Answer:
True
Explanation:
its true because a lot of drugs are bad technically all drugs are bad.
Answer:
T.
Explanation:
This is a symptom of untreated diabetes 1. The body's, endocrine system is unable to process carbohydrates, over time leads to ketoacidosis. the reaction is the cells in the body cannot absorb or benefit from all the extra sugars, in turn, the cells waste can only be secreted in the urine, hense unquenchable thirst of the patient(symptom). turns the blood acidic...
Answer:
I'm assuming the joint pain was related to a homeostatic imbalance. I believe the answer is C.
Explanation:
A is wrong but not false. Your kidneys (and other organs) can be affected, but the patient said that the doctor told them their pain will start to go away and they'll reach homeostasis. They didn't mention a problem with getting there.
Option B is patently false.
Option D is a little silly. Same sort of reasons with A.
Answer:
Multiple myeloma is a B-cell malignancy characterized by an excess of monotypic plasma cells in the bone marrow. The molecular mechanisms that are involved in disease progression depend on the interaction between the multiple myeloma cells and the bone microenvironment. Because these mechanisms have been well characterized, it is possible to develop regimens that are more specific to pathways involved in the pathogenesis of multiple myeloma than is typical for conventional chemotherapy in disease management. Thalidomide and immunomodulatory drugs (IMiDs) have now been shown to block several pathways important for disease progression in multiple myeloma. First established as agents with antiangiogenic properties, thalidomide and IMiDs inhibit the production of interleukin (IL)-6, which is a growth factor for the proliferation of myeloma cells. In addition, they activate apoptotic pathways through caspase 8-mediated cell death. At the mitochondrial level, they are responsible for c-jun terminal kinase (JNK)-dependent release of cytochrome-c and Smac into the cytosol of cells, where they regulate the activity of molecules that affect apoptosis. By activating T cells to produce IL-2, thalidomide and IMiDs alter natural killer (NK) cell numbers and function, thus augmenting the activity of NK-dependent cytotoxicity. Data delineating these events have been derived from experiments done in resistant and sensitive multiple myeloma cell lines. Although thalidomide and IMiDs demonstrate similar biologic activities, IMiDs are more potent than thalidomide and achieve responses at lower doses. Lenalidomide, a thalidomide derivative, has also been shown to have a different toxicity profile. Our understanding of the mechanism of action of these agents has provided a platform for exciting clinical trials evaluating combinations of thalidomide and lenalidomide with both conventional chemotherapy and newer targeted agents.
Explanation: