[Study on the molecular mechanism of autophagy and apoptosis induced by ultrafine carbon black in human bronchial epithelial cells and the intervention effect of N-acetylcysteine].

Objective: To investigate the molecular mechanism of autophagy and apoptosis induced by ultrafine carbon black in human bronchial epithelial cells (BEAS-2B cells), and to study the intervention effect and mechanism of N-acetylcysteine (NAC) on ultrafine carbon black-induced oxidative damage in BEAS-2B cells. Methods: In March 2023, BEAS-2B cells were used as research object, an in vitro airway model exposed to ultrafine carbon black was constructed. A control group and three carbon black exposure groups (50, 100, 200 µg/ml) were set up, and the cells were treated with corresponding concentrations of ultrafine carbon black for 24 hours. In addition, the experiment was divided into control group, NAC+ control group, 100 µg/ml carbon black exposure group and NAC+ exposure group. The corresponding groups were treated with 2 mmol/L NAC for 1 h and 100 µg/ml ultrafine carbon black for 24 h, respectively. Cell viability was measured by CCK-8 assay. Intracellular reactive oxygen species (ROS) level was detected by chemical fluorescence method. The activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT), as well as the content of malondialdehyde (MDA) were detected by colorimetry. The mRNA and protein expressions of autophagy-related genes[Atg5, Atg7, Beclin1, microtubule-associated protein light chain 3B (LC3B), p62 and lysosome-associated membrane protein 2 (LAMP2) ] and apoptosis-related genes [B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), Caspase3, Caspase9 and poly (ADP-ribose) polymerase 1 (PARP1) ] were determined by fluorescence quantitative PCR and Western blot. Cell apoptosis was determined by flow cytometry. Results: Compared with the control group, the relative survival rates of BEAS-2B cells in 50, 100, 200 µg/ml carbon black exposure groups were significantly decreased, the levels of ROS and MDA were significantly increased, and the activities of SOD, GSH-Px and CAT were significantly decreased (P<0.05). The relative survival rate, ROS and MDA levels, SOD, GSH-Px and CAT activities were significantly correlated with the exposure dose of ultrafine carbon black (r(s)=-0.755, 0.826, 0.934, -0.810, -0.880, -0.840, P<0.05). Compared with the control group, the relative expression levels of Atg5, Atg7, Beclin1, LC3B, p62, LAMP2, Bax, Caspase3, Caspase9, PARP1 mRNA and Atg5, Atg7, Beclin1, LC3BⅡ, p62, LAMP2, Bax, cleaved Caspase3 (C-Caspase3), cleaved Caspase9 (C-Caspase9), cleaved PARP1 (C-PARP1) protein and the ratio of LC3BⅡ/LC3BⅠ in 50, 100 and 200 µg/ml carbon black exposure groups were significantly increased, while the relative expression levels of Bcl-2 mRNA and protein were significantly decreased (P<0.05). The changes of the above indexes were significantly correlated with the exposure dose of carbon black (r(s)=0.892, 0.879, 0.944, 0.892, 0.828, 0.880, 0.814, 0.794, 0.931, 0.918, 0.813, 0.866, 0.774, 0.695, 0.918, 0.761, 0.794, 0.944, 0.833, 0.866, 0.905, -0.886, -0.748, P<0.05). Compared with 100 µg/ml carbon black exposure group, the relative survival rate, the activities of SOD, GSH-Px and CAT in NAC+exposure group were significantly increased, while the levels of ROS and MDA were significantly decreased, and the relative expression levels of LC3B, p62 and Caspase3 mRNA and protein as well as the ratio of LC3BⅡ/LC3BⅠ were significantly decreased, and the differences were statistically significant (P<0.05). Compared with the control group, the apoptosis rates of BEAS-2B cells in 50, 100, 200 µg/ml carbon black exposure groups were significantly increased (P<0.05), and there was a significant positive correlation between ultrafine carbon black exposure dose and cell apoptosis rate (r(s)=0.944, P<0.05). While compared with 100 µg/ml carbon black exposure group, the apoptosis rate of NAC+exposure group was significantly decreased, and the difference was statistically significant (P<0.05) . Conclusion: Cell autophagy and apoptosis may be important pathophysiological mechanisms of ultrafine carbon black-induced oxidative damage in BEAS-2B cells. NAC can alleviate the occurrence of BEAS-2B cell damage caused by ultrafine carbon black by regulating oxidative stress and the cascading autophagy and apoptosis pathways.

Sudden stoppage of rotor in a thermally driven rotary motor made from double-walled carbon nanotubes.

In a thermally driven rotary motor made from double-walled carbon nanotubes, the rotor (inner tube) can be actuated to rotate within the stator (outer tube) when the environmental temperature is high enough. A sudden stoppage of the rotor can occur when the inner tube has been actuated to rotate at a stable high speed. To find the mechanisms of such sudden stoppages, eight motor models with the same rotor but different stators are built and simulated in the canonical NVT ensembles. Numerical results demonstrate that the sudden stoppage of the rotor occurs when the difference between radii is near 0.34 nm at a high environmental temperature. A smaller difference between radii does not imply easier activation of the sudden rotor stoppage. During rotation, the positions and electron density distribution of atoms at the ends of the motor show that a sp(1) bonded atom on the rotor is attracted by the sp(1) atom with the biggest deviation of radial position on the stator, after which they become two sp(2) atoms. The strong bond interaction between the two atoms leads to the loss of rotational speed of the rotor within 1 ps. Hence, the sudden stoppage is attributed to two factors: the deviation of radial position of atoms at the stator's ends and the drastic thermal vibration of atoms on the rotor in rotation. For a stable motor, sudden stoppage could be avoided by reducing deviation of the radial position of atoms at the stator's ends. A nanobrake can be, thus, achieved by adjusting a sp1 atom at the ends of stator to stop the rotation of rotor quickly.

Impact of blood tube additives and timing of sampling on blood taurine concentrations in clinically healthy dogs.

INTRODUCTION: Dilated cardiomyopathy can be associated with taurine deficiency in dogs. Blood taurine concentrations can be analyzed in whole blood (WB) and plasma. The study objectives were to investigate agreement between taurine concentrations measured in WB, heparin plasma, and EDTA plasma, determine intraindividual variation in healthy dogs, and evaluate if time from feeding to sampling impacts concentrations. ANIMALS: Ten English Cocker spaniels and 10 dogs of various breeds. MATERIALS AND METHODS: Dogs were fasted 12 h prior to initial blood sampling, and the blood was collected at five occasions over eight h. Food was offered immediately after first and one h after fourth sampling time point. RESULTS: Agreement between taurine concentrations in EDTA plasma and heparinized plasma was good (mean difference 4.5 nmol/mL, 95% confidence interval (CI) 36.8-45.8 nmol/mL). Whole blood concentrations were systematically higher than EDTA and heparin plasma concentrations (mean difference 132.7 nmol/mL, 95% CI 23.6-241.8 nmol/mL, and 127.6 nmol/mL, 95% CI 28.6-226.6 nmol/mL, respectively, all P < 0.001). Intraindividual daily variations in taurine concentration were seen in all additives, with largest variations in plasma (P < 0.001). Taurine concentration in heparinized plasma was higher at first and fifth sampling time points compared to the fourth (P = 0.014). DISCUSSION: Agreement was found between taurine concentrations measured in different additives, with expected higher concentration in WB than plasma. Taurine concentrations measured in heparinized plasma varied with sampling time point. Intraindividual daily variations were observed in all additives, but mainly in plasma samples. CONCLUSION: Taurine concentrations in dogs with suspected deficiency should be interpreted with caution.

[Predictor of clinical response to subcutaneous immunotherapy with dust mites in polysensitized allergic rhinitis patients].

Objective: To evaluate the efficacy of 1-year subcutaneous immunotherapy (SCIT) with dust mites in polysensitized allergic rhinitis (AR) patients and to analyze the serological markers associated with clinical response. Methods: A retrospective analysis of data from 69 polysensitized AR patients who completed 1-year SCIT with dust mites from Oct 2020 to Mar 2022 in Shandong Provincial ENT Hospital was conducted. The median patient age was 21 years, including 41 males and 28 females. The changes in symptoms and serum IgE, IgG4 assessed before and after treatment were evaluated. The differences in serological markers between effective and ineffective groups were analyzed. Multivariate regression analysis was used to investigate the predictors of clinical response. SPSS 22.0 software was used for data processing. Results: After immunotherapy, there was a significant reduction in symptom scores and a substantial improvement in the quality of life of polysensitized AR patients (all P<0.001). Dust mite specific IgG4 (sIgG4) significantly increased and dust mite specific IgE (sIgE)/sIgG4 significantly decreased (all P<0.05). sIgE, total IgE (tIgE), sIgE/tIgE and sIgE/sIgG4 were significantly lower in ineffective group than those in effective group (all P<0.05). The clinical response of SCIT related only to dust mite sIgE (r=0.29, P=0.036), and sIgE≥53.86 kU/L had the best sensitivity (77.78%) and specificity (57.89%) to predict effective SCIT in polysensitized AR patients. Conclusions: One-year dust mite SCIT is effective for polysensitized AR patients. Pre-treatment serum dust mite sIgE≥53.86 kU/L may play a role in predicting clinical response of dust mite SCIT in polysensitized AR patients.

Molecular diversity and association mapping of fiber quality traits in exotic G. hirsutum L. germplasm.

The narrow genetic base of cultivated cotton germplasm is hindering the cotton productivity worldwide. Although potential genetic diversity exists in Gossypium genus, it is largely 'underutilized' due to photoperiodism and the lack of innovative tools to overcome such challenges. The application of linkage disequilibrium (LD)-based association mapping is an alternative powerful molecular tool to dissect and exploit the natural genetic diversity conserved within cotton germplasm collections, greatly accelerating still 'lagging' cotton marker-assisted selection (MAS) programs. However, the extent of genome-wide linkage disequilibrium (LD) has not been determined in cotton. We report the extent of genome-wide LD and association mapping of fiber quality traits by using a 95 core set of microsatellite markers in a total of 285 exotic Gossypium hirsutum accessions, comprising of 208 landrace stocks and 77 photoperiodic variety accessions. We demonstrated the existence of useful genetic diversity within exotic cotton germplasm. In this germplasm set, 11-12% of SSR loci pairs revealed a significant LD. At the significance threshold (r(2)>/=0.1), a genome-wide average of LD declines within the genetic distance at <10 cM in the landrace stocks germplasm and >30 cM in variety germplasm. Genome wide LD at r(2)>/=0.2 was reduced on average to approximately 1-2 cM in the landrace stock germplasm and 6-8 cM in variety germplasm, providing evidence of the potential for association mapping of agronomically important traits in cotton. We observed significant population structure and relatedness in assayed germplasm. Consequently, the application of the mixed liner model (MLM), considering both kinship (K) and population structure (Q) detected between 6% and 13% of SSR markers associated with the main fiber quality traits in cotton. Our results highlight for the first time the feasibility and potential of association mapping, with consideration of the population structure and stratification existing in cotton germplasm resources. The number of SSR markers associated with fiber quality traits in diverse cotton germplasm, which broadly covered many historical meiotic events, should be useful to effectively exploit potentially new genetic variation by using MAS programs.

[Osteogenic potential of the Schneiderian membrane and its factors].

Insufficient bone quantity in the posterior region of the maxilla is one of the difficulties for dental implant placement. Maxillary sinus augmentation is considered to be a reliable treatment to solve the problem of insufficient bone quantity. With the increase of researches on maxillary sinus elevation, the debate over osteogenesis potential of Schneiderian membrane is getting more attention. Therefore, this article will review the current research on osteogenic potential of the Schneiderian membrane and its influence factors.

Intracellular calcium levels are unchanged in the diabetic heart.

The quality control indices of myocyte isolation (viability, yield, survival time, cell response, etc.) suggest that the adult rat myocyte model is stable and useful in [Ca2+]i measurements and functional studies at the cellular level. Moreover, diabetic cardiomyocytes are a valuable model for studying cellular functions of the diabetic heart as they retain most of the features of cardiac dysfunction of intact rat. Data from our studies indicate that the basal [Ca2+]i in both quiescent and electrically-stimulated cells is not changed. Thus, resting levels of [Ca2+]i and basal [Ca2+]i transients may not reflect the abnormalities observed in diabetes until the system is challenged by certain stimuli. [Ca2+]i responses to isoproterenol are depressed in both resting and stimulated diabetic cells. This suggests an alteration in the beta-adrenergic pathway, possibly related to the beta-adrenoceptor deficiency reported in the diabetic heart. SR Ca-ATPase is also involved in the isoproterenol-induced [Ca2+]i changes. Moreover, the decreased maximum response to 8-bromo-cAMP provides evidence of a post-receptor alteration in the pathway. Diabetic myocytes are more sensitive to ouabain, whereas the maximum response to ouabain was depressed. This may be the result of depressed Na-K ATPase and increased [Na+]i. In diabetic myocytes, rapid cooling contractures and caffeine contractures are depressed, whereas caffeine-induced Ca2+ transients are decreased. Ryanodine binding suggests a decreased number of high-affinity binding sites in the SR of diabetic myocytes. Additionally, there are indications that SR releasable calcium is reduced and that the major functions of SR, notably uptake, release and storage, may be depressed in diabetic myocytes. Finally, L-type Ca(2+)-channels are quantitatively and qualitatively altered in diabetes. Insulin treatment normalizes most of the diabetes-induced changes in cardiomyocytes, suggesting that metabolic alterations due to insulin deficiency play an important role in diabetic cardiomyopathy. Results from several studies show that in diabetes the function of major organelles which handle [Ca2+]i in myocytes is depressed, which in turn causes the alteration of [Ca2+]i mobilization in myocytes. Different second messenger systems involved in E-C coupling may also be altered due to the metabolic impairments. The rapid increase in our understanding of the pathophysiology of calcium homeostasis in cardiomyocytes will be forthcoming as the powerful new tools of molecular and structural biology are used to investigate the regulation of the Ca2+ transport system.

Secondary heterotypic versus homotypic infection by Coxsackie B group viruses: impact on early and late histopathological lesions and virus genome prominence.

The impact of prior exposure to a different or identical strain of Coxsackievirus B (CVB) on murine CVB myocarditis was studied using a susceptible murine host (A/J[H-2a]) and myocarditic CVB3 or avirulent CVB2 as primary or secondary infectants. The effects of secondary heterotypic infection (CVB2 followed by CVB3) and homotypic infection (CVB3 followed by CVB3) 28 days after primary inoculation, versus CVB2 or CVB3 alone, on injury and viral genomic replication, both early (day 7) and late (days 28 and 56), were evaluated. After the primary infection by CVB2, trivial viral RNA was present in the heart and other organs, and a substantial positivity was observed with CVB3 infection. Seven days after secondary heterotypic (CVB2-CVB3) infection, the quantity of CVB genome in heart, pancreas, liver, and spleen was increased compared with the virus genome in the CVB3-CVB3 group and in the group with primary CVB3 infection alone. This phenomenon was seen in the heart and spleen up to day 28 postsecondary infection. Tissue inflammation and necrosis in heart and pancreas were prominent 7 days postsecondary infection with CVB2-CVB3 and correlated well with an increased quantity of CVB genome. Virus genome was present in heart and spleen 28 days after CVB3 infection alone. Serum CVB3 neutralization titer was increased to 1:128 in CVB2-CVB3 group at days 7 and 28 postsecondary infection, and serum completely neutralized cytopathological effects of CVB3 in the CVB3-CVB3 group at day 7 and 28 postsecondary infection. Our results indicate that secondary heterotypic infection by CVB causes increased injury, inflammation, and CVB replication in target organs such as the heart and pancreas, as well as in immune compartments like the spleen. Compared with CVB3 alone, the intense inflammatory infiltriate in the CVB2-CVB3 group is as not due solely to postviral sensitization of the immune system, but rather to the inability of the host to eradicate the virus.

Altered [Ca2+]i mobilization in diabetic cardiomyocytes: responses to caffeine, KCl, ouabain, and ATP.

To study the mechanisms mediating intracellular calcium transients involved in diabetic cardiac dysfunction, changes in intracellular calcium concentration ([Ca2+]i) in response to stimulation by caffeine, ouabain, KCl and ATP were studied in single cardiomyocytes (quiescent or electrically-stimulated) isolated from streptozotocin (STZ) diabetic rats. [Ca2+]i was measured by fluorescence microscopy using fura-2. Peak [Ca2+]i response to caffeine (20 mM) and decline of [Ca2+]i (-peak d[Ca2+]i/dt) were decreased in diabetic myocytes. Insulin treatment corrected these depressed [Ca2+]i responses. The data suggest a reduced sarcoplasmic reticulum (SR) calcium content and a depressed Na-Ca exchange activity in diabetic myocytes. Insulin deficiency may play a causal role in these changes. The maximum [Ca2+]i increase in response to ouabain was reduced in diabetic cells while the sensitivity of diabetic myocytes to ouabain was increased. This may be a result of depressed Na-K ATPase and elevated [Na+]i as previously reported. The KCl (12.5-50 mM)-induced [Ca2+]i increase was enhanced in diabetic cells. Caffeine (20 mM) and dichlorobenzamil (DCB, 10 microM) blocked this [Ca2+]i transient to a smaller degree in diabetic cells, but nitrendipine effects were similar in diabetic and control cells. These effects may be due to the increased L-channel activity and altered features, such as different responses to Ca-channel blockers, in diabetes which has previously been reported. The maximum response of [Ca2+]i to exogenous ATP was increased in diabetic cells while the sensitivity remained unchanged. The mechanisms underlying this enhanced response may be similar to the KCl-induced [Ca2+]i changes in diabetes.

[Effects of L-arginine on pulmonary circulation and cerebral blood flow in acute and chronic hypoxic rats].

The effects of L-arginine (L-Arg) on pulmonary circulation and cerebral blood flow in acute and chronic hypoxic rats and their mechanism were studied. The results showed that bolus injection of L-Arg 400mg.kg-1 did not inhibit acute hypoxic pulmonary vasoconstriction (HPV), while 800mg.kg-1 could inhibit HPV. Neither of these two doses of L-Arg was found to have any influence on the change in cerebral blood flow during acute hypoxia. Long-term administration of L-Arg (300mg.kg-1/d) could attenuate chronic hypoxic pulmonary hypertension, the increase in pulmonary vascular resistance and right ventricular hypertrophy, and the HPV as well. It did not influence the cerebral blood flow. Since the inhibitor of NO synthetase, NG-nitro-L-arginine methyl ester, could antagonize the effect of L-Arg, it is suggested that an increase in the synthesis of NO might contribute to the effect of L-Arg.

Effects of diabetes and hypertension on myocardial Na+-Ca2+ exchange.

Abnormalities in cardiac function have been extensively documented in experimental and clinical diabetes. These aberrations are well known to be exaggerated when hypertension and diabetes co-exist. The objective of the present study was to examine whether alterations in the activity of the myocardial Na+-Ca2+ exchanger (NCX) can account for the deleterious effects of diabetes and (or) hypertension on the heart. To this aim, the following experimental groups were studied: (i) control; (ii) diabetic; (iii) hypertensive; and (iv) hypertensive-diabetic. Wistar rats served as the control group (C) while Wistar rats injected with streptozotocin (STZ, 55 mg/kg) served as the diabetic (D) group. Spontaneously hypertensive (SH) rats were used as the hypertensive group (H) while SH rats injected with STZ served as the hypertensive-diabetic (HD) group. Sarcolemma was isolated from the ventricles of the C, D, H, and HD groups and NCX activity was examined using rapid quenching techniques to study initial rates over a [Ca2+]o range of 10-160 microM. The Vmax of NCX was lower in the D group when compared with the C group (D, 2.96 +/- 0.26 vs. C, 4.0 +/- 0.46 nmol x mgprot(-1) x s(-1), P < 0.05), however combined diabetes and hypertension (HD) did not affect the Vmax of NCX activity (HD, 3.84 +/- 0.88 vs. H, 3.59 +/- 0.24 nmol x mgprot(-1) x s(-1), P > 0.05). However, analysis of the Km values for Ca2+ indicated that both the D and HD groups exhibited a significantly lower Km when compared with their respective control groups (D, 42 +/- 4 vs. C, 56 +/- 4 microM, P < 0.05; HD, 33 +/- 7 vs. H, 51 +/- 8 microM, P < 0.05). Immunoblotting using polyclonal antibodies (against canine cardiac NCX) exhibited the typical banding of 160, 120, and 70 kDa. The 120 kDa band is believed to represent the native exchanger with its post-translational modifications. Examination of the blots revealed a lower intensity of the 120 kDa band in the D group when compared with the C group, however, no significant difference in the HD group was observed. We speculate that the lower Vmax in the D group may be due to a reduced concentration of exchanger protein in the membrane. The absence of this defect in the HD group may be a result of compensatory mechanisms to the overall hemodynamic overload, however, this remains to be determined. The increased affinity for Ca2+ in both the D and HD groups (determined by the lower Km values) is an interesting finding and may be due to changes in sarcolemmal lipid bilayer composition secondary to diabetes-induced hyperlipidemia.

Nitric oxide inhibits Ca(2+) mobilization through cADP-ribose signaling in coronary arterial smooth muscle cells.

The present study was designed to determine whether the cADP-ribose-mediated Ca(2+) signaling is involved in the inhibitory effect of nitric oxide (NO) on intracellular Ca(2+) mobilization. With the use of fluorescent microscopic spectrometry, cADP-ribose-induced Ca(2+) release from sarcoplasmic reticulum (SR) of bovine coronary arterial smooth muscle cells (CASMCs) was determined. In the alpha-toxin-permeabilized primary cultures of CASMCs, cADP-ribose (5 microM) produced a rapid Ca(2+) release, which was completely blocked by pretreatment of cells with the cADP-ribose antagonist 8-bromo-cADP-ribose (8-Br-cADPR). In intact fura 2-loaded CASMCs, 80 mM KCl was added to depolarize the cells and increase intracellular Ca(2+) concentration ([Ca(2+)](i)). Sodium nitroprusside (SNP), an NO donor, produced a concentration-dependent inhibition of the KCl-induced increase in [Ca(2+)](i), but it had no effect on the U-46619-induced increase in [Ca(2+)](i). In the presence of 8-Br-cADPR (100 microM) and ryanodine (10 microM), the inhibitory effect of SNP was markedly attenuated. HPLC analyses showed that CASMCs expressed the ADP-ribosyl cyclase activity, and SNP (1-100 microM) significantly reduced the ADP-ribosyl cyclase activity in a concentration-dependent manner. The effect of SNP was completely blocked by addition of 10 microM oxygenated hemoglobin. We conclude that ADP-ribosyl cyclase is present in CASMCs, and NO may decrease [Ca(2+)](i) by inhibition of cADP-ribose-induced Ca(2+) mobilization.

Serum from patients with chronic renal insufficiency alters growth characteristics and ANP mRNA expression of adult rat cardiac myocytes.

Left ventricular hypertrophy is very prevalent among patients with renal insufficiency. Known hypertrophic factors, such as systemic hypertension, do not adequately account for the prevalence of left ventricular hypertrophy in these patients. Circulating growth factors may stimulate cardiomyocyte growth and contribute to the development of left ventricular hypertrophy. The effects of sera from patients with (n = 30) and without (n = 5) chronic renal insufficiency on the growth of cultured adult cardiomyocytes were compared. An adult rat cardiomyocyte primary culture system was established with a high purity of cardiomyocyte population as confirmed by immunocytochemical staining of cardiac contractile proteins. Myocytes responded with increased [3H]thymidine incorporation when treated with angiotensin II, epidermal growth factor, hydrocortisone and insulin, and with increased [3H]phenylalanine incorporation when treated with parathormone, isoproterenol, phenylephrine and insulin. Renal insufficiency serum stimulated [3H]thymidine incorporation was 1.5 times that of the control (P < 0.02) and also tended to increase incorporation of [3H]phenylalanine compared to the control (P = N.S.). Increased [3H]thymidine incorporation by renal insufficiency serum did not correlate with serum insulin, parathormone or glucose in the renal insufficiency patients. A quantitative reverse transcriptase polymerase chain reaction (RT-PCR) method was used to measure renal insufficiency serum-induced atrial natriuretic peptide mRNA expression in cultured cardiomyocytes. Atrial natriuretic peptide (ANP) mRNA was increased 1-3-fold in cardiomyocytes treated with renal insufficiency sera in comparison to control sera. These data suggest that circulating growth factor(s) may contribute to the development of cardiac hypertrophy in patients with renal insufficiency.

In vivo effects of peroxovanadium compounds in BB rats.

Peroxovanadium compounds, each containing an oxo ligand, one or two peroxo anions, and an ancillary ligand in the inner coordination sphere of vanadium, were synthesized, crystallized and characterized by 51V NMR as > 95% pure. They markedly decreased plasma glucose in insulin-deprived diabetic BB rats, with a nadir occurring between 60 and 100 min after intravenous, intraperitoneal or subcutaneous administration. Plasma glucose was reduced after oral administration in insulin-treated and in insulin-deprived BB rats. When compared to sodium orthovanadate, peroxovanadium compounds exhibited a markedly greater potency on a molar basis, and in relation to their toxicity. The in vivo potency can be predicted by the degree of phosphotyrosine phosphatase inhibition observed in vitro. These are the first agents other than insulin that can acutely and markedly reduce plasma glucose in hypoinsulinemic diabetic BB rats.

HMW and LMW glutenin alleles among putative tetraploid and hexaploid European spelt wheat (Triticum spelta L.) progenitors.

The allelic compositions of high- and low-molecular-weight subunits of glutenins (HMW-GS and LMW-GS) among European spelt ( Triticum spelta L.) and related hexaploid and tetraploid Triticum species were investigated by one- and two-dimensional polyacrylamide-gel electrophoresis (PAGE) and capillary electrophoresis (CE). A total of seven novel glutenin alleles (designated A1a*, B1d*, B1g*, B1f*, B1j*, D1a* at Glu-1 and A3h at the Glu-3 loci, respectively) in European spelt wheat were detected by SDS-PAGE, which were confirmed further by employing A-PAGE and CE methods. Particularly, two HMW-GS alleles, Glu-B1d* coding the subunits 6.1 and 22.1, and Glu-B1f* coding the subunits 13 and 22*, were found to occur in European spelt with frequencies of 32.34% and 5.11%, respectively. These two alleles were present in cultivated emmer (Triticum dicoccum), but they were not observed in bread wheat (Triticum aestivum L.). The allele Glu-B1g* coding for 13* and 19* subunits found in spelt wheat was also detected in club wheat (Triticum compactum L.). Additionally, two alleles coding for LMW-GS, Glu-A3h and Glu-B3d, occurred with high frequencies in spelt, club and cultivated emmer wheat, whereas these were not found or present with very low frequencies in bread wheat. Our results strongly support the secondary origin hypothesis, namely European spelt wheat originated from hybridization between cultivated emmer and club wheat. This is also confirmed experimentally by the artificial synthesis of spelt through crossing between old European emmer wheat, T. dicoccum and club wheat, T. compactum.

ACE-Asia intercomparison of a thermal-optical method for the determination of particle-phase organic and elemental carbon.

A laboratory intercomparison of organic carbon (OC) and elemental carbon (EC) measurements of atmospheric particulate matter samples collected on quartz filters was conducted among eight participants of the ACE-Asia field experiment The intercomparison took place in two stages: the first round of the intercomparison was conducted when filter samples collected during the ACE-Asia experiment were being analyzed for OC and EC, and the second round was conducted after the ACE-Asia experiment and included selected samples from the ACE-Asia experiment Each participant operated ECOC analyzers from the same manufacturer and utilized the same analysis protocol for their measurements. The precision of OC measurements of quartz fiber filters was a function of the filter's carbon loading but was found to be in the range of 4-13% for OC loadings of 1.0-25 microg of C cm(-2). For measurements of EC, the precision was found to be in the range of 6-21% for EC loadings in the range of 0.7-8.4 microg of C cm(-2). It was demonstrated for three ambient samples, four source samples, and three complex mixtures of organic compounds that the relative amount of total evolved carbon allocated as OC and EC (i.e., the ECOC split) is sensitive to the temperature program used for analysis, and the magnitude of the sensitivity is dependent on the types of aerosol particles collected. The fraction of elemental carbon measured in wood smoke and an extract of organic compounds from a wood smoke sample were sensitive to the temperature program used for the ECOC analysis. The ECOC split for the three ambient samples and a coal fly ash sample showed moderate sensitivity to temperature program, while a carbon black sample and a sample of secondary organic aerosol were measured to have the same split of OC and EC with all temperature programs that were examined.