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101.
Infant autonomic reactivity to stress is a potential predictor of later life health complications, but research has not sufficiently examined sympathetic activity, controlled for effects of physical activity and respiration, or studied associations among autonomic adjustments, cardiac activity, and affect in infants. We studied 278 infants during the repeated Still-Face Paradigm, a standardized stressor, while monitoring cardiac activity (ECG) and respiratory pattern (respiratory inductance plethysmography). Video ratings of physical activity and affect were also performed. Respiratory sinus arrhythmia (RSA) and T-wave amplitude (TWA) served as noninvasive indicators of cardiac parasympathetic and sympathetic activity, respectively. Responses were compared between infants who completed two still-face exposures and those who terminated after one exposure due to visible distress. Findings, controlled for physical activity, showed robust reductions in respiration-adjusted RSA and TWA, with more tonic attenuation of TWA. Infants completing only one still-face trial showed more pronounced autonomic changes and less recovery from stress. They also showed elevated minute ventilation, suggesting hyperventilation. Both reductions in adjusted RSA and TWA contributed equally to heart rate changes and were associated with higher negative and lower positive affect. These associations were more robust in the group of distressed infants unable to complete both still-face trials. Thus, cardiac sympathetic activation and parasympathetic withdrawal are part of the infant stress response, beyond associated physical activity and respiration changes. Their association with cardiac chronotropy and affect increases as infants' distress level increases. This excess reactivity to social stress should be examined as a predictor of future cardiovascular disease.  相似文献   
102.

Background

Early environmental exposures may help shape the development of the autonomic nervous system (ANS) and hypothalamic–pituitary–adrenal (HPA) axis, influencing vulnerability for health problems across the lifespan. Little is known about the role of maternal sensitivity in influencing the development of the ANS in early life.

Aims

To examine associations among maternal sensitivity and infant behavioral distress and ANS and HPA axis reactivity to the Repeated Still-Face Paradigm (SFP-R), a dyadic stress task.

Study design

Observational repeated measures study.

Subjects

Thirty-five urban, sociodemographically diverse mothers and their 6-month-old infants.

Outcome measures

Changes in infant affective distress, heart rate, respiratory sinus arrhythmia (RSA), and T-wave amplitude (TWA) across episodes of the SFP-R were assessed. A measure of cortisol output (area under the curve) in the hour following cessation of the SFP-R was also obtained.

Results

Greater maternal insensitivity was associated with greater infant sympathetic activation (TWA) during periods of stress and tended to be associated with greater cortisol output following the SFP-R. There was also evidence for greater affective distress and less parasympathetic activation (RSA) during the SFP-R among infants of predominantly insensitive mothers.

Conclusions

Caregiving quality in early life may influence the responsiveness of the sympathetic and parasympathetic branches of the ANS as well as the HPA axis. Consideration of the ANS and HPA axis systems together provides a fuller representation of adaptive versus maladaptive stress responses. The findings highlight the importance of supporting high quality caregiving in the early years of life, which is likely to promote later health.  相似文献   
103.
International Journal of Clinical Pharmacy - Background Potentially inappropriate prescribing is increasingly common in older patients with falls. However, published indicators to assess...  相似文献   
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Pituitary adenylate cyclase-activating polypeptide-38 (PACAP-38) and its receptors have been shown in the spinal dorsal horn, on capsaicin-sensitive sensory neurons and inflammatory cells. The role of PACAP in central pain transmission is controversial, and no data are available on its function in peripheral nociception. Therefore, the aim of the present study was to analyze the effects of locally or systemically administered PACAP-38 on nocifensive behaviors, inflammatory/neuropathic hyperalgesia and afferent firing. Intraplantar PACAP-38 (0.2 nmol) injection inhibited carrageenan-evoked inflammatory mechanical allodynia, mild heat injury-induced thermal hyperalgesia, as well as nocifensive behaviors in the early and late phases of the formalin test in rats. However, the above dose did not alter basal mechanical or heat thresholds. In mice, PACAP-38 (0.2 nmol/kg s.c.) significantly diminished acetic acid-induced abdominal contractions, but exerted no effect on sciatic nerve ligation-induced neuropathic mechanical hyperalgesia. In contrast, local PACAP-38 injection markedly increased rotation-induced afferent firing in the inflamed rat knee joint clearly demonstrating a peripheral sensitization in this organ. These actions were blocked by VPAC1/VPAC2 receptor antagonist pretreatment, but were not altered by PAC1 receptor antagonism. This paper presents the first data for the peripheral actions of PACAP-38 on nociceptive transmission mediated by VPAC receptors. These effects seem to be divergent depending on the mechanisms of nociceptor activation and the targets of PACAP actions. In acute somatic and visceral inflammatory pain models, PACAP exerts anti-nociceptive, anti-hyperalgesic and anti-allodynic effects. It has no significant peripheral role in traumatic mononeuropathy, but induces mechanical sensitization of knee joint primary afferents.  相似文献   
107.

Aim  

To determine the effect of anticoagulants and antiplatelet medications on the positive-predictive-value of fecal occult blood test (FOBT).  相似文献   
108.
ABSTRACT Benzoporphyrin derivative monoacid ring A (Verteporfin, BPD-MA), a photosensitizing drug, has been suggested as having inhibitory effects on smooth muscle cell (SMC) proliferation in rabbit aortic intimal injuries. The effect of BPD-MA on vascular SMCs in the absence of light stimulation in vitro and in vivo was studied using models of intimal hyperplasia. Human SMCs were incubated with BPDMA for 4 h in darkness. A small (20%) but significant decrease in viability (n = 42, p < .05) was noted for BPD-MA concentrations above 15 mu g/mL. This was an all-or-none phenomenon with no further decrease in viability at higher concentrations. Treatment with BPD-MA was also carried out in vivo using a balloon injury model of intimal hyperplasia in rabbit aortas. Thirty-three rabbits were randomized into five groups and given intravenous BPD-MA (2 mg/kg) according to the following schedule: Group 1 (n = 8), BPD-MA 25 min prior to injury; Group 2 (n = 8), BPD-MA 25 min prior to injury plus a second dose 4 weeks later; Group 3 (n = 4), BPD-MA immediately postinjury; Group 4 (n = 7), BPD-MA immediately postinjury plus a second dose 4 weeks later; or Group 5 (n = 6), no drug (control group). No statistically significant difference was seen in the amount of intimal hyperplasia that developed in the five groups.  相似文献   
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