Dyspnea in pregnancy.

Dyspnea in pregnancy is common. It can result from adaption to body changes in pregnancy and also from complications therein. Understanding the mechanisms of change in the respiratory system during pregnancy helps with the differential diagnosis of dyspnea in normal pregnancy as opposed to pathological dyspnea.

Do elderly females have a higher risk of acute myocardial infarction? A retrospective analysis of 329 cases at an emergency department.

OBJECTIVE: Acute myocardial infarction (AMI) is a medical emergency; a missed or delayed diagnosis of this disease may contribute to a poor outcome and even death. Several studies have found elderly patients with AMI have atypical presentations for diagnosis, therefore we undertook this study to determine the risks among the elderly population, especially in female patients. MATERIALS AND METHODS: In this one-year retrospective study, we reviewed the cases of AMI patients who had visited the emergency department at Mackay Memorial Hospital, Taiwan, and who had either been discharged or had died following a diagnosis of AMI (ICD code 410). We compared the differences between the clinical presentations of these two groups as well as the risk factors, medical management, and outcomes. RESULTS: In our study, only 329 patients (164 elderly; 165 adults) met the defined criteria. The most common symptom of AMI was chest pain, and this was more common in adult patients than in elderly patients (81.8% vs. 60.4%, p < 0.001). In comparison with patients in the adult group, the patients in the elderly group had a significantly higher proportion of females (46.3% vs. 12.7%), non-ST-elevation myocardial infarction (NSTEMI) (71.3% vs. 46.7%), presenting with no chest pain (39.6% vs. 18.2%), shortness of breath (17.7% vs. 8.8%), nausea/vomiting/dizziness (7.9% vs. 2.4%), abdominal pain (4.3% vs. 0.6%), diabetes mellitus (45.1% vs. 26.1%), cerebrovascular disease (22.6% vs. 6.1%), longer hospital stays (18.2 ± 31.0 days vs. 9.8 ± 8.2 days), and increased in-hospital mortality rates (15.9% vs. 6.7%). CONCLUSION: Compared with the adult AMI group, the elderly AMI group had a higher proportion of females, electrocardiography with NSTEMI and no chest-pain complaints, and a larger proportion of elderly patients with diabetes, ischemic heart disease, heart attacks at home and cardiac shock, which had longer hospital stays, and higher mortality rates.

Involvement of protein phosphatases in the destabilization of methamphetamine-associated contextual memory.

Destabilization refers to a memory that becomes unstable when reactivated and is susceptible to disruption by amnestic agents. Here we delineated the cellular mechanism underlying the destabilization of drug memory. Mice were conditioned with methamphetamine (MeAM) for 3 d, and drug memory was assessed with a conditioned place preference (CPP) protocol. Anisomycin (ANI) was administered 60 min after the CPP retrieval to disrupt reconsolidation. We found that destabilization of MeAM CPP after the application of ANI was blocked by the N-methyl-d-aspartate receptor (NMDAR) antagonist MK-801 and the NR2B antagonist ifenprodil (IFN) but not by the NR2A antagonist NVP-AAM077 (NVP). In addition, decrease in the phosphorylation of GluR1 at Serine845 (p-GluR1-Ser845), decrease in spine density, and a reduction in the AMPAR/NMDAR ratio in the basolateral amygdala (BLA) were reversed after the MK-801 treatment. The effect of ANI on destabilization was prevented by the protein phosphatase 2B (calcineurin, CaN) inhibitors cyclosporine A (CsA) and FK-506 and the protein phosphatase 1 (PP1) inhibitors calyculin A (CA) and okadaic acid (OA). These results suggest that memory destabilization involves the activation of NR2B-containing NMDARs, which in turn allows the influx of Ca(2+) Increased intracellular Ca(2+) stimulates CaN, leading to the dephosphorylation and inactivation of inhibitor 1 and the activation of PP1. PP1 then dephosphorylates p-GluR1-Ser845 to elicit AMPA receptor (AMPAR) endocytosis and destabilization of the drug memory.

Involvement of metabotropic glutamate receptor 5 in the inhibition of methamphetamine-associated contextual memory after prolonged extinction training.

Addiction is thought to be a memory process between perception and environmental cues and addicted patients often relapse when they come into contact with the drug-related context once again. Here, we used a conditioned place preference protocol to seek a more effective extinction methodology of methamphetamine (METH) memory and delineate its underlying mechanism. Conditioning METH for 3 days in mice markedly increased the time spent in the METH-paired compartment. Then the mice were conditioned with saline for 6 days, from day 6 to day 11, a procedure termed extinction training. However, METH memory returned after a priming injection of METH. We prolonged extinction duration from 6 to 10 days and found that this extensive extinction (EE) training prevented priming effect. At the molecular level, we discovered that prolonged extinction training reversed the METH-conditioned place preference-induced increase in surface expression of GluA2 and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA)/NMDA ratio in the basolateral amygdala. In addition, we found that extinction with metabotropic glutamate receptor 5 (mGluR5) activation had similar results to EE: reduced relapse after extinction, decreased synaptic AMPA receptors AMPARs and the AMPA/NMDA ratio. On the contrary, EE with mGluR5 inhibition suppressed the results of EE. These data indicate that EE training-elicited inhibition of METH-primed reinstatement is mediated by the mGluR5. Conditioning mice with methamphetamine place preference (METH CPP) increases surface expression of AMPA receptors (AMPARs) in the basolateral amygdala. We found prolongation of extinction duration from 6 to 10 days prevented priming effect. At the molecular level, we discovered that extensive extinction (EE) reversed the METH CPP-induced increase in surface expression of GluA2 and AMPA/NMDA ratio. In addition, we found that extinction with the metabotropic glutamate receptor 5 (mGluR5) activation had similar results to EE: reduced relapse after extinction, decreased synaptic AMPARs and the AMPA/NMDA ratio. On the contrary, EE with mGluR5 inhibition suppressed the results of EE. These data indicate that EE training-elicited inhibition of METH-primed reinstatement is mediated by mGluR5 (PAM: positive allosteric modulator).