Occupational contact dermatitis in manufacture of vanillin.
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Biomedical subjects
Publications and source records attributed to H Zhu.
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Radio-binding assay, bioassay and HPLC detection were used to observe the antagonistic effects of dextrorphan on PCP's actions. Dextrorphan displayed high affinity to PCP receptors and it had weak PCP-like bioactivity, but could antagonize PCP's action dose-dependently in vitro and shift the dose-response curve to the right. PCP increased the contents of norepinephrine in bath medium, which was reversed by dextrorphan. Thus, the results suggest that dextrorphan is a partial antagonist for PCP receptors.
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Aromatase is an enzyme complex that is composed of a specific form of cytochrome P-450 and a flavoprotein, NADPH-cytochrome P-450 reductase. Aromatase activity of granulosa cells is increased markedly by follicle-stimulating hormone (FSH) and by analogs of cyclic AMP. It was the objective of the present study to investigate the effects of FSH and dibutyryl cyclic AMP (Bt2cAMP) on the synthesis of NADPH-cytochrome P-450 reductase in rat granulosa cells maintained in vitro. Granulosa cells were obtained from the ovaries of diethylstilbestrol (DES)-treated immature rats and were incubated in the presence of DES (10(-7) M), DES + FSH (250 ng/ml), or DES + Bt2cAMP (1 mM) for up to 72 h. After 72 h of incubation, aromatase activity of cells incubated with DES alone was 5 pmoles estrogen formed 2 h-1 mg-1 protein and was increased greater than 60-fold in cells incubated with FSH or Bt2cAMP. NADPH-cytochrome P-450 reductase was immunoisolated from [35S]methionine-labeled lysates of granulosa cells incubated for 72 h in the absence or presence of stimulatory factors. The rate of synthesis of reductase was found to be increased about 3-fold in cells incubated with DES + FSH or DES + Bt2cAMP as compared to cells incubated with DES alone. By immunoblot analysis we found that the cellular content of reductase was increased about 2-fold by FSH and Bt2cAMP treatment. Reductase specific activity was 10 nmoles min-1 mg-1 protein in membrane fractions of DES-treated cells and was increased 1.6-fold by FSH treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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Worn nozzles on spray equipment severely affect the efficiency of crop management systems while causing unnecessary pesticide contamination of non target areas. Scanning electron microscopy (SEM) that has been applied for direct measurement of pesticide deposition, was used to observe worn and unused brass and stainless steel fan-pattern spray nozzles. Wear and other changes were observed in both nozzle materials. Scanning electron microscopy can provide nozzle manufacturers with greater insight and needed information on nozzle mechanics to improve performance. More reliable delivery of pesticide spray should enhance integrated pest and disease management and crop protection for growers.
The effects of a single or repeated dermal administration of methyl parathion on motor function, learning and memory were investigated in adult female rats and correlated with blood cholinesterase activity. Exposure to a single dose of 50 mg/kg methyl parathion (75% of the dermal LD(50)) resulted in an 88% inhibition of blood cholinesterase activity and was associated with severe acute toxicity. Spontaneous locomotor activity and neuromuscular coordination were also depressed. Rats treated with a lower dose of methyl parathion, i.e. 6.25 or 12.5 mg/kg, displayed minimal signs of acute toxicity. Blood cholinesterase activity and motor function, however, were depressed initially but recovered fully within 1-3 weeks. There were no delayed effects of a single dose of methyl parathion on learning acquisition or memory as assessed by a step-down inhibitory avoidance learning task. Repeated treatment with 1 mg/kg/day methyl parathion resulted in a 50% inhibition of blood cholinesterase activity. A decrease in locomotor activity and impairment of memory were also observed after 28 days of repeated treatment. Thus, a single dermal exposure of rats to doses of methyl parathion which are lower than those that elicit acute toxicity can cause decrements in both cholinesterase activity and motor function which are reversible. In contrast, repeated low-dose dermal treatment results in a sustained inhibition of cholinesterase activity and impairment of both motor function and memory.
Increased platelet activation has been suggested as a possible reason for the increased vulnerability of depressed patients to ischemic heart disease (IHD). Translocation of P-selectin, an integral alpha-granule membrane protein, to the platelet surface is a measure of platelet activation. Herein, western blots of platelet plasma membranes containing P-selectin were quantified in patients with major depression (n=19; mean age=39 +/- 2 years) and healthy comparison subjects (n=17; mean age=36 +/- 2 years). None evidenced clinical signs of IHD, and only two patients had a lifestyle IHD risk factor (smoking). Blood was obtained from all 19 depressed patients before treatment, and 15 returned after 6-8 weeks of open-label bupropion treatment. Bupropion was chosen as the antidepressant because it did not elevate plasma norepinephrine or serotonin, endogenous agonists that can induce platelet degranulation. Western blotting revealed more P-selectin immunoreactivity (75 kD band) in depressed patients compared to healthy controls (P=0.003). After bupropion treatment, P-selectin remained high in depressed patients. beta3-Integrin, a reference plasma membrane protein that does not translocate during activation, was of equivalent density in depressed patients and healthy control subjects, and was unchanged after treatment with bupropion. P-Selectin failed to correlate with severity of illness based on the Hamilton Depression scale, or with the post-treatment plasma concentration of bupropion. The results suggest an elevation in P-selectin on platelet plasma membranes might be a trait marker for depression.
A comparison is presented between plasma catecholamine concentrations and platelet [125I]-p-iodoclonidine binding sites in 16 healthy women. Blood samples were obtained at six regularly spaced intervals over two consecutive menstrual cycles from healthy women with regular menstrual periods. Although no cycle-related changes were observed per se, there were significant correlations between the platelet binding sites and plasma norepinephrine and epinephrine concentrations. The densities of platelet alpha 2-adrenoceptors were negatively correlated in an exponential fashion (r2 = 0.694, P = 0.009) with plasma epinephrine concentrations, implying agonist-induced downregulation. On the other hand, platelet I1-imidazoline binding sites were positively correlated with plasma concentrations of norepinephrine in a linear fashion (r2 = 0.326, P = 0.021). This is the first indication that I1 binding sites might be upregulated by a physiological factor. Furthermore, the data suggest that elevations in plasma norepinephrine might explain reports of upregulated I1 binding sites in depressed patients.
A substantial number of studies have demonstrated increased imidazoline receptors (I1 binding sites) on platelets of depressed patients and downregulation following antidepressant treatments. Herein, imidazoline receptor binding protein (IRBP) antiserum was used to quantify imidazoline receptors on platelets of depressed patients before and after treatment with the atypical aminoketone antidepressant, bupropion. Western blots revealed an increase in IRBP-immunodensity (p = 0.01, two-tailed) in a 33 kDa protein band in untreated depressed patients (n = 21) as compared with controls (n = 17). This band has been positively correlated with I1 binding sites on platelets. Following 6 weeks' treatment with bupropion, IRBP-immunodensity was downregulated in depressed patients (p = 0.03, paired t-test); predominantly in responders (p = 0.005). Patients non-responsive to bupropion (n = 5) were significantly different from responders (p = 0.05) by exhibiting no elevation in IRBP-immunodensity at pre-treatment and no downregulation of the 33 kDa band after treatment. IRBP-immunodensity was negatively correlated (r = -0.79, p = 0.01) with plasma concentrations of bupropion and its metabolites at week-4 of BUP treatment. Thus, a 33-kDa IRBP on platelet plasma membranes is elevated in depression and normalized in responders to bupropion.
Several group contribution methods to estimate the aqueous solubility of organic molecules are proposed and evaluated for their ability to predict the water solubility of new molecules. The learning set consisted of 1168 organic compounds with experimental data taken from the literature after critical evaluation. The best method, based on a new fragment atom scheme, leads to a squared correlation coefficient of 0.95 and an average absolute calculation error of 0.50 log unit, which is superior to other group contribution methods currently available. One of the advantages of this model is that it has upper and lower limits so that the predicted solubilities cannot be unrealistily high or low.
Cultured hepatocytes derived from the newborn mutant c14CoS/c14CoS mouse (14CoS/14CoS cells) have 3-fold higher levels of reduced glutathione (GSH) and greater resistance to menadione toxicity than hepatocytes derived from the wild-type cch/cch mouse (ch/ch cells). Therefore, we used these cell lines to examine mechanisms of oxidative stress produced by iron and tert-butyl hydroperoxide (TBHP). Both cell types were resistant to 25 microM Fe2+ toxicity in the absence of added TBHP. However, in the presence of Fe2+, striking differences in susceptibility to TBHP toxicity between the cell types were observed. With 25 microM Fe2+, ch/ch cells showed TBHP concentration-dependent toxicity, with total lethality at 500 microM; in contrast, 14CoS/14CoS cells were completely resistant to the lethal effects of this concentration of TBHP. Concentration-dependent TBHP-mediated increases in cytosolic Ca2+, pH, and GSSG/GSH ratios, and decreases in GSH levels, were evident in ch/ch cells. 14CoS/14CoS cells exhibited concentration-dependent TBHP-mediated changes in GSH and GSSG/GSH ratios, but cytosolic Ca2+ and pH remained at control levels. Mitochondrial GSH pools were also diminished by TBHP, although there was no selective depletion; mitochondrial GSH remained at about 14% of total cellular GSH. Both cell types exhibited the same time-dependent decrease in plasma membrane protein thiols and a time-dependent increase in plasma membrane protein carbonyls. However, only ch/ch cells displayed a time-dependent depletion of mitochondrial protein thiols, concomitant with an increase in mitochondrial protein carbonyls, while 14CoS/14CoS cells were resistant to such changes. All of the effects produced by TBHP were prevented by desferoxamine.(ABSTRACT TRUNCATED AT 250 WORDS)
Staphylococcus epidermidis and Staphylococcus aureus are two of the commonest bacteria isolated from corneal ulcers. The aim of the current investigation was to determine the frequency of potentially pathogenic traits in the two staphylococcal species. Strains of both species, some isolated from eyes during active corneal inflammation, were screened for their ability to degrade a variety of proteins and hyaluronic acid and the production of cytotoxins. S. aureus produced more tissue-destructive enzymes than the S. epidermidis. S. aureus strains more commonly synthesized the cytotoxin, alpha-toxin. The production of elastase was more common among S. aureus strains isolated from ulcerative events. The production of alpha-toxin was inversely correlated with isolation from keratitis. This study has demonstrated that S. aureus is better equipped with a range of potentially damaging enzymes and toxins than S. epidermidis and that S. aureus elastase may be involved in the production of corneal ulcers.
PURPOSE: We investigated the correlation between the production of superantigens in Staphylococcus-aureus-induced ulcer and contact-lens-induced peripheral ulcer (CLPU) and infiltrative keratitis (IK). METHODS: Twenty-five S. aureus strains used in the study were isolated either from CLPU cases (six), or IK events (13) or asymptomatic eyes (six). A polymerase chain reaction (PCR) was employed to detect genes for superantigenic staphylococcal enterotoxins A-D, toxic shock syndrome toxin-1 and exfoliative toxins A and B. Reversed passive latex aggregation, enzyme-linked immunosorbent assay (ELISA) and immunoblot were used to examine the production of staphylococcal enterotoxins A-D and toxic shock syndrome toxin-1. RESULTS: The frequency of the superantigenic genes was not significantly different among the clinical isolates when asymptomatic isolates were compared with the strains isolated from CLPU and IK events. ELISA and immunoblot showed non-specific protein cross-reactions. CONCLUSIONS: The results suggest that detection of superantigenic toxin genes in ocular strains of S. aureus by PCR is a specific, sensitive, rapid and inexpensive alternative to traditional immunological assays. The role, if any, of the S. aureus superantigens in the production of CLPU/IK remains uncertain.
Pro-inflammatory mediators, including interleukin-6 (IL-6), IL-8, and complement C3a, are released after cardiac surgery as part of the inflammatory response related to blood-biomaterial interaction in the cardiopulmonary bypass circuit. Post operative time course data for these mediators are not fully defined in patients receiving left ventricular assist device (LVAD) support. The authors performed enzyme linked immunosorbent assays for concentrations of IL-6, IL-8, and C3a in plasma in six HeartMate LVAD recipients at the following times: pre operatively; 4, 8, 16, 24, 36, and 48 hr post operatively; daily through the first week; and weekly thereafter for 6 weeks. All patients survived without major complications during the study. Pre operative concentrations of IL-6 and C3a in plasma were significantly increased compared with age matched controls. Post operatively, the concentrations of IL-6 and IL-8 in plasma took longer to return to baseline values after insertion of the LVAD than the trends reported in the literature after routine cardiopulmonary bypass alone. Concentrations of IL-6 and complement C3a continued to decrease to lower than baseline post operatively, reaching statistical significance after 6 weeks of LVAD support. The authors conclude that the presence of the HeartMate LVAD delays the return of pro-inflammatory mediator concentrations back to baseline values compared with routine cardiopulmonary bypass alone, but the device does not appear to be an ongoing source of cytokine release or complement activation.
Cavitation is implicated as the cause of pitting and erosion of explanted mechanical heart valves that failed. Previous in vitro studies demonstrated transient negative pressure spikes upstream of mechanical heart valves at the instant of leaflet closure. When the magnitude of the transient negative pressure spike is below the vapor pressure of the fluid flowing across the mechanical valve, cavitation bubbles have been documented near the valve housing or occluder disc. To test for the presence of transient negative pressure spikes that are conducive to cavitation in vivo, we measured left atrial pressure at the valve orifice after mitral valve replacement. Mitral valves were replaced with 27 mm prostheses in 10 goats (50-60 kg). Control animals (Group 1, n = 5) received pericardial valves. Study animals (Group 2, n = 5) received bileaflet pyrolytic carbon valves. Pressure was recorded from a high frequency atrial transducer at hyperdynamic and hypodynamic states. Transient negative pressure spikes did not occur in any Group 1 animal. Transient negative pressure spikes below the vapor pressure of blood (-713 mm Hg) were recorded in four of five Group 2 animals at the hyperdynamic state: -900, -950, -800, -400, and -1,400 mm Hg (p = 0.048 Group 1 versus Group 2, Fisher's exact test). No cavitation potential exists in vivo after bioprosthetic valve implantation. Transient negative pressure spikes below the vapor pressure of blood occur in vivo at hyperdynamic physiologic states when this bileaflet pyrolytic carbon valve is implanted in the mitral position. These studies demonstrate the potential for cavitation with implanted mechanical valves in vivo.