Mechanism of Action. Blood pressure measurement typically involves the occlusion of the brachial artery at ap- proximately the height of the heart using an inflatable cuff. The cuff is slowly deflated, and the device detects the pressure at which blood flow resumes (systolic pressure) and the pressure at which it is fully unencumbered by the cuff (diastolic pressure). In the auscula- tory method, the caregiver uses a stethoscope to listen to the Korotkoff sounds as the cuff deflates, noting the pressure at each sound. In the oscillometric method, a pressure transducer in the cuff measures oscillations in the cuff pressure (caused by blood flow) as it deflates. The device then calculates blood pressure and displays it on a digital read out. While these automatic devices do not require the skill and related accuracy challenges of manual devices, some models systematically under report blood pressure. Current use in high-resource settings Several authors have noted the inaccuracy of blood pressure measurement around the Generic kit with stethoscope - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - GLOBAL ANNUAL DEATHS ASSOCIATED WITH HYPERTENSIVE DISEASES OF PREGNANCY PERCENT (%) NUMBER - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - Maternal 10-18% 35,800-64,440 - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - 370,000- Neonatal 10-15% 555,000 - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - 320,000- Stillbirth 10-15% 480,000 world, citing relatively low levels of agreement between sequential observers using manual equipment. Automated, oscillometric equipment is gradually replacing manual equipment, although it must be validated for use with pregnant women and calibrated at regular intervals. There is also movement to phase out mercury sphygmomanometers due to mercury concerns. Application in low-resource settings Manual, ausculatory cuffs are most commonly used in low-resource settings. Given the high level of user error associated with the aus- cultatory technique, the WHO recommends validated, low cost oscillometric blood pressure measurement devices replace older equip- ment. The WHO further recommends all devices be solar powered due to concerns over batteries and battery maintenance. Such devices are not yet common on the market. REPRESENTATIVE DEVICES MAKE MODEL PRICE* TECH STATUS NOTES ...
Mechanism of Action. The Ulthera® System images and delivers focused ultrasound energy to a specific soft tissue layer under the superficial layers of epidermis. Ultrasound treatment creates focal micro-coagulation zones in the skin, causing thermally induced contraction of tissue and a “wound-healing” response to stimulate the formation of new tissue and collagen, and to cause a skin-tightening/wrinkle-reduction effect. As stated earlier, it is hypothesized that the creation of focal lesions at the depth of the sweat glands, will effectively damage the glands without surface effects and result in a reduction of sweat. The device is designed and configured to produce small (approximately 1mm3) micro-coagulation zones in the mid to deep reticular layer of dermis and sub-dermis, while sparing overlying papillary dermal and epidermal layers of skin. The device also incorporates an ultrasound imaging capability to evaluate the skin tissue. Protocol Number ULT-218 FINAL v1_07SEP2016 P a g e | 3 Similar findings have been confirmed in human cadaver studies at the University of California at San Diego (UCSD, MEEI, and Xxxxxxx Lab – Harvard Medical School). Cadaver skin tissue was treated using the Ulthera® System at frequencies of 4-7 MHz. The focal depths of the 4 MHz transducer were 4.5mm and 6mm. The focal depths of the 7MHz transducer were 3mm and 4.5mm. These studies further demonstrated that the Ulthera® System reliably creates small, well-confined micro-coagulative zones.
Mechanism of Action. Local anesthetics block the generation and the conduction of nerve impulses presumably by increasing the threshold for electrical excitation in the nerve, by slowing the propagation of the nerve impulse, and by reducing the rate of rise of the action potential. In general, the progression of anesthesia is related to the diameter, myelination, and conduction velocity of affected nerve fibers. Clinically, the order of loss of nerve function is as follows: (1) pain, (2) temperature,
Mechanism of Action. Sulbactam Although sulbactam is classified as a BLI of several Class A enzymes, it also has intrinsic antibacterial activity against A. baumannii. This intrinsic activity has been shown by target-binding studies, cytological profiling, and resistance mapping to be primarily due to its inhibition of PBP3, a transpeptidase that is essential for the final step of bacterial peptidoglycan synthesis (Xxxxxxx 2015).
Mechanism of Action. Figure 1. Proposed mechanism of action for pelareorep.
Mechanism of Action. Benzhydrocodone Benzhydrocodone is a prodrug of hydrocodone. Hydrocodone Hydrocodone is a full opioid agonist with relative selectivity for the mu-opioid receptor, although it can interact with other opioid receptors at higher doses. The principal therapeutic action of hydrocodone is analgesia. Like all full opioid agonists, there is no ceiling effect for analgesia with hydrocodone. Clinically, dosage is titrated to provide adequate analgesia and may be limited by adverse reactions, including respiratory and CNS depression. The precise mechanism of the analgesic action is unknown. However, specific CNS opioid receptors for endogenous compounds with opioid-like activity have been identified throughout the brain and spinal cord and are thought to play a role in the analgesic effects of this drug.
Mechanism of Action. Taxol has a unique mechanism of action in that rather than inhibiting tubulin polymerization, it markedly enhances the reaction, and microtubules formed in the presence of taxol are unusually stable. Taxal blocks cell replication in HeLa cells, mainly during mitosis. (13) Studies with purified microtubule protein have demonstrated that taxol promotes the assembly of tubulin into calcium-stable microtubules in vitro in the presence or absence of GTP or microtubule-associated proteins.(13,15,18) Taxol binds directly to polymerized tubulin (17,18) with saturation occurring at approximate stoichiometry with tubulin dimer concentration. These activities of taxol are in contrast to other known mitotic spindle poisons such as colchicine, podophyllotoxin, and the vinca alkaloids which inhibit microtubule formation.
Mechanism of Action. Atezolizumab is an Fc-engineered, humanized, non-glycosylated IgG1 kappa monoclonal antibody that inhibits programmed death ligand 1 (PD-L1) interactions with the PD-1 and B7.1 receptors. PD-L1 may be expressed on tumor cells and/or tumor-infiltrating immune cells, and can contribute to inhibition of the anti-tumor immune response in the tumor microenvironment; PD-1 and B7.1 receptors are found on T-cells and antigen-presenting cells. The PD-1 pathway regulates the balance between T-cell activation and protection of healthy tissues from immune-mediated damage. In cancer, the PD-1 pathway is thought to play an important role in the interaction of tumor cells with the host immune response. Binding of PD-L1 to the PD-1 and B7.1 receptors suppresses cytotoxic T-cell activity, T-cell proliferation, and cytokine production; PD-L1 expression in a tumor cell may provide adaptive immune resistance and lead to poor outcomes. Atezolizumab binds to PD-L1 and prevents its interaction with both PD-1 and B7.1 receptors, releasing the PD-L1/PD-1 mediated inhibition of an anti-tumor immune response without inducing antibody-dependent cellular cytotoxicity. In syngeneic mouse tumor models, blocking PD-L1 activity resulted in decreased tumor growth.
Mechanism of Action. Similar to other azole derivatives, posaconazole inhibits the enzyme lanosterol 14α-demethylase and consequently inhibits the biosynthesis of ergosterol which is an essential component of fungal cell membrane (see in Fig. 1). This results in an accumulation of methylated sterol precursors and a depletion of ergosterol within the cell membrane, thereby weakening the structure and function of the fungal cell membrane, which is considered to be responsible for the antifungal activity of posaconazole [2].
