Explore the people, places, events, achievements, struggles and stories that shaped our journey.
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Movements, leaders, victories and the continuing fight for equality.
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Meet the people whose lives, choices and achievements shaped the journey.
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Black towns, communities, institutions and places where history happened.
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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.
In August 1908, a white mob attacked Springfield, Illinois’s Black community, destroying homes and businesses and lynching two Black men. National outrage over the violence helped spur the movement that created the NAACP the following year.
Reflects the personal views, recollections, and perspective of the author, Mike Davis.
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.
BHP gathered finds from its connected research sources.
Showing the 4
strongest Black History matches.
Zolmitriptan is contraindicated in patients with cerebrovascular or cardiovascular disease because serotonin5-HT1B receptors are present in coronary arteries. Such conditions include, but are not limited to, coronary artery disease, stroke, and peripheral vascular disease.[8] It is also contraindicated in hemiplegic migraine.[8]
There is limited experience with overdose of zolmitriptan and there is no specific antidote for zolmitriptan overdose.[5] A dose of zolmitriptan of 50mg, which is 10- to 40-fold the clinically used dose range of 1.25 to 5mg, commonly resulted in sedation in patients in a clinical study.[5] Zolmitriptan has a relatively short elimination half-life of 3hours, and so symptoms of overdose may be expected to resolve within around 15hours post-intake.[5]
Zolmitriptan's major metabolite, N-desmethylzolmitriptan (183C91), is also active and has about 2- to 6-fold the affinity of zolmitriptan for the serotonin 5-HT1B and 5-HT1D receptors.[4]
Zolmitriptan has a rapid onset of action and has been detected in the brain as early as within 5minutes of intranasal administration. On average, zolmitriptan has an oralbioavailability of 40%, a mean volume of distribution of 8.3L/kg after oral administration, and 2.4L/kg after intravenous administration.[8] According to a study of healthy volunteers, food intake seems to have no significant effect on the effectiveness of zolmitriptan in both men and women.[29]
The experimental log P of zolmitriptan is 1.6 to 1.8.[6][35] For comparison, the experimental log P of sumatriptan is 0.8 to 0.93.[36][35] Zolmitriptan is much more lipophilic than sumatriptan.[13][35]
In 2008, Zomig generated nearly $154 million in sales.[41]
AstraZeneca's U.S. patent on Zomig tablets expired on November 14, 2012, and its pediatric exclusivity extension expired on May 14, 2013.[42] The patent in certain European countries has already expired too, and generic drug maker Actavis released a generic version in those countries, starting in March 2012.[43]
In Russia, versions of zolmitriptan which are not registered in the National registry of medications may be regarded as narcotic drugs (derivatives of dimethyltriptamine (DMT)).[44]
^ abcdefghYu AM (June 2008). "Indolealkylamines: biotransformations and potential drug-drug interactions". AAPS J. 10 (2) 242: 242–253. doi:10.1208/s12248-008-9028-5. PMC2751378. PMID18454322. [...] the N-demethylated metabolites from zolmitriptan and eletriptan are both active at the 5-HT1B/1D sites. In particular, the N-desmethyl-zolmitriptan acts on 5-HT1B/1D receptors with an affinity about two- to six-fold of that of zolmitriptan and its steady state concentration is also higher than the parent drug. Therefore, N-desmethyl-zolmitriptan may have important contribution to the overall zolmitriptan drug effects. This active metabolite undergoes selective MAO-A-mediated deamination metabolism, resulting in an inactive indole acetic acid derivative (21) (Fig. 3). Because zolmitriptan is extensively N-demethylated and N-desmethyl-zolmitriptan is primarily excreted via deamination, potent MAO-A inhibitors are anticipated to alter the pharmacokinetics of N-desmethyl-zolmitriptan in humans. Indeed, concurrent use of selective MAO-A inhibitor, moclobemide, has been shown to cause 1.5- to 3-fold increase in the systemic exposure (AUC) and peak drug concentration (Cmax) of N-desmethyl-zolmitriptan (25).
^Newman LC, Lipton RB (2001). "Migraine MLT-Down: An Unusual Presentation of Migraine in Patients With Aspartame-Triggered Headaches". Headache: The Journal of Head and Face Pain (abstract). 41 (9): 899–901. doi:10.1046/j.1526-4610.2001.01164.x (inactive 5 August 2025). PMID11703479.{{cite journal}}: CS1 maint: DOI inactive as of August 2025 (link)
^van den Brink M (22 December 1999). "Coronary Side Effects of Antimigraine Drugs From Patient to Receptor". RePub, Erasmus University Repository. Retrieved 19 June 2025. Table 1.2 Receptor binding properties (pKi values) of sumatriptan and second-generation triptans at 5-HT receptors. [...]
^Pauwels PJ, Tardif S, Palmier C, Wurch T, Colpaert FC (1997). "How efficacious are 5-HT1B/D receptor ligands: an answer from GTP gamma S binding studies with stably transfected C6-glial cell lines". Neuropharmacology. 36 (4–5): 499–512. doi:10.1016/s0028-3908(96)00170-0. PMID9225275.
^Glen RC, Martin GR, Hill AP, Hyde RM, Woollard PM, Salmon JA, et al. (September 1995). "Computer-aided design and synthesis of 5-substituted tryptamines and their pharmacology at the 5-HT1D receptor: discovery of compounds with potential anti-migraine properties". Journal of Medicinal Chemistry. 38 (18): 3566–3580. doi:10.1021/jm00018a016. PMID7658443.
^Perez M, Fourrier C, Sigogneau I, Pauwels PJ, Palmier C, John GW, et al. (September 1995). "Synthesis and serotonergic activity of arylpiperazide derivatives of serotonin: potent agonists for 5-HT1D receptors". Journal of Medicinal Chemistry. 38 (18): 3602–3607. doi:10.1021/jm00018a020. PMID7658447.
^Perez M, Pauwels PJ, Fourrier C, Chopin P, Valentin JP, John GW, et al. (March 1998). "Dimerization of sumatriptan as an efficient way to design a potent, centrally and orally active 5-HT1B agonist". Bioorganic & Medicinal Chemistry Letters. 8 (6): 675–680. doi:10.1016/s0960-894x(98)00090-0. PMID9871581.
^Nelson DL, Phebus LA, Johnson KW, Wainscott DB, Cohen ML, Calligaro DO, et al. (October 2010). "Preclinical pharmacological profile of the selective 5-HT1F receptor agonist lasmiditan". Cephalalgia. 30 (10): 1159–1169. doi:10.1177/0333102410370873. PMID20855361.
^ abcRubio-Beltrán E, Labastida-Ramírez A, Haanes KA, van den Bogaerdt A, Bogers AJ, Zanelli E, et al. (December 2019). "Characterization of binding, functional activity, and contractile responses of the selective 5-HT1F receptor agonist lasmiditan". British Journal of Pharmacology. 176 (24): 4681–4695. doi:10.1111/bph.14832. PMC6965684. PMID31418454. TABLE 1 Summary of pIC50 (negative logarithm of the molar concentration of these compounds at which 50% of the radioligand is displaced) and pKi (negative logarithm of the molar concentration of the Ki ) values of individual antimigraine drugs at 5‐HT receptors [...] TABLE 2 Summary of pEC50 values of cAMP (5‐HT1A/B/E/F and 5‐HT7), GTPγS (5‐HT1A/B/D/E/F), and IP (5‐HT2) assays of individual antimigraine drugs at 5‐HT receptors [...]
^Perez, M., Halazy, S., Pauwels, P.J., Colpaert, F.C., John, G.W. (1999). "F-11356". Drugs of the Future. 24 (6): 0605. doi:10.1358/dof.1999.024.06.537284. Retrieved 23 June 2025.
^Martin GR (October 1997). "Pre-clinical pharmacology of zolmitriptan (Zomig; formerly 311C90), a centrally and peripherally acting 5HT1B/1D agonist for migraine". Cephalalgia. 17 (Suppl 18): 4–14. doi:10.1177/0333102497017S1802. PMID9399012.
^Lionetto L, Casolla B, Mastropietri F, D'Alonzo L, Negro A, Simmaco M, et al. (August 2012). "Pharmacokinetic evaluation of zolmitriptan for the treatment of migraines". Expert Opin Drug Metab Toxicol. 8 (8): 1043–1050. doi:10.1517/17425255.2012.701618. PMID22762358.
^ abDeen M, Christensen CE, Hougaard A, Hansen HD, Knudsen GM, Ashina M (March 2017). "Serotonergic mechanisms in the migraine brain - a systematic review". Cephalalgia. 37 (3): 251–264. doi:10.1177/0333102416640501. PMID27013238. The central mechanisms of triptans are a subject of intense debate and have been investigated in several studies. Brain PET studies reported that zolmitriptan crosses the BBB and binds to central 5-HT1B receptors with relatively low occupancy (77,78). It is still unknown whether sumatriptan has a central effect.
^ abWall A, Kågedal M, Bergström M, Jacobsson E, Nilsson D, Antoni G, et al. (2005). "Distribution of zolmitriptan into the CNS in healthy volunteers: a positron emission tomography study". Drugs in R&D. 6 (3): 139–147. doi:10.2165/00126839-200506030-00002. PMID15869317.
^Varnäs K, Jučaite A, McCarthy DJ, Stenkrona P, Nord M, Halldin C, et al. (July 2013). "A PET study with [11C]AZ10419369 to determine brain 5-HT1B receptor occupancy of zolmitriptan in healthy male volunteers". Cephalalgia. 33 (10): 853–860. doi:10.1177/0333102413476372. PMID23430984.
^ abcdTekes K, Szegi P, Hashemi F, Laufer R, Kalász H, Siddiq A, et al. (2013). "Medicinal chemistry of antimigraine drugs". Curr Med Chem. 20 (26): 3300–3316. doi:10.2174/0929867311320260012. PMID23746273.
^Goadsby PJ, Edvinsson L (1994). "Joint 1994 Wolff Award Presentation. Peripheral and central trigeminovascular activation in cat is blocked by the serotonin (5HT)-1D receptor agonist 311C90". Headache. 34 (7): 394–399. doi:10.1111/j.1526-4610.1994.hed3407394.x. PMID7928323.
^Martin GR (1994). "Pre-clinical profile of the novel 5-HT 1D receptor agonist 311C90". New Advances in Headache Research. 4: 3–4.
^Peck R, Dixon R, Seaber E, On N, Mercer J, Posner J, et al. (1994). "Clinical pharmacology of 311C90". New Advances in Headache Research. 4: 9–10.
^Boshuisen ML, den Boer JA (September 2000). "Zolmitriptan (a 5-HT1B/1D receptor agonist with central action) does not increase symptoms in obsessive compulsive disorder". Psychopharmacology (Berl). 152 (1): 74–79. doi:10.1007/s002130000529. PMID11041318.
^ ab"ML 004". AdisInsight. 8 June 2023. Retrieved 27 October 2024.
^Wang L, Clark EA, Hanratty L, Koblan KS, Foley A, Dedic N, et al. (August 2024). "TAAR1 and 5-HT1B receptor agonists attenuate autism-like irritability and aggression in rats prenatally exposed to valproic acid". Pharmacol Biochem Behav. 245 173862. doi:10.1016/j.pbb.2024.173862. PMID39197535. Interest in 5-HT1B as a target for ASD is further evidenced by the ongoing Phase 2 clinical trial of ML-004, a modified release form of the 5-HT1B/1D agonist zolmitriptan, which is being evaluated for the treatment of social communication deficits in adolescent and adult subjects with ASD (NCT05081245).
^"Maplight Autism Study". Cortica. Retrieved 27 October 2024. Purpose: The purpose of this study is to find out whether ML-004, an extended-release version of zolmitriptan, can support with sociability and emotional regulation in adults with ASD.
^Rasia-Filho AA, Giovenardi M, de Almeida RM (January 2008). "Drugs and aggression". Recent Pat CNS Drug Discov. 3 (1): 40–49. doi:10.2174/157488908783421456. PMID18221240. In addition, the 5-HT1B receptors are of potential importance as target for treatment of different disorders such as depression, schizophrenia, Parkinson's disease, and impulsive disorders [133]. Drugs acting as agonists at 5- HT1B receptors, when administered systemically, potently and efficaciously inhibit several types of aggressive behavior in mice [17,135; and for review see 63]. Systemically administered 5-HT1B receptor agonists such as CP-94,253, ampirtoline and zolmitriptan exert anti-aggressive effects in mice with moderate or high levels of aggression, without impairing non-aggressive activities [17, 23, 129,135]. Further support for the significant role of this receptor subtype derives from the finding of increased aggression in mutant 129Sv mice lacking the 5-HT1B receptor gene [136, and see 137].
^de Boer SF, Koolhaas JM (December 2005). "5-HT1A and 5-HT1B receptor agonists and aggression: a pharmacological challenge of the serotonin deficiency hypothesis". Eur J Pharmacol. 526 (1–3): 125–139. doi:10.1016/j.ejphar.2005.09.065. PMID16310183. Using such an ethopharmacological approach in either rats or mice, it has recently been claimed that only certain specific 5-HT1A receptor agonists (i.e., alnespirone and S-15535; de Boer et al., 1999, 2000), a mixed 5-HT1A/1B receptor agonist (i.e., eltoprazine; Olivier et al., 1995) and several specific 5-HT1B receptor agonists (i.e., CGS12066b, CP-94,253, anpirtoline, zolmitriptan, sumatriptan; Bell and Hobson, 1994; Fish et al., 1999; De Almeida et al., 2001; Miczek et al., 2004) exert behavioral specific anti-aggressive effects. In particular, it was claimed that agonists acting on the 5-HT1B receptors have more selective anti-aggressive effects in mice than those acting on 5-HT1A receptors (Miczek et al., 2004; Olivier, 2004).
^de Almeida RM, Nikulina EM, Faccidomo S, Fish EW, Miczek KA (September 2001). "Zolmitriptan--a 5-HT1B/D agonist, alcohol, and aggression in mice". Psychopharmacology (Berl). 157 (2): 131–141. doi:10.1007/s002130100778. PMID11594437.
^Tricklebank MD, Robbins TW, Simmons C, Wong EH (June 2021). "Time to re-engage psychiatric drug discovery by strengthening confidence in preclinical psychopharmacology". Psychopharmacology (Berl). 238 (6): 1417–1436. doi:10.1007/s00213-021-05787-x. PMC7945970. PMID33694032. A high proportion of violent acts are committed under the influence of alcohol. Aggressive behaviour can also be primed in the mouse by exposure to alcohol (De Almeida et al. 2001). In findings that are consistent with our knowledge of the relationship between serotonin and aggression (Pihl and Lemarquand 1998), this impact of alcohol can be ameliorated by treatment with the 5-HT1B/1D receptor agonist zolmitriptan, an approved anti-migraine drug. However, these findings have seemingly been overlooked despite the consistency of rodent and human data (Gowin et al. 2010).
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.
Which Supreme Court case ruled state-sponsored public-school segregation unconstitutional?
Brown v. Board of Education in 1954.
HAVE YOU CHECKED OUT...?
What Happened in Wilmington in 1898?
A thriving Black political and business community in Wilmington, North Carolina was attacked as white supremacists seized control of local government. Black citizens were killed and expelled, and elected leadership was overthrown. The event reshaped the city and suppressed Black political power for generations.
Text was copied from this source, which is available under a Creative Commons Attribution 4.0 International License.
