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Biomedical subjects

Hong Qian

Publications and source records attributed to Hong Qian.

At least 37 records · Page 2Linked to original sources

The role of exotic species in homogenizing the North American flora.

Exotic species have begun to homogenize the global biota, yet few data are available to assess the extent of this process or factors that constrain its advance at global or continental scales. We evaluate homogenization of vascular plants across America north of Mexico by comparing similarity in the complete native and exotic floras between states and provinces of the USA and Canada. Compared with native species, exotic plants are distributed haphazardly among areas but spread more widely, producing differentiation of floras among neighbouring areas but homogenization at greater distance. The number of exotic species is more closely associated with the size of the human population than with ecological conditions, as in the case of native species, and their distributions are less influenced by climate than those of native species.

Biodiversity↗

In vitro and in vivo activity of R547: a potent and selective cyclin-dependent kinase inhibitor currently in phase I clinical trials.

The cyclin-dependent protein kinases are key regulators of cell cycle progression. Aberrant expression or altered activity of distinct cyclin-dependent kinase (CDK) complexes results in escape of cells from cell cycle control, leading to unrestricted cell proliferation. CDK inhibitors have the potential to induce cell cycle arrest and apoptosis in cancer cells, and identifying small-molecule CDK inhibitors has been a major focus in cancer research. Several CDK inhibitors are entering the clinic, the most recent being selective CDK2 and CDK4 inhibitors. We have identified a diaminopyrimidine compound, R547, which is a potent and selective ATP-competitive CDK inhibitor. In cell-free assays, R547 effectively inhibited CDK1/cyclin B, CDK2/cyclin E, and CDK4/cyclin D1 (K(i) = 1-3 nmol/L) and was inactive (K(i) > 5,000 nmol/L) against a panel of >120 unrelated kinases. In vitro, R547 effectively inhibited the proliferation of tumor cell lines independent of multidrug resistant status, histologic type, retinoblastoma protein, or p53 status, with IC(50)s </= 0.60 mumol/L. The growth-inhibitory activity is characterized by a cell cycle block at G(1) and G(2) phases and induction of apoptosis. R547 reduced phosphorylation of the cellular retinoblastoma protein at specific CDK phosphorylation sites at the same concentrations that induced cell cycle arrest, suggesting a potential pharmacodynamic marker for clinical use. In vivo, R547 showed antitumor activity in all of the models tested to date, including six human tumor xenografts and an orthotopic syngeneic rat model. R547 was efficacious with daily oral dosing as well as with once weekly i.v. dosing in established human tumor models and at the targeted efficacious exposures inhibited phosphorylation of the retinoblastoma protein in the tumors. The selective kinase inhibition profile and the preclinical antitumor activity of R547 suggest that it may be promising for development for use in the treatment of solid tumors. R547 is currently being evaluated in phase I clinical trials.

Animals↗

Health disparities between island and mainland Puerto Ricans.

OBJECTIVE: To detect health disparities among three populations--Puerto Ricans living in Puerto Rico as well as Puerto Ricans and non-Hispanic whites living on the United States (U.S.) mainland. METHODS: Data from two similarly designed surveys conducted in 1999-2000 were analyzed. The Behavioral Risk Factor Surveillance System (BRFSS) provided data on Puerto Ricans living on the island and on non-Hispanic whites in the U.S. Another survey of Puerto Ricans living in New York City provided data on mainland Puerto Ricans. The age- and sex-standardized weighted prevalences of various health parameters (e.g., obesity, diabetes, smoking, and physical illness) and indicators of access to health care (e.g., frequencies of routine checkups and diabetes care) were compared between populations by means of standardized rate ratios (SRR). RESULTS: Puerto Ricans living on the mainland and those living on the island had a similar prevalence of obesity (21% to 22%). Compared with islanders, mainland Puerto Ricans had a higher prevalence of diabetes (SRR = 1.4; 95% confidence interval [95% CI] = 1.01 to 2.0); those with diabetes also showed higher prevalences of smoking (SRR = 4.2; 95% CI = 2.3 to 7.7) and physical illness (SRR = 1.5; 95% CI = 1.1 to 2.0) than Puerto Ricans living on the island. While mainland Puerto Ricans were similar to non-Hispanic whites in terms of their utilization of primary prevention and diabetes care, island Puerto Ricans trailed behind significantly. CONCLUSIONS: Puerto Ricans living on the U.S. mainland and those living in Puerto Rico both need to target lowering their prevalence of obesity and diabetes. For island Puerto Ricans, improved education about the significance of primary prevention and diabetes care is needed. For mainland Puerto Ricans, the accessibility of the primary health care system renders it a potentially effective venue for interventions, particularly for smoking cessation. More studies are warranted to identify factors associated with the poor health status observed in mainland Puerto Ricans.

Adolescent↗

Nonequilibrium potential function of chemically driven single macromolecules via Jarzynski-type Log-Mean-Exponential Heat.

Applying the method from recently developed fluctuation theorems to the stochastic dynamics of single macromolecules in ambient fluid at constant temperature, we establish two Jarzynski-type equalities: (1) between the log-mean-exponential (LME) of the irreversible heat dissiption of a driven molecule in nonequilibrium steady-state (NESS) and ln P(ness)(x) and (2) between the LME of the work done by the internal force of the molecule and nonequilibrium chemical potential function mu(ness)(x) identical with U(x) + k(B)T ln P(ness)(x), where P(ness)(x) is the NESS probability density in the phase space of the macromolecule and U(x) is its internal potential function. Psi = integral mu(ness)(x) P(ness)(x) dx is shown to be a nonequilibrium generalization of the Helmholtz free energy and DeltaPsi = DeltaU - TDeltaS for nonequilibrium processes, where S = - kB integralP(x) ln P(x) dx is the Gibbs entropy associated with P(x). LME of heat dissipation generalizes the concept of entropy, and the equalities define thermodynamic potential functions for open systems far from equilibrium.

Journal Article↗

Down-regulation of delta-opioid receptors in Na+/H+ exchanger 1 null mutant mouse brain with epilepsy.

Mice lacking Na+/H+ exchanger 1 (NHE1) show a unique epilepsy phenotype although the underlying mechanisms remain unclear. Since expression of delta-opioid receptor (DOR) may be involved in control of epileptic activity, we conducted immunohistochemistry and autoradiography to investigate whether DOR expression is dys-regulated in the brain of NHE1 null mouse. Immunohistochemistry showed a decline in DOR expression in hippocampus and cortex. Autoradiographic results confirmed that the density of DOR was decreased in most cortical and hippocampal regions such as striate and temporal cortex, hippocampal CA1 and CA3 regions (reduced by 27.7 +/- 6.4%, 29.4 +/- 5.1%, 40.7 +/- 4.4% and 20.6 +/- 5.7%, respectively, P < 0.05). These data demonstrate that NHE1 null mutation leads to a reduction of DOR expression in the cortical and hippocampal regions, which provides a new clue for the genesis of epilepsy.

Animals↗

Oxygen-sensitive {delta}-opioid receptor-regulated survival and death signals: novel insights into neuronal preconditioning and protection.

The detrimental effect of severe hypoxia (SH) on neurons can be mitigated by hypoxic preconditioning (HPC), but the molecular mechanisms involved remain unclear, and an understanding of these may provide novel solutions for hypoxic/ischemic disorders (e.g. stroke). Here, we show that the delta-opioid receptor (DOR), an oxygen-sensitive membrane protein, mediates the HPC protection through specific signaling pathways. Although SH caused a decrease in DOR expression and neuronal injury, HPC induced an increase in DOR mRNA and protein levels and reversed the reduction in levels of the endogenous DOR peptide, leucine enkephalin, normally seen during SH, thus protecting the neurons from SH insult. The HPC-induced protection could be blocked by DOR antagonists. The DOR-mediated HPC protection depended on an increase in ERK and Bcl 2 activity, which counteracted the SH-induced increase in p38 MAPK activities and cytochrome c release. The cross-talk between ERK and p38 MAPKs displays a "yinyang" antagonism under the control of the DOR-G protein-protein kinase C pathway. Our findings demonstrate a novel mechanism of HPC neuroprotection (i.e. the intracellular up-regulation of DOR-regulated survival signals).

Animals↗

Nonequilibrium thermodynamics and nonlinear kinetics in a cellular signaling switch.

We develop a rigorous nonequilibrium thermodynamics for an open system of nonlinear biochemical reactions responsible for cell signal processing. We show that the quality of the biological switch consisting of a phosphorylation-dephosphorylation cycle, such as those in protein kinase cascade, is controlled by the available intracellular free energy from the adenosine triphosphate (ATP) hydrolysis in vivo: DeltaG=k(B)Tln(([ATP]/K(eq)[ADP]), where K(eq) is the equilibrium constant. The model reveals the correlation between the performance of the switch and the level of DeltaG. The result demonstrates the importance of nonequilibrium thermodynamics in analyzing biological information processing, provides its energetic cost, establishes an interplay between signal transduction and energy metabolism in cells, and suggests a biological function for phosphoenergetics in the ubiquitous phosphorylation signaling.

Adenosine Diphosphate↗

Ab initio prediction of thermodynamically feasible reaction directions from biochemical network stoichiometry.

Analysis of the stoichiometric structure of metabolic networks provides insights into the relationships between structure, function, and regulation of metabolic systems. Based on knowledge of only reaction stoichiometry, certain aspects of network functionality and robustness can be predicted. Current theories focus on breaking a metabolic network down into non-decomposable pathways able to operate in steady state. The physics underlying these theories is based on mass balance and the laws of thermodynamics. However, due to the inherent nonlinearity of the thermodynamic constraints on metabolic fluxes, computational analysis of large-scale biochemical systems can be expensive. In this study, it is shown how the feasible reaction directions may be determined by either computing the allowable ranges under the mass-balance and thermodynamic constraints or by analyzing the stoichiometric structure of the network. The computed reaction directions translate into a set of linear constraints necessary for thermodynamic feasibility. This set of necessary linear constraints is shown to be sufficient to guarantee feasibility in certain cases, thus translating the nonlinear thermodynamic constraints to linear. We show that for a reaction network of 44 internal reactions representing energy metabolism, the computed linear inequality constraints represent necessary and sufficient conditions for thermodynamic feasibility.

Cell Physiological Phenomena↗

Nonequilibrium steady state of a nanometric biochemical system: determining the thermodynamic driving force from single enzyme turnover time traces.

A single enzyme molecule in a living cell is a nanometric system that catalyzes biochemical reactions in a nonequilibrium steady-state condition. The chemical driving force, Deltamu, is an important thermodynamic quantity that determines the extent to which the reaction system is away from equilibrium. Here we show that Deltamu for an enzymatic reaction in situ can be determined from the nonequilibrium time traces for enzymatic turnovers of individual enzyme molecules, which can now be recorded experimentally by single-molecule techniques. Three different Deltamu estimators are presented from principles of nonequilibrium statistical mechanics: fluctuation theorem, Kawasaki identity, and fluctuation dissipation theorem, respectively. In particular, a maximum likelihood estimation method of Deltamu has been derived based on fluctuation theorem. The statistical precisions of these three Deltamu estimators are analyzed and compared for experimental time traces with finite lengths.

Computer Simulation↗

GABA and glycine are protective to mature but toxic to immature rat cortical neurons under hypoxia.

Although recent studies suggest that gamma-aminobutyric acid (GABA) and glycine may be 'inhibitory' to mature neurons, but 'excitatory' to immature neurons under normoxia, it is unknown whether inhibitory neurotransmitters are differentially involved in neuronal response to hypoxia in immature and mature neurons. In the present study, we exposed rat cortical neurons to hypoxia (1% O2) and examined the effects of three major inhibitory neurotransmitters (GABA, glycine and taurine) on the hypoxic neurons at different neuronal ages [days in vitro (DIV)4-20]. Our data showed that the cortical neurons expressed both GABA(A) and glycine receptors with differential developmental profiles. GABA (10-2000 microm) was neuroprotective to hypoxic neurons of DIV20, but enhanced hypoxic injury in neurons of DIV4. In comparison with delta-opioid receptor (DOR)-induced protection in DIV20 neurons exposed to 72 h of hypoxia, glycine-induced protection was weaker than that of DOR but stronger than that of GABA and taurine. These data suggest that the effects of the inhibitory neurotransmitters on hypoxic cortical neurons are age-dependent, with GABA and glycine being neurotoxic to immature neurons and neuroprotective to mature neurons.

Animals↗

Multiscale modeling of cardiac cellular energetics.

Multiscale modeling is essential to integrating knowledge of human physiology starting from genomics, molecular biology, and the environment through the levels of cells, tissues, and organs all the way to integrated systems behavior. The lowest levels concern biophysical and biochemical events. The higher levels of organization in tissues, organs, and organism are complex, representing the dynamically varying behavior of billions of cells interacting together. Models integrating cellular events into tissue and organ behavior are forced to resort to simplifications to minimize computational complexity, thus reducing the model's ability to respond correctly to dynamic changes in external conditions. Adjustments at protein and gene regulatory levels shortchange the simplified higher-level representations. Our cell primitive is composed of a set of subcellular modules, each defining an intracellular function (action potential, tricarboxylic acid cycle, oxidative phosphorylation, glycolysis, calcium cycling, contraction, etc.), composing what we call the "eternal cell," which assumes that there is neither proteolysis nor protein synthesis. Within the modules are elements describing each particular component (i.e., enzymatic reactions of assorted types, transporters, ionic channels, binding sites, etc.). Cell subregions are stirred tanks, linked by diffusional or transporter-mediated exchange. The modeling uses ordinary differential equations rather than stochastic or partial differential equations. This basic model is regarded as a primitive upon which to build models encompassing gene regulation, signaling, and long-term adaptations in structure and function. During simulation, simpler forms of the model are used, when possible, to reduce computation. However, when this results in error, the more complex and detailed modules and elements need to be employed to improve model realism. The processes of error recognition and of mapping between different levels of model form complexity are challenging but are essential for successful modeling of large-scale systems in reasonable time. Currently there is to this end no established methodology from computational sciences.

Algorithms↗

[Studies on administration of in-vitro diagnostic reagents].

This article introduces the definition, classification, premarket admission and other administering specialities about In-Vitro Diagnostic Reagents in the U.S.A. and China. And by analyzing manufacture and administration of In-Vitro Diagnostic Reagents in our country, It is pointed out that a suitable administering model in accordance with the characteristics of In-Vitro Diagnostic Reagents should be adopted to perfect the administration.

China↗

Thermodynamics of stoichiometric biochemical networks in living systems far from equilibrium.

The principles of thermodynamics apply to both equilibrium and nonequilibrium biochemical systems. The mathematical machinery of the classic thermodynamics, however, mainly applies to systems in equilibrium. We introduce a thermodynamic formalism for the study of metabolic biochemical reaction (open, nonlinear) networks in both time-dependent and time-independent nonequilibrium states. Classical concepts in equilibrium thermodynamics-enthalpy, entropy, and Gibbs free energy of biochemical reaction systems-are generalized to nonequilibrium settings. Chemical motive force, heat dissipation rate, and entropy production (creation) rate, key concepts in nonequilibrium systems, are introduced. Dynamic equations for the thermodynamic quantities are presented in terms of the key observables of a biochemical network: stoichiometric matrix Q, reaction fluxes J, and chemical potentials of species mu without evoking empirical rate laws. Energy conservation and the Second Law are established for steady-state and dynamic biochemical networks. The theory provides the physiochemical basis for analyzing large-scale metabolic networks in living organisms.

Animals↗

Thermodynamic-based computational profiling of cellular regulatory control in hepatocyte metabolism.

Thermodynamic-based constraints on biochemical fluxes and concentrations are applied in concert with mass balance of fluxes in glycogenesis and glycogenolysis in a model of hepatic cell metabolism. Constraint-based modeling methods that facilitate predictions of reactant concentrations, reaction potentials, and enzyme activities are introduced to identify putative regulatory and control sites in biological networks by computing the minimal control scheme necessary to switch between metabolic modes. Computational predictions of control sites in glycogenic and glycogenolytic operational modes in the hepatocyte network compare favorably with known regulatory mechanisms. The developed hepatic metabolic model is used to computationally analyze the impairment of glucose production in von Gierke's and Hers' diseases, two metabolic diseases impacting glycogen metabolism. The computational methodology introduced here can be generalized to identify downstream targets of agonists, to systematically probe possible drug targets, and to predict the effects of specific inhibitors (or activators) on integrated network function.

Algorithms↗

Entropy production of Brownian macromolecules with inertia.

We investigate the nonequilibrium steady-state thermodynamics of single Brownian macromolecules with inertia under feedback control in an isothermal ambient fluid. With the control being represented by a velocity-dependent external force, we find such an open system can have a negative entropy production rate, and we develop a mesoscopic theory consistent with the second law. We propose an equilibrium condition and define a class of external force, which includes the transverse Lorentz force, leading to equilibrium.

Journal Article↗

Thermodynamic constraints for biochemical networks.

The constraint-based approach to analysis of biochemical systems has emerged as a useful tool for rational metabolic engineering. Flux balance analysis (FBA) is based on the constraint of mass conservation; energy balance analysis (EBA) is based on non-equilibrium thermodynamics. The power of these approaches lies in the fact that the constraints are based on physical laws, and do not make use of unknown parameters. Here, we show that the network structure (i.e. the stoichiometric matrix) alone provides a system of constraints on the fluxes in a biochemical network which are feasible according to both mass balance and the laws of thermodynamics. A realistic example shows that these constraints can be sufficient for deriving unambiguous, biologically meaningful results. The thermodynamic constraints are obtained by comparing of the sign pattern of the flux vector to the sign patterns of the cycles of the internal cycle space via connection between stoichiometric network theory (SNT) and the mathematical theory of oriented matroids.

Energy Metabolism↗

Taxon richness and climate in angiosperms: is there a globally consistent relationship that precludes region effects?

We comment on a recent paper by Francis and Currie that reports a globally consistent relationship between plant family diversity in large geographic grid cells and factors in the physical environment. This relationship was interpreted as demonstrating local ecological determination of diversity, leaving little room for regional and historical effects. We suggest that using family richness to describe patterns of diversity reduces regional effects owing to the lower endemism of plants at the family compared with the species level. Regardless of the taxonomic level of analysis, we further point out that unless regional effects are tested explicitly, statistically significant differences in diversity between regions can be overlooked. Finally, even correlations between diversity and physical conditions of the environment can have primarily historical and evolutionary origins when lineages diversify within ecological zones of origin and spread more slowly to diverse environments. Thus, local ecological determinism should not have primacy over evolutionary-historical explanations for patterns of diversity between or within regions. Ecologists must evaluate patterns in local diversity within historical and geographic, as well as ecological, contexts.

Biodiversity↗

Fluorescence correlation spectroscopy with high-order and dual-color correlation to probe nonequilibrium steady states.

In living cells, biochemical reaction networks often function in nonequilibrium steady states. Under these conditions, the networks necessarily have cyclic reaction kinetics that are maintained by sustained constant input and output, i.e., pumping. To differentiate this state from an equilibrium state without flux, we propose a microscopic method based on concentration fluctuation measurements, via fluorescence correlation spectroscopy, and statistical analyses of high-order correlations and cross correlations beyond the standard fluorescence correlation spectroscopy autocorrelation. We show that, for equilibrium systems with time reversibility, the correlation functions possess certain symmetries, the violation of which is a measure of steady-state fluxes in reaction cycles. This result demonstrates the theoretical basis for experimentally measuring reaction fluxes in a biochemical network in situ and the importance of single-molecule measurements in providing fundamental information on nonequilibrium steady-states in biochemistry.

Enzymes↗