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One reason for conflicting results may be that prior studies of -AP-induced microglial neurotoxicity largely ignored important costimulatory agents present in the AD brain. The extracellular environment surrounding neuritic plaques in the AD brain is rich in a variety of proinflammatory agents including cytokines, 6 which are likely to augment the effects of -AP on microglia. It has been reported that interferon-, phorbol ester, and lipopolysaccharide LPS ; all augment the effects of -AP on microglia and monocytic cells.27, 38, 46 However, none of these augmenting stimuli have a physiologic role in AD. Our group has focused on two cytokines known to be increased in the central nervous system CNS ; in AD, macrophage colony-stimulating factor M-CSF ; and interleukin-1 IL-1 ; , both of which are microglial activators. M-CSF produced by neurons, astrocytes, and endothelial cells ; 47-52 induces proliferation, migration, and activation of microglia.53-56 After traumatic brain injury, microglial expression of the M-CSF receptor c-fms ; is greatly increased.57 M-CSF treatment of microglia induces increased expression of macrophage scavenger receptors MSRs ; .52 Microglial adhesion to -AP, internalization of -AP, and possibly -AP-induced microglial activation may be mediated by MSR class A.58, 59 -AP also interacts with neuronal receptors for advanced glycation end products RAGEs ; to increase neuronal MCSF expression, 52 which causes further microglial activation. Neuropathologic studies show increased. PROGESTERONE AND GRANULOSA CELL APOPTOSIS transcription. As part of this proposed mechanism, estrogen could stimulate the synthesis of EGF and or a related growth factor, transforming growth factor alpha TGFt ; [21], since both are produced in the ovary [22, 23]. Both EGF and TGFa stimulate P4 secretion within the first 24 h of culture present study, [12] ; . It appears that enhanced P4 synthesis is an essential part of the mechanism through which EGF and presumably TGFax maintain large GC viability. This conclusion is based on the observations that the anti-apoptotic action of EGF is inhibited by both RU 486, a progesterone receptor antagonist, and AG, which reduces basal and EGFinduced P4 secretion. Further, P4 alone is sufficient to extend large GC survival in vitro, and its action is attenuated only by RU 486 and not by AG. P4 also prevents apoptosis in other systems. For example, administration of P4 prevents and RU 486 triggers apoptosis within the uterine epithelium [24]. In addition, a decline in P4 secretion precedes apoptotic changes within luteal cells [25]. Taken together, these studies indicate that P4 acts as an autocrine paracrine factor to maintain cell viability within the ovary and uterus and that factors inhibiting P4 secretion ultimately induce apoptotic changes in these cells. While previous work has shown that a decline in serum P4 precedes apoptosis within the corpus luteum and uterine epithelium, serum P4 levels increase as the GCs of eCGinduced preovulatory follicles undergo DNA fragmentation [2]. The reason for this contradiction is mostly likely that the enzyme responsible for the conversion of pregnenolone to P4 , 3-hydrosteroid dehydrogenase 3p-HSD ; , is expressed in the GCs of healthy preovulatory follicles as well as the associated thecal and interstitial cells [26]. As these follicles undergo atresia, GCs, but not the thecal and interstitial cells, lose their ability to express 3-HSD [26]. This selective loss of 313-HSD within the GCs of atretic follicles could result in a decrease in P4 in the GC component of the follicle. Since P4 maintains GC viability in vitro, the putative decline in P4 within the GC layers could result in a corresponding increase in GC DNA fragmentation, even in the presence of elevated serum P4 levels. These experiments clearly indicate that P4 plays a pivotal role in regulating large GC survival. Previous work with luteal cells has shown that prostaglandin F2, induces an increase in [Ca 2 + ]i that lasts for 20-30 min prior to decreasing P4 synthesis [27]. A similar transient increase in [Ca2 + ]i is observed as the large GCs undergo apoptosis present study ; . Not only does the apparent [Ca 2 + ]i increase, but the calcium distribution changes prior to the large GCs' becoming apoptotic. In the presence of P4, large GC viability is maintained, and calcium is localized to cytoplasmic foci. This pattern of calcium distribution is also observed in GCs that are isolated and immediately loaded with fluo-3 unpublished observation ; . When apoptosis is initiated by inhibiting the action of P4 with RU 486, calcium becomes uniformly distributed throughout the cytoplasm. At this stage, the apparent [Ca2 + ]i is relatively low, as judged by intensity. Dual-purpose otc medicines and products may be reimbursed under a hcfsa with a licensed health care provider's note stating your specific diagnosis or medical condition, a recommendation to take the specific otc medicine to treat your condition, and documentation of the product and cost. THE TOP 100 FALSE CLAIMS ACT SETTLEMENTS: THE CASE HISTORIES 1 ; HCA 1, 400, 000 ; * In December 2000, HCA The Healthcare Company formerly known as Columbia HCA ; , the largest for profit hospital chain in the United States, agreed to plead guilty to criminal conduct and pay more than 0 million in criminal fines, civil penalties and damages for alleged unlawful billing practices. Under the agreement, HCA will pay a total of 5 million to resolve five allegations regarding the manner in which it bills the U.S. government and the states for health care costs. The agreement does not resolve allegations that HCA unlawfully charged for the costs of running its hospitals on cost reports submitted to the government, and that it paid kickbacks to physicians to get Medicare and Medicaid patients referred to its facilities. Of the 5 million, the settlement requires HCA to pay: * more than million to resolve civil claims arising from the company's outpatient laboratory billing practices, which included billing to Medicare, Medicaid, the Defense Department's TRICARE health care program, and the Federal Employees' Health Benefits Program, for lab tests that were not medically necessary, not ordered by physicians, as well as other billing violations; * more than 3 million to resolve civil claims arising from "upcoding, " where false diagnosis codes were assigned to patient records in order to increase reimbursement to the hospitals by Medicare, Medicaid, TRICARE and the Federal Employees' Health Benefits Program. The guilty plea includes one count relating to this upcoding practice; * million to resolve civil claims that the company illegally claimed non reimbursable marketing and advertising costs it disguised as community education. Medicare reimburses providers for "community education" - costs to educate the community at large about public health issues - but not for advertising and marketing a hospital's services; * million to resolve civil claims that HCA illegally charged Medicare for non reimbursable costs incurred in the purchase of home health agencies owned by the Olsten Corporation, as well as other agencies in Florida, Georgia and Alabama. According to the government, HCA devised an elaborate scheme to hide these costs in reimbursable "management fees" paid to third parties. In 1999, a subsidiary of Olsten Corporation, Kimberly Quality Care, entered into criminal plea agreements in three districts and paid more than million in criminal fines. Olsten paid nearly million as part of a civil settlement arising from its collusion with HCA for that conduct. HCA has now agreed to pay million to settle this issue, and 6 million to resolve civil claims for billing Medicare, Medicaid and TRICARE for home health visits for patients who did not qualify to receive them or were not performed and for committing other billing violations. Many of the civil issues resolved as part of the agreement arose from lawsuits filed by relators, commonly known as "whistleblowers, " under the False Claims Act. This law allows whistleblowers who qualify under the statute to receive up to 25 percent of the settlement recovery in cases the government pursues. In addition to the civil settlement, two subsidiaries of Tennessee based HCA, Columbia Homecare Group Inc. and Columbia Management Companies Inc. entered into a criminal plea agreement in which they agreed to pay , 336, 432 in criminal fines and plead guilty to several charges involving a wide range of criminal conduct which occurred at HCA's hospitals nationwide. "HCA To Pay 0 Million, " 15 Corporate Crime Reporter 1 5 ; , January 1, 2001. 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