The Dubin–Johnson Syndrome is a rare hereditary disease, which is associated with hyperbilirubinemia (high bilirubin and bilirubin-glucuronide plasma  concentrations).

• The disease is caused by loss of function mutations in the ABCC2 gene, which is coding for the ABC-transporter MRP2 (also termed as multispecific organic anion transporter (MOAT)).

• Normally, this transporter is localized in the canalicular membrane of hepatocytes, where it eliminates bilirubin-glucuronide and other organic anions into the bile.

Dyskinesias are abnormal movements, usually caused by neurological diseases or by drugs used to treat neurological (e.g., levodopa) or psychiatric diseases (e.g., neuroleptics).

Desmoplakin is the most abundant desmosomal component that plays a critical role in linking intermediate filament networks to the desmosomal plaque. Desmoplakin
forms rod-like dimers that bind to intermediate filaments and to the cadherin-associated proteins plakoglobin and plakophilin. Gene knock-out experiments have revealed an essential role of desmoplakin in establishing cell–cell contacts in early mouse embryos.

A condition in which a receptor is unresponsive despite the presence of agonist; also referred to as a ‘refractory state’. Typically this state is the consequence of prolonged exposure to agonist, and occurs after receptor activation; it is a built in mechanism to limit a receptor’s effects.

Mechanistically the desensitised state differs from the resting, closed state of a receptor because in the latter state, a receptor can respond to agonist. This difference predicts that these states are structurally distinct.

• The desensitised state may also be stabilised by very low concentrations of agonist, such that no measurable activation of the receptor precedes it.
• Desensitisation is an intrinsic property of many receptors but can also be influenced by other interactions or modifications, such as phosphorylation.

Desensitization is the rapidly attenuation of receptor activation as a result of stimulation of cells and occurs in seconds to minutes. Receptor phosphorylation by  G-protein-coupled receptor kinases and secondmessenger- regulated kinases as well as receptor/ G-protein uncoupling contribute to this process.

In the continued presence or at high concentrations of agonistic ligands, ligand gated ion channels may undergo desensitization by entering a permanently closed state.While the ligand binding domain is occupied by the agonist, the desensitized channel is unable to re-open. For ligandgated ion channels, the structural basis of desensitization is not understood. For voltage-gated K+ channels, the ‘ball and chain’ model suggests a mechanism of ion channel desensitization.

Dependence is a somatic state which develops after chronic administration of certain drugs.

• This condition is characterized by the necessity to continue administration of the drug to avoid the appearance of withdrawal symptoms.

• Withdrawal symptoms are relieved by the administration of the drug upon which the body was  “dependent”.

• Psychological dependence is due to (e.g., social) reinforcement processes in the maintenance of drug-seeking behavior.

Defensins are a group of antimicrobial and cytotoxic peptides made by immune cells. There are seven defensins in humans, six alpha-defensins and one beta-defensin, which are involved in the innate immune defense at the surface of epithelia from the respiratory tract, the intestinal tract or the urinary tract.

A comprehensive textbook covering the design of dosage forms and all aspects of drug delivery systems. ‘Pharmaceutics’ in its broadest sense is the ‘art of the apothecary’ or, in simple terms, pharmaceutical preparations. It remains a diverse subject in the pharmacy curriculum, encompassing design of drugs, their manufacture, and the elimination of micro-organisms from the products. This books encompasses all those areas and pays particular attention to the design of dosage forms and their manufacture.

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Disorder characterized by atrophy of the choroid (the thin membrane covering most of the posterior of the eye between the retina and sclera) and degeneration of the retinal pigment epithelium resulting in night blindness. The disease is caused by mutations in Rab escort protein Rep1  (component A of Rab geranylgeranyl transferase).

Chorionic gonadotropin (CG) is produced in the placenta. Together with the pituitary hormones, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), it constitutes the glycoprotein family of gonadotropins. The actions of CG are mediated by the LH receptor, both belonging to the superfamily of G-protein Coupled Receptors.

Cholecystokinin (CCK) is produced in the intestine and the brain. It appears to be an important mediator of anxiety.

• It also stimulates vasopressin secretion and slows gastric emptying.
• In addition, it is an important humoral satiety signal (appetite control).
• Various antagonists have been developed and are currently being investigated with regard to their therapeutic potential.