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PubMed1987

Effects of intracellular and extracellular calcium blockers on the pulmonary vascular responses to PGF2 alpha and U46619.

In this study, TMB-8, an intracellular calcium antagonist, and verapamil, an extracellular calcium antagonist, were used simultaneously to elucidate the role of calcium in the pulmonary vasopressor response induced by PGF2 alpha and U46619. The pulmonary vasoconstrictor action of these two agonists was evaluated in the canine isolated lung lobe preparation. Lobar arterial pressure was constantly monitored and changes in arterial pressure were recorded as a percentage from baseline. Control responses to PGF2 alpha (42.0 +/- 8.2%) and U46619 (47.2 +/- 7.0%) were obtained prior to the administration of TMB-8 and verapamil. After administration of TMB-8 and verapamil, the PGF2 alpha (7.4 +/- 3.1%) and U46619 (28.8 +/- 6.2%) responses were significantly attenuated. We conclude that the PGF2 alpha pressor response is dependent on a TMB-8-sensitive intracellular calcium pool and a verapamil-sensitive slow-channel calcium influx. In contrast, the degree of attenuation of the U46619 response was similar to the vasopressor response in the presence of verapamil alone, as described previously. This indicates a direct dependence on extracellular calcium. An additional source of calcium insensitive to verapamil and TMB-8 may also be activated and contribute to the pulmonary vasoconstrictor action. These results suggest that each agonist possesses a mechanism of action distinctly different from the other.

Animals↗
PubMed1978

Tetramethyl benzidine for horseradish peroxidase neurohistochemistry: a non-carcinogenic blue reaction product with superior sensitivity for visualizing neural afferents and efferents.

Tetramethyl benzidine (TMB) is a presumptively non-carcinogenic chromogen which yields a blue reaction-product at sites of horseradish peroxidase activity. Sixty-six distinct procedures were performed in rats and monkeys in order to determine the optimal incubation parameters for TMB. As a result, a procedure is recommended whose sensitivity greatly surpasses that of a previously described benzidine dihydrochloride method. Indeed, the sensitivity of this new method in demonstrating retrograde transport is markedly superior to that of the previously described benzidine dihydrochloride method. Furthermore, as a consequence of this enhanced sensitivity, many efferent connections of the injection site are also visualized. The injection site demonstrated by this TMB procedure is significantly larger than the one demonstrated when benzidine dihydrochloride or diaminobenzidine is used as a chromogen. Finally, this TMB procedure has been compared to two other TMB procedures and found to provide superior morphology and sensitivity.

Animals↗
PubMed1981

Comparison of horseradish peroxidase visualization methods: quantitative results and further technical specifics.

Four methods used for the neurohistochemical demonstration of horseradish peroxidase (HRP) were quantitatively compared by counting retrogradely labeled neurons found after each method was used. HRP used as a retrograde marker is an important neuroanatomical tracing method, and maximum sensitivity in its demonstration of retrogradely, labeled neurons is important if these neuroanatomical studies are to completely demonstrate afferent neurons. The four methods compared were a diaminobenzidine (DAB) procedure, a Hanker-Yates procedure using P-phenylenediamine and pyrocatechol, an o-dianisidine procedure, and a tetramethyl benzidine (TMB) procedure. The TMB procedure resulted in a more complete topography of neurons afferent to the HRP application site, and demonstrated many more neurons in all afferent cell groups that either of the three other procedures. Use of the TMB method was especially critical in the cases of small HRP applications, a size useful for neuroanatomical studies, where the other methods demonstrated very few or no retrogradely labeled neurons. Neurons were judged to be retrogradely HRP labeled if they had small granules of the reaction product (the color varying with the chromogen) describing the somal shape, usually extending into the processes, and a clear nucleus. In addition, after the o-dianisidine or the TMB reaction a small number of retrogradely labeled neurons had soma and processes especially well filled with reaction product, giving the appearance of neurons from Golgi preparations. For a sensitive TMB reaction giving good results, exact H2O2 concentration, freshly prepared solutions, minimal postreaction exposure to alcohol, counterstaining, and clean glassware were each found to be important.

3,3'-Diaminobenzidine↗
PubMed1993

Opposite, phase-dependent effects of 3,4,5-trimethoxybenzoic acid 8-(diethylamino) octyl ester or tetracaine on islet function during three phases of glucose-stimulated insulin secretion.

The spontaneous decline of insulin secretion which occurs under a variety of secretory conditions is well documented and suggests a general desensitization of the secretory process distal to signal recognition. Accordingly, we have investigated the effects of agents thought to mobilize intracellular Ca++ on insulin secretion over 24 h, which includes periods of rising secretory activity (second phase) and desensitized secretory activity (third phase). During the first 3 h of glucose stimulation of freshly isolated rat islets, insulin secretion was strongly inhibited by 30 microM 3,4,5-trimethoxybenzoic acid 8-(diethylamino) octyl ester (TMB) or 300 microM tetracaine hydrochloride (TC). However, when either of these agents was added for the first time to islets at h 20 when insulin secretion was at a low steady rate (third phase), insulin secretion was greatly enhanced. Both these inhibitory and stimulatory effects declined with continued administration. Removal of TMB and rechallenge with high glucose plus forskolin uncovered a residual inhibition in both chronically and acutely treated islets. Coadministration of forskolin with either TMB or TC blunted both inhibitory and stimulatory effects. Pertussis toxin pretreatment, however, did not alter subsequent response of islets to either agent. Thus TMB or TC have opposite, phase-dependent effects on glucose-stimulated insulin secretion. We postulate that potentiators of glucose-stimulated insulin secretion, which are increased during second phase, are most sensitive to inhibitory effects of TMB or TC, and that the low steady rate of third phase permits their stimulatory component(s) to become apparent.

Animals↗
PubMed2026

Genetic insights into lung squamous cell carcinoma: how TP53 and CSMD3 co-mutations shape prognosis and immune response.

BACKGROUND: Lung squamous cell carcinoma (LUSC) accounts for a significant proportion of lung cancer cases and is often associated with smoking and various environmental factors. The prognostic and immunologic implications of TP53 and CSMD3 co-mutations in LUSC remain poorly understood. This study aimed to investigate the role of TP53/CSMD3 co-mutations in LUSC using comprehensive bioinformatics analyses. METHODS: Data from 487 LUSC patients were obtained from The Cancer Genome Atlas (TCGA) database, with external validation performed using the combined cohort. Patients were stratified into TP53/CSMD3 co-mutation, single-mutation, and wild-type (WT) groups. Prognostic analysis was conducted using Kaplan-Meier survival curves. Tumor mutational burden (TMB) was calculated, and immune cell infiltration was assessed using multiple algorithms. Differentially expressed genes (DEGs) between co-mutated and WT groups were identified, followed by Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. A nomogram incorporating mutation status, gender, age, and tumor stage (T stage) was developed for individualized prognostic prediction. RESULTS: The TP53/CSMD3 co-mutated group exhibited significantly better overall survival (OS) compared to single-mutation and WT groups. TMB scores were markedly higher in co-mutated patients, suggesting potential sensitivity to immune checkpoint inhibitors. Immune infiltration analysis revealed distinct profiles, including elevated CD8 T cells and reduced immunosuppressive components, in the co-mutation group. A total of 403 DEGs were identified between co-mutated and WT groups, with significant enrichment in immune-related pathways. Mechanistically, the co-mutation was associated with distinct downregulation of complement negative regulators (CFH/CFI), indicating complement hyperactivation independent of TMB. The constructed nomogram provided accurate individualized prognostic assessments. CONCLUSIONS: The co-mutation of TP53 and CSMD3 identifies a distinct LUSC subtype with favorable survival, marked by high TMB and an immune-activated microenvironment. Beyond TMB-driven neoantigen generation, the significant downregulation of complement negative regulators (CFH/CFI) reveals an independent complement hyperactivation pathway associated with CSMD3 loss. The constructed nomogram provides accurate individualized survival prediction. These findings establish TP53/CSMD3 co-mutation as a promising prognostic biomarker and offer mechanistic insights for personalized immunotherapy strategies. Future prospective cohorts are warranted to validate its predictive value.

Lung squamous cell carcinoma (LUSC)↗
PubMed2000

The treatment of delayed polyneuropathy induced by diisopropylfluorophosphate in hens.

This study was undertaken to examine the influence of atropine, oximes and benzodiazepine on organophosphate-induced delayed polyneuropathy (OPIDP) in hens, which were poisoned with diisopropylfluorophosphate (DFP). The birds were treated with a standard neuropathic dose of DFP (1.1 mg/kg, s.c.), which produced typical signs of OPIDP. The development of OPIDP was observed within the followings 22 days. All drugs were given subcutaneously (s.c.), intramuscularly (i.m.) or intraperitoneally (i.p.), 20 min before the poison. The results obtained have shown that atropine (20 mg/kg, i.p.) only in combination with oxime TMB-4 (15 mg/kg, i.m.) produced significant improvement of OPIDP symptoms in comparison with positive control. Clinical signs and symptoms of OPIDP in the group which was treated with atropine (20 mg/kg, i.p.), TMB-4 (15 mg/kg, i.m.) and midazolam (2.5 mg/kg, i.m.) were more improved than that in the presence of a combination of atropine and TMB-4. The results of these experiments have shown that it is possible to prevent the development of DFP-induced OPIDP in hens by treatment with atropine and TMB-4 or atropine, TMB-4 and midazolam when given before DFP.

Animals↗
PubMed1998

[Effect of 8-(N,N'-diethylamino)-n-octyl-3,4,5-trimethoxybenzoate on [Ca2+]i and the release of NO in cultured endothelial cells of the calf middle cerebral artery].

The effect of 8-(N,N'-diethylamino)-n-octyl-3,4,5-trimethoxybenzoate(TMB-8) on [Ca2+]i and the release of NO in cultured endothelial cells of the calf middle cerebral artery was studied by a system of measurement of AR-CM-MIC, using Fura-2/AM as a fluorescent indicator and the oxy-haemoglobin method. In the presence of extracellular Ca2+ 1.3 mmol.L-1, the resting [Ca2+]i and the extinction difference(delta E) of between 401 and 410 nm were not changed by TMB-8 12.5 and 25 mumol.L-1, but were increased by TMB-8 50 and 100 mumol.L-1. The rise of delta E induced by TMB-8 50 and 100 mumol.L-1 was blocked completely by L-NAME. The elevation of [Ca2+]i was related to the release of NO. The result suggested that TMB-8 increased resting [Ca2+]i of endothelial cells of the calf middle cerebral artery and induced NO release.

Animals↗
PubMed1992

Modulation of human basophil histamine release by protein kinase C inhibitors differs with secretagogue and with inhibitor.

To assess possible involvement of protein kinase C (PKC) in human basophil degranulation, the present work compared effects of various purported PKC inhibitors on leukocyte histamine release triggered by different stimuli. The effects recorded varied with the inhibitor and the secretagogue used; moreover, with a given secretagogue, different inhibitors often displayed different activities. Thus, histamine release triggered by the PKC activator 4 beta-phorbol 12-myristate 13-acetate was blocked by K252a, staurosporine and the purported specific PKC inhibitor Ro 31-7549, and reduced by calphostin C, H-7, TMB-8 and W-7 but not affected by polymyxin B; it was augmented by 2.1 microM palmitoyl carnitine. The leukocyte response induced by another putative activator of PKC, 1,2-isopropylidene-3-decanoyl-sn-glycerol, was also enhanced by 2.1 microM palmitoyl carnitine, slightly increased by staurosporine, TMB-8 and W-7 but not affected by calphostin C, H-7, K252a or Ro 31-7549, whereas the hyperosmolar mannitol-induced response was reduced by H-7, calphostin C, TMB-8 and W-7 and slightly augmented by staurosporine. Anti-IgE-induced histamine release was blocked by staurosporine and K252a and reduced by calphostin C, sphingosine, TMB-8 and W-7 but not affected by H-7, polymyxin B or retinal. It was enhanced by Ro 31-7549. In contrast, leukocyte histamine release induced by calcium ionophore A23187 or by ionomycin was blocked by retinal, TMB-8 and W-7 and reduced by calphostin C and palmitoyl carnitine but enhanced by H-7, staurosporine and polymyxin B; K252a and Ro 31-7549 did not affect such responses. Formyl-methionyl-leucyl-phenylalanine-triggered histamine release was barely affected by any agent used. Thus, the specific PKC inhibitor Ro 31-7549 selectively blocked 4 beta-phorbol 12-myristate 13-acetate-triggered leukocyte histamine release. These results imply that examined secretagogues trigger human leukocyte histamine release through partly separate pathways probably involving different kinase activities (PKC isozymes?). Moreover, the distinct effect patterns recorded for most purported PKC inhibitors imply a functional selectivity between these compounds.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1990

Comparison of particulate 3,3',5,5'-tetramethylbenzidine and 3,3'-diaminobenzidine as chromogenic substrates for immunoblot.

In horseradish peroxidase (EC: 1.11.1.7)-dependent immunoblot assays, particulate 3,3',5,5'-tetramethylbenzidine (TMB) is shown to be a more efficient immunoblot substrate than the standard substrate 3,3'-diaminobenzidine (DAB), because TMB is easily prepared, stable, and less carcinogenic than is DAB. Assays of antibody in a serially diluted human immunodeficiency virus (HIV) control serum (CDC reference CAT# VS2151) have the same sensitivity limits with both DAB and TMB (1:312,500). Complete, working substrate solutions of H2O2/TMB/enhancer and of H2O2/DAB were stored at room temperatures and at 48 degrees C respectively. Periodic tests showed the TMB substrate system to be functional after four weeks at 48 degrees C and after eight weeks at room temperature, while the DAB system was functional after one week at 48 degrees C and after four weeks at room temperature. The stability, safety, and convenience of the commercially available TMB kits make this substrate ideal for immunoblot tests.

3,3'-Diaminobenzidine↗
PubMed1989

[Mode of action of trimebutine: involvement if opioid receptors].

Several studies in dogs, cats, rabbits and humans have suggested that the motility-stimulating properties of trimebutine (TMB) are mediated by peripheral opiate receptors. The present work deals with the capacity of the drug and its N-desmethyl metabolite (NDTMB) to displace mu, delta and kappa specific ligands from their receptors using guinea-pig whole brain membranes and ileum myenteric plexus synaptosomes membranes. The activity of both compounds on the twitch response induced by transmural stimulation of the guinea-pig ileum and of the mouse and rabbit vas deferens was also investigated. These preparations have been claimed to be specific for the mu, delta and kappa receptor subtypes respectively. TMB (0.2 to 1.8 microM) and NDTMB (0.3 to 6 microM) displayed a good affinity for all receptor subtypes in brain and myenteric plexus preparations. The decreasing order of IC50 (50 per cent inhibitory concentration)'S of TMB ranged from 0.75 microM in the guinea-pig ileum to 7.1 and 39 microM in the vas deferens of the rabbit and the mouse respectively. These results indicate that TMB and NDTMB possess mu, delta as well as kappa agonistic properties without true specificity for one or the other of these subtypes. They also confirm that activation of peripheral mu, delta and kappa opiate receptors mediate the gastrointestinal motility effect of TMB.

Animals↗
PubMed1997

Retardation of the age-related increase in spontaneous cortical spike-wave discharges (SWD) in rats after a 28-day inhalation (SWD) in rats after a 28-day inhalation exposure to an industrial solvent, pseudocumene (1,2,4-trimethylbenzene).

It has been hypothesized that exposure to neurotoxins may hasten the process of brain ageing. Volatile hydrocarbons are in common use as solvents and their neurotoxic properties are acknowledged. In the rat, the age-related neurodegenerative changes in the brain develop together with an increased occurrence of bursts of spontaneous spike-wave discharges (SWD) in the neocortex. Therefore, the number and/or duration of SWD bursts may serve as an index allowing to distinguish between young and old brains (7). Measuring the SWD activity after exposure may thus reveal the effect of the studied neurotoxicant on brain ageing. Pseudocumene (1,2,4-trimethylbenzene, TMB), is a component of industrial solvent mixtures. The present study investigated the effect of a 4-week (6h/day, 5 days/week) inhalation exposure to TMB at concentrations of 0, 25, 100 or 250 ppm on the occurrence of SWD bursts. EEG recordings were performed before and one day, 30 days and 4 months after exposure. In rats exposed to TMB at 0 and 25 ppm, the level of the SWD activity increased progressively after exposure. In rats exposed to TMB at 100 or 250 ppm, the SWD activity did not increase during the post-exposure period or even dropped below the pre-exposure level. This result indicates that the persistent changes in the rat central nervous system (CNS), following the exposure to TMB, differ in some respects from those which develop in the course of normal ageing.

Administration, Inhalation↗
PubMed1987

Angioarchitecture of the CNS, pituitary gland, and intracerebral grafts revealed with peroxidase cytochemistry.

Blood vessels of the fetal, neonatal, and adult subprimate and primate CNS, including circumventricular organs (e.g., median eminence, pituitary gland, etc.), and of solid CNS and nonneural (anterior pituitary gland) allografts placed within brains of adult mammalian hosts were visualized with peroxidase cytochemistry applied in three ways: to tissues from animals injected systemically with native horseradish peroxidase (HRP) or peroxidase conjugated to the lectin wheat germ agglutinin (WGA) prior to perfusion fixation; to tissues from animals infused with native HRP into the aorta subsequent to perfusion fixation; and to tissues from animals fixed by immersion and incubated for endogenous peroxidase activity in red cells retained within blood vessels. In neonatal and adult animals receiving native HRP intravascularly, non-fenestrated vessels contributing to a blood-brain barrier were outlined with HRP reaction product when tetramethylbenzidine (TMB) as opposed to diaminobenzidine (DAB) was used as the chromogen; fenestrated vessels of circumventricular organs were not discernible due to the density of extravascular reaction product. Fenestrated and non-fenestrated cerebral and extracerebral blood vessels exposed to bloodborne WGA-HRP were visible when incubated in TMB and DAB solutions. Native HRP infused into the aorta of fixed animals likewise labeled non- fenestrated vessels throughout the brain upon exposure to TMB or DAB but obscured fenestrated vessels of the circumventricular organs. Endogenous peroxidase activity of red cells, seen equally well with TMB and DAB, outlined blood vessels throughout the cerebral gray and white matter and all circumventricular organs in fetal, neonatal, and adult animals. Application of the three peroxidase cytochemical approaches to study the development or absence of a blood-brain barrier in intracerebral allografts demonstrated that the vascularization of day 16-19 fetal/1 day neonatal CNS allografts is not well defined prior to 7 days following intracerebral placement of the grafts. CNS allografts secured from donor sites expected to possess a blood-brain barrier exhibited blood vessels that were not leaky to HRP injected intravenously in the host. Fenestrated blood vessels associated with anterior pituitary allografts were evident prior to 3 days posttransplantation within the host brain and permitted blood-borne HRP in the host to enter the graft and surrounding host brain parenchyma.

Animals↗
PubMed1985

Mitogen and co-mitogen stimulation of lymphocytes inhibited by three Ca++ antagonists.

The Ca++ requirement for in vitro lymphocyte stimulation by lectins is well known and can be demonstrated by the use of Ca++ chelators. In this study, three Ca++ antagonists were examined for their effects on lymphocyte proliferation. [3H]-thymidine incorporation was employed to measure DNA synthesis in several systems. Stimulation and proliferation were achieved by the addition of one of the following: the mitogenic lectin concanavalin A (ConA); the combination of two co-mitogens, the calcium ionophore A23187 and the phorbol ester, 12-0-tetradecanoylphorbol-13-acetate (TPA), neither of which is mitogenic alone; or the non-mitogenic lectin, wheat germ agglutinin (WGA) with TPA. These mitogenic systems were tested for their sensitivity to the Ca++ channel blockers verapamil and nicardipine and the intracellular Ca++ antagonist TMB-8. We found that the ConA and WGA plus TPA treated cells were inhibited approximately 50% by 10 microM verapamil, nicardipine or TMB-8. The stimulation caused by A23187 and TPA was only inhibited by TMB-8 and nicardipine. The inhibitory effects caused by the Ca++ antagonists could not be reversed by the addition of exogenous Ca++ (0.1-1.5 mM), but were reversed by repeated washings in antagonist free media. Using TMB-8 we saw an apparent intracellular Ca++ dependence throughout the G1 phase. Previous studies using Ca++ chelators or Ca++ antagonists suggested an endpoint at about halfway through this period.

Animals↗
PubMed1985

Cortical granule exocytosis in sea urchin eggs is inhibited by drugs that alter intracellular calcium stores.

In sea urchin eggs fertilization is accompanied by cortical granule exocytosis, a secretory event thought to be initiated by release of intracellularly sequestered calcium. We have examined the effect of two drugs on this process: chlortetracycline (CTC), a known chelator of intracellular calcium, and 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8), an antagonist of intracellular calcium release in both skeletal and smooth muscle. Preincubation of eggs for 10 min with either CTC or TMB-8 blocked sperm entry, inhibited the burst of 45Ca2+ efflux normally seen postinsemination, and prevented fertilization envelope elevation. Half-maximal inhibition occurred with 200 microM CTC and 60 microM TMB-8. Electron microscopy confirmed that cortical granule exocytosis had been blocked, although inhibition was not due to a direct effect on exocytosis. CTC and TMB-8 had no effect on Ca2+-stimulated granule fusion in isolated egg cortices. Rather, these drugs block the early events in egg activation: sperm incorporation and triggering of exocytosis. These two effects appear to be independent since addition of either drug just before insemination permits sperm entry but inhibits calcium release and cortical granule exocytosis.

Animals↗
PubMed2005

Investigation of limiting metabolic steps in the utilization of xylose by recombinant Saccharomyces cerevisiae using metabolic engineering.

A Saccharomyces cerevisiae screening strain was designed by combining multiple genetic modifications known to improve xylose utilization with the primary objective of enhancing xylose growth and fermentation in xylose isomerase (XI)-expressing strains. Strain TMB 3045 was obtained by expressing the XI gene from Thermus thermophilus in a strain in which the GRE3 gene coding for aldose reductase was deleted, and the genes encoding xylulokinase (XK) and the enzymes of the non-oxidative pentose phosphate pathway (PPP) [transaldolase (TAL), transketolase (TKL), ribose 5-phosphate ketol-isomerase (RKI) and ribulose 5-phosphate epimerase (RPE)] were overexpressed. A xylose-growing and fermenting strain (TMB 3050) was derived from TMB 3045 by repeated cultivation on xylose medium. Despite its low XI activity, TMB 3050 was capable of aerobic xylose growth and anaerobic ethanol production at 30 degrees C. The aerobic xylose growth rate reached 0.17 l/h when XI was replaced with xylose reductase (XR) and xylitol dehydrogenase (XDH) genes expressed from a multicopy plasmid, demonstrating that the screening system was functional. Xylose growth had not previously been detected in strains in which the PPP genes were not overexpressed or when overexpressing the PPP genes but having XR and XDH genes chromosomally integrated. This demonstrates the necessity to simultaneously increase the conversion of xylose to xylulose and the metabolic steps downstream of xylulose for efficient xylose utilization in S. cerevisiae.

Aldehyde Reductase↗
PubMed1994

Determination of 3,4-dimethylhippuric acid as a biological monitoring index for trimethylbenzene exposure in transfer printing workers.

The relationship between exposure to 1,2,4-trimethylbenzene (1,2,4-TMB) and urinary concentration of 3,4-dimethylhippuric acid (3,4-DMHA), one of its metabolites, was studied in workers involved in transfer printing. Airborne TMBs were sampled by an organic vapor monitoring badge and analyzed by capillary gas chromatography. Urinary 3,4-DMHA and creatinine were analyzed under the same conditions of high-performance liquid chromatography. The exposure concentration of 1,2,4-TMB among workers was around 25 ppm, the threshold limit value (TLV). The urinary concentration of 3,4-DMHA was low at the start of each shift and high at the end. Exposure to the TLV (25 ppm) of 1,2,4-TMB results in a urinary 3,4-DMHA concentration of 410 mg/g creatinine (r = 0.897, P < 0.001). Urinary 3,4-DMHA concentration could be used as a biological monitoring index for 1,2,4-TMB exposure.

Adult↗
PubMed2002

Fermentation performance and intracellular metabolite patterns in laboratory and industrial xylose-fermenting Saccharomyces cerevisiae.

Heterologous genes for xylose utilization were introduced into an industrial Saccharomyces cerevisiae, strain A, with the aim of producing fuel ethanol from lignocellulosic feedstocks. Two transformants, A4 and A6, were evaluated by comparing the performance in 4-l anaerobic batch cultivations to both the parent strain and a laboratory xylose-utilizing strain: S. cerevisiae TMB 3001. During growth in a minimal medium containing a mixture of glucose and xylose (50 g/l each), glucose was preferentially consumed. During the first growth phase on glucose, the specific growth rates were 0.26, 0.32, 0.27 and 0.30 h(-1) for strains TMB 3001, A (parental strain), A4, and A6, respectively. The specific ethanol productivities were 0.04, 0.13, 0.04 and 0.03 g/g.per hour, for TMB 3001, A, A4 and A6, respectively. The specific xylose consumption rates were 0.06, 0.21 and 0.14 g/g.per hour, respectively for strains TMB 3001, A4 and A6. Xylose consumption resulted mainly in the formation of xylitol, with biomass and ethanol being minor products. The metabolite profile of intermediates in the pentose phosphate pathway and key glycolytic intermediates were determined during growth on glucose and xylose, respectively. The metabolite pattern differed depending on whether glucose or xylose was utilized. The levels of intracellular metabolites were higher in the industrial strains than in the laboratory strain during growth on xylose.

Anaerobiosis↗
PubMed1997

Age-related changes in the brain transfer of blood-borne horseradish peroxidase in the hippocampus of senescence-accelerated mouse.

Age-related changes in the brain transfer of blood-borne horseradish peroxidase (HRP) were examined by light microscopy in senescence-accelerated prone mice (SAMP8) and senescence-accelerated resistant mice (SAMR1). The intracerebral HRP transferred from the blood stream was reacted with tetramethyl benzidine (TMB) and the area showing the presence of HRP-TMB reaction products was morphometrically evaluated. Areas containing HRP reaction products in the medial CA1 region and medial dentate gyrus of the hippocampus were observed in 3- and 13-month-old SAMP8 and SAMR1. The mean percentage of the positive area for the HRP to the area of interest was significantly higher in the rostral portion of the hippocampus in 13-month-old than in 3-month-old SAMP8. On the other hand, age-related changes in the area positive for HRP-TMB reaction products in the cortices and the caudal portion of the hippocampus in SAMP8 were not observed. In addition, positive staining reaction for HRP was also observed in the dorsal portion of the thalamus of 13-month-old SAMP8. There were no significant age-related changes in the area positive for HRP-TMB reaction products in rostral and caudal portions of the cortices and the hippocampus of SAMR1. These findings suggest that blood-borne macromolecules have access to the medial and rostral portion of the hippocampus, that this phenomenon becomes more pronounced during the process of senescence in the SAMP8 brain and, moreover, that intravascular macromolecules have access to the dorsal portion (periventricular area) of the thalamus of 13-month-old SAMP8.

Aging↗