c_Jun (Phospho_Tyr170) Antibody
- Known as:
- c_Jun (Phospho_Tyr170) Antibody
- Catalog number:
- E011023-2
- Product Quantity:
- 100ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- c_Jun (Phospho_Tyr170) Antibody
Related products to: c_Jun (Phospho_Tyr170) Antibody
Related articles to: c_Jun (Phospho_Tyr170) Antibody
- Calcium is an essential element for normal physiologic function. Normal serum calcium is maintained within a close range of 8.4 to 10.4 mg/dL, and acute or severe changes can result in serious cardiac, musculoskeletal, and neurologic consequences. Normal calcium levels are maintained by interactions of parathyroid hormone and vitamin D. Parathyroid hormone regulates calcium levels via bone resorption, renal calcium reabsorption, and enhanced calcium absorption in the small intestine. Causes of hypocalcemia include hypoparathyroidism (often postsurgical), severe chronic kidney disease, and vitamin D deficiency. Laboratory testing for serum parathyroid hormone, kidney function, vitamin D metabolites, and serum phosphorus can help differentiate among causes. Acutely symptomatic patients require inpatient treatment with intravenous calcium gluconate, cardiac monitoring, and correction of hypomagnesemia. Hypercalcemia is most often due to primary hyperparathyroidism or malignancy. In the evaluation, hypercalcemia should first be confirmed by measurement of ionized calcium or repeat measurement of total serum calcium and correction for albumin. Obtaining a serum parathyroid hormone level is the next step. Asymptomatic, chronic mild hypercalcemia is often caused by primary hyperparathyroidism, which can be observed or treated surgically. Patients with severe hypercalcemia may have profound dehydration and require inpatient treatment with intravenous fluids, bisphosphonates, and calcitonin. - Source: PubMed
Wipperman Jennifer - Maintaining a normal physiologic acid-base balance is essential for the functioning of every organ system in the body. The renal and pulmonary systems are the primary regulators of acid-base balance. There are four principal acid-base disorders: metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis. A systematic approach to evaluation is critical to identify potential etiologies. A history, physical examination, metabolic profile, and arterial blood gas measurement provide a full assessment of acid-base status. However, availability of arterial blood gas measurements is usually limited outside of inpatient and emergency department settings. Calculation of an anion gap is a crucial first step for evaluating laboratory test results. Changes in serum pH, Pco, serum bicarbonate concentration, and anion gap suggest the primary disorder, and predictable compensatory changes indicate whether a secondary acid-base disturbance is present. Mixed acid-base disorders involving the renal and pulmonary systems can occur, underscoring the importance of a systematic approach to evaluation. In the outpatient setting, primary care physicians play a vital role in identifying and treating these disorders based on initial evaluation. Prompt recognition and management of acid-base disorders can help prevent morbidity and mortality. - Source: PubMed
Regehr Jared - A normal serum potassium level of 3.5 to 5.0 mEq/L is maintained via potassium ingestion, excretion, and distribution between intra- and extracellular fluid. Potassium balance is essential for maintenance of normal resting cell membrane potential in excitatory tissues. Abnormalities in serum potassium, whether low or high, can cause life-threatening complications due to cardiac, respiratory, or neurologic compromise. Hypokalemia results from renal or gastrointestinal losses, or transcellular shifts. In the absence of an identified cause, evaluation of urinary potassium excretion and acid-base status can help determine the etiology. Patients with severe (ie, serum potassium less than 2.5 mEq/L) or symptomatic hypokalemia should be admitted to the hospital for intravenous potassium replacement and cardiac monitoring. Patients with mild to moderate hypokalemia are often asymptomatic and can be treated with oral potassium while the underlying cause is addressed. Hyperkalemia is usually due to low urinary excretion, and less often to cellular release and transcellular shifts. Patients with acute hyperkalemia with associated electrocardiography findings and those with potassium levels 6.5 mEq/L or greater require inpatient treatment with calcium gluconate and other measures. Asymptomatic patients with chronic mild to moderate hyperkalemia can be managed as outpatients with dietary modification, diuretics, and medication adjustments. - Source: PubMed
Beekhuizen Jeff - Sodium disorders are commonly encountered in clinical practice and are frequently misunderstood. Abnormal serum sodium levels are due to an imbalance in free water. Hyponatremia and hypernatremia can be asymptomatic if mild and chronic; however, acute and severe changes in sodium levels may cause substantial symptoms. In acute mild hyponatremia, symptoms can include confusion, vomiting, and weakness. In severe cases, seizures can occur. Determining the patient's volume status helps to determine the underlying etiology and appropriate treatment strategy. Euvolemic hyponatremia is the most common presentation due to the prevalence of syndrome of inappropriate antidiuretic hormone. Depending on severity, hyponatremia can be managed in the outpatient or inpatient setting. Management is directed at treating underlying causes and relieving severe symptoms while decreasing the risk of serious adverse effects from treatment. In patients with chronic hyponatremia without severe symptoms, rapid correction of serum sodium should be avoided to minimize the risk of osmotic demyelination syndrome. Hypernatremia is caused by a loss of free water, inadequate water intake, or salt overload. Patients with acute hypernatremia may present with fatigue, signs of dehydration, and weakness. Symptomatic acute and severe hypernatremia require inpatient admission and management of free water deficit with intravenous hypotonic fluids. - Source: PubMed
Olson Aaron - - Source: PubMed
Kauffman Ryan D