Fatigue marks

Work at high altitudes can bring on headaches, increased muscular fatigue, marked mental function deterioration (i.e., memory and computation), impairments in decision making and judgment, and poor sleep quality. These symptoms result from reduced barometric pressure and oxygen intake. 

Which of the following elements responsible for corrosion fatigue Mark YES or NO)... 

Normally, dietary tyramine is broken down in the gastrointestinal tract by MAO and is not absorbed. In the presence of MAOI, however, all of its potent sympathomimetic actions are seen. Other side effects of MAOI include excessive CNS stimulation, orthostatic hypotension, weight gain, and in rare cases hepatotoxicity. Because the monoamine oxidase inhibitors exhibit greater toxicity, yet no greater therapeutic response than other, newer agents, clinical use has been markedly curtailed. The primary use for MAOIs is in the treatment of atypical depressions, eg, those associated with increased appetite, phobic anxiety, hypersomnolence, and fatigues, but not melancholia (2). 

Change in section at weld bead. Gives stress concentration. In the case of butt welds this can be removed by grinding back the weld until flush with the parent plates. Grinding marks must be parallel to loading direction otherwise they can initiate fatigue cracks. 

Often contain defects (hydrogen cracks, slag inclusions, stop-start marks). Help initiate fatigue cracks. Critical welds must be tested non-destructively and defects must be gouged out. 

Figure 21-21. Cross seotion of fatigued biade. Note ehevron markings near the traiiing edge indieating eyeiie fatigue.

Another important factor in the selection of a lead alloy is fatigue strength, which may arise from high-frequency vibration from pumps and stirrers or from differential expansion from heat and cooling cycles. The marked increase of fatigue strength obtained by alloying with copper, silver and tellurium can be seen from Table 3.25. 

A metal s resistance to fatigue is markedly reduced in a corrosive environment. Many welded structures are subjected to fluctuating stresses which, with the superimposed tensile residual stress of the joint, can be dangerous. In addition to this a welded joint is a discontinuity in an engineering structure containing many possible sites of stress concentration, e.g. toe or root of the joint, weld ripple. 

In vivo, patients treated with AZT develop a mitochondrial myopathy with mitochondrial DNA depletion, deficiency of cytochrome c oxidase (complex IV), intracellular fat accumulation, high lactate production and marked phosphocreatine depletion (Lewis and Dalakas 1995 Dalakas 2001). Clinically, the patient presents with fatigue, myalgia, muscle weakness, wasting and elevated serum creatine kinase. Muscle biopsy shows ragged red fibers , the characteristic histopathologic changes of mitochondrial myopathy, cansed by subsarcolemmal accumulation of mitochondria (Lewis and Dalakas 1995). 

When fever resolves, it is followed by marked fatigue and drowsiness, warm dry skin, tachycardia, cough, headache, nausea, vomiting, abdominal pain, diarrhea and delirium, anemia, and splenomegaly... 

The term corrosion fatigue is used to describe the premature failure of materials in corrosive environments caused by cyclic stresses. Even mildly corrosive conditions can markedly reduce the fatigue life of a component. Unlike stress corrosion cracking, corrosion fatigue can occur in any corrosive environment and does not depend on a specific combination of corrosive substance and metal. Materials with a high resistance to corrosion must be specified for critical components subjected to cyclic stresses. 

Herbal remedies that have been reported to be he-patotoxic include chaparral (Larrea tridentata), germander (Teucrium chamaedrys), and life root (Senecio aureus) [18]. Cases reported patients developing jaundice, fatigue, pruritus, markedly elevated serum liver enzyme levels, severe cholestasis, hepatitis, and hepatocellular injury or necrosis documented by serial liver biopsies [19-21]. Signs and symptoms may occur as early as 3 weeks to as late as 7 months following ingestion [20,21]. 

Glutaric aciduria type II, which is a defect of P-oxida-tion, may affect muscle exclusively or in conjunction with other tissues. Glutaric aciduria type II, also termed multiple acyl-CoA dehydrogenase deficiency (Fig. 42-2), usually causes respiratory distress, hypoglycemia, hyperammonemia, systemic carnitine deficiency, nonketotic metabolic acidosis in the neonatal period and death within the first week. A few patients with onset in childhood or adult life showed lipid-storage myopathy, with weakness or premature fatigue [4]. Short-chain acyl-CoA deficiency (Fig. 42-2) was described in one woman with proximal limb weakness and exercise intolerance. Muscle biopsy showed marked accumulation of lipid droplets. Although... 

Further observations. Wilson3 studied the effect of D.F.P. in myasthenia gravis and found on prolonged administration in one case there was a marked diminution of the prostigmine requirements (a fall from 2 to 0-2 mg. after 3 weeks of daily D.F.P.). Another case was able to perform muscular movements without undue fatigue after a course of D.F.P. alone. 

In the endurance event, the pH does not change but the content of phosphate increases whereas the contents of glycogen and phosphocreatine decrease markedly. The change in phosphate is considered to be responsible for fatigue. Studies using P NMR spectroscopy indicate that the resting content of phosphate is about 1 mmol/L and increases more than 20 fold at exhaustion in these physical activities. 

Hypertension, ulcer, hemolytic anemia (marked by fatigue)... 

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