The association between height and birth order: evidence from 652 518 Swedish men
"birth orders 2, 3 and 4 were associated with 0.4, 0.7 and 0.8 cm shorter height than birth order 1, respectively{Being the first or only child is important for greater height}. The associations were similar in large and small and high-SEP[socioeconomic position] and low-SEP families, but were attenuated[diminished] in recent cohorts[groups]. Birth characteristics did not explain these associations. "
There is one study mentioned that shows the reverse trend where children born after other kids are taller.
I'm not sure exactly what conclusion you can draw but it shows the importance of the maternal conditions on the health of the child.
Saturday, May 23, 2009
MT1-MMP
MT1-MMP-Dependent Control of Skeletal Stem Cell Commitment via a β1-Integrin/YAP/TAZ Signaling Axis.
"conditional deletion of the membrane-anchored metalloproteinase MT1-MMP (Mmp14){so inhibiting MMP14 could be one way to induce chondrogenesis?} in mesenchymal progenitors, but not in committed osteoblasts, redirects SSC fate decisions from osteogenesis to adipo- and chondrogenesis. By effecting ECM remodeling, MT1-MMP regulates stem cell shape, thereby activating a β1-integrin/RhoGTPase signaling cascade and triggering the nuclear localization of the transcriptional coactivators YAP and TAZ, which serve to control SSC lineage commitment. These data identify a critical MT1-MMP/integrin/YAP/TAZ axis operative in the stem cell niche that oversees SSC fate determination."
Illustration of how MMP14 may inhibit chondrogenesis:
However MMP14 knockout results in defects including death.
" commitment to either the adipogenic or chondrogenic pathways results in decreased MT1-MMP expression" Despite this the conditional MMP14 knockout mice seemed to develop some defects in terms of body height.
"MT1-MMP knockout transgenic mice engineered to overexpress MT1-MMP in chondrocytes to [are unable to] resorb the expanded cartilage network "
"conditional deletion of the membrane-anchored metalloproteinase MT1-MMP (Mmp14){so inhibiting MMP14 could be one way to induce chondrogenesis?} in mesenchymal progenitors, but not in committed osteoblasts, redirects SSC fate decisions from osteogenesis to adipo- and chondrogenesis. By effecting ECM remodeling, MT1-MMP regulates stem cell shape, thereby activating a β1-integrin/RhoGTPase signaling cascade and triggering the nuclear localization of the transcriptional coactivators YAP and TAZ, which serve to control SSC lineage commitment. These data identify a critical MT1-MMP/integrin/YAP/TAZ axis operative in the stem cell niche that oversees SSC fate determination."
Illustration of how MMP14 may inhibit chondrogenesis:
However MMP14 knockout results in defects including death.
" commitment to either the adipogenic or chondrogenic pathways results in decreased MT1-MMP expression" Despite this the conditional MMP14 knockout mice seemed to develop some defects in terms of body height.
"MT1-MMP knockout transgenic mice engineered to overexpress MT1-MMP in chondrocytes to [are unable to] resorb the expanded cartilage network "
Wednesday, May 20, 2009
ACTN3
ACTN3 is a gene that is beneficial for endurance athletes but is it good for height growth?
α-Actinin-3 deficiency is associated with reduced bone mass in human and mouse.
This study found ACTN3 to be associated with reduced bone mass. ACTN3-KO mice resulted in a non-statistically significant increase in Sox9. I emailed to find out.
"no evidence for an association between R577X and height, weight, BMI, or WHR in either males or females" was found in the study ACTN3 Genotype, Athletic Status, and Life Course Physical Capability: Meta-Analysis of the Published Literature and Findings from Nine Studies. Looking directly at the data in the supplement data, the height variation was minor between the various gene expression variations.
α-Actinin-3 deficiency is associated with reduced bone mass in human and mouse.
This study found ACTN3 to be associated with reduced bone mass. ACTN3-KO mice resulted in a non-statistically significant increase in Sox9. I emailed to find out.
"no evidence for an association between R577X and height, weight, BMI, or WHR in either males or females" was found in the study ACTN3 Genotype, Athletic Status, and Life Course Physical Capability: Meta-Analysis of the Published Literature and Findings from Nine Studies. Looking directly at the data in the supplement data, the height variation was minor between the various gene expression variations.
Wednesday, May 6, 2009
Acid Ceramidase
Acid ceramidase maintains the chondrogenic phenotype of expanded primary chondrocytes and improves the chondrogenic differentiation of bone marrow-derived mesenchymal stem cells.
"Acid ceramidase is required to maintain the metabolic balance of several important bioactive lipids, including ceramide, sphingosine and sphingosine-1-phosphate. Addition of recombinant acid ceramidase (rAC) to primary chondrocyte culture media maintained low levels of ceramide and led to elevated sphingosine by 48 hours. Surprisingly, after three weeks of expansion the chondrogenic phenotype of these cells also was markedly improved, as assessed by a combination of histochemical staining (Alcian Blue and Safranin-O), western blotting (e.g., Sox9, aggrecan, collagen 2A1), and/or qPCR. The same effects were evident in rat, equine and human cells, and were observed in monolayer and 3-D cultures. rAC also reduced the number of apoptotic cells in some culture conditions, contributing to overall improved cell quality. In addition to these effects on primary chondrocytes, when rAC was added to freshly harvested rat, equine or feline bone marrow cultures an ∼2-fold enrichment of mesenchymal stem cells (MSCs) was observed by one week. rAC also improved the chondrogenic differentiation of MSCs, as revealed by histochemical and immunostaining. These latter effects were synergistic with TGF-beta1. Short-term changes in sphingolipid metabolism may lead to longer-term effects on the chondrogenic phenotype."
"rAC was taken up by rat chondrocytes and retained biological activity by hydrolyzing ceramide and producing sphingosine and S1P. The fact that AC levels returned to baseline by 7 days was consistent with its expected intracellular half-life of 48–72 h"
rAC was tested on human osteoarthritic patient cultures and pro-chondrogenic gene expression increased although there was no difference in cell number.
"Sphingosine may have a protective effect on chondrocytes."
"Acid ceramidase is required to maintain the metabolic balance of several important bioactive lipids, including ceramide, sphingosine and sphingosine-1-phosphate. Addition of recombinant acid ceramidase (rAC) to primary chondrocyte culture media maintained low levels of ceramide and led to elevated sphingosine by 48 hours. Surprisingly, after three weeks of expansion the chondrogenic phenotype of these cells also was markedly improved, as assessed by a combination of histochemical staining (Alcian Blue and Safranin-O), western blotting (e.g., Sox9, aggrecan, collagen 2A1), and/or qPCR. The same effects were evident in rat, equine and human cells, and were observed in monolayer and 3-D cultures. rAC also reduced the number of apoptotic cells in some culture conditions, contributing to overall improved cell quality. In addition to these effects on primary chondrocytes, when rAC was added to freshly harvested rat, equine or feline bone marrow cultures an ∼2-fold enrichment of mesenchymal stem cells (MSCs) was observed by one week. rAC also improved the chondrogenic differentiation of MSCs, as revealed by histochemical and immunostaining. These latter effects were synergistic with TGF-beta1. Short-term changes in sphingolipid metabolism may lead to longer-term effects on the chondrogenic phenotype."
"rAC was taken up by rat chondrocytes and retained biological activity by hydrolyzing ceramide and producing sphingosine and S1P. The fact that AC levels returned to baseline by 7 days was consistent with its expected intracellular half-life of 48–72 h"
rAC was tested on human osteoarthritic patient cultures and pro-chondrogenic gene expression increased although there was no difference in cell number.
"Sphingosine may have a protective effect on chondrocytes."