benefit from the exact same pills. Finding the right drug for each patient is often a matter of trying different ones until one works.So a genetic test to work out whether a certain drug will help a particular person would be really useful. Not to mention really profitable for whoever patented it. Three recent papers, published in three major journals, all claim to have found genes that predict antidepressant response. Great! The problem is, they were different genes.
First up, American team Binder et al looked at about 200 variants in 10 genes involved in the corticosteroid stress response pathway. They found one, in a gene called CRHBP, that was significantly associated with poor response to the popular SSRI antidepressant citalopram (Celexa), using the large STAR*D project data set. But this was only true of African-Americans and Latinos, not whites.
Garriock et al used the exact same dataset, but they did a genome-wide association study (GWAS), which looks at variants across the whole genome, unlike Binder et al who focussed on a small number of specific candidate genes. Sadly no variants were statistically significantly correlated with response to citalopram, although in a GWAS, the threshold for genome-wide significance is very high due to multiple comparisons correction. Some were close to being significant, but they weren't obviously related to CRHBP, and most weren't anything to do with the brain.
Uher et al did another GWAS of response to escitalopram and nortriptyline in a different sample, the European GENDEP study. Escitalopram is extremely similar to citalopram, the drug in the STAR*D studies; nortriptyline however is very different. They found one genome-wide significant hit. A variant in a gene called UST was associated with response to nortriptyline, but not escitalopram. No variants were associated with response to escitalopram, although one in the gene IL11 was close. There were some other nearly-significant results, but they didn't overlap with either of the STAR*D studies.
Finally, one of the STAR*D studies found a variant significantly linked to tolerability (side effects) of citalopram. GENDEP didn't look at this.
*
The UST link to nortriptyline finding is the strongest thing here, but for citalopram / escitalopram, no consistent pharmacogenetic results emerged at all. What does this mean? Well, it's possible that there just aren't any genes for citalopram response, but that seems unlikely. Even if you believe that antidepressants only work as placebos, you'd expect there would be genes that alter placebo responses, or at the very least, that affect side-effects and hence the active placebo improvement.
The thing is that the "antidepressant response" in these studies isn't really that: it's a mix of many factors. We know that a lot of the improvement would have happened even with placebo pills, so much of it isn't a pharmacological effect. There are probably genes associated with placebo improvement, but they might not be the same ones that are associated with drug improvement and a gene might even have opposite effects that cancel out (better drug effect, worse placebo effect). Some of the recorded improvement won't even be real improvement at all, just people saying they feel better because they know they're expected to.
If I were looking for the genes for SSRI response, not that I plan to, here's what I'd do. To stack the odds in my favour, I'd forget people with an moderate or partial response, and focus on those who either do really well, or those who get no benefit at all, with a certain drug. I'd also want to exclude people who respond really well, but not due to the specific effects of the drug.
That would be hard but one angle would be to only include people whose improvement is specifically reversed by acute tryptophan depletion, which reduces serotonin levels thus counteracting SSRIs. This would be a hard study to do, though not impossible. (In fact there are dozens of patients on record who meet my criteria, and their blood samples are probably still sitting in freezers in labs around the world... maybe someone should dig them out).
Still, even if you did find some genes that way, would they be useful? We'd have had to go to such lengths to find them, that they're not going to help doctors decide what to do with the average patient who comes through the door with depression. That's true, but they might just help us to work out who will respond to SSRIs, as opposed to other drugs.
Binder EB, Owens MJ, Liu W, Deveau TC, Rush AJ, Trivedi MH, Fava M, Bradley B, Ressler KJ, & Nemeroff CB (2010). Association of polymorphisms in genes regulating the corticotropin-releasing factor system with antidepressant treatment response. Archives of general psychiatry, 67 (4), 369-79 PMID: 20368512Uher, R., Perroud, N., Ng, M., Hauser, J., Henigsberg, N., Maier, W., Mors, O., Placentino, A., Rietschel, M., Souery, D., Zagar, T., Czerski, P., Jerman, B., Larsen, E., Schulze, T., Zobel, A., Cohen-Woods, S., Pirlo, K., Butler, A., Muglia, P., Barnes, M., Lathrop, M., Farmer, A., Breen, G., Aitchison, K., Craig, I., Lewis, C., & McGuffin, P. (2010). Genome-Wide Pharmacogenetics of Antidepressant Response in the GENDEP Project American Journal of Psychiatry DOI: 10.1176/appi.ajp.2009.09070932
Garriock, H., Kraft, J., Shyn, S., Peters, E., Yokoyama, J., Jenkins, G., Reinalda, M., Slager, S., McGrath, P., & Hamilton, S. (2010). A Genomewide Association Study of Citalopram Response in Major Depressive Disorder Biological Psychiatry, 67 (2), 133-138 DOI: 10.1016/j.biopsych.2009.08.029
The Hunt for the Prozac Gene
One of the difficulties doctors face when prescribing antidepressants is that they're unpredictable.
One person might do well on a certain drug, but the next person might get no benefit from the exact same pills. Finding the right drug for each patient is often a matter of trying different ones until one works.
So a genetic test to work out whether a certain drug will help a particular person would be really useful. Not to mention really profitable for whoever patented it. Three recent papers, published in three major journals, all claim to have found genes that predict antidepressant response. Great! The problem is, they were different genes.
First up, American team Binder et al looked at about 200 variants in 10 genes involved in the corticosteroid stress response pathway. They found one, in a gene called CRHBP, that was significantly associated with poor response to the popular SSRI antidepressant citalopram (Celexa), using the large STAR*D project data set. But this was only true of African-Americans and Latinos, not whites.
Garriock et al used the exact same dataset, but they did a genome-wide association study (GWAS), which looks at variants across the whole genome, unlike Binder et al who focussed on a small number of specific candidate genes. Sadly no variants were statistically significantly correlated with response to citalopram, although in a GWAS, the threshold for genome-wide significance is very high due to multiple comparisons correction. Some were close to being significant, but they weren't obviously related to CRHBP, and most weren't anything to do with the brain.
Uher et al did another GWAS of response to escitalopram and nortriptyline in a different sample, the European GENDEP study. Escitalopram is extremely similar to citalopram, the drug in the STAR*D studies; nortriptyline however is very different. They found one genome-wide significant hit. A variant in a gene called UST was associated with response to nortriptyline, but not escitalopram. No variants were associated with response to escitalopram, although one in the gene IL11 was close. There were some other nearly-significant results, but they didn't overlap with either of the STAR*D studies.
Finally, one of the STAR*D studies found a variant significantly linked to tolerability (side effects) of citalopram. GENDEP didn't look at this.
The UST link to nortriptyline finding is the strongest thing here, but for citalopram / escitalopram, no consistent pharmacogenetic results emerged at all. What does this mean? Well, it's possible that there just aren't any genes for citalopram response, but that seems unlikely. Even if you believe that antidepressants only work as placebos, you'd expect there would be genes that alter placebo responses, or at the very least, that affect side-effects and hence the active placebo improvement.
The thing is that the "antidepressant response" in these studies isn't really that: it's a mix of many factors. We know that a lot of the improvement would have happened even with placebo pills, so much of it isn't a pharmacological effect. There are probably genes associated with placebo improvement, but they might not be the same ones that are associated with drug improvement and a gene might even have opposite effects that cancel out (better drug effect, worse placebo effect). Some of the recorded improvement won't even be real improvement at all, just people saying they feel better because they know they're expected to.
If I were looking for the genes for SSRI response, not that I plan to, here's what I'd do. To stack the odds in my favour, I'd forget people with an moderate or partial response, and focus on those who either do really well, or those who get no benefit at all, with a certain drug. I'd also want to exclude people who respond really well, but not due to the specific effects of the drug.
That would be hard but one angle would be to only include people whose improvement is specifically reversed by acute tryptophan depletion, which reduces serotonin levels thus counteracting SSRIs. This would be a hard study to do, though not impossible. (In fact there are dozens of patients on record who meet my criteria, and their blood samples are probably still sitting in freezers in labs around the world... maybe someone should dig them out).
Still, even if you did find some genes that way, would they be useful? We'd have had to go to such lengths to find them, that they're not going to help doctors decide what to do with the average patient who comes through the door with depression. That's true, but they might just help us to work out who will respond to SSRIs, as opposed to other drugs.
Binder EB, Owens MJ, Liu W, Deveau TC, Rush AJ, Trivedi MH, Fava M, Bradley B, Ressler KJ, & Nemeroff CB (2010). Association of polymorphisms in genes regulating the corticotropin-releasing factor system with antidepressant treatment response. Archives of general psychiatry, 67 (4), 369-79 PMID: 20368512
Uher, R., Perroud, N., Ng, M., Hauser, J., Henigsberg, N., Maier, W., Mors, O., Placentino, A., Rietschel, M., Souery, D., Zagar, T., Czerski, P., Jerman, B., Larsen, E., Schulze, T., Zobel, A., Cohen-Woods, S., Pirlo, K., Butler, A., Muglia, P., Barnes, M., Lathrop, M., Farmer, A., Breen, G., Aitchison, K., Craig, I., Lewis, C., & McGuffin, P. (2010). Genome-Wide Pharmacogenetics of Antidepressant Response in the GENDEP Project American Journal of Psychiatry DOI: 10.1176/appi.ajp.2009.09070932
Garriock, H., Kraft, J., Shyn, S., Peters, E., Yokoyama, J., Jenkins, G., Reinalda, M., Slager, S., McGrath, P., & Hamilton, S. (2010). A Genomewide Association Study of Citalopram Response in Major Depressive Disorder Biological Psychiatry, 67 (2), 133-138 DOI: 10.1016/j.biopsych.2009.08.029
One person might do well on a certain drug, but the next person might get no benefit from the exact same pills. Finding the right drug for each patient is often a matter of trying different ones until one works.So a genetic test to work out whether a certain drug will help a particular person would be really useful. Not to mention really profitable for whoever patented it. Three recent papers, published in three major journals, all claim to have found genes that predict antidepressant response. Great! The problem is, they were different genes.
First up, American team Binder et al looked at about 200 variants in 10 genes involved in the corticosteroid stress response pathway. They found one, in a gene called CRHBP, that was significantly associated with poor response to the popular SSRI antidepressant citalopram (Celexa), using the large STAR*D project data set. But this was only true of African-Americans and Latinos, not whites.
Garriock et al used the exact same dataset, but they did a genome-wide association study (GWAS), which looks at variants across the whole genome, unlike Binder et al who focussed on a small number of specific candidate genes. Sadly no variants were statistically significantly correlated with response to citalopram, although in a GWAS, the threshold for genome-wide significance is very high due to multiple comparisons correction. Some were close to being significant, but they weren't obviously related to CRHBP, and most weren't anything to do with the brain.
Uher et al did another GWAS of response to escitalopram and nortriptyline in a different sample, the European GENDEP study. Escitalopram is extremely similar to citalopram, the drug in the STAR*D studies; nortriptyline however is very different. They found one genome-wide significant hit. A variant in a gene called UST was associated with response to nortriptyline, but not escitalopram. No variants were associated with response to escitalopram, although one in the gene IL11 was close. There were some other nearly-significant results, but they didn't overlap with either of the STAR*D studies.
Finally, one of the STAR*D studies found a variant significantly linked to tolerability (side effects) of citalopram. GENDEP didn't look at this.
*
The UST link to nortriptyline finding is the strongest thing here, but for citalopram / escitalopram, no consistent pharmacogenetic results emerged at all. What does this mean? Well, it's possible that there just aren't any genes for citalopram response, but that seems unlikely. Even if you believe that antidepressants only work as placebos, you'd expect there would be genes that alter placebo responses, or at the very least, that affect side-effects and hence the active placebo improvement.
The thing is that the "antidepressant response" in these studies isn't really that: it's a mix of many factors. We know that a lot of the improvement would have happened even with placebo pills, so much of it isn't a pharmacological effect. There are probably genes associated with placebo improvement, but they might not be the same ones that are associated with drug improvement and a gene might even have opposite effects that cancel out (better drug effect, worse placebo effect). Some of the recorded improvement won't even be real improvement at all, just people saying they feel better because they know they're expected to.
If I were looking for the genes for SSRI response, not that I plan to, here's what I'd do. To stack the odds in my favour, I'd forget people with an moderate or partial response, and focus on those who either do really well, or those who get no benefit at all, with a certain drug. I'd also want to exclude people who respond really well, but not due to the specific effects of the drug.
That would be hard but one angle would be to only include people whose improvement is specifically reversed by acute tryptophan depletion, which reduces serotonin levels thus counteracting SSRIs. This would be a hard study to do, though not impossible. (In fact there are dozens of patients on record who meet my criteria, and their blood samples are probably still sitting in freezers in labs around the world... maybe someone should dig them out).
Still, even if you did find some genes that way, would they be useful? We'd have had to go to such lengths to find them, that they're not going to help doctors decide what to do with the average patient who comes through the door with depression. That's true, but they might just help us to work out who will respond to SSRIs, as opposed to other drugs.
Binder EB, Owens MJ, Liu W, Deveau TC, Rush AJ, Trivedi MH, Fava M, Bradley B, Ressler KJ, & Nemeroff CB (2010). Association of polymorphisms in genes regulating the corticotropin-releasing factor system with antidepressant treatment response. Archives of general psychiatry, 67 (4), 369-79 PMID: 20368512Uher, R., Perroud, N., Ng, M., Hauser, J., Henigsberg, N., Maier, W., Mors, O., Placentino, A., Rietschel, M., Souery, D., Zagar, T., Czerski, P., Jerman, B., Larsen, E., Schulze, T., Zobel, A., Cohen-Woods, S., Pirlo, K., Butler, A., Muglia, P., Barnes, M., Lathrop, M., Farmer, A., Breen, G., Aitchison, K., Craig, I., Lewis, C., & McGuffin, P. (2010). Genome-Wide Pharmacogenetics of Antidepressant Response in the GENDEP Project American Journal of Psychiatry DOI: 10.1176/appi.ajp.2009.09070932
Garriock, H., Kraft, J., Shyn, S., Peters, E., Yokoyama, J., Jenkins, G., Reinalda, M., Slager, S., McGrath, P., & Hamilton, S. (2010). A Genomewide Association Study of Citalopram Response in Major Depressive Disorder Biological Psychiatry, 67 (2), 133-138 DOI: 10.1016/j.biopsych.2009.08.029
Abercrombie Fitch Miami Outlet
On Sunday morning I called Cynthia to give me the sad news that Cami was hospitalized in intensive care. For those who do not know, I invite you to stop by her blog to learn more of their history and their daddies Nati and Norberto: "smile for the soul"
Cami is a beautiful princess who always gives us her smile, which always has the surface, hence the name of your blog. It's a super brave and feisty girl who has spent all, but still went ahead aided by the tremendous love of their parents and the people around her.
I have the pleasure of knowing her and to Nati, his mother. We knew "cyber" through the blogs of sin and the truth without seeing the faces and we joined a very special affection. It was because I could finally know Cindy personally to the two so we can hug and talk a great time with Nati and die of love with the smile and the mischievous look of Cami.
Alicia's mom Manu, in his blog explains a bit better than I can do the situation that Cami went into intensive care on Sunday 11 April (two days ago)
"Cami is admitted to the Hosp. Garraham since Friday, is based pneumonia in both lungs. She had been hospitalized last week went well and after 3 days began to feel ill with high fever, a virus apparently grabbed hospital when he was there, they are doing studies to find that virus is not yet known. This afternoon I stopped by the hosp. to see how he was and spending some time with Natalie and Norberto, their parents, who do not understand how this situation came to Cami, saturating was very low, making much effort to breathe with the mustache, so they decided to intubation, it is with respirator and her drug induced coma. Doctors are optimistic because they say that Cami previously never had problems breathing, so it has the potential to recover from this. Yesterday I had very low platelets, but it rose nearly to the normal amount. And today in the afternoon had problems of low pressure, but it was stabilizing. You have to wait for the next party is Monday at noon. I ask you to do a prayer chain to pray for the health of Camilla, who have the strength to overcome this situation, and by parents who also have strength ... "
text message today I Contacted back to Alice to see if I was new, told me that the medical report yesterday said that the gordita is stable and that any studies conducted to detect what type of virus was affecting gave negative, ie, they found none. He also told me he was better with the respirator saturating 60%.
I urge you to join this prayer chain for Cami to succeed, and that while improved, is still in a delicate situation may change at any moment. Let us ask this not to happen and the continued progress minute by minute.
us pray also for Nati and Norberto continue having faith and hope that everything will go well and have the strength to endure this difficult time.
I'll be uploading anything new that I got the blog to keep up to date.
THANKS!
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