Answer:
it is a failure of tolerance (self-tolerance) and specificity (recognition)
Explanation:
Type 1 diabetes is a chronic disease caused by the selective destruction of β cells that are involved in the production of insulin in the pancreas. Type 1 diabetes can be classified into two types: Type 1A diabetes (the immune form of the disease) and Type 1B diabetes (the non-immune form of the disease). Type 1A diabetes is considered an autoimmune disorder where immune responses against pathogens suffer a failure of tolerance to antigens in the β-cells of the pancreatic islets. Thus, Type 1A diabetes is characterized by the process of recognition of β-cell antigens (autoantigens) by the immune system. This disease is often caused by genetic factors associated with mutations in the human leukocyte antigen (HLA) class II region located on chromosome 6.
Meningitis is an inflammation of the membranes (meninges) surrounding your brain and spinal cord. ... Most cases of meningitis in the United States are caused by a viral infection, but bacterial, parasitic and fungal infections are other causes. Some cases of meningitis improve without treatment in a few weeks.
Should be prophase because chromatin coils up, becoming shorter and thicker, thick enough to become visible when stained.
Long-term potentiation (LTP) is considered a cellular correlate of learning and memory. The presence of G protein-activated inwardly rectifying K(+) (GIRK) channels near excitatory synapses on dendritic spines suggests their possible involvement in synaptic plasticity. However, whether activity-dependent regulation of channels affects excitatory synaptic plasticity is unknown. In a companion article we have reported activity-dependent regulation of GIRK channel density in cultured hippocampal neurons that requires activity oF receptors (NMDAR) and protein phosphatase-1 (PP1) and takes place within 15 min. In this study, we performed whole-cell recordings of cultured hippocampal neurons and found that NMDAR activation increases basal GIRK current and GIRK channel activation mediated by adenosine A(1) receptors, but not GABA(B) receptors. Given the similar involvement of NMDARs, adenosine receptors, and PP1 in depotentiation of LTP caused by low-frequency stimulation that immediately follows LTP-inducing high-frequency stimulation, we wondered whether NMDAR-induced increase in GIRK channel surface density and current may contribute to the molecular mechanisms underlying this specific depotentiation. Remarkably, GIRK2 null mutation or GIRK channel blockade abolishes depotentiation of LTP, demonstrating that GIRK channels are critical for depotentiation, one form of excitatory synaptic plasticity.
Learn more about receptors here:
brainly.com/question/11985070
#SPJ4
In four o'clock flowers, red petals show incomplete dominance over white petals. If two pink flowers are crossed, 50 percent of the flowers will be homozygous, and 25 percent of the flowers will be heterozygous.
