|
Citrus
|
B01.650.940.800.575.912.250.875.177 |
|
|
Carbonic Anhydrase IV
|
D08.811.520.241.300.150.400 |
|
|
Viral Packaging Sequence
|
D000086502 |
[Specific sequences in the viral nucleic acid that are involved in packaging the viral genome (VIRAL GENOME PACKAGING) into the VIRUS PARTICLES.
] |
|
Brucellosis
|
C01.150.252.400.167 |
|
|
Retinoblastoma-Binding Protein 7
|
D12.644.360.024.328.700 |
|
|
Prometaphase
|
G05.113.220.781.812 |
|
|
Mitosis
|
G05.113.220.781 |
|
|
Anion Transport Proteins
|
D12.776.157.530.450.074 |
|
|
Ion Pumps
|
D12.776.157.530.450 |
|
|
Pseudogenes
|
D011544 |
[Genes bearing close resemblance to known genes at different loci, but rendered non-functional by additions or deletions in structure that prevent normal transcription or translation. When lacking introns and containing a poly-A segment near the downstream end (as a result of reverse copying from processed nuclear RNA into double-stranded DNA), they are called processed genes.
] |
|
Pseudohypoaldosteronism
|
D011546 |
[Rare autosomal disorder of renal electrolyte transport dysfunctions. The Type I features HYPERKALEMIA with sodium wasting; Type II, HYPERKALEMIA without sodium wasting. Loss of function mutations in EPITHELIAL SODIUM CHANNELS subunits (autosomal dominant) or MINERALOCORTICOID RECEPTORS (autosomal recessive) cause the disorder. Different mutations in EPITHELIAL SODIUM CHANNELS subunits cause Liddle syndrome.
, A heterogeneous group of disorders characterized by renal electrolyte transport dysfunctions. Congenital forms are rare autosomal disorders characterized by neonatal hypertension, HYPERKALEMIA, increased RENIN activity and ALDOSTERONE concentration. The Type I features HYPERKALEMIA with sodium wasting; Type II, HYPERKALEMIA without sodium wasting. Pseudohypoaldosteronism can be the result of a defective renal electrolyte transport protein or acquired after KIDNEY TRANSPLANTATION.
, Autosomal dominant syndrome of renal electrolyte transport dysfunctions. The clinical features include salt-sensitive hypertension, renal HYPERKALEMIA without sodium wasting, normal glomerular filtration rate and metabolic acidosis (hyperchloremic acidemia and HYPERCALCIURIA). Wnk1 and Wnk4 mutations are responsible for the disorder.
] |
|
Pseudohypoparathyroidism
|
D011547 |
[A syndrome characterized by variable features such as short stature, obesity, round face, subcutaneous ossifications, and BRACHYDACTYLY. It is associated with resistance to PARATHYROID HORMONE and THYROTROPIN. The autosomal dominant inherited form (PSEUDOHYPOPARATHYROIDISM, TYPE IA) is caused by mutations in the GNAS gene. OMIM: 103580.
, A hereditary syndrome clinically similar to HYPOPARATHYROIDISM. It is characterized by HYPOCALCEMIA; HYPERPHOSPHATEMIA; and associated skeletal development impairment and caused by failure of response to PARATHYROID HORMONE rather than deficiencies. A severe form with resistance to multiple hormones is referred to as Type 1a and is associated with maternal mutant allele of the ALPHA CHAIN OF STIMULATORY G PROTEIN.
] |
|
Pseudomonadaceae
|
D011548 |
[A family of gram-negative bacteria usually found in soil or water and including many plant pathogens and a few animal pathogens.
, A subfamily of motile, gram-negative bacteria found in SOIL and WATER and capable of fixing atmospheric nitrogen.
] |
|
Brenner Tumor
|
C04.557.450.565.590.595.150 |
|
|
Pseudomonas
|
D011549 |
[A genus of gram-negative, aerobic, rod-shaped bacteria widely distributed in nature. Some species are pathogenic for humans, animals, and plants.
] |
|
Miller Fisher Syndrome
|
C10.668.829.350.500 |
|
|
Guillain-Barre Syndrome
|
C10.668.829.350 |
|
|
Lignin
|
D05.750.078.562.180.515 |
|
|
Licensure, Hospital
|
N03.706.110.510.290 |
|
|
Licensure
|
N03.706.110.510 |
|
