The microstructure of amorphous polymers-- a wide angle x-ray diffraction study

Imperial Users onl

Franks family papers, 1711-1821, [1965-1968].

Contains business correspondence, accounts and documents relating to Jacob Franks of New York, his two sons, Moses and David, a nephew, Isaac, and a John Franks of Halifax, possibly a member of the family.The collection is subdivided according to the individuals concerned, as follows: Jacob Franks, 1687-1769, includes a paper fragment with his signature (n.d.), and a "Recognizance of Abraham De Lucena to prosecute Jacob Franks for an assault" (1711); Moses Franks, 1718-1789, includes a Kings Warrant for payment to Sir James Colebrooke et al., contractors for victualling British forces in North America. Among the signatures appearing are those of King George II, Holles, Duke of Newcastle, prime minister, and Moses Franks (1760), photocopies of handwritten copies of two letters from James Parker to Moses Franks (1762), and letters of administration granted to John Ashley, Phineas Bond and Charles Jervis for the estate of Moses Franks (1790); David Franks, 1720-1793, includes letters of administration issued to David Franks and Nathan Levy for the estate of William Hale (1744), a sworn deposition by James Lowry of Lancaster County, Indian trader, regarding a business transaction involving, among others, Joseph Simon and David Franks (1754), an order to Jacob Franks for payment (1762), a letter from Bartram Galbriath to Jonathan Logan regarding a real estate matter involving David Franks and Nathan Levy (1767), a business letter (1770), a letter to Franks from George Croghan regarding a contract in which Barnard and Michael Gratz are mentioned (1775), a journal containing handwritten copies of three indentures, one partnership agreement and one power of attorney.Among the names appearing are David Franks, Joseph Simons, Levy Andrew Levy, B. Franklin, and William Franklin (1776), "Mr. David Franks's Account with Joseph Simon for Supplying the Prisoners at Lancaster, Pa. with Necessary's" (1777), a typewritten copy of an announcement appearing in Towne's Penna. Evening post alleging that David Franks had been disloyal to the United States (1778), a letter signed by Myer Hart, an agent for David Franks, certifying that the prisoners in the British Service under his care at Easton, Pa. were well-cared for (1778), and a sworn deposition signed by David Franks attesting to the birth dates of his sister, Phila, and himself (1792).Isaac Franks, 1759-1822, includes a letter from William Morrison, written from Charleston, S.C., expressing thanks for his letter of introduction to M. Zirzedas (?Moses Sarzedas) (1784), a handwritten copy of the account of Isaac Franks as settled by Jonathan Burrall, Commissioner for the Quartermaster Dept., the copy was made March 25, 1812, with added comments by Isaac Franks as to its accuracy (1788), a second somewhat different handwritten copy of the same account, submitted to the Claims Commission for settlement, both dealing with Franks' service at West Point during the Revolutionary War (1788), five documents pertaining to land and property transactions (1878-1794), one involving Dr. Benjamin Rush and bearing the signatures of William Bradford and James Mease, three other items of correspondence (1811-1817), a handwritten copy of "A Narrative of the Revolutionary Services of Isaac Franks" (1818), a letter from the judges of the Supreme Court of Pennsylvania to Franks in his capacity as clerk (1821), and a genealogy of Samuel Davison, father-in-law of Isaac Franks, prepared by John Clagett Proctor; John Franks, 18th century, includes a business letter from Halifax (1758).Also includes a flyleaf of a Hebrew book with signatures of Jacob Franks, his son Moses, in Hebrew and English, another son, David, and a grandson, Jacob Jr.Contains Hart's signature in Hebrew and English on verso of title page of a prayer book published in Amsterdam in 1687. (All except title page are missing). Below is signature of Jacob Franks.Consists of two items: a bill submitted by Benjamin Dunn to Arnold (1778), and the other a cash account of money evidently paid or owed by Arnold (undated). David Salisbury Franks is mentioned in both as a payee.Consists of a letter from Franks in London to David Vanderheyden Senior in Albany regarding sales of "Furs, Castorum & Jenseng."Original manuscript: Laing III, 452--"Poems on Several Occasions by Archibald Home, Esqr. ..."--At the University of Edinburgh.Consists of 31 letters written by Mrs. Jacob Franks and 1 letter written by Jacob Franks in New York City to their son, Naphtali, in England. The greater bulk of the collection consists of research notes and copies of primary source material collected initially by Lee M. Friedman and ultimately by Leo Hershkowitz and by Isidore Meyer, who prepared these letters for publication under the title The Lee Max Friedman collection of American Jewish colonial correspondence : letters of the Franks family (1733-1748) (New York : American Jewish Historical Society, 1968).Gifts, in part, of Mendes Cohen, Bert Handelsman, M. Jastrow, John W. Jordan, Simon Rosendale, and the Elsie O. and Philip D. Sang Foundation.Gift, in part, of the Elsie O. and Philip D. Sang Foundation,Gift, in part, of Leo Hershkowitz,Gift, in part, of Dr. David S. Shields.far0315digitize

Animal models of Parkinson's disease: a source of novel treatments and clues to the cause of the disease

Animal models of Parkinson's disease (PD) have proved highly effective in the discovery of novel treatments for motor symptoms of PD and in the search for clues to the underlying cause of the illness. Models based on specific pathogenic mechanisms may subsequently lead to the development of neuroprotective agents for PD that stop or slow disease progression. The array of available rodent models is large and ranges from acute pharmacological models, such as the reserpine- or haloperidol-treated rats that display one or more parkinsonian signs, to models exhibiting destruction of the dopaminergic nigro-striatal pathway, such as the classical 6-hydroxydopamine (6-OHDA) rat and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse models. All of these have provided test beds in which new molecules for treating the motor symptoms of PD can be assessed. In addition, the emergence of abnormal involuntary movements (AIMs) with repeated treatment of 6-OHDA-lesioned rats with L-DOPA has allowed for examination of the mechanisms responsible for treatment-related dyskinesia in PD, and the detection of molecules able to prevent or reverse their appearance. Other toxin-based models of nigro-striatal tract degeneration include the systemic administration of the pesticides rotenone and paraquat, but whilst providing clues to disease pathogenesis, these are not so commonly used for drug development. The MPTP-treated primate model of PD, which closely mimics the clinical features of PD and in which all currently used anti-parkinsonian medications have been shown to be effective, is undoubtedly the most clinically-relevant of all available models. The MPTP-treated primate develops clear dyskinesia when repeatedly exposed to L-DOPA, and these parkinsonian animals have shown responses to novel dopaminergic agents that are highly predictive of their effect in man. Whether non-dopaminergic drugs show the same degree of predictability of response is a matter of debate. As our understanding of the pathogenesis of PD has improved, so new rodent models produced by agents mimicking these mechanisms, including proteasome inhibitors such as PSI, lactacystin and epoximycin or inflammogens like lipopolysaccharide (LPS) have been developed. A further generation of models aimed at mimicking the genetic causes of PD has also sprung up. Whilst these newer models have provided further clues to the disease pathology, they have so far been less commonly used for drug development. There is little doubt that the availability of experimental animal models of PD has dramatically altered dopaminergic drug treatment of the illness and the prevention and reversal of drug-related side effects that emerge with disease progression and chronic medication. However, so far, we have made little progress in moving into other pharmacological areas for the treatment of PD, and we have not developed models that reflect the progressive nature of the illness and its complexity in terms of the extent of pathology and biochemical change. Only when this occurs are we likely to make progress in developing agents to stop or slow the disease progression. The overarching question that draws all of these models together in the quest for better drug treatments for PD is how well do they recapitulate the human condition and how predictive are they of successful translation of drugs into the clinic? This article aims to clarify the current position and highlight the strengths and weaknesses of available models. LINKED ARTICLES: This article is part of a themed issue on Translational Neuropharmacology. To view the other articles in this issue visit http://dx.doi.org/10.1111/bph.2011.164.issue-