Anaerobic degradation of di-n-butyl phthalate and di-(2-ethylhexyl) phthalate in sludge.
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Biomedical subjects
Publications and source records attributed to G S Liao.
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This work experimentally elucidates the effects of ultrasonic treatment on the physical, chemical, and biological characteristics of a waste-activated sludge. A critical ultrasonic power level exists above which, accompanied with the release of divalent cations from the sludge body, the floc structure effectively disintegrated, microbial level acceptably disinfected, and particulate organic compounds sufficiently transformed into soluble state. Both ultrasonic vibration and bulk temperature rise contribute to the treatment efficiency. Possible mechanisms of ultrasonic treatment are discussed.
Sleep disordered breathing (SDB) and hypertension are commonly associated. In this study, we assessed how longitudinal measures of SDB predict a 24-h ambulatory blood pressure monitoring (ABPM) profile. Participants (n = 82) were recruited from a community-based urban (26% African American) sample and included family members of patients with laboratory diagnosed SDB (cases) and family members of neighborhood control subjects evaluated at baseline and at 5 years. Nearly all participants were normotensive and were not receiving therapy for SDB. During both examinations, the respiratory distress index (RDI) was assessed with overnight in-home polysomnography. Seated blood pressure (BP) was assessed at a baseline examination (t,) and after a 5-year follow-up period (t5), when 24-h ABPM also was performed. The change in RDI (t5-t1) over 5 years was significantly associated with 24-h mean systolic blood pressure (SBP) (P = .04), 24-h maximum diastolic blood pressure (DBP) (P = .03), sleep mean SBP (P = .05), sleep mean DBP (P < .05), and sleep maximum SBP (P = .02). Regression analysis revealed that average 24-h mean arterial pressure (MAP) and mean 24-h DBP were each best predicted by change in RDI, explaining 5% of the variance in these 24-h BP readings, and by current smoking status. After accounting for these variables, BP was not predicted by any of the other potential confounders (all P > .10). Mean RDI (averaged between t5 and t1) was associated with mean MAP, mean SBP, and maximal SBP measured during sleep. This study documents for the first time the association between changes in sleep apnea activity and BP and in a community-based normotensive sample. Further long-term evaluation of the effects of these findings and the long-term consequences of hypertension are needed.
Transferrin (Tf) undergoes receptor-mediated transport through the blood-brain barrier in vivo. This property allows transferrin to act as a vector for drug transport to the brain. The present investigation examines both the profile of brain delivery of nerve growth factor (NGF)-transferrin conjugate, and its therapeutic effects on CNS neurodegeneration, which affect locomotion and memory. Delivery of NGF-Tf conjugate to the brain was measured and found to be 0.075% of the injected dose per gram of brain, which is 5-fold higher than that of biotin-NGF. The increased delivery using the NGF-Tf conjugate can be attributed to an increased BBB permeability surface area product, which is about 8-fold higher than that of biotin-NGF. Intravenous injection of biotin-NGF/Tf-avidin conjugate significantly increased neuronal survival in the substantia nigra of a Parkinson's disease mouse model. In addition, this conjugate also improved recognition and memory in Alzheimer's disease rat model. In summary, these results demonstrate that using transferrin as a delivery vector is effective in targeting NGF to the central nervous system (CNS), and may optimize the therapy of age-related neurodegenerative diseases.
Recent study showed that transferrin receptors were concentrated on the plasma membrane of brain endothelia cells and mediated transcytosis of transferrin (Tf) through the blood-brain barrier (BBB). This property allows the transferrin to act as the brain drug transporter vector. The present investigation examined the pharmacokinetic behavior of nerve growth factor (NGF), which was conjugated to transferrin by the avidin/biotin technology, especially its brain-uptake efficiency. The area under the plasma concentration curve and the mean residence time were not significantly different for either bio-NGF or bio-NGF/AV-Tf. At the first hour after single intravenous injection, the BBB permeability surface area product of bio-NGF/AV-Tf was 0.77 microliter/min/g; it was about 8-fold higher than that of bio-NGF, and equal to that of AV-OX26. The delivery of bio-NGF/AV-Tf to brain was 0.075% of injected dose per gram brain, and it was 5-fold higher than that of bio-NGF, and 2-fold higher than that of AV-OX26. In summary, these studies demonstrated that the use of Tf as brain drug delivery vector was as effective in transporting biotinylated therapeutics as OX26, and avoided the disadvantages of its antigenicity.
The nerve growth factor, NGF, from Chinese cobra Naja naja atra venom was isolated by gel-filtration and ion-exchange chromatography. Cobra NGF was characterized by analytical HPLC techniques as well as SDS-PAGE, and was proven to be a glycoprotein with a mol. wt. of 23 (+/- 2) kD and a pI of 9.2. The amino acid analysis and N-terminal sequencing were performed using conventional methods. Bioassays with cultured chick embryos ganglia and rat pheochromocytoma PC-12 cells revealed a promotion of fiber outgrowth, which is typical of NGF activity. Absence of enzymatic, toxicological, and teratogenic activities were shown by quality inspection. Since 1994, many clinical cases about volunteers receiving NGF treatment have been reported in mainland China. Bioactivities of NGF deal with a wide range of disciplines and technologies. In this paper we will discuss neuronal and non-neuronal effects of NGF treatment. Does the NGF cross the blood-brain barrier by transcytosis into the brain tissue? How is NGF important in wound healing, especially in peripheral nerve injury and diabetic neuritis? NGF may also be useful for male volunteers suffering from sterility, because it is possible that the sexual cells of testis can be promoted to maturity.
Rat superior cervical ganglia infected with herpes virus suis (pseudorabies virus) display a spontaneous bursting activity of still unknown origin. Previous intracellular recordings from the ganglionic neurons combined with pharmacological studies showed that the postganglionic action potentials are induced by acetylcholine release spontaneously from the preganglionic nerve. In this study we investigated whether the acetylcholine release is caused by mechanisms which are dependent on action potentials spontaneously generated on the preganglionic nerve or by mechanisms which occur without any changes in the excitability of presynaptic fibers. Simultaneous intra- and extracellular recordings from the ganglion cells and from the preganglionic nerve, respectively, were performed 32-38 h after the inoculation of herpes virus suis (strain Aujeszky) into the anterior chamber of one eye of the rat. Tetrodotoxin, well known to prevent the generation of action potentials by blocking the fast sodium channels, completely and reversibly abolished, whereas the potassium channel blockers 4-aminopyridine and apamin, enhanced the spontaneous, bursting activity at pre- and postsynaptic levels. The nicotinic receptor antagonist hexamethonium abolished the postsynaptic discharges and reduced the preganglionic activity by 50%. Pre- and postsynaptic electrical activities were suppressed in low calcium Krebs' solution, demonstrating that extracellular calcium is required not only for acetylcholine release but also for triggering the presynaptic action potentials. It is concluded that in the infected ganglia the spontaneous acetylcholine release is due to the generation of action potentials in the preganglionic nerve. Voltage-gated sodium and calcium channels contribute to the presynaptic electrogenesis, while the latter appears to be damped by the activation of voltage- and calcium-dependent potassium channels. Possible factors as well as mechanisms inducing such an increase in excitability are discussed.