Jeffery Amherst, Baron Amherst (1717-1797), was commanding general of the British forces in North America and then governor general of British North America.

Born on Jan. 29, 1717, at Riverhead, Kent County, England, Jeffery, or Jeffrey, Amherst became a page to the 1st Duke of Dorset. Entering the army in 1731, he served as an aide to Gen. John Ligonier in the War of the Austrian Succession and participated in the battles of Dettingen, Roucoux, and Fontenoy. On Dec. 25, 1745, he became lieutenant colonel of the 1st Regiment of Foot Guards, and as an aide to the Duke of Cumberland he was present at the Battle of Laffeldt in 1747. Promoted to the colonelcy of the 15th Regiment of Foot, he accompanied Cumberland as commissary at the Battle of Hastenbeck.

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Amherst was recalled to England in January 1758 and was given the rank of major general and command of an army of 14,000 men. His mission was to take the French fort of Louisbourg in Canada, which had been besieged since June 1, 1758; the garrison surrendered on July 26, giving the British their first important victory in the Seven Years War. After securing the Gulf of St. Lawrence, Amherst moved to Albany as commanding general in North America. His task was to drive the French from Lake George and Lake Champlain prior to joining forces with James Wolfe to besiege Quebec.

Ticonderoga fell to Amherst on July 27, 1759, and Crown Point on August 4. After he reached the northern limits of Lake Champlain, he learned of the fall of Quebec and closed his campaign. In recognition of his services, George III appointed him to the sinecure governorship of Virginia. In 1760 Amherst drove down the St. Lawrence from Oswego, meeting British forces from Quebec and from Lake Champlain, to take Montreal, which fell September 8. His conduct of operations during the Indian uprising led by Pontiac in 1763 has usually been criticized as inept. Amherst returned to England during the winter of 1763-1764.

In 1768, when George III decided that all governors should reside in the Colonies, Amherst resigned as governor of Virginia, giving up his military commissions as well. Several months later he was given additional military commissions and 20,000 acres in New York and was appointed to the sinecure governorship of the island of Guernsey. He declined to command the British forces in New England during the American Revolution. In 1776 Amherst served as
military adviser to the Cabinet and was made Baron Amherst. After France entered the war in 1778, he was appointed commander of the military forces in England and was active in the suppression of the Gordon riots. After the war he retired; in view of the approaching war with France in 1792, he was recalled to active duty. He left the army in 1795. A year later he was made a field marshal, the highest rank in the British army. He died on Aug. 31, 1797.

The components from exotic fruit Spondias mombin were analyzed by GC and GC/MS. A total of 261 compounds were identified, accounting for 18.6 ppm of the extracted fruit. They were identified according to their GC retention time on a polar column and their mass spectra. They are divided as follows: 32 hydrocarbons (4.1%), three sulfur compounds (trace), 126 esters (56.2%), eight lactones (10.4%), 22 carbonyl compounds (3.2%), 16 acids (19.5%), 37 alcohols and ethers (5.5%) and 17 miscellaneous compounds (1.1%). Of these 261 compounds, 83 have already been described in the literature to be present in Spondias mombin aroma. The major volatile products identified were γ-hexalactone (0.9 ppm), 2(5H)-furanone (0.7 ppm), methyl hexadecanoate (0.6 ppm) and ethyl 3-hydroxyhexanoate (0.5 ppm).

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Key Word Index

Spondias mombin, Anacardiaceae, fruit volatiles, yellow mombin, hog plum, γ-hexalactone, 2(5H)-furanone, methyl hexadecanoate, ethyl 3-hydroxyhexanoate.

Introduction

Spondias mombin is one of the two Spondias species with S. cytherea Sonn., which grows in the French Polynesian islands. Mombin fruit is eaten by a few persons as an intact fruit or in juice form. Its single natural production is at the end of the warm period (April-May).

Yellow mombin from African, Mexican and Brazilian trees have been examined (1-3). Adedeji et al. reported the presence of 46 free or glycosidically bound compounds in African fruit (1). Sagrero-Nieves et al. identified 48 compounds in Mexican mombin (2). More recently, analysis of volatile compounds of taperebá and cajá, two varieties of Brazilian mombin, were performed by Ceva-Antunes et al., using simultaneous distillation and extraction (SDE) and solid phase microextraction (SPME). In taperebá, 46 substances were identified by SDE and 48 by SPME. In cajá fruit, 42 compounds were analyzed by SDE and 47 by SPME (3). Some changes in physical and chemical composition during maturation of fruits were also analyzed by Bora et al. (4). In addition, the essential oil composition of leaves of S. mombin from Brazil has been described by Lemos et al. (5).

While mombin fruit flavor and leaf oil composition have already been analyzed in previous studies, this work presents a distinctive extraction method, already tested for the determination of the aromatic composition of pineapple (6). Moreover, the aroma compound extract was chromatographed on silica gel low pressure column prior to GC and GC/MS analysis. The silica gel chromatographic fractionation has led to the determination of some newly identified compounds in the fresh pulp of yellow inombin.

Experimental

Reagents: The solvents (acetone, dichloromethane, hexane, diethyl ether and methanol) were Normapur grade from Prolabo (Prolabo, Paris cedex, France) and were redistilled prior to use. The calcium and sodium chloride salts, anhydrous magnesium sulfate, silica gel C60 were purchased from Prolabo, and tetradecane from Aldrich (Aldrich, Chemical Co., Gillingham Dorset, England). Fresh mature ripe fruits were collected in April 2002 from trees growing in Atimaono Golf Club (Tahiti Island, French Polynesia).

Sample extraction and preparation: Ten kg of fresh ripe mombin were manually triturated to give 6.6 kg of pulp and peel. The homogenized mixture was blended with 20% volume of 1.0 M CaCl^sub 2^, for 1 min to inactivate enzymes (6-8), yielding 8.25 L of nectar juice (V). The batch of the nectar juice was extracted with acetone (2.5 x 5) during 5 inin, at room temperature. The extract was passed through a paper filter to discard all trie insoluble material. Sodium chloride was then added to the clear mombin juice leading to aqueous and organic separated phases. These two phases were extracted simultaneously with dichloromethane ( 2/1 ). The organic phase (a dichloromethane-acetone mixture) was dried with anhydrous magnesium sulfate. The anhydrous organic phase was carefully concentrated to ca. 2 mL using a rotary evaporator at 40°C. The aliquot of the organic phase led to an estimated weight of 1.08 g for 10 kg of fresh ripe mombin.

The organic aroma extract was then chromatographied on

a silica gel column (150 mm x 10 mm) using 100 mL of hexane (Fl), dichloromethane (F2), diethyl ether (F3) and methanol (F4). The four eluted fractions were slowly evaporated under dried nitrogen gas to approximately 100 µL.

Objective: To evaluate the role of resident pleural macrophages in the initiation of inflammation.

Methods: We have used a conditional macrophage ablation strategy to determine the role of resident pleural macrophages in the regulation of neutrophil recruitment in a murine model of experimental pleurisy induced by the administration of carrageenan and formalin-fixed Staphylococcus aureus.

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Measurements and Main Results: Conditional macrophage ablation mice express the human diphtheria toxin receptor under the control of the CD11b promoter such that the administration of diphtheria toxin induces ablation of nearly 97% of resident macrophages. Ablation of resident pleural macrophages before the administration of carrageenan or S. aureus dramatically reduced neutrophil influx into the pleural cavity. In the carrageenan model, the reduction in neutrophil infiltration was associated with marked early reduction in the level of macrophage inflammatory protein 2 as well as reduced levels of various cytokines, including tumor necrosis factor α, interleukin 6, and interleukin 10. Adoptive transfer of nontransgenic macrophages partially restored neutrophil infiltration. We also stimulated macrophage-depleted and nondepleted pleural cell populations with carrageenan in vitro and determined the production of chemokines and cytokines. Chemokine and cytokine production was markedly reduced by macrophage depletion, reinforcing the role of resident pleural macrophages in the generation of mediators that initiate acute inflammation.

Conclusion: These studies indicate a critical role for resident pleural macrophages in sensing perturbation to the local microenvironment and orchestrating subsequent neutrophil infiltration.

Keywords: inflammation; macrophage; pleural diseases

The pleural membranes and associated cells are important because they are metabolically active and act as a barrier to invading pathogens by generating an innate and adaptive immunologic response. The pleural cavity is lined with mesothelium and contains resident macrophages (M[straight phi]), mast cells, and lymphocytes (1, 2). During pleural inflammation, it has been reported that mesothelial cells are predominantly responsible for the secretion of C-X-C chemokines, such as interleukin 8 (IL-8), and C-C chemokines, such as macrophage inflammatory protein 1α (MIP-1α) and macrophage chemoattractant protein 1 (MCP-1), which act to recruit neutrophils (polymorphonuclear leukocytes [PMNs]) and mononuclear cells (3-6). In addition, a recent study demonstrated that activated pleural fibroblasts may also be a source of C-X-C and C-C chemokine production (7).

Previous work suggested that the initiation of inflammation is dependent on endogenous IL-6 secretion that subsequently stimulates the additional production of tumor necrosis factor α (TNF-α) and IL-1β from resident pleural cells (8). In contrast, increased IL-1β levels have been reported to precede elevated IL-6 levels (9), thereby suggesting that IL-1β might induce IL-6 production. There is no doubt that TNF-α and IL-1β are key cytokines in the development of pleural inflammation because they act to enhance IL-8 and MCP-1 production from mesothelial cells (3, 5, 10-12). In addition, studies using function-blocking antibodies suggest that activated resident M[straight phi] could be responsible for this TNF-α and IL-1β secretion (10, 12).

Carrageenan-induced pleurisy is a well-established model of acute inflammation (13) and is characterized by a rapid influx of PMNs followed by mononuclear cell infiltration (14, 15). This model is often used to assess the antiinflammatory effects of pharmaceutical agents (16-20) and to assess the in vivo importance of established inflammatory mediators (21-23). Although the neutrophil influx evident in this model is generally used as an experimental readout of acute inflammation, there are data indicating that neutrophils are involved in the release of injurious enzymes and modulation of vascular permeability in carrageenan-mediated pleural inflammation (24, 25).

To date, there has been little study of the role of the resident pleural M[straight phi] in the initiation of inflammation and orchestration of PMN recruitment. Previous work demonstrated a reduced eosinophil influx after administration of LPS to mice that had been previously treated with diphosphonate-containing liposomes to deplete resident pleural M[straight phi] (26). Although this suggests that resident pleural M[straight phi] may play a key role in the initiation of pleural inflammatory responses, there are no definitive data available for PMN infiltration and proinflammatory cytokine production.