Peripheral Tissue Equivalent

Peripheral Tissue Equivalent (PTE) module a three-dimensional construct that recapitulates the innate arm of the immune system... 

Figure 19-4 Reactogenicity of commercial vaccines in the PTE module and by monocytes alone. Vaccines hepatitis B virus (FIBV 1 200), influenza virus vaccine (Fluzone 1 400), and tetanus toxoid vaccine (DTaP 1 200) were used in the study. PTE is the peripheral tissue equivalent module containing CD33+ positively selected cells (left). CD33+ monocytes alone do not produce any appreciable cytokines nor chemokines when stimulated with the vaccines (right).

Depending on the status of the liver, acetoacetate can now be reduced to give D-betfl-hydroxybutyrate, which delivers more reducing equivalents, and thus ATP equivalents, to the peripheral tissues at the expense of the liver ... 

These reactions can be thought of as giving the liver overall control of fat metabolism. Lower vertebrates store fat in the liver. In a sense adipose tissue can be thought of then as "extended liver" tissue metabolically. Note that the liver can adjust the amount of reducing equivalents, and thus ATP equivalents, it sends to the peripheral tissues by adjusting the amounts of acetoacetate vs. beta-hydroxybulyrate it exports. Thus, the percentage of the free energy distributed between the tissues is shown below as Table 10.2 ... 

No inhibition of COX in peripheral tissues and lacks significant anti-inflammatory effects. Equivalent analgesic and antipyretic activity to ASA, probably due to inhibition of cyclooxygenases in the CNS. 

It is clear from these data that for AEA the relative regional abundance in the brain does not correlate with the distribution of CBIR. AEA levels in the brain are equivalent to those of other neurotransmitters such as dopamine and serotonin, but at least 10-fold lower than the levels reported for GABA and glutamate. AEA has also been found in peripheral tissues such as human and rat spleen, which expresses high levels of CB2R. Small amounts of AEA were also detected in human serum, plasma, and cerebrospinal fluid (Felder et al., 1996). 

Among the different peripheral cells expressing APP, platelets are particularly interesting because they show concentrations of its isoforms equivalent to those found in the brain [96]. Some differences between these two cellular populations are nevertheless present both at mRNA and at protein levels the isoform 695, lacking the Kuntiz Protease Inhibitor (KPI) domain, is by far the most abundant in neuronal tissue, whereas its expression is nearly undetectable in platelets in whom the major isoform is APP 770 [97]. After the platelets are activated, soluble forms of cleaved APP are released, analogous to processing in neurons. 

In rhesus monkeys (Macaca mulatta), Pb(C2H5)4 has a greater toxic potential than Pb(CH3)4 [70, 76]. Intravenous Pb(CH3)4 doses of 6 mg kg d caused disturbances of patellar reflexes, peripheral nerve damage, and degeneration of skeletal muscle. Transient clinical abnormalities In peripheral nerve reflexes were detected when 1.2 to 2.4 mg kg d were given. All reflexes were normal after a recovery period [70]. Six months at a dose level equivalent to 6 pg kg d of Pb did not induce clinical manifestations of toxicity [76]. No evidence was found that sublethal exposure to Pb(CH3)4 causes permanent damage to any tissue [70, 76]. The rate of clearance of tissue lead is slower for Pb(CH3)4 than for Pb(C2H5)4 [70]. For lead levels in tissue, blood, urine, and feces, see [70, 76]. 

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