Clinical symptoms

Other nootropic agents in some stage of clinical development include nebracetam (9), nefinacetam (10), and BMY 21502 (11). Nebracetam, an aminomethyl pyrrolidinone derivative, is expected to be approved in Japan in 1994 (73). In clinical studies involving patients having cerebrovascular or senile dementia of the Alzheimer s type, clinical symptoms such as spontaneous or emotional expression were enhanced in up to 71% of cases. Long-term treatment using nebracetam in patients with cerebral infarction also afforded marked improvement in most cases with few side effects (74). A review of this compound has beenpubUshed (75). 

Physiological functions as well as clinical symptoms that occur in humans deficient in specific vitamins are given in Table 6. It is becoming more authenticated that vitamins have additional potential health benefits when adrninistered, via the diet or by supplementation, at levels above those required for obviating deficiency. Although for most vitamins the optimal levels are not yet estabUshed, some of the potential health benefits to be derived from vitamins are indicated (16). In one case, the level of scientific proof is such that the U.S. FDA has allowed "a health cl aim that women who are capable of... 

Thrombolytic Enzymes. Although atherosclerosis and the accompanying vascular wall defects are ultimately responsible for such diseases as acute pulmonary embolism, arterial occlusion, and myocardial infarction, the lack of blood flow caused by a fibrin clot directly results in tissue injury and in the clinical symptoms of these devastating diseases (54). Thrombolytic enzyme therapy removes the fibrin clot by dissolution, and has shown promise in the treatment of a number of thrombo-occlusive diseases (60). 

The most serious acute Type I reaction is the generalized reaction, the anaphylactic shock. Anaphylactic shock results from a generalized release of mediators from mast cells and basophils. The clinical symptoms are manifested predominantly in... 

Four different protozoa of the genus Plasmodium -P. falciparum, P. vivax, P. ovale and P malariae - can cause malaria. P. falciparum is the most virulent, being responsible for virtually all fatal malaria cases. Humans are infected by a feeding female Anopheles mosquito (Fig. 2). The clinical symptoms of malaria are associated with the development of the parasite within human red blood cells, while the liver stages remain asymptomatic. The following dtugs (in alphabetical order) are currently in use for the treatment of malaria [5]. 

Delayed type hypersensitivty (DTH) reactions (synonym type IV allergic reactions) are exaggerated, T-lymphocyte mediated, cellular immune reactions to foreign substances, which require one to two days to manifest clinical symptoms. 

Hyperkalemia is an excess of potassium in the blood. Clinical symptoms are muscle weakness and cardiac arrhythmias. It is caused by, e.g., hyperaldosteronism and angiotensin-converting enzyme (ACE) inhibitors. 

Raynaud s phenomenon is an exaggerated vascular-response to cold temperature or emotional stress. Clinical symptoms are sharply demarcated color-changes in the skin of the digits. The underlying disorder consists of abnormal vasoconstriction of digital arteries and cutaneous arterioles due to a local defect in normal vascular responses. 

Type I allergic reactions are inappropriate immune responses to an allergen with preferential synthesis of immunoglobulin E (IgE), a special antibody class, which binds to mast cells and basophilic granulocytes via Fee receptors. Binding of the allergen to the cell-bound IgE initiates the rapid release of allergic mediators, most prominently histamine, and the de novo synthesis of arachidonic acid metabolites and cytokines, which are responsible for the clinical symptoms. 

In a study of 135 workers in the ehemical industry who handle methyl parathion, the methyl parathion concentration in plasma, the 4-nitrophenol concentration in urine, and the cholinesterase and acetylcholinesterase activities were determined to assess the pesticide burden in such workers (Leng and Lewalter 1999). The mean concentration of methyl parathion in the plasma of the workers was 233 pg/L no clinical symptoms were reported by the workers. In an additional group of 19 workers handling methyl parathion, who were also exposed to the pyrethroid cyfluthrin, the mean concentrations of methyl parathion in plasma were 269 and 241 pg/L (for groups without and with clinical S5miptoms, respectively), and 7 of the workers exhibited skin paraesthesia, while none of the 427 workers exposed only to the pyrethroid experienced the symptom (Leng and Lewalter 1999). 

Tables. Classification of anaphylactic reactions according to severity of clinical symptoms [35]... 

According to the different intensity of clinical symptoms, several attempts have been made to classify anaphylaxis according to severity, the most common scales have been published by Mueller [26] and Ring and Messmer [35] (table 3). 

Immediate hypersensitivity reactions to RCM are associated with histamine release from basophils and mast cells [27], and extensive mast cell activation in vivo associated with clinical symptoms has been demonstrated by Earoche et al. [31]. Patients with hypersensitivity reactions after contrast medium exposure had increased plasma levels of both histamine and tryptase, and levels correlated with severity. Also other investigators have reported high levels of tryptase in connection with severe or fatal reactions [21, 33]. 

LA preparations are common elicitors of adverse reactions, i.e. ca. 0.1-1% of applications in dental and other procedures. The clinical symptoms often correspond to anaphylactic reactions with tachycardia, hypotension, and subjective feelings such as... 

Disease Enzyme Deficiency Lipid Accumulating Clinical Symptoms... 

All defects in urea synthesis result in ammonia intoxication. Intoxication is more severe when the metabolic block occurs at reactions 1 or 2 since some covalent linking of ammonia to carbon has already occurred if citrulline can be synthesized. Clinical symptoms common to all urea cycle disorders include vomiting, avoidance of high-protein foods, intermittent ataxia, irritability, lethargy, and mental retardation. The clinical features and treatment of all five disorders discussed below are similar. Significant improvement and minimization of brain damage accompany a low-protein diet ingested as frequent small meals to avoid sudden increases in blood ammonia levels. 

Tetrodotoxin poisoning has been recogniz for more than two thousand years. Japanese historical records show that the consumption of certain species of pufferOsh (Tetraodon spp.) resulted in paralytic intoxication (8), This problem continues in modern times in various i ian countries, especially Japan, where pufferfish are still regarded as a delicacy. Clinical symptoms of TTX intoxication include numbness, paralysis, and in some instances death. In fact, the "zombie state described in the Voodoo religion has been attributed to TTX in potions derived from pufferOsh (9). 

The serum from patients with clinical symptoms of hepatitis B commonly contain three distinct structures that possess HBsAg (section 3.8.5 above). The effects of different concentrations of various disinfectants on the structure of Dane particles have been studied, but it is unlikely that morphological changes can be related to virucidal activity. 

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