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This paper discusses a component of the research study conducted to provide construction organizations with a genetic benchrnarking framework to assess their extent of information communication technology (ICT) adoption for building project management processes. It defines benchmarking and discusses objectives of the required benchmarking framework and development of the framework. The study focused on ICT adoption by small and medium enterprises (SMEs) in the construction industry and with respect to SMEs it is important to understand processes, their indicators, and measures in the local context. Structure of the suggested benchmarking framework has been derived after extensive literature survey and a questionnaire survey conducted in the Indian construction industry. The suggested benchmarking process is an iterative process divided into four stages. It can be implemented at organization and industry levels for rating the construction organizations for ICT adoption and performance measurement. The framework has a genetic structure and can be generalized and applied for other countries with due considerations. CE Database subject headings: Bench marks; Buildings; Communication; Construction management. Author keywords: Benchmarks; Buildings; Communication; Construction management. DOI: 10.1061/(ASCE)CO.1943-7862.0000155

Reactive airway disease predisposes patients to episodes of acute smooth muscle mediated bronchoconstriction. We have for the first time recently demonstrated the expression and function of endogenous ionotropic [GABA.sub.A] channels on airway smooth muscle cells. We questioned whether endogenous [GABA.sub.A] channels on airway smooth muscle could augment [beta]-agonist-mediated relaxation. Guinea pig tracheal tings or human bronchial airway smooth muscles were equilibrated in organ baths with continuous digital tension recordings. After pretreatment with or without the selective [GABA.sub.A] antagonist gabazine (100 [micro]M), airway muscle was contracted with acetylcholine or [beta]-ala neurokinin A, followed by relaxation induced by cumulatively increasing concentrations of isoproterenol (1 nM to 1 [micro]M) in the absence or presence of the selective [GABA.sub.A] agonist muscimol (10-100 [micro]M). In separate experiments, guinea pig tracheal tings were pretreated with the large conductance [K.sub.Ca] channel blocker iberiotoxin (100 nM) after an [EC.sub.50] contraction with acetylcholine but before cumulatively increasing concentrations of isoproterenol (1 nM to 1 uM) in the absence or presence of muscimol (100 uM). [GABA.sub.A] activation potentiated the relaxant effects of isoproterenol after an acetylcholine or tachykinin-induced contraction in guinea pig tracheal rings or an acetylcholine-induced contraction in human endobronchial smooth muscle. This muscimol-induced potentiation of relaxation was abolished by gabazine pretreatment but persisted after blockade of the maxi [K.sub.Ca] channel. Selective activation of endogenous [GABA.sub.A] receptors significantly augments [beta]-agonist-mediated relaxation of guinea pig and human airway smooth muscle, which may have important therapeutic implications for patients in severe bronchospasm. guinea pig; organ bath; gabazine; muscimol

[gamma]-Aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the mammalian central nervous system and exerts its actions via both ionotropic ([GABA.sub.A]) channels and metabotropic ([GABA.sub.B]) receptors. [GABA.sub.A] channels are ubiquitously expressed in neuronal tissues, and in mature neurons modulate an inward chloride current resulting in neuronal inhibition due to membrane hyperpolarization. In airway smooth muscle (ASM) cells, membrane hyperpolarization favors smooth muscle relaxation. Although [GABA.sub.A] channels and [GABA.sub.B] receptors have been functionally identified on peripheral nerves in the lung, [GABA.sub.A] channels have never been identified on ASM itself. We detected the mRNA encoding of the [GABA.sub.A] [[alpha].sub.4]-, [[alpha].sub.5]-, [[beta].sub.3]-, [[delta], [[gamma].sub.1-3]-[pi]-, and [theta]-subunits in total RNA isolated from native human and guinea pig ASM and from cultured human ASM cells. Selected immunoblots identified the [GABA.sub.A] [[alpha].sub.4]-, [[alpha].sub.5]-, [[beta].sub.3]-, and [[gamma].sub.2]-subunit proteins in native human and guinea pig ASM and cultured human ASM cells. The [GABA.sub.A] [[beta].sub.3]-subunit protein was immunohistochemically localized to ASM in guinea pig tracheal rings. While muscimol, a specific [GABA.sub.A] channel agonist, did not affect the magnitude or the time to peak contractile effect of substance P, it directly concentration dependently relaxed a tachykinin-induced contraction in guinea pig tracheal rings, which was inhibited by the [GABA.sub.A]-selective antagonist gabazine. Muscimol also relaxed a contraction induced by an alternative contractile agonist histamine. These results demonstrate that functional [GABA.sub.A] channels are expressed on ASM and suggest a novel therapeutic target for the relaxation of ASM in diseases such as asthma and chronic obstructive lung disease. RT-PCR; immunoblot; tachykinin; guinea pig; organ bath', histamine

Neuropeptide tachykinins (substance P, neurokinin A, and neurokinin B) are present in peripheral terminals of sensory nerve fibers within the respiratory tract and cause airway contractile responses and hyperresponsiveness in humans and most mammalian species. Three subtypes of neurokinin receptors ([NK.sub.1] R, [NK.sub.2]R, and [NK.sub.3]R) classically couple to [G.sub.q] protein-mediated inositol 1,4,5-trisphosphate ([IP.sub.3]) synthesis and liberation of intracellular [Ca.sup.2+], which initiates contraction, but their expression and calcium signaling mechanisms are incompletely understood in airway smooth muscle. All three subtypes were identified in native and cultured human airway smooth muscle (HASM) and were subsequently overexpressed in HASM cells using a human immunodeficiency virus-l-based lentivirus transduction system. Specific NKR agonists {[NK.sub.1]R, [[Sar.sup.9],Met[([O.sub.2]).sup.11]] substance P; [NK.sub.2]R, [beta]-[Ala.sup.8]]-neurokinin A(4-10); [NK.sub.3]R, senktide} stimulated inositol phosphate synthesis and increased intracellular [Ca.sup.2+] concentration ([[[Ca.sup.2+].sub.i]]) in native HASM cells and in HASM cells transfected with each NKR subtype. These effects were blocked by NKR-selective antagonists ([NK.sub.1]R, L-732138; [NK.sub.2]R, GR-159897, [NK.sub.3]R, SB-222200). The initial transient and sustained phases of increased [[[Ca.sup.2+]].sub.i] were predominantly inhibited by the [IP.sub.3] receptor antagonist 2-aminoethoxydiphenyl borate (2-APB) or the store-operated [Ca.sup.2+] channel antagonist SKF-96365, respectively. These results show that all three subtypes of NKRs are expressed in native HASM cells and that [IP.sub.3] levels are the primary mediators of NKR-stimulated initial [[[Ca.sup.2+]].sub.i] increases, whereas store-operated [Ca.sup.2+] channels mediate the sustained phase of the [[[Ca.sup.2+]].sub.i] increase. intracellular calcium: ryanodine: actin: myosin; lentivirus

The role of renal [A.sub.1] adenosine receptors (AJAR) in the pathogenesis of radiocontrast nephropathy is controversial. We aimed to further elucidate the role of [A.sub.1] AR in the pathogenesis of radiocontrast nephropathy and determine whether renal proximal tubule [A.sub.1]AR contribute to the radiocontrast nephropathy. To induce radiocontrast nephropathy, [A.sub.1]AR wild-type (WT) or knockout (KO) mice were injected with a nonionic radiocontrast (iohexol, 1.5-3 g iodine/kg). Some [A.sub.1]WT mice were pretreated with 8-cyclopentyl-1, 3-dipropylxanthine (DPCPX; a selective [A.sub.1]AR antagonist) before iohexol injection. [A.sub.1]AR contribute to the pathogenesis of radiocontrast nephropathy in vivo as the [A.sub.1]WT mice developed significantly worse acute renal failure, more renal cortex vacuolization, and had lower survival 24 h after iohexol treatment compared with the [A.sub.1]KO mice. DPCPX pretreatment also protected the [A.sub.1]WT mice against radiocontrastinduced acute renal failure. No differences in renal cortical apoptosis or inflammation were observed between [A.sub.1]WT and [A.sub.1]KO mice. To determine whether the proximal tubular [A.sub.1]AR mediate the direct renal cytotoxicity of radiocontrast, we treated proximal tubules in culture with iohexol with or without 2-chloro-[N.sup.6]-cyclopentylad-enosine (a selective [A.sub.1]AR agonist) or DPCPX pretreatment. We also subjected cultured proximal tubule cells overexpressing [A.sub.1]AR or lacking [A.sub.1]AR to radiocontrast injury. Iohexol caused a direct dosedependent reduction in proximal tubule cell viability as well as proliferation. Neither the [A.sub.1]AR agonist nor the antagonist treatment affected proximal tubule viability or proliferation. Moreover, overexpression or lack of [A.sub.1]AR failed to impact the iohexol toxicity on proximal tubule cells. Therefore, we conclude that radiocontrast causes acute renal failure via mechanisms dependent on [A.sub.1]AR; however, renal proximal tubule AjAR do not contribute to the direct tubular toxicity of radiocontrast. acute renal failure; HK-2 cells; iohexol; knockout mice; LLC-P[K.sub.1] cells; vasoconstriction