Issue 01 My Childhood.rar
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Yes. You can use your own Transparent Table instead of BRF+ account determination table also. But I am surprised about your issue as I don't have that in my system. The account determination works fine. Did you try the simulation in BRF+ with the values that are passed to brf+?
Thanks. Yes, I am getting this while processing the Invoice RAI's. I have as such changed my event type from Manual to Goods Issue under POB and the error has gone. Still, some further issues wherein the fulfillments are not being reflected on the POB's.
This deception fooled the Yuuzhan Vong, but Rar was faced with other, more personal issues. Her partisan war against the enemy was drawing her close to the dark side of the Force, and Master Skywalker, the head of the Jedi Order, felt that Rar was putting her integrity as a Jedi at risk. The Rar sisters soon suffered another loss; the New Plympto resistance became successful enough that the frustrated Yuuzhan Vong decided to raze the planet, rather than continue to attempt subjugation. All life was wiped from the surface of the planet, rendering it uninhabitable and killing seven million sentients. The Rar sisters were only just able to flee in time, hiding with several thousand other beings aboard a fleet of intrasystem ore miners until help arrived in the form of the Corellian cruiser Nebula Chaser, already loaded with refugees. The captain of the Nebula Chaser, Pollux, promised the Jedi sisters safe asylum. Many during the war had sought personal gain in turning wanted Jedi over to the Yuuzhan Vong, but the Rar sisters accepted the captain's offer and boarded the cruiser.
There was little to be done but complete the mission as swiftly as possible, and with Drark's longblaster Rar prepared for the attack on the cloning grashal. She supported her fellow team members as they entered, using the longblaster to kill Yuuzhan Vong warriors who came too close. Ultimately, Anakin Solo surrendered himself to the Force and let its energy control him, using the vast power to fight off the Yuuzhan Vong and wipe out all the voxyn cloning tissue reserves. At some point, Rar handed the longblaster over to Jaina Solo, who protected her brother as he died. With the voxyn queen on the run, the surviving members of the team relocated to a hidden warren while Tesar Sebatyne sought to find the queen. Lowbacca reported back that the Yuuzhan Vong were moving Solo's body, and Alema Rar, along with Zekk, Jaina Solo and Tahiri Veila, set off to recover the young Jedi's corpse.
The campaign for Borleias was ultimately successful, and granted the New Republic government enough time to set up its new headquarters on the water world of Dac, home to the Quarren and Mon Calamari species. The Myrkr survivors, in the meantime, were again reduced in number with the death of Ganner Rhysode on conquered Coruscant, before being replenished by the return of Jacen Solo, whose life Rhysode had fought to save. Rar, who had been traveling with Tahiri Veila and Zekk as their temporary leader, took her small group to Dac on a refugee convoy, as she had no duties or a Jedi Master to issue her with directives. On Dac, Luke Skywalker had acted alongside the new Chief of State, the Alderaanian Cal Omas, to create a High Council, with Jedi and non-Jedi representatives in equal numbers. Rar contacted Jedi Master Tresina Lobi, who held a seat on the Council, and asked the Chev woman to query Skywalker on what her next actions should be. It was decided by Omas and Skywalker that a ceremony would be held to honor the Myrkr strike team, and that the survivors would be elevated to the status of Jedi Knight.
Without the leader of the Order, or knowledge of the whereabouts or status of the missing Jedi, a meeting was convened in the apartment of Master Tresina Lobi in Coral City's Quarren Tower. Rar attended alongside a group of whichever Jedi could be mustered, and Master Kenth Hamner addressed the assembled Knights and Masters on the issue of the Skywalkers and their companions. The group discussed the idea of inserting a strike team onto Coruscant to interrogate a mysterious figure, the Prophet Yu'shaa, who was leading a resistance movement against the Yuuzhan Vong rulers and was suspected to hold knowledge on the whereabouts of Zonama Sekot. The similarity of the plan to that of the Mission to Myrkr was obvious, as were the risks, and it was intended as a last resort; if Skywalker and his companions failed to make contact within a week, Hamner planned to assemble the strike team of Jedi, of which Rar would be a member.
Tenel Ka Djo still remained the Hapan Queen Mother, Jacen Solo had vanished on a five year journey to explore the Force, and Tekli and Tahiri spent the years on Zonama Sekot. For Rar, as with Jaina Solo, Zekk, Lowbacca and Tesar, moving on was difficult. The Jedi Knight carried out an extensive intelligence-gathering mission on the Bothans, who had since the death of Chief of State Borsk Fey'lya during the Battle of Coruscant wished to enact speciecide against the Yuuzhan Vong. A Bothan politician, Reh'mwa, formed a faction of fundamentalists known as the True Victory Party in order to hunt down Zonama Sekot and eliminate the species. By 35 ABY, Rar had discovered that Reh'mwa and his followers had intelligence pertaining to the living planet's location and were provisioning a cruiser, the Avengeance, for an attack on the exiled Yuuzhan Vong. The Twi'lek duly issued a report to the Jedi High Council.
Rar responded with scorn to Skywalker's overtures and instead began discussing R2-D2, Skywalker's parents, and the sequestered recordings the droid possessed. Despite Solo's skepticism, Skywalker granted Rar a hearing, and the Twi'lek explained that she could reveal the identity of the Jedi Master's mother via the codes she possessed. She issued a code to R2-D2, and the droid played a holorecording of Anakin Skywalker and Padmé Amidala together in the latter's apartment, days before the enaction of Order 66 and the near-extinction of the Jedi Order.
If a response is received within 30 calendar days, it will be reviewed and the BCRC will issue a demand (request for repayment) as applicable. If a response is not received in 30 calendar days, a demand letter will automatically be issued without any reduction for fees or costs. For more information about the CPN, refer to the document titled Conditional Payment Notice (Beneficiary) in the Downloads section at the bottom of this page.
The BCRC will apply a termination date (generally the date of settlement, judgment, award, or other payment) to the case. The BCRC will identify any new, related claims that have been paid since the last time the CPL was issued up to and including the settlement/judgment/award date. Once this process is complete, the BCRC will issue a formal recovery demand letter advising you of the amount of money owed to the Medicare program. The amount of money owed is called the demand amount. The demand letter includes the following:
Obesity [MIM 601665] appears when energy intake exceeds energy expenditure, which leads to an abnormal accumulation of fat in the adipocyte tissue. Both genetic and environmental factors contribute to this multifactorial condition. Candidate genes for obesity can be involved in three fundamental mechanisms; (i) relative increase in energy intake, (ii) relative decrease in energy expenditure and (iii) preferential partitioning of ingested calories to fat storage. Animal models have shown that defects in genes involved in any of these mechanisms are sufficient to cause an obese phenotype.1 Monogenic obesity in mice has led to the discovery of a total of nine single-gene mutation models: diabetes, fatty liver dystrophy, fat, OLETF, little, obese, tubby, mahogany and agouti.2 The first two of these to be characterised were obese, which is caused by a defect in the leptin (LEP [MIM 164160]) gene,3 and diabetes, due to a mutation in the leptin receptor (LEPR [MIM 601007]).4 In humans, seven genes have been identified that are related to obesity, of which six are related to the leptin pathway.5, 6 Leptin induces, through the leptin receptor, the prohormone pro-opiomelanocortin (POMC [MIM 176830]).7, 8 The POMC prohormone is processed into α-MSH by the interacting proteins prohormone convertase I (PCSK1 [MIM 162150]) and carboxypeptidase E.9, 10 α-MSH is an agonist of the predominant neuronal melanocortin receptor isoforms, melanocortin 3 receptor (MC3R [MIM 155540]) and melanocortin 4 receptor (MC4R [MIM 155541]).11, 12, 13 The MC4R regulates food intake and energy expenditure, whereas MC3R influences feeding efficiency and the partitioning of fuel stores into fat.14 The most recent gene to be associated with obesity in humans encodes the transcription factor Drosophila single-minded gene 1 (SIM1 [MIM 603128]). This gene was identified from a balanced chromosomal translocation and haploinsufficiency for the gene causes obesity in mice.15, 16
A detailed characterisation of both breakpoints revealed that the only gene disrupted by the translocation is the RAR-related orphan receptor alpha gene (RORa; MIM 600825) on chromosome 15. The breakpoint is located in the first intron and predicts the loss of the isoform 1 of RORa (RORa1); the other isoforms are not directly affected by the breakpoint. The RORa gene encodes four alternative transcripts (termed RORa1, -a2, -a3, and -a4) and the corresponding proteins are members of the NR1 subfamily of nuclear hormone receptors. The nuclear receptors are composed of a variable N-terminal region, a DNA-binding domain (DBD), and a conserved region that contains the ligand binding domain (LBD). The LBD contains an activation function motif (AF-2) responsible for ligand-dependent transcriptional activation.22 The RORa acts as a monomer or homodimer with the ROR response element (RORE) sequence within the promoter regions upstream of several genes to enhance their expression. An N-terminal modulator region varies between the four RORa splice isoforms which allows for isoform-specific interactions with AT-rich sequences just upstream of the RORE motif. The RORa transcript variants are under control of separate promoter sequences, which gives specific expression patterns. There is little knowledge about the function of the individual RORa isoforms but a targeted disruption of the RORa gene with a loss of all four isoforms in mouse causes the staggerer (sg) phenotype. The sg/sg-mutant mice fed a high fat diet develop atherosclerosis and show hypoalphalipoproteinaemia associated with a decrease in apolipoprotein A-I gene (APOA1 [MIM 107680]) transactivation. The mice also show an aberrant blood plasma lipid profile with lowered levels of circulating HDL and triglycerides.23 The REV-ERB-alpha binds to an element in the proximal promoter of the apolipoprotein C-III (APOC3 [MIM 107720]) gene that is also a RORalpha1-binding element. Recent data have provided evidence for a crosstalk between REV-ERB-alpha and RORalpha1 in the modulation of the APOC3 promoter.24 The APOC3 gene promoter and a distal regulatory region acts as a common enhancer for the three genes of the apolipoprotein cluster on 11q23 (APOC3, APOA1, and APOA4 [MIM 107690]), which could explain the decrease in APOA1 transactivation in the staggerer mouse.25 The role of RORa in lipid regulation in skeletal muscle has also been implicated and thereby suggesting that RORa could be a critical regulator of energy homeostasis in this major mass of lean tissue.26 Presence of a putative responsive element (RORE) specific for RORa isoform 1 also exists in the PPARγ promoter.27 PPARγ is a key regulator of adipocyte differentiation and factors interfering with the PPARγ pathway are strong candidates for an obese phenotype. A regulation of APOC3 and PPARγ by RORa1 provides a direct link to lipid and adipocyte metabolism. Interestingly, three cases with interstitial deletions of 15q have previously been reported in patients with mental retardation and late onset obesity.28, 29, 30 A more recent report also supports the presence of a microdeletion-syndrome involving obesity at 15q21, which possibly overlaps with our breakpoint region on chromosome 15.31 2b1af7f3a8