Virus: Vaccine, Antibiotics are not useful, Is not an organism
Both: Curable, Harmful to humans, Deadly
Bacteria: No vaccine, Antibiotics are useful, Is an organism
Answer: 1300 kg m- and in the lower layer is
Explanation:
Answer:
The correct answer is option E.
Explanation:
Voluntary hyperventilation results in alkalosis, not in acidosis. Alkalosis takes place when the body possesses too many bases. It can take place due to decreased levels of carbon dioxide or due to enhanced level of bicarbonates in the blood, that is, a base.
Emphysema directly impairs exhalation more than it directly impairs inhalation. Emphysema refers to a lung disorder, which leads to shortness of breath. In the individuals suffering from the condition, the air sacs in the lungs, that is, alveoli get damaged.
The hemoglobin-oxygen dissociation curve shifts to the right at the time of metabolic acidosis. The low partial pressure of oxygen within the lungs results in the constriction of pulmonary arterioles. Thus, all the mentioned statements are false.
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.
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