Frequency-to-voltage conversion in the pyramidal tract neuron: an important role of the inhibitory postsynaptic potential

Frequency-coded impulses are known to be converted into postsynaptic potentials (PSPs) at the synapse of a target neuron. This can be termed frequency-voltage (F-V) conversion. Studies on this problem in pyramidal tract neurons (PTNs) showed that not only the amplitude but also the duration of depolarizing PSPs was determined as a function of the input impulse frequency. Two opposite patterns of F-V conversion were observed following activation of two input systems to PTNs. Inhibitory postsynaptic potentials were found to play an important role in the regulation of the duration of PSPs by curtailing excitatory post-synaptic potentials.     

TGFβ1基因对血管内皮细胞细胞外基质表达及与基质黏附的影响

了解TGFβ1基因对血管内皮细胞表达细胞外基质蛋白及与基质黏附力的影响。用DOTAP脂质体转染p MAMneo TGFβ1于原代培养的脐静脉内皮细胞,经G4 18筛选,TGFβ1表达经免疫荧光鉴定。Western blot确定 型胶原、纤黏连蛋白的表达,微管吸吮系统确定内皮细胞与基质的黏附力。结果表明生理情况下的内皮细胞能表达少量的TGFβ1及胶原、纤黏连蛋白。经G4 18筛选,外源性TGFβ1在血管内皮细胞中稳定表达,能显著提高胶原、纤黏连蛋白纤维的表达及细胞与基质的黏附。说明TGFβ1在血管组织工程中促进内皮细胞的黏附具有一定的应用价值。     

Isometric and isokinetic torque curves at the knee joint

Isometric and isokinetic torques of bilateral quadriceps and hamstrings were measured with Isokinetic Rehabilitation and Testing System (Model No. Cybex 340) on 40 normal untrained subjects, 20 males and 20 females, ranging between the ages of 23 and 35 years. The mean peak isometric and isokinetic torque values of both muscle groups showed no significant differences between dominant (right) and nondominant (left) limbs in both sexes; however there were significant differences between the male and the female. As the angular velocity increased, the peak torque significantly decreased, and the point of peak torque output occurred significantly later in the range of motion for quadriceps and hamstrings (p less than 0.01). There were no significant changes in the hamstrings to quadriceps (H/Q) ratios as the angular velocity increased. However, there were significant differences of mean H/Q ratio between male and female (p less than 0.01). Height had significant positive correlation with peak isometric and isokinetic torques for both quadriceps and hamstrings (p less than 0.01). Weight was found to correlate significantly with peak isometric and isokinetic torques (p less than 0.01). The mean isometric torques were significantly higher than the mean isokinetic torques for any joint angles in both sexes (p less than .01).     

Characteristics and diagnoses of cockroach-sensitive bronchial asthma.

Bronchial asthma with cockroach hypersensitivity is prevalent among urban asthmatic populations. To elucidate characteristics of cockroach asthma, we analyzed 592 consecutive urban Chicago asthmatic patients retrospectively. Allergy skin testing (AST) with common inhalants, serum total IgE, and cockroach-specific IgE (IgE-CR) antibodies were measured. Some cockroach asthmatics were studied further for bronchial reactivity in vivo and histamine releasability (HR) in vitro against cockroach allergen (CRa), and diagnostic accuracy for asthma was analyzed. Clinical characteristics were evaluated and compared with those of ragweed asthmatics and asthmatics in general. Two hundred eighty-three (196 women, 87 men) were reactive to CRa by AST. The average age and duration of cockroach asthma were 30.4 and 15.1 years, respectively. Steroid dependency of the cockroach asthma was higher (32%) than those of general asthmatics (P less than .05) and ragweed asthma (P less than .05). IgE level was elevated (geometric mean 413.2 IU/mL), higher than that of general asthmatics (P less than .001), and 87% showed IgE level higher than 100 IU/mL. IgE-CR and BPT-CR were positive in 61% (175 tested) and in 87% (166 tested), respectively. Sensitivity and specificity of skin test were 99% and 40%, while those of IgE-CR were 91% and 58%, respectively. IgE-CR increased probability of cockroach asthma from 87% to 91%. BPT with CRa was correlated well with the HR of leukocytes (P less than .0001). Thus, cockroach asthma is a severe allergic asthma and can be diagnosed accurately by skin test plus BPT or skin test plus HR.     

DNA prime followed by protein boost enhances neutralization and Th1 type immunity against FMDV

Prime-boost strategy has been exhibited its potency to enhance immune responses, which would be important to the success to develop a vaccine against the foot-and-mouth disease virus (FMDV). An eukaryotic expression construct encoding the FMDV capsid VP1 protein with a recombinant VP1 protein or a commercial FMDV vaccine were tested in the prime-boost strategy in mice and cattle trials. The levels of induced specific antibodies, T cell proliferations, and DTH activities were significantly higher in the prime-boost groups than in those vaccinated with DNA, protein or FMDV vaccine alone. More importantly, the levels of neutralizing antibodies in the former groups were significantly higher than others and could last for at least four months in cattle trials. This study suggests that the prime-boost strategy significantly improves the effective immunity and may provide a longer protection against FMDV infection.     

Influence of GnRH agonist and neural antagonists on stress-blockade of LH and prolactin surges induced by 17beta-estradiol in ovariectomized rats

In our previous study, we demonstrated that immobilization stress blocked estrogen-induced luteinizing hormone (LH) surge possibly by inhibiting the synthesis and release of gonadotropin-releasing hormone (GnRH) at the hypothalamic level and by blocking estrogen-induced prolactin (PRL) surge by increasing the synthesis of dopamine receptor at the pituitary level in ovariectomized rats. The present study was performed to determine whether immobilization stress affects pituitary LH responsiveness to GnRH, and whether endogenous opioid peptide (EOP) and dopamine systems are involved in blocking LH and PRL surges during immobilization stress. Immobilization stress was found to inhibit basal LH release and to completely abolish LH surge. However, the intravenous application of GnRH agonist completely restored immobilization-blocked LH surge and basal LH release. Treatment with naloxone did not exert any effect on immobilization-blocked LH surge but increased basal LH release during immobilization stress. Pimozide did not affect immobilization-blocked LH surge or basal LH release. Naloxone also decreased immobilization-induced basal PRL release, but had no effect on immobilization-blocked PRL surge. Immobilization-increased basal PRL levels were augmented by pimozide treatment and immobilization-blocked PRL surge was dramatically restored by pimozide. We conclude that immobilization stress does not impair pituitary LH response to GnRH, and that the immobilization stress-induced blockage of LH surge is probably not mediated by either the opioidergic or the dopaminergic system. However, immobilization-blockade of PRL surge may be partly mediated by the dopaminergic system.     

Induction of 4-1BB (CD137) expression by DNA damaging agents in human T lymphocytes

4-1BB(CD137) is a member of the tumour necrosis factor receptor superfamily and is expressed on activated T cells, monocytes and natural killer (NK) cells. The interaction of 4-1BB and 4-1BB ligand provides a costimulatory signal leading to T-cell activation. The expression of 4-1BB has been known to be activation dependent. Interestingly, we found that expression of 4-1BB increased in human peripheral blood mononuclear cells after exposure to mitomycin C. Thus, we tested whether the treatment with other DNA-damaging agents, such as doxorubicin, bleomycin, and gamma-irradiation, could induce 4-1BB expression. The data indicated that 4-1BB expression increased dose-dependently by these agents reaching maximum at 2-3 days after the exposure. We found that the major 4-1BB-expressing population was CD3+ T cells, although a moderate number of CD14+ cells and a few NKB1+ cells also expressed 4-1BB. The levels of 4-1BB expression induced by anticancer drugs, were relatively lower than that induced by CD3 ligation. Interestingly, at subcytotoxic concentrations, doxorubicin and bleomycin considerably enhanced 4-1BB expression induced by CD3 ligation in CEM cells. The ligation of the damage-induced 4-1BB by monoclonal antibody enhanced the viability and proliferating capacity of the cells. In conclusion, the expression of 4-1BB might be one of the cellular responses of the immune cells against various genotoxic stresses.     

Immunocytochemical localization of metallothionein and its relation to doxorubicin toxicity in transgenic mouse heart

Previous studies using a cardiac-specific metallothionein-overexpressing transgenic mouse model have demonstrated that metallothionein protects the heart from doxorubicin toxicity. The present study was undertaken to determine cellular and subcellular distribution of metallothionein and located the antioxidant action of this protein in the transgenic heart. Using light microscopic immunoperoxidase method, it was identified that the overexpressed metallothionein is localized exclusively in cardiomyocytes. The electron microscopic immunogold method revealed that elevated metallothionein is in nucleus, myofibers, and sarcoplasm. In contrast with these distributions, metallothionein in nontransgenic myocardium was undetectable by immunoperoxidase light microscopy and was seldom found in nucleus and myofibers by immunogold electron microscopy. Treatment with doxorubicin induced cytoplasmic vacuolization and severe damages in myofilaments and nucleus in nontransgenic myocardium. The most prominent injury, however, occurred in mitochondria, including striking size and shape changes, focal swelling and loss of cristae. These damages were rarely found in the doxorubicin-treated transgenic myocardium. In particular, the internal morphology of mitochondria was maintained essentially normal, although metallothionein was not localized in this compartment in transgenic hearts. This study thus demonstrates that although the subcellularly localized action of metallothionein is important, it also plays a significant role in protection against oxidative injury by doxorubicin in remote organelles.     

Effect of ketamine on apoptosis by energy deprivation in astroglioma cells using flow cytometry system

Apoptosis is a programmed, physiologic mode of cell death that plays an important role in tissue homeostasis. As for the central nervous system, ischemic insults can induce pathophysiologic cascade of apoptosis in neurophils. Impairment of astrocyte functions during brain ischemia can critically influence neuron survival by neuronglia interactions. We aimed to elucidate the protective effect of ketamine on apoptosis by energy deprivation in astrocytes. Ischemic insults was induced with iodoacetate/ carbonylcyanide m-chlorophenylhydrazone (IAA/CCCP) 1.5 mM/20 microm or 150 microm/2 microm for 1 hr in the HTB-15 and CRL-1690 astrocytoma cells. Then these cells were reperfused with normal media or ketamine (0.1 mM) containing media for 1 hr or 24 hr. FITC-annexin-V staining and propidium iodide binding were determined by using flow cytometry. Cell size and granularity were measured by forward and side light scattering properties of flow cytometry system, respectively. An addition of ketamine during reperfusion increased the proportion of viable cells. Ketamine alleviated cell shrinkage and increased granularity during the early period, and ameliorated cell swelling during the late reperfusion period. Ketamine may have a valuable effect on amelioration of early and late apoptosis in the astrocytoma cells, even though the exact mechanism remains to be verified.