Brain secondary

Radium was also used as a "rejuvenating" tonic in the 1920s and was available to the general public in bottled water. Gettler and Norris (1933) described a case of a 52-year-old man who drank about 1,400 bottles of "Radithor", containing radium at 2 pg/60 ml bottle, over a 5-year period (total dose approximately 2,800 pCi or 56 pCi/kg or 2,074 kBq/kg for a 50-kg man). The cause of death was stated to be a combination of necrosis of the jaw, abscess of the brain, secondary anemia and terminal bronchopneumonia. However, it is important to note that each of these effects can also be attributed to other etiologies. 

In 74 patients over the age of 18 years with possible metastatic brain disease, a total cumulative dose of 0.2 mmol/kg of gadobenate dimeglumine injected intravenously over 20 minutes was safe and enhanced the assessment of brain secondaries (8). 

In the rat, the most often studied animal species, whose tryptophan metabolism resembles closely that of humans, acute ethanol administration, as described earlier, induces a biphasic effect on serum tryptophan levels, an initial increase followed by a later inhibition. Similarly, acute ethanol administration exerts a biphasic effect on brain serotonin synthesis and turnover, an initial enhancement followed by a later inhibition.111 The initial enhancement is caused by an increase in circulating free tryptophan availability to brain, probably secondary to a catecholamine-dependent lipolysis and a nonesteri-fied fatty acid-mediated displacement of the albumin-bound amino acid, whereas the later inhibition of serotonin synthesis and turnover is the result of a decrease in circulating free and albumin-bound tryptophan availability to the brain secondary to activation of hepatic tryptophan 2,3-dioxygenase (TP) by the earlier increase in free tryptophan to the liver. The activation of hepatic TP by acute ethanol administration, which is substrate (tryptophan) mediated, has been described in rats by Badawy and Evans.111127128... 

Badawy et al.131 attributed the enhanced rat brain serotonin synthesis and turnover by chronic ethanol administration to the increased circulating tryptophan availability to the brain secondary inhibition of hepatic TP activity (NAD(P)H-dependent allosteric inhibition). 

Demethylation of the tricyclic antihistamine 9, with cyanogen bromide gives the secondary amine 10 acylation of that intermediate with ethyl chloroformate affords the nonsedating H-1 antihistaminic agent loratidine (11) [3], It is of interest that this compound does not contain the zwitterionic funcrion which is thought to prevent passage through the blood-brain barrier, characteristic of this class of compounds. 

Somatostatin. Figure 1 Somatostatin-like im mu noreactivity in neurons of the periventricular hypothalamic nucleus of the rat. Coronal brain cryostat sections have been processed for im mu nohistochemistry and sequentially incubated with a primary monoclonal mouse anti human somatostatin antibody and secondary antimouse antibody conjugated with the fluorescence-dye Cy-3. Images have been taken with a Zeiss Axioplan fluorescence microscope. Scale bar, 100 pM. 

Early studies indicate that combined GP Ilb/IIIa inhibition with rt-PA thrombolysis may improve clinical and MRI outcomes after acute ischemic stroke, with an acceptable safety prohle. The dual targeting of platelets and hbrin by combination therapy may provide synergistic benefits, including increased arterial recanalization, reduced microvascular thrombosis, reduced arterial reocclusion, and less rt-PA-mediated blood-brain barrier injury and secondary activation of the coagulation system. 

If a subconvulsive stimulus is applied, generally in rats, at regular intervals, e.g. daily for some two weeks to a specific brain area, especially the amygdala or hippocampus, then eventually full localised (partial) or secondary generalised seizures develop. A similar effect can be obtained by the repeated localised injection of subconvulsive doses of some convulsants. The ability of a drug to reduce the kindled seizure itself may be indicative of value in partial seizure but if it slows the actual development of kindling that may indicate some ability to retard epileptogenesis. 

In contrast, iproniazid, introduced in 1951 for treatment of tuberculosis, induced euphoria and was described as a psychic energiser . In fact, these patients, when given iproniazid, could become quite disruptive and this action was regarded as an undesirable side-effect However, its beneficial effects in depression were soon recognised and it was regarded as the first effective antidepressant drug. Studies of peripheral sympathetic neurons, later extended to noradrenergic neurons in the brain, showed that iproniazid irreversibly inhibits the catalytic enzyme, monoamine oxidase (MAO). Because only cytoplasmic monoamines are accessible to MAO, inhibition of this enzyme first increases the concentration of the pool of soluble transmitter but this leads to a secondary increase in the stores of vesicle-bound transmitter i.e. the pool available for impulse-evoked release (Fillenz and Stanford 1981). 

Neuritic or senile plaques are extracellular protein deposits of fibrils and amorphous aggregates of P-amyloid protein.11 This formed protein is central to the pathogenesis of AD. The P-amyloid protein is present in a non-toxic, soluble form in human brains. In AD, conformational changes occur that render it insoluble and cause it to deposit into amorphous diffuse plaques associated with dystrophic neuritis.14 Over time, these deposits become compacted into plaques and the P-amyloid protein becomes fibrillar and neurotoxic. Inflammation occurs secondary to clusters of astrocytes and microglia surrounding these plaques. 

Abused drugs generally produce pleasant effects that are desired by the user. However, while most individuals will experience these pleasant effects, not everyone abuses these drugs, and not everyone who abuses them becomes dependent on them. Why some persons abuse drugs while most people do not is a complex area of research. It appears that genetic, environmental, and cultural factors may all interact to predispose some individuals to substance abuse and subsequent dependence. The initial hedonic experiences secondary to use of drugs appear to be primarily due to their ability to activate the primary reward circuits in the brain. These same reward circuits operate under normal circumstances to reinforce certain activities that promote survival, such as food, social affiliation, or sexual activity. 

T. pallidum rapidly penetrates intact mucous membranes or microscopic dermal abrasions, and within a few hours, enters the lymphatics and blood to produce systemic illness. During the secondary stage, examinations commonly demonstrate abnormal findings in the cerebrospinal fluid (CSF). As the infection progresses, the parenchyma of the brain and spinal cord may subsequently be damaged. 

BZ is usually disseminated as an aerosol with the primary route of entry into the body through the respiratory system the secondary route is through the digestive tract. BZ blocks the action of acetylcholine in both the peripheral and central nervous systems. As such, it lessens the degree and extent of the transmission of impulses from one nerve fiber to another through their connecting synaptic junctions. It stimulates the action of noradrenaline (norepinephrine) in the brain, much as do amphetamines and cocaine. Thus, it may induce vivid hallucinations as it sedates the victim. Toxic delirium is very common. 

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