Increasing synthesis

S. Increased synthesis of transforming growth factor-beta , which blocks cell division and promote.s apoptosis by interacting with its own membrane recepror,... 

One of the questions confronting investigators in the HS field is whether fever or other acute phase reactants can induce HS gene expression. In vitro studies utilize extraordinary temperatures of 42 °C and higher. Core body temperatures may approach 40 °C as a result of fever. In most in vitro systems, this temperature does not lead to the HS response. However, there are reports that fever induces the increased synthesis of hsps in peripheral blood lymphocytes (Ciavarra, 1990). This response was observed in mononuclear cells exposed to febrile temperatures and in cells isolated from a medical intern who developed fever. 

Downing, J.F., Taylor, M.W., Wie, K.-M., Elizondo, R.S. (1987). In vivo hyperthermia enhances plasma antiviral activity and stimulates peripheral lymphocytes for increased synthesis of interferon gamma. J. Interferon Res. 7, 185-193. 

Perez, N., Sugar, J., Chatya, S., Johnson, G., Merril, C., Bierer, L., Perl, D., Haroutunian, V., Wallace, W. (1991). Increased synthesis and accumulation of heat shock proteins in Alzheimer s disease Brain Res. Mol. Brain Res. 11,249-254. 

Zhang, J. Davies, W.J. (1987). Increased synthesis of ABA in partially dehydrated root tips and ABA transport from roots to leaves. Journal of Experimental Botany, 38, 2015-23. 

Considering the example of drought-induced increase in monodehydroa-scorbate reductase activity (Fig. 8) and assuming the increased activity reflects increased synthesis, isolation of the corresponding genes via the cDNA route should give us access to another set of stress-inducible... 

When bacterial cells are shifted directly from a low growth temperature to a lethal temperature, the cells are rapidly killed. However, if the cells are first preadapted by growth at a non-lethal temperature for 30 min, the rate of killing upon a shift to lethal temperature is dramatically decreased these cells have acquired thermotolerance. During the pre-adaptation phase a heat shock response is induced which leads to increased synthesis of heat shock proteins. 

Synthesis of the transferrin receptor (TfR) and that of ferritin are reciprocally linked to cellular iron content. Specific untranslated sequences of the mRNAs for both proteins (named iron response elements) interact with a cytosolic protein sensitive to variations in levels of cellular iron (iron-responsive element-binding protein). When iron levels are high, cells use stored ferritin mRNA to synthesize ferritin, and the TfR mRNA is degraded. In contrast, when iron levels are low, the TfR mRNA is stabilized and increased synthesis of receptors occurs, while ferritin mRNA is apparently stored in an inactive form. This is an important example of control of expression of proteins at the translational level. 

Fig. 3. A proposed signal transduction pathway regarding the external Ca effect on ginsenoside Rb synthesis by P. notoginseng cells. Ca signal changes are triggered by external Ca concentrations. The calcium signatures are decoded by calcium sensors, CaM and CDPK. UGRdGT is possibly modulated by the sensors in a direct or indirect (dashed lines) way. Changes of CDPK activity may result from increased synthesis or posttranslational modification of the enzyme (shown as CDPK ).

Increase synthesis. This may be achieved by giving the precursor, if it crosses the blood-brain barrier. Whether this works will depend on (i) how many neurons remain to synthesise the NT, unless this can be performed extraneuronally and (ii) the availability of synthesising enzymes. Thus if synthesis is a complicated multistage process or is controlled by the availability of enzymes that are already reduced or working maximally in remaining neurons, this approach may prove difficult. 

Evidence for a neuroimmunological involvement in Alzheimer s disease is accumulating. Activation of the complement cascade by beta amyloid (Rogers et al., 1992), the recruitment, proliferation and activation of microglia in intimate juxtaposition to the senile plaques (Davis et al., 1992), and the increased synthesis of microglia-derived pro-inflammatory cytokine interleukin-1 (Griffin et al., 1989) is indicative of a chronic inflam-... 

Kraan MC, Patel DD, Haringman JJ, et al. The development of clinical signs of rheumatoid synovial inflammation is associated with increased synthesis of the chemokine CXCL8 (interleukin-8). Arthritis Res 2001 3(1) 65-71. 

Another vasoactive substance produced by the endothelium is thromboxane A2 (TxA2). Normally, small amounts of TxA2 are released continuously however, increased synthesis appears to be associated with some cardiac diseases. Synthesized from arachidonic acid, a plasma membrane phospholipid, TxA2 is a potent vasoconstrictor. Furthermore, this substance stimulates platelet aggregation, suggesting that it plays a role in thrombotic events such as myocardial infarction (heart attack). Nonsteroidal anti-inflammatory drugs such as aspirin and ibuprofen block formation of TxA2 and reduce formation of blood clots. 

Figure 3A shows the kinetics of poly(3HB) accumulation for several specific formation rates, depending on the duration of accumulation. As can be seen, the poly(3HB) content approaches a value of 100% asymptotically. However - and this might be considered trivial - how closely the upper limit is reached is ruled by the fact that an increasing content requires increasing synthesis while the capacity is decreasing (Fig. 3B). Economically acceptable contents are reached after very different periods of accumulation this means that the specific formation rate is a very important parameter which depends on the organism involved and, with a given genotype, on the substrate used. Hence we should fo-...

Two main factors have guided the need for optimization of the early screening techniques on one hand the use of simple, quick and high-capacity cell monolayer methods, e.g., Caco-2 cell and MDCK and on the other hand the increased synthesis of more lipophilic, insoluble compounds from combinatorial libraries. This has created a vast number of different variants of cell-based assays and has resulted in variability among the data obtained. A need for optimization of as many as possible of the different parameters in order to increase the predictivity and throughput of the model has been suggested in the literature [98-100]. 

The a ns wer is a. (Hardman, pp 1525-1528.) Pa r a thyroid ho r m o ne is synthesized by and released from the parathyroid gland increased synthesis of PTI1 is a response to low serum Ca concentrations. Resorption and mobilization of Ca and phosphate from bone are increased in response to elevated PTI1 concentrations. Replacement of body stores of Ca is enhanced by the capacity of PTH to promote increased absorption of Ca by the small intestine in concert with vitamin D, which is the primary factor that enhances intestinal Ca absorption. Parathyroid hormone also causes an increased renal tubular reabsorption of Ca and excretion of phosphate. As a consequence of these effects, the extracellular Ca concentration becomes elevated. 

The effect of diet on vulnerability to lead makes interpretation of published information on experimental lead poisoning in waterfowl extremely difficult (Chasko et al. 1984). For example, many mallards on a diet of com die within 10 to 14 days after ingesting a single lead shot, whereas similar birds on a balanced commercial duck ration appear outwardly normal after ingesting as many as 32 pellets of the same size (Wobeser 1981). Also, multiple nutritional deficiencies may have additional effects in potentiating the toxicity of lead in mallards (Carlson and Nielsen 1985). Under conditions of reduced dietary calcium availability, such as can occur in acid-impacted environments, birds risk increased uptake of lead (and other metals) and may accumulate toxic concentrations more rapidly (Scheuhammer 1996). Enhanced accumulation of lead was accompanied by an increased synthesis of metallothioneins and a greater inhibition of ALAD activity (Scheuhammer 1996). 

Increases GABA levels in plasma and CNS inhibits GABA catabolism, increases synthesis, and release can prevent GABA reuptake enhances the action of GABA at the GABAa receptor ... 

The plasma Hp level rises in disease, like the concentration of fibrinogen and orosomucoid (J8, N5), and this is most likely the result of increased synthesis. The degree of abnormality seems largely to follow the activity of the inflammatory reaction of the disease (infections, tumors, aseptic necrosis). Treatment with cortisol will normalize all three of the above-mentioned plasma proteins. We do not yet know the link between inflammatory reaction and the changed synthesis of Hp and the other plasma proteins. A deeper knowledge of Hp synthesis and the pathophysiology of the inflammatory reaction is necessary for proper utilization in clinical work of the individual Hp values found in diseased subjects. 

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