top of page

Emma Patrick Group

Public·29 members
Jameson Bennett
Jameson Bennett

1997 - No 6.rar 'LINK'

The 8th/9th Battalion, Royal Australian Regiment (8/9 RAR) is a motorised infantry battalion of the Australian Army. It was originally formed in 1973 by linking together both the 8th and 9th Battalions of the Royal Australian Regiment. Over the next twenty-four years the battalion would remain on the Australian Order of Battle based at Enoggera Barracks in Brisbane, Queensland, until it was disbanded in 1997 amid a number of Defence-wide cutbacks introduced by the Howard government. In 2006 it was announced that the battalion would be re-raised as part of a plan to expand the size of the Army and since then it established itself as a fully deployable motorised infantry battalion as part of 7th Brigade.

1997 - No 6.rar

In January 1992, the battalion took on the role of a Ready Reserve unit.[1] Under this scheme Ready Reserve soldiers were posted to the battalion for an initial 12-month full-time period, followed by a further period of four years part-time. On 10 October 1992, the battalion received the Right to the Freedom of Entry to the City of Brisbane.[2] In 1996, the Ready Reserve scheme was abolished by the incoming Howard government,[3] and shortly after this, as part of a restructuring of the Army, 8/9 RAR was disbanded on 30 June 1997.[1]

The Battalion Association was created to perpetuate the memory of the unit when it was initially disbanded in 1997. With resurrection in 2007, the association now serves as the conduit for past, present and future members.[18]

The Bcl-2 family of pro- and anti-apoptotic proteins plays an important role in apoptosis induced by a large variety of stimuli (Gross et al, 1999). We show here that overexpression of Bcl-2 in T3M-4 cells efficiently inhibits induction of apoptosis by 9cRA. Treatment of parental T3M-4 cells with 9cRA also causes a decrease in the Bcl-2/Bax ratio, which may facilitate cell death. It may be hypothesised that this is important for the ability of retinoids to enhance the sensitivity of pancreatic cancer cells to other cytotoxic drugs (Pettersson et al, 2001). Until now, the relationship between apoptosis induced by retinoic acid and expression of Bcl-2 has been explored mainly in leukaemic cells. In agreement with the results presented here, down-regulation of Bcl-2 expression by retinoids has been observed in acute promyelocytic and myeloid leukaemic cells, and stable overexpression of Bcl-2 has been shown to confer resistance to apoptosis (Nagy et al, 1996; Bocchia et al, 1997; Bruel et al, 1997).

A major aim of this study was to investigate the role of different retinoid receptor subtypes in activation of the apoptotic response to the pan-agonist 9cRA. We determined that the four cell lines studied showed similar receptor expression patterns, with one important exception. That is, 9cRA-resistant A818-4 cells express almost undetectable levels of RAR-γ. RAR-α, RAR-γ and RXR-α were expressed in all cells but weak expression of RAR-β could be detected in T3M-4 cells only. This is in agreement with previous reports, which have shown that RAR-β expression is generally low or absent in pancreatic cancer cells (Kaiser et al, 1997). Although induction of RAR-β has been reported to be an indicator of retinoid response (Seewaldt et al, 1995; Lee et al, 2000; Sun et al, 2000), we could detect no induction of either RAR subtype upon retinoid treatment. This may seem surprising, but is likely to be due to methylation of the RAR-beta gene (Ueki et al, 2000).

Among the receptor subtype selective compounds tested, only two had inhibitory activity as single agents. "type":"entrez-nucleotide","attrs":"text":"LG101093","term_id":"1041427333"LG101093, which binds selectively to RAR-γ and the pan RAR-agonist LGD1550 both caused significantly reduced cell viability and induced nuclear fragmentation, characteristic of apoptosis. Furthermore, an RAR-β/γ selective antagonist ("type":"entrez-nucleotide","attrs":"text":"LG030403","term_id":"972843834"LG030403) was shown to counteract the effect of "type":"entrez-nucleotide","attrs":"text":"LG101093","term_id":"1041427333"LG101093, LGD1550, as well as 9cRA. Taken together, these results demonstrate that activation of RAR-γ is essential for induction of apoptosis by retinoids in pancreatic adenocarcinoma cells. This is also supported by the fact that A818-4 are resistant to the effects of 9cRA. A number of earlier studies have established a connection between RAR-γ and retinoid induced growth arrest and apoptosis in various cell types. Expression of RAR-β is often lost or decreased in tumour cells (Seewaldt et al, 1995; Wan et al, 1999; Lee et al, 2000; Sun et al, 2000). However, results from a study in melanoma cells showed that, although RAR-β expression was induced by activation of any of the RAR or RXR subtypes, only RAR-γ selective compounds were able to induce differentiation followed by apoptosis. This suggests a critical role for RAR-γ in apoptosis (Spanjaard et al, 1997). The same finding has been observed in neuroblastoma cells. In contrast to ATRA, which induces differentiation in these cells, RAR-γ selective retinoids were shown to induce apoptotic cell death (Meister et al, 1998).

Rev. Proc. 97-27, 1997-21 I.R.B. 10 - This advance consent (voluntary change) revenue procedure provides the general procedures under Treas. Reg. 1.446-1(c) for obtaining the consent of the Commissioner of Internal Revenue to change a method of accounting for federal income tax purposes. Rev. Proc. 97-27 was modified by Rev. Proc. 2002-19, Rev. Proc. 2007-67 and Rev. Proc. 2009-39, and superseded by Rev. Proc. 2015-13. 041b061a72


Welcome to the group! You can connect with other members, ge...


bottom of page