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Geodyne Resources Inc. (\"Geodyne\") (ASE:GDR) announced Wednesday that Geodyne has entered into an agreement with Samson Investment Co. and one of Samson's subsidiaries, both of Tulsa, Okla., whereby Samson will acquire Geodyne by merger for cash in the amount of $1.22 per share of outstanding common stock of Geodyne. Geodyne has 16,635,376 common shares outstanding. Under the agreement, the subsidiary of Samson will be merged into Geodyne which will survive as a wholly-owned subsidiary of Samson Investment Co. (excerpt)

Geodyne Resources Inc. (AMEX: GDR) reported a net loss of $2,682,544, or 17 cents per common share for its fiscal year ended Feb. 29, 1992, a decrease from the net income of $4,196,128, or 24 cents per common share from the previous fiscal year. The company reported revenues of $9,582,422 for fiscal year 1992, down 53 percent from the $20,356,702 reported for fiscal 1991. \"The loss is the result of the continued downturn in the energy income program market,\" says Michael W. Tomasso, president and CEO of Geodyne Resources. (excerpt)

Geodyne Resources Inc. (AMEX:GDR), Thursday announced the formation of PaineWebber/Geodyne Institutional/Pension Energy Income Limited Partnership P-7 and P-8 with aggregate subscriptions of approximately $30.5 million. Activated on Feb. 28, the partnerships include subscriptions from approximately 1,427 investors totaling $18,870,200 for P-7 and 1,280 investors totaling $11,616,800 for P-8. Upon activation, the partnership purchased $21.4 million in natural gas and oil properties which Geodyne had acquired on their behalf. The purchase allowed Geodyne to retire $23.6 million in short-term debt originally incurred to purchase the properties in November 1991. (excerpt)

Geodyne Resources Inc. (AMEX:GDR) reported a net loss of $385,437, or 3 cents a share, for the third quarter ended Nov. 30, 1991 compared with net income of $1,517,780, or 9 cents per share, reported in fiscal 1991. Revenues for the third quarter of fiscal 1992 decreased 54 percent to $2,472,091 from $5,428,454 reported for the same period last year. In addition, the company reported revenues for the nine months ended Nov. 30, 1991 of $5,538,088 as compared to $14,324,828 for the same period last year. (excerpt)

Geodyne Resources Inc. (NASDAQ:GEOD) reported record net income of $7,388,581, or 43 cents per common share, for the year ended Feb. 28, 1989, an increase of 65.5 percent from $4,463,135, or 25 cents per common share, for the year ended Feb. 29, 1988. The company also reported record revenues for fiscal 1989 of $20,189,818, up 44 percent from $14,016,907 reported for fiscal 1988. Revenues from management fees for fiscal 1989 were $11.7 million, resulting from the acquisition of approximately $101 million in producing oil and gas properties on behalf of the company's partnerships. (excerpt)

Geodyne Resources Inc. (NASDAQ:GEOD) Friday announced it had completed the offering of interests in the PaineWebber/Geodyne Energy Income II-G limited partnership with total subscriptions of approximately $37.2 million from approximately 3,700 investors. The II-G limited partnership is the seventh offered under the $300 million registration for this program. The company also sponsors the PainWebber/Geodyne Institutional/Pension Energy Income Partners Program, a $150 million partnership offering. (excerpt)

Geodyne Resources Inc. Tuesday announced that Mesa Limited Partnership's G. Shell Boudreaux has joined Geodyne in the capacity of senior vice president -- chief operations officer. In this newly created position at the company's Tulsa office, Boudreaux will supervise Geodyne's production, operations, land, geological, gas contracts and partnership management departments. \"We are extremely pleased that an oil and gas professional with the depth of experience of Shell Boudreaux has joined Geodyne,\" said Michael W. Tomasso, president and chief executive officer. \"With his operational leadership we believe Geodyne is poised to become a major independent energy company in the 1990s.\" (excerpt)

Using both confocal immunofluorescence microscopy and biochemical approaches, we have examined the role of β-arrestins in the activation and targeting of extracellular signal-regulated kinase 2 (ERK2) following stimulation of angiotensin II type 1a receptors (AT1aR). In HEK-293 cells expressing hemagglutinin-tagged AT1aR, angiotensin stimulation triggered β-arrestin-2 binding to the receptor and internalization of AT1aR-β-arrestin complexes. Using red fluorescent protein-tagged ERK2 to track the subcellular distribution of ERK2, we found that angiotensin treatment caused the redistribution of activated ERK2 into endosomal vesicles that also contained AT1aR-β-arrestin complexes. This targeting of ERK2 reflects the formation of multi-protein complexes containing AT1aR, β-arrestin-2, and the component kinases of the ERK cascade, cRaf-1, MEK1, and ERK2. Myc-tagged cRaf-1, MEK1, and green fluorescent protein-tagged ERK2 coprecipitated with Flag-tagged β-arrestin-2 from transfected COS-7 cells. Coprecipitation of cRaf-1 with β-arrestin-2 was independent of MEK1 and ERK2, whereas the coprecipitation of MEK1 and ERK2 with β-arrestin-2 was significantly enhanced in the presence of overexpressed cRaf-1, suggesting that binding of cRaf-1 to β-arrestin facilitates the assembly of a cRaf-1, MEK1, ERK2 complex. The phosphorylation of ERK2 in β-arrestin complexes was markedly enhanced by coexpression of cRaf-1, and this effect is blocked by expression of a catalytically inactive dominant inhibitory mutant of MEK1. Stimulation with angiotensin increased the binding of both cRaf-1 and ERK2 to β-arrestin-2, and the association of β-arrestin-2, cRaf-1, and ERK2 with AT1aR. These data suggest that β-arrestins function both as scaffolds to enhance cRaf-1 and MEK-dependent activation of ERK2, and as targeting proteins that direct activated ERK to specific subcellular locations.

Contrast-enhanced magnetic resonance imaging is an essential tool for disease diagnosis and management; all marketed clinical magnetic resonance imaging (MRI) contrast agents (CAs) are gadolinium (Gd) chelates and most are extracellular fluid (ECF) agents. After intravenous injection, these agents rapidly distribute to the extracellular space and are also characterized by low serum protein binding and predominant renal clearance. Gd is an abiotic element with no biological recycling processes; low levels of Gd have been detected in the central nervous system and bone long after administration. These observations have prompted interest in the development of new MRI contrast agents based on biotic elements such as iron (Fe); Fe-HBED (HBED = N,N′-bis(2-hydroxyphenyl)ethylenediamine-N,N′-diacetic acid), a coordinatively saturated iron chelate, is an attractive MRI CA platform suitable for modification to adjust relaxivity and biodistribution. Compared to the parent Fe-HBED, the Fe-HBED analogs reported here have lower serum protein binding and higher relaxivity as well as lower relative liver enhancement in mice, comparable to that of a representative gadolinium-based contrast agent (GBCA). Fe-HBED analogs are therefore a promising class of non-Gd ECF MRI CA.

Objective: Since peritoneal dialysis causes peritoneal fibrosis, we examined how glucose (osmotic factor), mannitol (osmotic control), and angiotensin II (AngII) regulate proinflammatory cyclooxygenase 2 (COX-2) in primary rat peritoneal mesothelial cells. Materials and Methods: For this study, we used the following material (n = 4-8 cell lines): cells, passages 1-2; 125I-AngII receptor surface binding (AT1R antagonist losartan, AT2R antagonist PD123319; both 10 µM ); intracellular calcium probe calcium-5; COX-2 immunoblotting (β-actin normalized); real-time PCR of COX-2 gene PTGS2, and NF-κB inhibitor Ro-1069920 (5 µM ). Results: AngII surface receptors were predominantly AT1R (minimally AT2R). AngII and glucose increased COX-2 protein expression concentration dependently; mannitol also increased COX-2 expression. Maximal COX-2 protein expression was observed after 6 h (AngII) and 24 h (glucose, mannitol). The time course of increases in PTGS2 mRNA levels reflected that of COX-2 protein expression. At optimal exposure conditions (time/concentration), glucose was 5-fold more efficacious in stimulating COX-2 protein expression than AngII or mannitol. Losartan fully inhibited COX-2 protein responses to AngII and mannitol, but minimally inhibited responses to glucose. Ro-1069920 fully inhibited COX-2 protein responses to each effector. Conclusion: AngII, glucose, and osmotic stress (mannitol) activate COX-2; NF-κB may be an ideal site for COX-2 blockade, and COX-2 activation by osmotic stress requires AT1R, but activation by glucose is more robust and mechanistically complex. © 2014 S. Karger AG, Basel