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MY'STORY

The MOVE Fire

This is a personal recollection on the Move fire on May 13, 1985 Philadelphia police fired thousands of rounds at the MOVE house, city officials approved dropping an explosive device on the roof, the resulting fire was allowed to burn, 11 people—including five children—died, and 61 homes were destroyed. Philadelphia City Council later called it a “brutal attack carried out by the City of Philadelphia on its own citizens” and acknowledged that no individual faced criminal consequences for the bombing. One timeline correction worth preserving for the BHP record: the major previous MOVE-police confrontation was August 8, 1978, about seven years before the bombing, not a year or two earlier. Officer James Ramp was killed, other police and firefighters were wounded, nine MOVE members were later convicted, and television cameras recorded police beating Delbert Africa during his arrest. The 1985 MOVE Commission later specifically criticized city planners for failing to adequately use lessons from that 1978 confrontation. And that actually strengthens the point you’re making: 1985 did not happen without precedent or institutional memory. There had already been a deadly confrontation with MOVE, years of conflict, negotiations and police involvement before Osage Avenue.

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BLACK FACTS
The Truths They Never Taught You...

Wilmington 1898 — An American Coup

Wilmington, North Carolina once had a thriving Black middle class and an elected interracial government. In 1898 white supremacists used violence to overthrow that government, kill Black residents and drive many others from the city.

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Wikipedia

TrkB IRES

TrkB IRES
Predicted secondary structure and sequence conservation of IRES_TrkB
Identifiers
SymbolIRES_TrkB
RfamRF00547
Other data
RNA typeCis-reg; IRES
DomainEukaryota
GOGO:0043022
SOSO:0000243
PDB structuresPDBe

The TrkB internal ribosome entry site (IRES) is an RNA element which is present in the 5' UTR sequence of the mRNA. TrkB is a neurotrophin receptor which is essential for the development and maintenance of the nervous system. The internal ribosome entry site IRES element allows cap-independent translation of TrkB which may be needed for efficient translation in neuronal dendrites.[1]

See also

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References

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  1. ^ Dobson T, Minic A, Nielsen K, Amiott E, Krushel L (2005). "Internal initiation of translation of the TrkB mRNA is mediated by multiple regions within the 5' leader". Nucleic Acids Research. 33 (9): 2929–2941. doi:10.1093/nar/gki605. PMC 1133793. PMID 15908588.
[edit]

Source: Wikipedia. Article content is retrieved live through the MediaWiki API.

Wikipedia

TrkB IRES

The TrkB internal ribosome entry site (IRES) is an RNA element which is present in the 5' UTR sequence of the mRNA. TrkB is a neurotrophin receptor which is essential for the development and maintenance of the nervous system. The internal ribosome entry site IRES element allows cap-independent translation of TrkB which may be needed for efficient translation in neuronal dendrites.

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Wikipedia

Brain-derived neurotrophic factor

Brain-derived neurotrophic factor (Bdnf), or abrineurin, is a protein that, in humans, is encoded by the BDNF gene. BDNF is a member of the neurotrophin family of growth factors, which are related to the canonical nerve growth factor (NGF), a family which also includes NT-3 and NT-4/NT-5. Neurotrophic factors are found in the brain and the periphery. BDNF was first isolated from a pig brain in 1982 by Yves-Alain Barde and Hans Thoenen. BDNF activates the TrkB tyrosine kinase receptor.

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Wikipedia

Tropomyosin receptor kinase B

Tropomyosin receptor kinase B (TrkB), also known as tyrosine receptor kinase B, or BDNF/NT-3 growth factors receptor or neurotrophic tyrosine kinase, receptor, type 2 is a protein that in humans is encoded by the NTRK2 gene. TrkB is a receptor for brain-derived neurotrophic factor (BDNF).

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Wikipedia

Tropoflavin

Tropoflavin, also known as 7,8-dihydroxyflavone (7,8-DHF), is a naturally occurring flavone found in Godmania aesculifolia, Tridax procumbens, and Primula vulgaris. It has been found to act as a potent and selective small-molecule agonist of the tropomyosin receptor kinase B (TrkB) (Kd ≈ 320 nM), the main signaling receptor of the neurotrophin brain-derived neurotrophic factor (BDNF). Tropoflavin is both orally bioavailable and able to penetrate the blood–brain barrier. A prodrug of tropoflavin with greatly improved potency and pharmacokinetics, R13 (and, formerly, R7), is under development for the treatment of Alzheimer's disease. Tropoflavin has demonstrated therapeutic efficacy in animal models of a variety of central nervous system disorders, including depression, Alzheimer's disease, cognitive deficits in schizophrenia, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, traumatic brain injury, cerebral ischemia, fragile X syndrome, and Rett syndrome. Tropoflavin also shows efficacy in animal models of age-associated cognitive impairment and enhances memory consolidation and emotional learning in healthy rodents. In addition, tropoflavin possesses powerful antioxidant activity independent of its actions on the TrkB receptor, and protects against glutamate-induced excitotoxicity, 6-hydroxydopamine-induced dopaminergic neurotoxicity, and oxidative stress-induced genotoxicity. It was also found to block methamphetamine-induced dopaminergic neurotoxicity, an effect which, in contrast to the preceding, was found to be TrkB-dependent. In 2017, evidence was published suggesting that tropoflavin and various other reported small-molecule TrkB agonists might not actually be direct agonists of the TrkB and might be mediating their observed effects by other means. Tropoflavin has been found to act as a weak aromatase inhibitor in vitro (Ki = 10 μM), though there is evidence to suggest that this might not be the case in vivo. In addition, it has been found to inhibit aldehyde dehydrogenase and estrogen sulfotransferase in vitro (Ki = 35 μM and 1–3 μM, respectively), although similarly to the case of aromatase, these activities have not yet been confirmed in vivo. Unlike many other flavonoids, tropoflavin does not show any inhibitory activity on 17β-hydroxysteroid dehydrogenase. Tropoflavin has also been observed to possess in vitro antiestrogenic effects at very high concentrations (Ki = 50 μM). A variety of close structural analogues of tropoflavin have also been found to act as TrkB agonists in vitro, including diosmetin (5,7,3'-trihydroxy-4'-methoxyflavone), norwogonin (5,7,8-trihydroxyflavone), eutropoflavin (4'-dimethylamino-7,8-dihydroxyflavone), 7,8,3'-trihydroxyflavone, 7,3'-dihydroxyflavone, 7,8,2'-trihydroxyflavone, 3,7,8,2'-tetrahydroxyflavone, and 3,7-dihydroxyflavone. The highly hydroxylated analogue gossypetin (3,5,7,8,3',4'-hexahydroxyflavone), conversely, appears to be an antagonist of TrkB in vitro. Tropoflavin was also found to decrease mouse sleep in dark phase and reduce hypothalamus level of orexin A, but not orexin B, in mice.

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TOPIC OF THE DAY

Greenwood / Black Wall Street

Before the 1921 destruction of Tulsa’s Greenwood District, Black residents had created a remarkable center of business and community life. The district included stores, professional offices, entertainment venues and homes owned by Black citizens. Understanding Greenwood means learning what was built—not only what was burned.

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TRIVIA QUESTION OF THE DAY

Which Supreme Court case ruled state-sponsored public-school segregation unconstitutional?

Brown v. Board of Education in 1954.