Justify the following:

1. TSH levels are low in grave's disease while in hashimoto's TSH levels are high.

TSH levels are low in grave's disease because the pituitary gland will try to compensate for the excess T3 and T4 hormones in the blood. It will stop producing TSH in an attempt to stop production of the thyroid hormones whereas, in hashimoto's disease, TSH levels are high because the brain thinks the pituitary gland is not making enough thyroid stimulating hormone which in return, is not producing enough thyroid hormones and needs stimulation.

2. All steroid hormone receptors have DNA binding domain.

Steroid hormones mediate their actions through genomic mechanisms. The hormone enters the cell by passive diffusion. It binds to the hormone-binding domain of the receptor. This binding results in a conformational change exposing the receptor's DNA binding domain and enabling it to bind to the nuclear chromatin. This binding to DNA initiate transcription of mRNA and ultimately translation into androgen-specific proteins.

The DNA-binding domain, a 66-68 amino acid sequence is encoded by exons B and C which code the first and second (C-terminal) zinc finger motifs respectively. The first zinc finger specifies the receptor's DNA recognition and the second is mainly responsible for dimerization of two receptor molecules during the association with DNA. The androgen binding C-terminal domain consists of about 252 amino acids and is encoded by exons D-H.

 3. DOPA is an important agent in the treatment of Parkinson disease.

Levodopa is the most commonly prescribed medicine for Parkinson's disease. It works when brain cells change it into dopamine. Dopamine is a neurotransmitter present in the brain which sends signals that helps in the movement of the body. People suffering from Parkinson's disease don't have enough dopamine in their brains to control their movements. There are many dopamine agonists available which are recommended first than levodopa therapy.

4. Ras protein requires Sos for its activation.

In the mechanism of activation of the INSR protein kinase, an adaptor protein functions to bring together two proteins: IRS-1 and the protein Sos that must interact to enable signal transduction. In addition to Grb2's SH2 domain, it also has SH3 that binds to proline-rich region of Sos recruiting Sos to the growing receptor complex. When bound to Grb2, Sos acts as a guanosine nucleotide exchange factor (GEF) catalyzing the replacement of bound GDP with GTP and hence Ras is activated. Ras can exist in two conformations either active GTP bound or GDP bound inactive.

5. Goiter is a symptom of both hyper and hypo-thyroidism.

Failure of the thyroid to produce T4 and T3 may lead to the development of a goiter since, in the absence of any negative feedback to the hypothalamus and pituitary gland, there is excessive secretion of TSH. In the absence of thyroid hormone production TSH stimulation leads to hypertrophy of the thyroid follicular cells which then causes the gland to enlarge.

Goiter may also develop under conditions of hyperthyroidism due to auto-antibodies against thyroid TSH- receptors causing it to produce excess thyroid. This overstimulation causes the thyroid to swell.

6. Hyperglycemia is not a confirmatory symptom for diabetes mellitus.

Hyperglycemia is an abnormally high blood glucose level. It is not always related to lack of insulin or insulin sensitivity and diabetes is characterized by high amounts of sugar in the bloodstream that occurs as a result of a lack of insulin or insulin sensitivity.