Lactose is the most important carbohydrate in the milk of most species. Its biosynthesis takes place in the mammary gland. The molecular structures of α- and β -lactose differ in the orientation of a hydrogen- and a hydroxyl group on carbon atom no.1 in the glucose moiety. Both forms change into one another continuously. At room temperature, the equilibrium results in a ratio of about 40% α-lactose and 60% β-lactose. The fact that two forms of lactose exist which differ in molecular structure has profound effects on various properties of lactose such as crystallization behavior, crystal morphology, solid-state properties, and solubility. The intestine does not actively absorb lactose unless it is split into its two-monosaccharide components, i.e. glucose and galactose. This hydrolysis of lactose is affected by the enzyme lactase, which is produced by the epithelium cells in the brush-border of the small intestine. Thus, the capacity of mammals to digest lactose is dependent on the lactase activity in the intestine. The maximum activity of the enzyme occurs shortly after birth and declines during the weaning period, after which it remains at a relatively constant level. Genetically determined factors governing residual lactase activity also exist. Individuals having low lactase activity are called lactose malabsorbers. Lactose intolerance is a condition in which people have symptoms due to the decreased ability to digest lactose. The principal symptom of lactose intolerance is an adverse reaction to products containing lactose (primarily milk), including abdominal bloating and cramps, flatulence, diarrhea, nausea, borborygmi, and vomiting (particularly in adolescents). These appear one-half to two hours after consumption.

Molybdenum-99 (99Mo, half-life = 66 h) is a parent radionuclide of a diagnostic nuclear isotope. It decays in technetium-99 m (half-life = 6 h), which is used in over 30 million procedures per year around the world. Between 95 and 98 percent of Mo-99 is currently being produced using highly enriched uranium (HEU) targets. Other medical isotopes such as iodine-131 (I-131) and xenon-133 (Xe-133) are by-products of the Mo-99 production process and will be sufficiently available if Mo-99 is available.

Molybdenum-99 (99Mo, half-life = 66 h) is a parent radionuclide of a diagnostic nuclear isotope. It decays in technetium-99 m (half-life = 6 h), which is used in over 30 million procedures per year around the world. Between 95 and 98 percent of Mo-99 is currently being produced using highly enriched uranium (HEU) targets. Other medical isotopes such as iodine-131 (I-131) and xenon-133 (Xe-133) are by-products of the Mo-99 production process and will be sufficiently available if Mo-99 is available.

Molybdenum-99 (99Mo, half-life = 66 h) is a parent radionuclide of a diagnostic nuclear isotope. It decays in technetium-99 m (half-life = 6 h), which is used in over 30 million procedures per year around the world. Between 95 and 98 percent of Mo-99 is currently being produced using highly enriched uranium (HEU) targets. Other medical isotopes such as iodine-131 (I-131) and xenon-133 (Xe-133) are by-products of the Mo-99 production process and will be sufficiently available if Mo-99 is available.

Tetraamminecopper dihydroxide also known as Schweizer's Reagent dissolves cellulose; used in rayon production.

Zinc monocarbonate (Zinc Carbonate) is an inorganic salt. In the United States, Zinc Carbonate may be used as an active ingredient in OTC drug products. When used as an active drug ingredient, the established name is Zinc Carbonate. Zinc monocarbonate is generally recognized as safe by FDA. It is used as skin protectant active ingredient. Zinc carbonate was found to retard the degradation of some poly(lactide-co-glycolide) (PLG) microspheres in vivo and in vitro. Adding Zinc Carbonate is essential during the preparation of PLGA microspheres. It can remarkably improve the stability of drugs in the acid microenvironment inside PLGA microspheres.

Angiotensin III (Ang III) is a bioactive heptapeptide that is formed from the degradation of the Angiotensin II peptide by aminopeptidase A. In peripheral Angiotensin systems, Angiotensin II is the main effector peptide in the systemic circulation, although exogenous Angiotensin III can be as potent as Angiotensin II in, for example, stimulating aldosterone secretion or inhibiting renin release. In the rat brain, Angiotensin III was found to be equipotent with Angiotensin II as a pressor agent or dipsogen and was bound as avidly to the nervous system as Angiotensin II. Angiotensin receptor subtype AT1 has the greater affinity towards Angiotensin II and is also responsive to Angiotensin III, while the AT2 receptor subtype appears to be more sensitive to Angiotensin III but less responsive to Angiotensin II. Angiotensin III enhances blood pressure, vasopressin release and thirst when it is centrally administrated. Angiotensin III infusion increases blood pressure in healthy volunteers and hypertensive patients as well as augments aldosterone release. Although Angiotensin III does not change renal function in humans, it induces natriuresis in AT, receptor-blocked rats likely by binding to AT2 receptors. In addition, in cultured renal cells, this peptide stimulates the expression of many growth factors, proinflammatory mediators, and extracellular matrix proteins.

Polidocanol is a non-ionic surfactant sclerosing agent indicated to treat uncomplicated spider veins and uncomplicated reticular veins in the lower extremity. Polidocanol also is indicated for the treatment of incompetent great saphenous veins, accessory saphenous veins, and visible varicosities of the great saphenous vein system above and below the knee. When administered, polidocanol locally damages blood vessel endothelium. Following the endothelial damage, platelets aggregate at the site and attach to the venous wall eventually resulting in a dense network of platelets, cellular debris, and fibrin that occludes the vessel. Eventually the vessel is replaced by connective fibrous tissue. Adverse reactions include pain in extremity, infusion site thrombosis, contusion/injection site hematoma, limb discomfort and some others.

Ferric chloride is a compound used as a food additive, a haemostatic or treatment for hypochromic anaemia. Ferric chloride induced vascular injury is a widely used model of occlusive thrombosis that reports platelet activation and aggregation in the context of an aseptic closed vascular system. Iron i.v. ferric chloride (960 mg) has being shown to be effective in correcting anaemia in HD patients with iron deficiency.

Ferric chloride is a compound used as a food additive, a haemostatic or treatment for hypochromic anaemia. Ferric chloride induced vascular injury is a widely used model of occlusive thrombosis that reports platelet activation and aggregation in the context of an aseptic closed vascular system. Iron i.v. ferric chloride (960 mg) has being shown to be effective in correcting anaemia in HD patients with iron deficiency.