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Many plants grown with low-millimolar concentration of NH4 + as a sole nitrogen source develop NH4 + -toxicity symptoms. To date, crucial molecular identities and a practical approach involved in the improvement of plant NH4 + -tolerance remain largely unknown. By phenotyping of upland cotton grown on varied nitrogen forms, we came across a phenomenon that caused sub-millimolar concentrations of urea (e.g., up 50 μM) to repress the growth inhibition of roots and whole plant cultivated in a NH4 + -containing nutrient solution. A growth-recovery assay revealed that the relief in NH4 + -inhibited growth required only a short-term exposure (≧12 h) of the roots to urea, implying that urea could elicit an internal signaling and be involved in antagonizing NH4 + -sensitivity. Intriguingly, split-root experiments demonstrated that low urea occurrence in one root-half could efficaciously stimulate not only supplied root but also the root-half grown in NH4 + -solution without urea, indicating the existence of urea-triggered local and systemic long-distance signaling. In the split-root experiment we also observed high arginase activity, strong arginine reduction and remarkable upregulation of polyamine biosynthesis-related genes (ADC1/2, SPDS and SPMS). Therefore, we suggest that external urea might serve as an effective cue (signal molecule) in an arginine-/polyamine-related process for ameliorating NH4 + -suppressed root growth, providing a novel aspect for deeper exploring and understanding plant NH4 + -tolerance.

To evaluate the effect of baicalin on subarachnoid hemorrhage (SAH) in rats and explore the potential mechanisms. Sprague-Dawley rats underwent experimental SAH and received treatment with baicalin at 10 or 50 mg/kg after 2 and 12 h of SAH. Neurological scores, brain water content, Evans-blue extravasation, and levels of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), myeloperoxidase (MPO), and malondialdehyde (MDA) were measured 24 h after SAH. Expression of nuclear factor erythroid-related factor 2 (Nrf2), NAD(P)H: quinone oxidoreductase 1 (NQO1), matrix metalloproteinase-9 (MMP-9), aquaporin 4 (AQP4), occludin, and zonulaoccludens-1 (ZO-1) were detected in the brain by Western blot. Heme oxygenase-1 (HO-1) was detected by quantitative polymerase chain reaction, and tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were assessed by enzyme-linked immunosorbent assay. Baicalin attenuated EBI 24 h after SAH in rats (P

Ammonium and nitrate are major soil inorganic-nitrogen sources for plant growth, but many species cultivated with even low millimolar NH4+ as a sole N form display a growth retardation. To date, critical biological components and applicable approaches involved in the effective enhancement of NH4+ tolerance remain to be thoroughly explored. Here, we report phenotypical traits of urea-dependent improvement of NH4+-suppressed plant/root growth. Urea at 0.1 mM was sufficient to remarkably stimulate NH4+ (3 mM)-fed cotton growth, showing a 2.5∼4-fold increase in shoot- and root-biomass and total root-length, 20 % higher GS activity, 18 % less NH4+-accumulation in roots, and a comparable plant total-N content compared to the control, implying a novel role for urea in cotton NH4+detoxification. A similar phenomenon was observed in tobacco and rice. Moreover, comparisons between twelve NH4+-grown Arabidopsis accessions revealed a great degree of natural variation in their root-growth response to low urea, with WAR and Blh-1 exhibiting the most significant increase in primary- and lateral-root length and numbers, and Sav-0 and Edi-0 being the most insensitive. Such phenotypical evidence suggests a common ability of plants to accommodate NH4+-stress by responding to exogenous urea, providing a novel aspect for further understanding the process of urea-dependent plant NH4+ tolerance.

Liraglutide, one of the glucagon-like peptide 1 receptor (GLP-1R) agonists, has been demonstrated to protect brain damage produced by ischemic stroke. However, it remains unknown whether liraglutide attenuates early brain injury after subarachnoid hemorrhage. The present study was performed to explore the effect of liraglutide on early brain injury after subarachnoid hemorrhage in rats, and further investigate the potential mechanisms. Sprague-Dawley rats underwent subarachnoid hemorrhage (SAH) by endovascular perforation, then received subcutaneous injection with liraglutide (50 or 100 μg/kg) or vehicle after 2 and 12 h of SAH. SAH grading, neurological scores, brain water content, and Evans Blue extravasation were measured 24 h after SAH. Immunofluorescent staining was performed to detect the extent of microglial activation in rat brain 24 h after SAH. TUNEL staining was performed to evaluate neuronal apoptosis in rat brain of SAH. Expression of GLP-1R, cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), Bcl-2, Bax, and cleaved caspase-3 in rat brain were determined by western blot. Expression of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in rat brain was assessed by ELISA. Neurological dysfunction, brain water content, Evans Blue extravasation, microglial activation, and neuronal apoptosis were significantly reduced by GLP-1R agonist liraglutide. Expression of GLP-1R in rat brain was decreased after SAH, which is significantly elevated by liraglutide. Expression of inflammatory mediates like COX-2, iNOS, TNF-α, and IL-1β was increased after SAH, which were significantly inhibited by liraglutide. Furthermore, SAH caused the elevated expression of pro-apoptotic factors Bax and cleaved caspase-3 in rat brain, both of which were inhibited by liraglutide. In addition, liraglutide reversed the expression of anti-apoptotic protein Bcl-2. Our results demonstrated that liraglutide reduces early brain injury and attenuates inflammatory reaction and neuronal apoptosis in rats of SAH. Liraglutide provides neuroprotection against SAH, which might be associated with the inhibition of inflammation and apoptosis.

Malignant gliomas are the most common brain tumors with high rates of recurrence and mortality. Novel approaches are in research, and immunotherapy emerges as a promising strategy. Recently, scientific attention has been focused on Ganoderma lucidum polysaccharides (GL-PS), one of the critical bioactive components of G lucidum, which have been recognized as a promising natural source of immunomodulatory and anticancer compounds. It remains unknown whether the GL-PS have any immunomodulatory and anticancer effects on brain glioma. This study was designed to identify and characterize the antitumor action and influence of immune system of GL-PS in glioma-bearing rats. Results showed that GL-PS increased the concentration of serum interleukin-2, tumor necrosis factor-α, and interferon-γ, and enhanced the cytotoxic activity of natural killer cells and T cells, promoting the functional maturation of dendritic cells, thus resulting in the inhibition of glioma growth and prolonged survival of rats. Therefore, GL-PS may be potentially useful as part of the treatment regimen to regulate host immune responses and increase the antitumor effects of immunotherapy for glioma.

Glioblastoma is one of the most fatal diseases in human central nerve system. However, the prognosis and treatment of glioblastoma still call for steady improvement. In recent years, increasing studies have revealed that the abnormal expression of long non-coding RNA (lncRNA) is closely related to carcinogenesis and prognosis. Unfortunately, many lncRNAs still need further research in their function and molecule mechanism. LncRNA TRG-AS1 hasn't been detected in any types of cancers before. TRG-AS1 is associated with poor prognosis and is upregulated in glioblastoma tissues and cells. TRG-AS1 can also accelerate glioblastoma cell proliferation in return. On the other hand, miRNA-877-5p expresses low in glioblastoma and contains binding sites with both TRG-AS1 and SUZ12. Furthermore, TRG-AS1 suppresses the expression of miR-877-5p while miR-877-5p suppresses SUZ12 expression. Overexpression of TRG-AS1 could promote the expression of SUZ12.Rescue assays demonstrates that overexpression of SUZ12 can counteract the decline of glioblastoma cell proliferation induced by knockdown of TRG-AS1. Based on all these assays, TRG-AS1 promotes glioblastoma cell proliferation by acting as a ceRNA of miR-877-5p to regulate SUZ12 expression. TRG-AS1 might serve as a new target in glioblastoma treatment.

Previous studies have demonstrated that inflammation and disruption of the blood-brain barrier (BBB) are important pathological processes during focal cerebral ischemia. Therefore, the present study evaluated the neuroprotective effects of resveratrol against brain damage, inflammation and BBB disruption in rats with focal cerebral ischemia and assessed the potential underlying molecular mechanisms. Sprague-Dawley rats underwent cerebral ischemia/reperfusion (IR) and then received intraperitoneal resveratrol (10 and 100 mg/kg) 2 h following the onset of ischemia. Following 24 h of ischemia, neurological deficit scores, cerebral infarctions, morphological characteristics, cerebral water content, myeloperoxidase (MPO) activity and Evans blue extravasation were assessed. Additionally, the protein expression levels of Toll-like receptor 4 (TLR4) and nuclear factor (NF)-κB p65 were detected using western blot analyses, the mRNA expression levels of cyclooxygenase-2 (COX-2) and matrix metalloproteinase-9 (MMP-9) were examined by reverse-transcription polymerase chain reaction, and tumor necrosis factor (TNF)-α and interleukin (IL)-1β blood levels were determined by ELISA. Resveratrol significantly reduced neurological deficit scores, cerebral infarct sizes, neuronal injury, MPO activity and EB content. Cerebral ischemia increased the expression levels of TLR4, NF-κB p65, COX-2, MMP-9, TNF-α and IL-1β, but all of these factors were reduced by resveratrol. In conclusion, the present data suggest that resveratrol reduces inflammation, BBB disruption and brain damage in rats following focal cerebral ischemia. Additionally, the neuroprotective effects of resveratrol against cerebral ischemia may be associated with downregulation of the TLR4 pathway.

Previous studies from our laboratories showed that an anti-inflammatory drug, 5-lipoxygenase inhibitor zileuton, attenuates ischemic brain damage via inhibiting inflammatory reaction. However, it was elusive whether zileuton attenuates inflammatory reaction and ischemic brain damage through the modulation of PI3K/Akt signaling pathway. In the present study, we, for the first time, investigated whether PI3K/Akt pathway was involved in zileuton's anti-inflammatory and neuroprotective properties against brain damage following experimental ischemic stroke. Adult male Sprague-Dawley rats underwent middle cerebral artery occlusion (MCAO), then received treatment with zileuton or vehicle after the onset of ischemia. LY294002 was injected intracerebroventricularly to inhibit the activation of PI3K/Akt signaling pathway selectively. Neurological deficit scores, cerebral infarct volume, morphological characteristic and cerebral water content were assessed 24 h after cerebral ischemia. The enzymatic activity of myeloperoxidase (MPO) was measured 24 h after cerebral ischemia. Expression of p-Akt, t-Akt and COX-2 in ischemic brain were determined by western blot. NF-κB p65 immuno-positive cells in ischemic brain were detected 24 h after cerebral ischemia. The content of TNF-α in blood was examined by ELISA. 5-LOX inhibitor zileuton significantly reduces neurological deficit scores, cerebral infarct volume, cerebral water content, ischemic neuronal injury and the enzymatic activity of MPO, all of which were abolished by LY294002 administration. Zileuton significantly up-regulates the expression of p-Akt, which was inhibited by LY294002 administration. Zileuton significantly down-regulates the over-expression of NF-κB p65 and COX-2, and attenuates the release of TNF-α, all of which were disminished by LY294002 administration. These results suggest that zileuton attenuates ischemic brain damage by inhibiting inflammatory reaction through the activation of PI3K/Akt signaling pathway.

The aim of the present study was to determine the effect of baicalin on the expression of miR-497 and its target B-cell lymphoma-2 (Bcl-2) in the hippocampus of kainic acid (KA)-induced epileptic mice. To establish status epilepticus (SE), 0.1 µg/5 µl KA was injected into the lateral cerebral ventricle in mice, which then received an intraperitoneal injection of baicalin (100 mg/kg) after 1 and 8 h. Hematoxylin and eosin staining was used to observe the pathological changes in morphology and neuronal apoptosis was determined by terminal transferase-mediated dUTP nick end-labeling staining. Western blot analysis was used to detect the expression of Bcl-2 and cleaved caspase-3 proteins in the hippocampus, while reverse transcription-quantitative polymerase chain reaction was used to quantify hippocampal miR-497 expression. The results showed that baicalin significantly attenuated neuronal damage and apoptosis in the hippocampus 72 h after SE. In addition, baicalin decreased SE-induced expression of miR-497 and cleaved caspase-3 protein, while upregulating the expression of Bcl-2 protein. In conclusion, the present results suggest that baicalin possesses potent antiapoptotic properties and attenuates hippocampal injury in mice after SE, which may be associated with the downregulation of miR-497 and cleaved caspase-3 and the upregulation of Bcl-2.

Ammonium (NH4 + ) represents a primary nitrogen source for many plants, its effective transport into and between tissues and further assimilation in cells determine greatly plant nitrogen use efficiency. However, biological components involved in NH4 + movement in woody plants are unclear. Here, we report kinetic evidence for cotton NH4 + uptake and molecular identification of certain NH4 + transporters (AMTs) from cotton (Gossypium hirustum). A substrate-influx assay using 15 N-isotope revealed that cotton possessed a high-affinity transport system with a Km of 58 μM for NH4 + . Sequence analysis showed that GhAMT1.1-1.3 encoded respectively a membrane protein containing 485, 509 or 499 amino acids. Heterologous functionality test demonstrated that GhAMT1.1-1.3 expression mediated NH4 + permeation across the plasma membrane (PM) of yeast and/or Arabidopsis qko-mutant cells, allowing a growth restoration of both mutants on NH4 + . Quantitative PCR measurement showed that GhAMT1.3 was expressed in roots and leaves and markedly up-regulated by N-starvation, repressed by NH4 + resupply and regulated diurnally and age-dependently, suggesting that GhAMT1.3 should be a N-responsive gene. Importantly, GhAMT1.3 expression in Arabidopsis improved plant growth on NH4 + and enhanced total nitrogen accumulation (∼50% more), conforming with the observation of 2-fold more NH4 + absorption by GhAMT1.3-transformed qko plant roots during a 1-h root influx period. Together with its targeting to the PM and saturated transport kinetics with a Km of 72 μM for NH4 + , GhAMT1.3 is suggested to be a high-affinity NH4 + permease that may play a significant role in cotton NH4 + acquisition and utilization, adding a new member in the plant AMT family.

To determine whether cholera toxin B subunit and active peptide from shark liver (CTB-APSL) fusion protein plays a role in treatment of type 2 diabetic mice, the CTB-APSL gene was cloned and expressed in silkworm (Bombyx mori) baculovirus expression vector system (BEVS), then the fusion protein was orally administrated at a dose of 100 mg/kg for five weeks in diabetic mice. The results demonstrated that the oral administration of CTB-APSL fusion protein can effectively reduce the levels of both fasting blood glucose (FBG) and glycosylated hemoglobin (GHb), promote insulin secretion and improve insulin resistance, significantly improve lipid metabolism, reduce triglycerides (TG), total cholesterol (TC) and low density lipoprotein (LDL) levels and increase high density lipoprotein (HDL) levels, as well as effectively improve the inflammatory response of type 2 diabetic mice through the reduction of the levels of inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). Histopathology shows that the fusion protein can significantly repair damaged pancreatic tissue in type 2 diabetic mice, significantly improve hepatic steatosis and hepatic cell cloudy swelling, reduce the content of lipid droplets in type 2 diabetic mice, effectively inhibit renal interstitial inflammatory cells invasion and improve renal tubular epithelial cell nucleus pyknosis, thus providing an experimental basis for the development of a new type of oral therapy for type 2 diabetes.

Our previous studies demonstrated that inflammatory reaction and neuronal apoptosis are the most important pathological mechanisms in ischemia-induced brain damage. Propofol has been shown to attenuate ischemic brain damage via inhibiting neuronal apoptosis. The present study was performed to evaluate the effect of propofol on brain damage and inflammatory reaction in rats of focal cerebral ischemia. Sprague-Dawley rats underwent permanent middle cerebral artery occlusion, then received treatment with propofol (10 or 50 mg/kg) or vehicle after 2 h of ischemia. Neurological deficit scores, cerebral infarct size and morphological characteristic were measured 24 h after cerebral ischemia. The enzymatic activity of myeloperoxidase (MPO) was assessed 24 h after cerebral ischemia. Nuclear factor-kappa B (NF-κB) p65 expression in ischemic rat brain was detected by western blot. Cyclooxygenase-2 (COX-2) expression in ischemic rat brain was determined by immunohistochemistry. ELISA was performed to detect the serum concentration of tumor necrosis factor-α (TNF-α). Neurological deficit scores, cerebral infarct size and MPO activity were significantly reduced by propofol administration. Furthermore, expression of NF-κB, COX-2 and TNF-α were attenuated by propofol administration. Our results demonstrated that propofol (10 and 50 mg/kg) reduces inflammatory reaction and brain damage in focal cerebral ischemia in rats. Propofol exerts neuroprotection against ischemic brain damage, which might be associated with the attenuation of inflammatory reaction and the inhibition of inflammatory genes.

Long-chain diols have been detected in a wide range of environments and have been used to reconstruct past environmental changes, however only a few long-term records exist to date. Here we reconstructed past environmental changes in the central Sea of Okhotsk over the last 1.5 million years, covering the Mid-Pleistocene Transition (MPT). Sea surface temperatures (SST) reconstructed using the Long-Chain Diol Index (LDI) reflects glacial/interglacial changes. However, when compared with other organic paleothermometers (Uk′37 and TEXL86) the LDI-SST is lower during interglacials and similar or higher during glacials, possibly suggesting a shift of diol production season during interglacials. The LDI-SST does not change in periodicity around the MPT as observed for the TEXL86, likely due to this seasonal shift. Diatom productivity, as recorded by 1,14-diols and biogenic opal content, increased during the main deglaciations with a succession from Proboscia diatoms to diatoms with a more heavily silicified shell, confirming that primary productivity in the central Sea of Okhotsk is driven by sea-ice progress and retreat. In contrast to the LDI-SST, the 1,14-diols record shows a change in periodicity around the MPT from 41- to 100-kyr cycle, suggesting an influence of orbital parameters on diatom productivity. In the central Sea of Okhotsk, the relative amount of C32 1,15-diol (FC32 1,15), a proxy for riverine input, correlates with sea-level change with more riverine-derived material reaching the core site when the Amur River mouth is closer at lower sea-levels. In agreement, FC32 1,15 shows a change in periodicity during the MPT, with the appearance of a 100-kyr cycle. Our results show that the long chain diols can provide important paleoceanographic information in subpolar environments over long time scales, but that temperature reconstructions can be severely impacted by changes in seasonality.

Previous studies from our laboratory demonstrated that zileuton, a selective 5-lipoxygenase (5-LOX) inhibitor, attenuates ischemic brain damage in rats of focal cerebral ischemia. Enormous evidences showed that inflammatory reaction and neuronal apoptosis are the two important pathophysiological events in ischemia-induced brain damage. Our previous studies demonstrate that zileuton attenuates ischemic brain damage via inhibiting inflammatory reaction. The present study was performed to explore whether 5-LOX inhibitor zileuton attenuates neuronal apoptosis following focal cerebral ischemia and further investigate the potent mechanisms underlying its neuroprotection. Adult male Sprague-Dawley rats underwent permanent middle cerebral artery occlusion (MCAO) for 72 h, then received intragastric gavage with zileuton or vehicle as a bolus after the onset of MCAO. Neurological deficit scores, cerebral infarct volume, and neuronal damage were measured 72 h after MCAO. TUNEL staining was performed to measure the extent of neuronal apoptosis. Reverse transcription-polymerase chain reaction was performed to determine the expression of caspase-1 mRNA. Western blot was performed to determine the expression of procaspase-3 and cleaved caspase-3 in rat brain. Neurological deficit scores, infarct volume, and neuronal damage were significantly attenuated by administration of zileuton. MCAO caused the elevation of neuronal apoptosis, which was significantly inhibited by the administration of zileuton. MCAO caused the over-expression of caspase-1 and cleaved caspase-3, both of which were significantly inhibited by the administration of zileuton. Expression of procaspase-3 was reduced after MCAO, which was significantly up-regulated by administration of zileuton. Our studies suggested that 5-LOX inhibitor zileuton reduces MCAO-induced brain damage and neuronal apoptosis, which might be associated with the inhibition of caspase-1 and the regulation of caspase-3.

Salidroside (SDS), a phenylpropanoid glycoside isolated from Rhodiola rosea L., has been reported to be neuroprotective in vitro, which raises the possibility of using SDS as a neuroprotective agent after nerve injuries. In the present study, the possibly beneficial effect of SDS on promoting nerve regeneration after sciatic nerve crush injury in rats was investigated. Rats with sciatic nerve crush injury were administered intraperitoneally daily with 5 or 10 mg/kg body weight of SDS for 4 weeks. Rats that received mecobalamin or saline were considered as a positive or a negative control, respectively. Morphometric analysis of regenerated nerves and Fluoro-Gold retrograde tracing was used to evaluate axonal regeneration, whereas walking track analysis, electrophysiological assessment, and histological appearance of target muscles were carried out to evaluate the recovery of motor function. The results showed that SDS achieved functionally successful nerve regeneration in the rat sciatic nerve crush injury model, indicating that SDS holds potential as a neuroprotective agent for peripheral nerve therapies.

A microcalorimetric technique was used to investigate the influence of Zn2+ on the growth metabolism of Bacillus thuringiensis. LKB-2277 Bioactivity Monitor was employed to obtain the power-time curves, from which the maximum peak-heat output power (Pmax) in the log phase, the growth rate constants (k), the inhibitory ratios (I), the generational time (tG) and the total heat effect (Qtotal) in 23 h for the growth metabolism of Bacillus thuringiensis at 28 °C can be evaluated. The results indicate that the concentration of Zn2+ affects its growth obviously. Low concentration (0–50 μg/mL) of Zn2+ promotes the growth of Bacillus thuringiensis while high concentration (50–500 μg/mL) of Zn2+ inhibits its growth. When the concentration reached up to 600 μg/mL, it can not grow at all.

By using an LKB-2277 bioactivity monitor, cycle-flow mode, the thermogenic curve of metabolism of Escherichia cou NCTC 10418 growth at 37°C in basic media was determined. The experimental results indicate that the relationship between cell concentration and power output can be characterized by the equations C = k'P + adC/dP0 = KC, n = 1 where P is the power output (μW), C is cell concentration (mg/mL), P0 is the power output produced by the metabolism of one unit of cell (P0 = P/0.6C), the order of metabolism n is 1, and k', a and K are constants which depend on the culture condition and phylogenic state of the cells. These equations are different from those of the non-growth metabolism of resting cells and endogenous metabolism of cells. For different kinds of metabolism of cells, the order of metabolism, n, is different. For endogenous metabolism, n = 0, for growth metabolism, n = 1, and for non-growth metabolism of resting cells, n = 2. The equations are general thermochemical equations for the various different kinds of metabolism of cells.

The metabolic thermogenic curves of liver mitochondria isolated from the livers of Cyprinus Carpio vol and its parents were determined at 28°C by using an LKB-2277 Bioactivity Monitor. The results indicated that their thermogenic curves are different The total heat output and total time of the metabolism of the liver mitochondria of the hybrid F1 (Cyprinus Carpio val) are more than those of its parents, and its maximum heat power is between that of the female parent and male parent. The relationship between their metabolic thermogenic curves and character of mitochondrial metabolism, and thermokinetics and the heterosis were analyzed and discussed. The character of the mitochondrial thermogenic curves reflected the physiologic character of heterosis. The microcalorimetric method proved to be a probable and sensitive tool for the assessment of heterosis.

Microcalorimetric bioassay for acute cellular toxicity is based on metabolic heat production from cultured cells. The biological response to toxicants is the inhibition of the heat production rate in cells, and toxicity is expressed as the concentration of toxicant that is 50% effective in this inhibition (IC50). In mis paper, the effect of Na2SeO3 on Bacillus subtilis growth was investigated at 37 °C by microcalorimetry. The relationship between growth rate constants (k) and concentration of Na2SeO3 (c) shows a logarithmic normal distribution, and lC50 is 20.3 μg/mL. All these thermokinetic information is readily obtained by an LKB 2277–204 heat conduction microcalorimeter. Microcalorimetry is a quantitative, inexpensive, and versatile method for toxicology research.

By using an LKB2277 Bioactivity Monitor, the power-time curves of Bacillus thuringiensis Cry B at 28°C effected by Na2SeO3 were determined. Some parameters, such as growth rate constants k, inhibitory ratio I, the maximum beat production rate Pmax, heat output Q, were obtained. Considering both the growth rate constant k and heat output Q, we found that a low concentration of Na2SeO3 had a promoting action on the growth of Bacillus thuringiensis Cry B, but a high concentration of Na2SeO3 had an inhibitory action. The toxicity of a toxicant can also be expressed as half inhibitory concentration IC50 of toxicant, i. e., 50% effective in this inhibition. The value of IC50 of Na2SeO3on Bacillus thuringiensis Cry B is 117 μg/mL. This microcalorimetric bioassay for cellular toxicity is based on metabolic heat evolution from cultured cells. The assay is quantitative, inexpensive, and versatile.

By using an LKB-2277 Bioactivity Monitor and cycle-flow method, the thermogenic curves of aerobic growth for Bacillus thuringiensis cry II strain at 28 °C have been obtained. The metabolic thermogenic curves of Bt cry II contain two distinct parts: the first part reflects the changes of bacterial growth phase and the second part corresponds to sporulation phase. From these thermogenic curves in the absence or presence of Sm3+, Dy3+ ions, the thermokinetic parameters such as the growth rate constants k, the interval time τI, the maximum power PMAX1 and heat-output QLOG for log phase, the maximum power PMAX2 and heat-output QSTAT for stationary phase, the heat-output QSPOR for sporulation phase and total heat effects QT were calculated. Sm3+ and Dy3+ ions have promoting action on the growth of Bt cry II in their lower concentration range, on the other hand, they have inhibitory action on the sporulation of Bt in their higher concentration range. It has also been found that the effects of Sm3+ and Dy3+ ions on Br firing the sporulation phase were far greater than those during the bacterial growth phase. It was concluded that the application of Bt for controlling insecticide could not be affected by the presence of the rare-earth elements in the environmental ecosystem.

Odontotermes formosanus (Shiraki) and O. hainanensis (Light) (Isoptera: Termitidae) are two dominant termite species that damage earthen dikes in China. This paper describes behavioral biology (mating, egg caring, hatching, and molting) and development of incipient colonies of these two species under laboratory conditions. Oviposition of O. formosanus and O. hainanensis began 8-11 d and 2-5 d after mating, respectively. The eggs of both species were laid in batches. Egg hatching of O. formosanus and O. hainanensis required assistance from parents or nestmates. Average hatching periods of these two species were 31 d and 27 d, respectively. The molting process of O. formosanus and O. hainanensis also required help from nestmates. Such assistance was more essential for O. hainanensis than for O. formosanus. Average developmental times from newly hatched O. formosanus to adult workers and to soldiers were 16.7 d and 23.8 d, respectively. For O. hainanensis, these times were 18.1 d and 19.6 d, respectively. The survival rate of the incipient colonies of O. formosanus at 6 mo after establishment was below 50%. Colony death probably was due to unsuccessful culture of the fungus, Termitosphaeria duthiei.

The interaction between methylene blue (MB) and bovine serum albumin (BSA) was investigated by fluorescence and UV–vis absorbance spectroscopy. In the mechanism discussion, it was proved that the fluorescence quenching of BSA by MB is mainly a result of the formation of MB–BSA complex and electrostatic interactions play an important role to stabilize the complex. The Stern–Volmer quenching constant K SV and corresponding thermodynamic parameters Δ H , Δ G , and Δ S were calculated. The distance r between donor (BSA) and acceptor (MB) was obtained according to fluorescence resonance energy transfer (FRET). The effect of MB on the conformation of BSA has been analyzed by means of UV–vis absorbance spectra and synchronous fluorescence spectroscopy.

A calorimetric method was used to monitor the relative promoter activity of the chromosome DNA fragments cloned from Pseudomonas maltophilia AT18 in Escherichia coli . The promoter probe vector, plasmid pKK232-8, was used to form the recombinants. Three recombinants were selected to study by calorimetric method and agar plate method. The relative strength of the promoter was represented by the resistance level to chloramphenicol. The results showed that the agar plate method could only provide the MIC of the antibiotic to the recombinants, but the calorimetric method not only provided a more precise MIC but also IC 50 that quantitates the activity of these promoter fragments.

Fluorescence quenching in solutions of bovine serum albumin has been investigated in the presence of 6-mercaptopurine and ionic surfactants. Spectroscopic analysis of the emission quenching at different temperatures revealed that the quenching mechanism of bovine serum albumin by 6-mercaptopurine was dynamic quenching mechanism. The Stern–Volmer quenching model has been successfully applied, and the activation energy of the interaction between 6-mercaptopurine and bovine serum albumin as much as 4.26 kJ mol−1 was calculated. The distance r between donor (bovine serum albumin) and acceptor (6-mercaptopurine) was obtained according to fluorescence resonance energy transfer (FRET). The result of synchronous fluorescence spectra shows that the conformation of bovine serum albumin has been changed at the present of 6-mercaptopurine.

The interaction between methylene blue (MB) and human serum albumin (HSA) was investigated by fluorescence spectroscopy and UV–vis absorbance spectroscopy. In the mechanism discussion, it was proved that the fluorescence quenching of HSA by MB is a result of the formation of MB–HSA complex and electrostatic interactions play a major role in stabilizing the complex. The Stern–Volmer quenching constant K SV and corresponding thermodynamic parameters Δ H , Δ G and Δ S were calculated. Binding studies concerning the number of binding sites n and apparent binding constant K b were performed by fluorescence quenching method. The distance r between the donor (HSA) and the acceptor (MB) was obtained according to fluorescence resonance energy transfer (FRET). Wavelength shifts in synchronous fluorescence spectra showed the conformation of HSA molecules is changed in the presence of MB.

The interaction between anti-tumor drug, 1-hexylcarbamoyl-5-fluorouracil (Carmofur), and bovine serum albumin (BSA) were studied by spectroscopic methods including fluorescence spectroscopy, circular dichroism (CD) and UV–Visible absorption spectrum. The quenching mechanism of fluorescence of BSA by Carmofur was discussed. The number of binding sites n and apparent binding constant K b was measured by fluorescence quenching method. The thermodynamic parameters Δ H , Δ G , Δ S at different temperatures were calculated and the results indicate the binding reaction is mainly entropy-driven and hydrophobic forces played major role in the reaction. The distance r between donor (BSA) and acceptor (Carmofur) was obtained according to Forster theory of non-radiation energy transfer. CD spectrum were used to investigate the structural change of BSA molecules with addition of Carmofur, the result indicates that the secondary structure of BSA molecules is changed in the presence of Carmofur.

A microcalorimetric technique was used to evaluate the influence of Er3+ on Halobacterium halobium R1 growth. By means of a LKB-2277 Bioactivity Monitor ampoule method, we obtained the thermogenic curves of H. halobium R1 growth at 37 degrees C. In order to analyze the results, the relationship between k and C was obtained. The addition of Er3+ in low concentration cause a decrease of the maximum heat production P max and growth rate constants k; however, Er3+ in a high concentration might promote growth of H. halobium R1. When Er3+ is in a much higher concentration, the growth of H. halobium R1 is inhibited completely. For comparison, the shapes of H. halobium R1 cells were observed by means of transmission electron microscope (TEM). According to the thermogenic curves and TEM photos of H. halobium R1 under different conditions, it is clear that the metabolic mechanism of H. halobium R1 growth has been changed with the addition of Er3+.

A microcalorimetric technique based on the bacterial heat output was applied to evaluate the influence of plasmid copy number and various promoters on the green fluorescent protein expression in Bacillus thuringiensis. The thermogenic curves of the aerobic metabolism of B. thuringiensis strains were determined by using an LKB-2277 bioactivity monitor at 28°C. The analysis of the thermogenic curves indicated for the first time that the more plasmid copy number per cell the more protein synthetization. Promoter BtI-BtII had a stronger impact on the gene expression than promoter 3A investigated by the method of microcalorimetry.

The interaction between monoammonium glycyrrhizinate (MAG) and bovine serum albumin (BSA) were studied by fluorescence and absorption spectroscopy. The quenching mechanism of fluorescence of bovine serum albumin by monoammonium glycyrrhizinate was discussed. The binding sites number n and apparent binding constant K were measured by fluorescence quenching method. The thermodynamic parameters Δ H ° , Δ G ° , Δ S ° at different temperatures were calculated. The distance r between donor (bovine serum albumin) and acceptor (monoammonium glycyrrhizinate) was obtained according to Főrster theory of non-radiation energy transfer. The results of synchronous fluorescence spectra and UV–vis absorption spectra show that the conformation of bovine serum albumin has been changed.

The binding of Schiff base selenide, (2-hydroxy-benzimido)ethyl-n-hexylselenide, to bovine serum albumin (BSA) was studied using fluorescence spectroscopy. The measurement was performed in Tris-HCl buffer aqueous medium at pH 7.4. Stern-Volmer graphs were plotted and quenching constants were estimated. The quenching constant at 303 K was (1.639 ± 0.046) × 1013 L mol−1 s−1. Decreased quenching was observed as temperature increased, but at the temperature range of 303–313 K, the association of Schiff base selenide to BSA was not significantly different. The static quenching presented in the system of Schiff base selenide and BSA. A complex was possibly formed between Schiff base selenide and BSA, which was responsible for the quenching of the fluorescence of BSA. This fact was also confirmed by differences in the absorption spectra of BSA before and after Schiff base selenide addition. The hydrophobic interaction was found to play a main role in the binding according to the thermodynamic parameters, enthalpy change (ΔH) and entropy change (ΔS) of reaction. Schiff base selenide most likely binds to the hydrophobic pockets within sub domain IIA of BSA, which can be proved by competition experiments for sodium dodecyl sulfate. By constant-wavelength synchronous fluorescence spectra, the influence of (2-hydroxy-benzimido)-ethyl-n-hexylselenide on the surrounding environment of tyrosine and tryptophan residues in BSA was also investigated. The red shift of the fluorescence peak of tryptophan residues indicated that the hydrophobic amino acid structure surrounding tryptophan residues in BSA collapsed slightly after the addition of (2-hydroxy-benzimido)ethyl-n-hexylselenide.

A novel microcalorimetric technique based on the bacterial heat output was applied to evaluate the special growth model, the protein expression and the generation time of Bacillus thuringiensis for the first time. The thermogenic curves of the aerobic metabolism of B. thuringiensis strains YBT-833, YBT-1520 and YBT-833-2-1 were determined by using an LKB-2277 BioActivity Monitor. The analysis of the thermogenic curves indicated both the mutant strain and the wild-type strains followed the same linear growth model during sporulation. The metabolism heat output revealed heat output was correlated to the yield of the insecticidal crystal proteins (ICPs) very well, the more protein product, and the less heat output. Based on the data acquired, we proposed that this method could be a useful tool in monitoring the fermentation of B. thuringiensis.

A series of microcalorimetric experiments were performed to investigate the effect of La3+ on the formation of the competent state of Escherichia coli HB101 by using a LKB-2277 BioActivity Monitor at 37°C. The thermogenic curves in the absence and in the presence of La3+ were obtained. Based on these curves, we calculated that the total heat effects (Q T) and the maximal power (P max) in the presence and absence of La3+. Our experiments indicate that the total heat effects in the presence of a low concentration of La3+ (≤ 100 µg/mL) are greater than those in the absence of La3+. Their trends are similar with respect to the increasing concentration of La3+. To the contrary, when the concentration of La3+ is greater than 100 µg/mL, the total heat effects decrease with the increasing concentration of La3+. Therefore, in the latter case, La3+ has inhibitory effects on the formation of competence. Our experimental results suggest that the La3+ ion in the environmental ecosystem can facilitate the formation of competence of E. coli HB101 and further stimulate the transfer of genetic materials between organisms.

The heat output of and the effect of manganese (II) on Tetrahymena shanghaiensis S(1)99 growth metabolism has been determined by means of a LKB-2277 BioActivity monitor. Different concentrations of manganese(II) ions have different effects on the growth of T. shanghaiensis. At low concentrations (0-40 mug/mL) culture growth is promoted, whereas high concentrations (60-800 mug/mL) slow growth. Furthermore, concentrations of 1200 mug/mL or greater stop the growth of this protozooa completely.

By using an LKB-2277 Bioactivity Monitor, cycle-flow method, the thermogenic curves of aerobic growth for Bacillus thuringiensis cry II strain at 28°C have been obtained. The metabolic thermogenic curves of B. thuringiensis cry II contained two distinct patterns: the first reflects the changes during the bacterial growth phase and the second corresponds to the sporulation phase. From these thermogenic curves in the absence and presence of Sm3+ ions, the thermokinetic parameters such as the growth rate constants k, the interval time τI, the maximum power Pmax 1 and heat-output Qlog for log phase, the maximum power Pmax 2 and heat-output Qstat for stationary phase, the heat-output Qspor for sporulation phase and total heat effects QT are calculated. Sm3+ ion has promoting action on the growth of B. thuringiensis cry II in its lower concentration range; on the other hand, this ion has inhibitory action on the sporulation of B. thuringiensis in its higher concentration range. We also found that the effects of Sm3+ ion on B. thuringiensis during the sporulation phase were far greater than that during the bacterial phase. It is concluded that the application of B. thruringiensis of controlling insecticides is not affected by the presence of the rare-earth elements in the environmental ecosystem.

By using an LKB-2277 Bioactivity Monitor, ampoule mode, the heat output of Bacillus thuringiensis growth metabolism is determined at 28°C and the effect of Cu2+ on B. thuringiensis growth is studied. Copper is regarded as an essential trace element for life. Its deficiency may be the cause of diseases. Cu2+ at different concentrations has different effects on B. thuringiensis growth metabolism: a low concentration (0–30 μg/ml) of Cu2+ can promote the growth of B. thuringiensis, a high concentration (40–120 μg/ml) can inhibit growth of the bacteria, and a concentration of Cu2+ of up to 130 μg/ml completely inhibits B. thuringiensis growth.

The effect of Na2SeO3 on the growth of Halobacterium halobium R1 was investigated by means of microcalorimetry at 37°C. The biological response to toxicants is observed as the inhibition of the rate constant of growth of living cells. A low concentration of Na2SeO3 stimulated the growth of H. halobium R1, and a high concentration of Na2SeO3 inhibited the growth of H. halobium R1. Toxicity may be expressed as the half-inhibition concentration (IC50). The rate constants of growth (k) and the concentrations of Na2SeO3 (c) shows a linear relationship: k=1.790 × 10−6 − 2.27 × 10−3 c. The value of IC50 obtained from the accompanying figure of I-c is 679 µg/mL.

The application of a microcalorimetric method to the study of extremophiles is described briefly. Using the LKB 2277 Bioactivity Monitor, the growth thermogenic curves of three strains of Halobacterium halobium were determined at 37°C, and compared with the spectrophotometric curves. Then the suitable growth thermokinetic equation was established based on the characteristics of growth thermogenic curves. By using cycle-flow method, all of the growth thermogenic curves of H. halobium strains displayed a brief lag phase before the onset of exponential growth when they were cultured in Halo-2 medium.

Hyperthermia is a useful adjunct in cancer therapy, as it can increase the effectiveness and decrease the toxicity of currently available cancer treatments such as chemotherapy and radiation. In this study we determined the power-time curves of U-937 cell line treated by the combination of hyperthermia and Carmofur by using an LKB 2277 Bioactivity Monitor. The maximal thermal power and the heat production were used to evaluate the antitumor effect. Our results show that the combined treatment of hyperthermia and Carmofur had a synergistic antitumor effect, which is consistent with the apoptosis ratio obtained by TUNEL assay. The results also indicate that the metabolic activity of apoptotic cells is lower than that of normal cells. Thus microcalorimetry is a powerful tool in fields of hyperthermia.

Microcalorimetry, UV–VIS spectroscopy and HPLC were used to conduct thermodynamic and kinetic investigations of the scission of calf thymus DNA catalyzed by bleomycin A 5 (BLM-A 5 ) in the presence of ferrous ion and oxygen. The molar reaction enthalpy for the cleavage, the Michaelis constant for calf thymus DNA and the turnover number of BLM-A 5 were calculated by a novel thermokinetic method for enzyme-catalyzed reactions to be −577±19 kJ mol −1 , (2.04±0.38)×10 −5 mol dm −3 and (2.28±0.49)×10 −2 s −1 , respectively, at 37.00 °C. This DNA cleavage was a fast and exothermic reaction. The catalytic efficiencies of BLM-A 5 and of some DNA-cleaving enzymes, such as Taq I restriction endonuclease and Nae I endonuclease, are of the same order of magnitude. By comparing the molar enthalpy change for the cleavage of calf thymus DNA induced by BLM-A 5 with those for the scission of calf thymus DNA mediated by adriamycin and by (1,10-phenanthroline)-copper, it was found that BLM-A 5 possessed the highest DNA cleavage efficiency among these DNA-damaging agents. The UV–VIS spectral experiments showed that BLM-A 5 itself remained unchanged chemically after the cleavage. The products of this scission, including four kinds of free nucleic acid bases, were separated and detected by HPLC. These results strongly suggest that BLM-A 5 is analogous in mechanism to a DNA-cleaving enzyme, although it is much smaller than such type of enzymes. A possible mechanism for the cleavage of DNA catalyzed by BLM was suggested in this paper.

A microcalorimetric technique based on the bacterial heat-output was explored to evaluate the effect of Mn(II) on Bacillus thuringiensis. The power-time curves of the growth metabolism of B. thuringiensis and the effect of Mn(II) on it were studied using an LKB-2277 BioActivity Monitor, ampoules method, at 28°C. For evaluation of the results, the maximum peak-heat output power (P max) in the growth phase, the growth rate constants (k), the log phase heat effects (Q log ), and the total heat effect in 23 h (Q T) for B. thuringiensis were determined. Manganese has been regarded as the essential biological trace element. Mn(II) of different concentration have different effects on B. thuringiensis growth metabolism. High concentration (800-1600 μg mL-1) of Mn(II) can promote the growth of B. thuringiensis; low concentration (500-800 μg mL-1) can inhabit its growth.

The action of three kinds of the selenomorpholine compounds on a strain ofEscherichia coli was studied by microcalorimetry. Differences in their capacities to affect the metabolism of this bacterium were observed. The extent and duration of the effect on the metabolism as judged from the rate constant (k) of Escherichia coli (in log phase) varied with the different drugs. The kinetics show that selenomorpholine compounds had an effect on the metabolism process of Escherichia coli. The k of Escherichia coli in the presence of the drugs increased with the increasing concentrations of the drugs (C) at low concentration; but at high concentration, the rate constant decreased with the increasing concentrations of the drugs. The experimental results reveal that the sequence of antibiotic activity of selenomorpholines is: N-selenomorpholinemethyl succinimide and its hydrochloride>N-(α-selenomorpholinebenzyl) succinimide.

In this paper, a promoter-probe plasmid pKK232-8 was used as a vector, which functioned in Escherichia coli TG1 host. The plasmid DNA fragments from Pseudomonas maltophilia AT18 chromosome DNA active as promoter inEscherichia coli TG1, the promoter function was studied by means of microcalorimetry, the promoter is about 800 bp DNA, it can promote the chloramphenicol (Cm) gene in plasmid pKK232-8, the Cm resistance level is about 80 μg mL–1, the promoter activity is high. It implicates that there are probably many promoters in Pseudomonas maltophilia AT18 chromosome. All these information is readily obtained by an LKB 2277-204 heat conduction microcalorimeter. Microcalorimetry is a quantitative, inexpensive, and versatile method for microbiological genetic research.

Toll-like receptors 2 and 4 (TLR2/4) and the downstream nuclear factor-kappa B (NF-κB) signaling pathway, which mediate the inflammatory reaction in cerebral ischemia, were demonstrated to be involved in the extension of cerebral infarction and the aggravation of ischemic brain damage. Reports showed that curcumin provides neuroprotection against ischemic brain damage. In this study, we investigated whether curcumin inhibits the activation of TLR2/4-NF-κB signaling pathway in rats of permanent focal cerebral ischemia. Adult male Sprague-Dawley rats underwent permanent middle cerebral artery occlusion (pMCAO). Curcumin was administered by intraperitoneal injection twice at 2 and 12 h after the onset of ischemia. Neurological deficit scores, cerebral infarct size, morphological characteristic, and cerebral water content were measured after 24 h of pMCAO. The enzymatic activity of myeloperoxidase (MPO) was assessed after 24 h of pMCAO. Expression of TLR2 and TLR4 in ischemic brain was determined by western blot. Expression of NF-κB p65 in ischemic brain was detected by immunohistochemistry and western blot. The release of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in blood was examined by ELISA. Curcumin significantly reduced neurological deficit scores, cerebral infarct size, neuronal damage, cerebral water content, and MPO activity. It also inhibited the expression of TLR2/4 and decreased the expression and activity of NF-κB p65 in rat brain. In addition, curcumin attenuated the release of TNF-α and IL-1β in blood. Our results suggest that curcumin reduces inflammatory reaction and brain damage in a rat model of permanent focal cerebral ischemia. The neuroprotective effect and anti-inflammatory property of curcumin in cerebral ischemia might be associated with the inhibition of TLR2/4-NF-κB signaling pathway.

This study was conducted to evaluate the role of tumor suppressor gene ras homologue member I (ARHI) in human glioma tumors. We examined expression of ARHI in human glioma tumors and normal brain tissue and also in 4 different glioma cell lines. Furthermore, the effects of ARHI over-expression produced by cellular transfection on the growth of human glioma U251 cells cultured in vitro were also studied. Expression of ARHI was evaluated in samples of glioma tumors obtained from 59 patients who underwent surgery at the Department of Neurosurgery, Fujian Medical University Union Hospital, Fuzhou, China. Ten samples of normal brain tissue were used as controls. Additionally, in vitro studies were conducted in which a recombinant vector carrying ARHI cDNA was constructed and transfected into U251 glioma cells with reduced expression of ARHI. Following transfection, the MTT assay, flow cytometry, TUNEL procedure, Transwell assay, and wound-healing test were employed to evaluate the biological functions of ARHI in U251 glioma cells in vitro. Analyses of mRNA and protein expression revealed that ARHI was significantly down-regulated in glioma tissues as well as in 4 malignant glioma cell lines. Over-expression of ARHI resulted in suppression of glioma cell proliferation, arrest of cell cycle progression, reduction in cell migration and invasion, and promotion of cell apoptosis. Collectively, our data highlight the importance of ARHI in glioma progression and provide the first biological basis for ARHI as a novel candidate target for gene therapy of glioma.

The thermodynamic and kinetic behaviors of energy release of mitochondria isolated from rice (Oryza sative L.) were studied by using a LKB 2277 Bioactivity Monitor under different conditions. The thermogenesis curves of energy release of the rice mitochondria (which had been kept at 0-3 degreesC for 15 h and 40 day before the determination) were determined respectively at 25 and 30 degreesC, and the difference in shape of the thermogenesis curves and thermodynamic and kinetic characteristics were compared. The thermodynamic and kinetic parameters of energy release of the mitochondria in the thermogenesis increasing stage have been calculated, and the experimental thermokinetic equations of the thermogenesis have been established. The results indicated that the lower the temperature, the slower the energy release of the rice mitochondria. Both the thermogenesis and the energy release late of the rice mitochondria increased after the mitochondria was kept at lower temperature for 40 days. One can use the methods to characterize the ability of the rice mitochondria to release energy under different conditions. (C) 2001 Published by Elsevier Science B.V.

The thermogenic curves of the metabolism of mitochondria isolated from the liver of chicken Star-Cross 288 and the effect of La3+ on it were studied by using an LKB-2277 BioActivity Monitor, ampoule method, at 37°C. After isolation from the chicken liver tissue, mitochondria still have metabolic activity and can live for a long time by using the stored nutrients. From the thermogenic curves, we obtained the thermokinetic equations under different condition. The kinetic study shows that La3+ has changed the metabolism completely.

Thermodynamics and kinetics of the dismutation of superoxide anion (O2·−) catalyzed by superoxide dismutase (SOD) in batch reactors has been studied by on-line reaction calorimetry. The decomposition of hydrogen peroxide catalyzed by catalase is utilized as a source of oxygen and the autoxidation of pyrogallol as a source of the substrate (O2·−) for SOD. The molar reaction enthalpies of the SOD reaction and the pyrogallol autoxidation have been measured as −160.1 and −218kJ/mol, respectively, at 298.15K and pH8.0. The experimental results showed that SOD had no effect on the kinetic parameters or the mechanism for pyrogallol autoxidation. This autoxidation followed second-order reaction kinetics in the presence of limited oxygen (first order with respect to both pyrogallol and O2), and the second-order rate constants were determined at 298.15K and pH 8.0 to be 1.25 and 1.30l/mols in the absence and presence of SOD, respectively. A possible mechanism for the autoxidation of pyrogallol inhibited by SOD was also suggested.

The microcalorimetric bioassay for acute cellular toxicity is based on metabolic heat production from cultured cells. Microcalorimetry is a quantitative, inexpensive, and versatile method for toxicology research. The biological response to toxicants is the inhibition of the heat production rate in cells and toxicity is expressed as the concentration of toxicant that is 50% effective in this inhibition (IC(50)). In this paper, the effect of Cd(2+) on Rhizopus nigricans growth was investigated at 25 degrees C. The relationship between growth rate constants (k) and concentration of Cd(2+) (C) shows a logarithmic normal distribution, and described as k=1. 2742x10(61)exp[-1.810x10(-3)(C+283.0)(2)], and IC(50) is 0.72 microg/ml. These signals are readily obtained by an LKB 2277-204 heat conduction microcalorimeter.

As Chance et al. [1] , [2] , [3] proposed, the decomposition of hydrogen peroxide catalyzed by catalase is an overall first-order reaction. In this paper, we have studied this enzyme-catalyzed reaction with a thermokinetic method. The rate constant and the molar reaction enthalpy of this reaction have been measured. At 310.15 K and pH=8.2, kcat=1.75×106 l mol−1 s−1, ΔrHm=88.99 kJ mol−1. Furthermore, we have studied the competitive inhibition of catalase by cyanide ion and reported some correlated parameters.