The specification mentions that the weight loss must not be greater than 0.04 mg/cm³ from the specimen surface, which is considered negligible from a clinical standpoint.

A wax pattern made in the mouth will shrink appreciably as it is cooled to room temperature because the coefficient of  thermal expansion of wax is very high.(This  is the property which describes the thermal energy transport in watts per second through a specimen 1cm thick with a cross sectional area of 1 cm² when the temperature differential between the surfaces of the specimen perpendicular to the heat flow 1⁰ K)  Co efficient of thermal expansion is defined  as the change in length  per unit of the original length  of a material when its temperature is raised 1⁰K.

The rate limiting step in cholesterol synthesis is HMG CoA reductase. Here's a detailed explanation:

Cholesterol synthesis is a complex process that involves multiple enzymatic steps. This process begins with the condensation of acetyl-CoA molecules to form acetoacetyl-CoA, which is then converted into HMG CoA (3-hydroxy-3-methylglutaryl-CoA) by the enzyme HMG CoA synthetase. HMG CoA is further converted to mevalonate by the action of HMG CoA reductase. This reaction is the rate limiting step of the cholesterol synthesis pathway. The rate limiting step is the slowest step in a metabolic pathway and is responsible for controlling the overall rate of the process.

HMG CoA reductase is a critical regulatory enzyme that is tightly controlled because it is the first committed step in the synthesis of cholesterol from acetate. This enzyme is responsible for reducing HMG CoA to mevalonate, which is the precursor of all isoprenoids, including cholesterol, steroids, and other important biological molecules. The rate limiting nature of this step is due to the fact that HMG CoA reductase is subject to both allosteric regulation and feedback inhibition.

Allosteric regulation involves the binding of regulatory molecules, such as ATP, citrate, and NADH, which can either activate or inhibit the enzyme. For example, when cellular ATP levels are high, the enzyme is inhibited, which reduces cholesterol synthesis. Conversely, when ATP levels are low, the enzyme is activated, leading to increased cholesterol production. Citrate, a molecule derived from the citric acid cycle, inhibits HMG CoA reductase when it builds up in the cytosol, indicating that the cell has enough energy and does not need to synthesize additional cholesterol.

Feedback inhibition occurs when the end product of the pathway, cholesterol, binds to the enzyme and reduces its activity. This is a form of negative feedback regulation that helps to maintain homeostasis of cholesterol levels within the cell. When cellular cholesterol levels are high, the enzyme is inhibited, which slows down the synthesis of new cholesterol molecules. Conversely, when cholesterol levels are low, the enzyme is less inhibited, and the synthesis rate increases.

The other enzymes listed, HMG CoA synthetase and mevalonate synthetase, are involved in the synthesis of HMG CoA and the subsequent transformation of mevalonate, but they are not the rate limiting steps. HMG CoA lyase, on the other hand, is part of an alternative pathway that breaks down HMG CoA into acetyl-CoA and acetoacetate. This enzyme is not directly involved in the rate limiting step of cholesterol synthesis.

Analgesics are not effective in reducing pain in trigeminal neuralgia.

According to gate control theory of pain, large fiber impulses tend to inhibit the effect of painful stimuli transmitted by small fibers.