2014 Group Project 8 - Revision history

Z8600021: /* Abnormalities */

2014-10-31T05:42:39Z

Abnormalities

← Older revision		Revision as of 15:42, 31 October 2014
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	Nemaline rod myopathy is congenital non-dystrophic muscle disease. Sufferers experience general muscle weakness, weakness is most severe in face, neck and limbs<ref name="PMID 14090530"><pubmed> 14090530</pubmed></ref>. Further clinical manifestations include feeding problems, scoliosis of spine, foot deformities and respiration difficulties. The disease is an inherited both autosomal dominant and recessive, 30% autosomal dominant, 20% autosomal recessive and 50% simplex. In total 6 genes have been associated with the formation of nemaline myopathy with the NEB and ACTA1 genes being the most prominent<ref name="PMID 10051637"><pubmed> 10051637</pubmed></ref> <ref name="PMID 15236405"><pubmed> 15236405</pubmed></ref>. Over 60 NEB mutations have been discovered which result in nemaline myopathy, it results in the decreased production and decreased length of the nebulin protein, half of all NM cases are associated with NEB mutations<ref name="PMID 10051637"><pubmed> 10051637</pubmed></ref>. About 140 mutations to ACTA1 can lead to formation of nemaline myopathy, this results in either aggregation of α-actin fibres preventing functional muscle contraction or total absence of α-actin production<ref name="PMID 15236405"><pubmed> 15236405</pubmed></ref>.		Nemaline rod myopathy is congenital non-dystrophic muscle disease. Sufferers experience general muscle weakness, weakness is most severe in face, neck and limbs<ref name="PMID 14090530"><pubmed> 14090530</pubmed></ref>. Further clinical manifestations include feeding problems, scoliosis of spine, foot deformities and respiration difficulties. The disease is an inherited both autosomal dominant and recessive, 30% autosomal dominant, 20% autosomal recessive and 50% simplex. In total 6 genes have been associated with the formation of nemaline myopathy with the NEB and ACTA1 genes being the most prominent<ref name="PMID 10051637"><pubmed> 10051637</pubmed></ref> <ref name="PMID 15236405"><pubmed> 15236405</pubmed></ref>. Over 60 NEB mutations have been discovered which result in nemaline myopathy, it results in the decreased production and decreased length of the nebulin protein, half of all NM cases are associated with NEB mutations<ref name="PMID 10051637"><pubmed> 10051637</pubmed></ref>. About 140 mutations to ACTA1 can lead to formation of nemaline myopathy, this results in either aggregation of α-actin fibres preventing functional muscle contraction or total absence of α-actin production<ref name="PMID 15236405"><pubmed> 15236405</pubmed></ref>.

	~~==Abnormalities==~~
	~~[[2014 Group Project 8 part 2]]~~

	==References==		==References==

	<references/>		<references/>

Z8600021: /* Current Research Models and Findings */

2014-10-31T05:40:53Z

Current Research Models and Findings

← Older revision		Revision as of 15:40, 31 October 2014
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	\|}		\|}

	~~==Current Research Models and Findings==~~
	==Current Research and Findings==		==Current Research and Findings==

Z8600021: /* Current Research Models and Findings */

2014-10-31T05:39:09Z

Current Research Models and Findings

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Z8600021: Protected "2014 Group Project 8" ([Edit=Allow only administrators] (indefinite) [Move=Allow only administrators] (indefinite))

2014-10-24T13:20:34Z

Protected "2014 Group Project 8" ([Edit=Allow only administrators] (indefinite) [Move=Allow only administrators] (indefinite))

← Older revision	Revision as of 23:20, 24 October 2014
(No difference)

Z3418989 at 09:03, 24 October 2014

2014-10-24T09:03:26Z

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Z3418989: /* Stapedius */

2014-10-24T06:45:42Z

Stapedius

← Older revision		Revision as of 16:45, 24 October 2014
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	===Stapedius===		===Stapedius===

	Rodri´guez-va´ zquez et al (2010) in order to understand the isolated case of a unilateral agenesia of the stapedius tendonduring week 14 of post-conception development (PCd), have tried to understand the way the stapedius muscle develops. The stapedius is essentially formed by two anlagen; one anlagen forms the tendon of the stapedius and the other forms the muscle belly of stapedius. The anlagen forming the tendon are derived from the internal segment of interhyale. The anlagen forming the muscle belly are derived from the 2nd pharyngeal arch near the interhyale, medial to the facial nerve. Interhyale is the internal part of the second branchial arch and it develops into stapedius’ tendon ~~(http://www.drugs.com/dict/interhyale.html )~~. The observed unilateral agenesia of the tendon of stapedius was found by Rodriguez-va et al (2010) to be due to the internal segment of the interhyale regression. Instead the belly of stapedius was accompanied with a pseudo tendon formed by the external segment of the interhyale. To come to this conclusion the formation of the stapedius and pyramidal eminence was tracked.		Rodri´guez-va´ zquez et al (2010) in order to understand the isolated case of a unilateral agenesia of the stapedius tendonduring week 14 of post-conception development (PCd), have tried to understand the way the stapedius muscle develops. The stapedius is essentially formed by two anlagen; one anlagen forms the tendon of the stapedius and the other forms the muscle belly of stapedius. The anlagen forming the tendon are derived from the internal segment of interhyale. The anlagen forming the muscle belly are derived from the 2nd pharyngeal arch near the interhyale, medial to the facial nerve. Interhyale is the internal part of the second branchial arch and it develops into stapedius’ tendon. The observed unilateral agenesia of the tendon of stapedius was found by Rodriguez-va et al (2010) to be due to the internal segment of the interhyale regression. Instead the belly of stapedius was accompanied with a pseudo tendon formed by the external segment of the interhyale. To come to this conclusion the formation of the stapedius and pyramidal eminence was tracked.<ref name="PMID19899117"><pubmed>19899117</pubmed></ref>

	Interhyale was observed as a mesenchymal condensation formed at O’Rahilly stage 16 at cranial component of the second branchial arch. The stapes and reichert cartilage are eventually differentiated from the interhyale. At Stage 18 and 19 a mesenchymal bridge forms by the interhyale which bridges stapes and cranial part laterohyale (Reichert’s cartilage). And by stage O’Rahilly stages 20 and 21 the interhyale fully develops.		Interhyale was observed as a mesenchymal condensation formed at O’Rahilly stage 16 at cranial component of the second branchial arch. The stapes and reichert cartilage are eventually differentiated from the interhyale. At Stage 18 and 19 a mesenchymal bridge forms by the interhyale which bridges stapes and cranial part laterohyale (Reichert’s cartilage). And by stage O’Rahilly stages 20 and 21 the interhyale fully develops.
	Rodriguez-va et al (2010) found the belly of stapedius to derive from a blastema which develops adjacent the interhyale to form its own anlage. In O’Rahilly stage 22 Rodriguez-va et al (2010) found that the interhyale began to take on an angular shape and the anlage of the stapedius belly connected with the vertex of the now angular interhyale.		Rodriguez-va et al (2010) found the belly of stapedius to derive from a blastema which develops adjacent the interhyale to form its own anlage. In O’Rahilly stage 22 Rodriguez-va et al (2010) found that the interhyale began to take on an angular shape and the anlage of the stapedius belly connected with the vertex of the now angular interhyale.<ref name="PMID19899117"/>

	Interhyale developed two segments; internal thick segment and an external thin segment. The thick internal segment as discussed contributes to the formation of the tendon of the stapedius muscle. The external segment begins to regress in the embryonic period and by the fetal period, week 9, the external segment was observed to be fully regressed.		Interhyale developed two segments; internal thick segment and an external thin segment. The thick internal segment as discussed contributes to the formation of the tendon of the stapedius muscle. The external segment begins to regress in the embryonic period and by the fetal period, week 9, the external segment was observed to be fully regressed.
	In weeks 10-11 a conical belly continuous with the stapedius tendon was observed and the stapedius tendon attached at the back of the stapes head.The anlage of the pyramidal eminence formed around week 12-14 and around the stapedius muscle belly. The mesenchymal condensation forming the pyramidal eminence grew until it was inhibited around week 15-17.		In weeks 10-11 a conical belly continuous with the stapedius tendon was observed and the stapedius tendon attached at the back of the stapes head.The anlage of the pyramidal eminence formed around week 12-14 and around the stapedius muscle belly. The mesenchymal condensation forming the pyramidal eminence grew until it was inhibited around week 15-17.
	After week 9 there was not much morphological change of the stapedius. From this study we can see how the stapedius muscle develops its shape and attachments in the embryonic and fetal periods.		After week 9 there was not much morphological change of the stapedius. From this study we can see how the stapedius muscle develops its shape and attachments in the embryonic and fetal periods.<ref name="PMID19899117"/>

	===Two studies on Triceps Brachii and Biceps Brachii and their parameters===		===Two studies on Triceps Brachii and Biceps Brachii and their parameters===

Z3418989: /* Pannexin 1 and Pannexin 3 and Myoblast differentiation and proliferation */

2014-10-24T06:03:00Z

Pannexin 1 and Pannexin 3 and Myoblast differentiation and proliferation

@@ Line 239: / Line 239: @@
 Pannexins have also been observed to play certain roles in contraction as studies showed that Panx channel blockers reduced ATP release from electrical stimulation of myotubes <ref name="PMID23321639"/> <ref name="PMID23583931"/> .The role however of pannexins in cell differentiation and proliferation is unknown and what Langlois et al (2014) investigate in this experiment. <ref name="PMID25239622"/>
 HSMM (primary Human Skeletal Muscle Myoblasts) was obtained from post quadriceps and psoas major. And SkMC (primary Human Skeletal Muscle cells) was got from upper arm or leg. <ref name="PMID25239622"/> Western Blot analysis confirmed the presence of Panx1, Panx2 and Panx3 in the human, rat and mouse skeletal muscle tissue samples. Pan1 and Panx3 was detected in the tissue samples but Panx2 wasn’t. Panx1 and Panx2 stained differently within skeletal muscle and hinted that they had different functions. <ref name="PMID25239622"/> It is known that in the fetal stage there is lots of proliferation whilst in the adult stages there is decreased proliferation. Decreased proliferation was indicated by decreased proliferating cell nuclear antigen (PCNA). Whilst increased differentiation resulted in increased myosin heavy chains (MHC). <ref name="PMID25239622"/> Panx1 of higher molecular weight is the main pannexin found in skeletal muscle, more so in fetal than adult cells. Lower molecular forms of both Panx1 and Panx3 are more increased in adult forms and the higher weight forms are more increased in fetal forms. This shift possibly suggests that Panx1 and Panx3 plays a role in skeletal muscle development. <ref name="PMID25239622"/> Langlois et al (2014) also found that Panx1 and Panx3 had a role to play in the sophisticated process of myogenesis, in particular myoblast proliferation and differentiation. Panx1 was low in in undifferentiated skeletal muscle cells and myoblasts but promoted myoblast differentiation and were thereafter more abundant. Panx3 of low molecular weight (~ 43 kDa) acted differently to higher weight species (~ 70 kDa). Expression of low molecular weight Panx3 promoted myoblast differentiation and repressed proliferation. Whilst expression of high molecular weight Panx3 coincided with proliferation and subsided with differentiation of myoblasts. Low molecular weight Panx3 were low in differentiated and undifferentiated HSMM but was expressed in skeletal muscle tissue which may indicate that lower molecular weight Panx3 plays a role more later on in differentiation. <ref name="PMID25239622"/> Langlois et al (2014) used 2 Panx3 shRNAs to reduce Panx3 expression and they observed an inhibition of Proliferation whilst not initiating differentiation. Other impacts on Panx were studied such as their glycosylation, phosphorylation and being sialylated are important in their functioning as membrane channels. Post-transcriptional modifications and molecular interactions of Panx are thus important in regulating Panx channel function and thus important in myoblast differentiation and proliferation. <ref name="PMID25239622"/> All evidences led to the conclusion that both Panx1 and Panx3 are expressed in skeletal muscle cells and participate in proliferation and differentiation of myoblast muscle cells.
 ==Abnormalities==

Z3418340: /* Pannexin 1 and Pannexin 3 and Myoblast differentiation and proliferation */

2014-10-24T05:21:15Z

Pannexin 1 and Pannexin 3 and Myoblast differentiation and proliferation

← Older revision		Revision as of 15:21, 24 October 2014
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	Pannexins are known to be present within skeletal muscle. Pannexins were found in mRNA of skeletal muscle <ref><pubmed>15028292</pubmed></ref>. And Panx1 in sarcolemma of rodent skeletal muscle <ref name="PMID23321639"><pubmed>23321639</pubmed></ref>		Pannexins are known to be present within skeletal muscle. Pannexins were found in mRNA of skeletal muscle <ref><pubmed>15028292</pubmed></ref>. And Panx1 in sarcolemma of rodent skeletal muscle <ref name="PMID23321639"><pubmed>23321639</pubmed></ref>
	Pannexins have also been observed to play certain roles in contraction as studies showed that Panx channel blockers reduced ATP release from electrical stimulation of myotubes <ref name="PMID23321639"/> <ref name="PMID23583931"/> .The role however of pannexins in cell differentiation and proliferation is unknown and what Langlois et al (2014) investigate in this experiment. <ref name="PMID25239622"/>		Pannexins have also been observed to play certain roles in contraction as studies showed that Panx channel blockers reduced ATP release from electrical stimulation of myotubes <ref name="PMID23321639"/> <ref name="PMID23583931"/> .The role however of pannexins in cell differentiation and proliferation is unknown and what Langlois et al (2014) investigate in this experiment. <ref name="PMID25239622"/>
			HSMM (primary Human Skeletal Muscle Myoblasts) was obtained from post quadriceps and psoas major. And SkMC (primary Human Skeletal Muscle cells) was got from upper arm or leg. <ref name="PMID25239622"/> Western Blot analysis confirmed the presence of Panx1, Panx2 and Panx3 in the human, rat and mouse skeletal muscle tissue samples. Pan1 and Panx3 was detected in the tissue samples but Panx2 wasn’t. Panx1 and Panx2 stained differently within skeletal muscle and hinted that they had different functions. <ref name="PMID25239622"/> It is known that in the fetal stage there is lots of proliferation whilst in the adult stages there is decreased proliferation. Decreased proliferation was indicated by decreased proliferating cell nuclear antigen (PCNA). Whilst increased differentiation resulted in increased myosin heavy chains (MHC). <ref name="PMID25239622"/> Panx1 of higher molecular weight is the main pannexin found in skeletal muscle, more so in fetal than adult cells. Lower molecular forms of both Panx1 and Panx3 are more increased in adult forms and the higher weight forms are more increased in fetal forms. This shift possibly suggests that Panx1 and Panx3 plays a role in skeletal muscle development. <ref name="PMID25239622"/> Langlois et al (2014) also found that Panx1 and Panx3 had a role to play in the sophisticated process of myogenesis, in particular myoblast proliferation and differentiation. Panx1 was low in in undifferentiated skeletal muscle cells and myoblasts but promoted myoblast differentiation and were thereafter more abundant. Panx3 of low molecular weight (~ 43 kDa) acted differently to higher weight species (~ 70 kDa). Expression of low molecular weight Panx3 promoted myoblast differentiation and repressed proliferation. Whilst expression of high molecular weight Panx3 coincided with proliferation and subsided with differentiation of myoblasts. Low molecular weight Panx3 were low in differentiated and undifferentiated HSMM but was expressed in skeletal muscle tissue which may indicate that lower molecular weight Panx3 plays a role more later on in differentiation. <ref name="PMID25239622"/> Langlois et al (2014) used 2 Panx3 shRNAs to reduce Panx3 expression and they observed an inhibition of Proliferation whilst not initiating differentiation. Other impacts on Panx were studied such as their glycosylation, phosphorylation and being sialylated are important in their functioning as membrane channels. Post-transcriptional modifications and molecular interactions of Panx are thus important in regulating Panx channel function and thus important in myoblast differentiation and proliferation. <ref name="PMID25239622"/> All evidences led to the conclusion that both Panx1 and Panx3 are expressed in skeletal muscle cells and participate in proliferation and differentiation of myoblast muscle cells.
	HSMM (primary Human Skeletal Muscle Myoblasts) was obtained from post quadriceps and psoas major. And SkMC (primary Human Skeletal Muscle cells) was got from upper arm or leg. <ref name="PMID25239622"/>

	==Abnormalities==		==Abnormalities==

Z3418989: /* Pannexin 1 and Pannexin 3 and Myoblast differentiation and proliferation */

2014-10-24T05:14:22Z

Pannexin 1 and Pannexin 3 and Myoblast differentiation and proliferation

← Older revision		Revision as of 15:14, 24 October 2014
Line 238:		Line 238:
	Pannexins are known to be present within skeletal muscle. Pannexins were found in mRNA of skeletal muscle <ref><pubmed>15028292</pubmed></ref>. And Panx1 in sarcolemma of rodent skeletal muscle <ref name="PMID23321639"><pubmed>23321639</pubmed></ref>		Pannexins are known to be present within skeletal muscle. Pannexins were found in mRNA of skeletal muscle <ref><pubmed>15028292</pubmed></ref>. And Panx1 in sarcolemma of rodent skeletal muscle <ref name="PMID23321639"><pubmed>23321639</pubmed></ref>
	Pannexins have also been observed to play certain roles in contraction as studies showed that Panx channel blockers reduced ATP release from electrical stimulation of myotubes <ref name="PMID23321639"/> <ref name="PMID23583931"/> .The role however of pannexins in cell differentiation and proliferation is unknown and what Langlois et al (2014) investigate in this experiment. <ref name="PMID25239622"/>		Pannexins have also been observed to play certain roles in contraction as studies showed that Panx channel blockers reduced ATP release from electrical stimulation of myotubes <ref name="PMID23321639"/> <ref name="PMID23583931"/> .The role however of pannexins in cell differentiation and proliferation is unknown and what Langlois et al (2014) investigate in this experiment. <ref name="PMID25239622"/>

			HSMM (primary Human Skeletal Muscle Myoblasts) was obtained from post quadriceps and psoas major. And SkMC (primary Human Skeletal Muscle cells) was got from upper arm or leg. <ref name="PMID25239622"/>

	==Abnormalities==		==Abnormalities==

Z3418989: /* Pannexin 1 and Pannexin 3 and Myoblast differentiation and proliferation */

2014-10-24T04:39:19Z

Pannexin 1 and Pannexin 3 and Myoblast differentiation and proliferation

← Older revision		Revision as of 14:39, 24 October 2014
Line 233:		Line 233:

	Panx1 and Panx3 are part of the pannexin channel protein family. Panx1 is known to play many roles, a few of which are vasodilation and inflammatory responses.<ref name="PMID25239622"/>		Panx1 and Panx3 are part of the pannexin channel protein family. Panx1 is known to play many roles, a few of which are vasodilation and inflammatory responses.<ref name="PMID25239622"/>

	Panx3 is known for fewer functions such as carcinogenesis and osteoprogenitor cell proliferation. <ref><pubmed>22947051</pubmed></ref> <ref><pubmed>24338011</pubmed></ref>		Panx3 is known for fewer functions such as carcinogenesis and osteoprogenitor cell proliferation. <ref><pubmed>22947051</pubmed></ref> <ref><pubmed>24338011</pubmed></ref>
			However recent studies have shown the potential role of Panx1 and Panx3 in skeletal muscle development.

	~~However recent~~ studies ~~have shown the potential~~ role of ~~Panx1~~ and ~~Panx3~~ in ~~skeletal muscle development~~.		Pannexins are known to be present within skeletal muscle. Pannexins were found in mRNA of skeletal muscle <ref><pubmed>15028292</pubmed></ref>. And Panx1 in sarcolemma of rodent skeletal muscle <ref name="PMID23321639"><pubmed>23321639</pubmed></ref>
			Pannexins have also been observed to play certain roles in contraction as studies showed that Panx channel blockers reduced ATP release from electrical stimulation of myotubes <ref name="PMID23321639"/> <ref name="PMID23583931"/> .The role however of pannexins in cell differentiation and proliferation is unknown and what Langlois et al (2014) investigate in this experiment. <ref name="PMID25239622"/>

	==Abnormalities==		==Abnormalities==