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Träfflista för sökning "hsv:(MEDICAL AND HEALTH SCIENCES) hsv:(Basic Medicine) hsv:(Physiology) "

Sökning: hsv:(MEDICAL AND HEALTH SCIENCES) hsv:(Basic Medicine) hsv:(Physiology)

  • Resultat 2901-2910 av 4938
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2901.
  • Lager, Susanne, 1978, et al. (författare)
  • Oleic acid stimulates system A amino acid transport in primary human trophoblast cells mediated by toll-like receptor 4
  • 2013
  • Ingår i: Journal of Lipid Research. - 0022-2275. ; 54:3, s. 725-733
  • Tidskriftsartikel (refereegranskat)abstract
    • Obese women have an increased risk to deliver large babies. However, the mechanisms underlying fetal overgrowth in these pregnancies are not well understood. Obese pregnant women typically have elevated circulating lipid levels. We tested the hypothesis that fatty acids stimulate placental amino acid transport, mediated via toll-like receptor 4 (TLR4) and mammalian target of rapamycin (mTOR) signaling pathways. Circulating NEFA levels and placental TLR4 expression were assessed in women with varying prepregnancy body mass index (BMI). The effects of oleic acid on system A and system L amino acid transport, and on the activation of the mTOR (4EBP1, S6K1, rpS6), TLR4 (IĸBɑ, JNK, p38 MAPK), and STAT3 signaling pathways were determined in cultured primary human trophoblast cells. Maternal circulating NEFAs (n = 33), but not placental TLR4 mRNA expression (n = 16), correlated positively with BMI (P < 0.05). Oleic acid increased trophoblast JNK and STAT3 phosphorylation (P < 0.05), whereas mTOR activity was unaffected. Furthermore, oleic acid doubled trophoblast system A activity (P < 0.05), without affecting system L activity. siRNA-mediated silencing of TLR4 expression prevented the stimulatory effect of oleic acid on system A activity. Our data suggest that maternal fatty acids can increase placental nutrient transport via TLR4, thereby potentially affecting fetal growth.
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2902.
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2903.
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2904.
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2905.
  • Lagercrantz, Hugo, et al. (författare)
  • Plötslig spädbarnsdöd
  • 1984
  • Ingår i: Paediatricus. ; 14:1, s. 3-18
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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2906.
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2907.
  • Lai, Jacqueline, 1980, et al. (författare)
  • Immune responses in perinatal brain injury.
  • 2017
  • Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 1090-2139 .- 0889-1591. ; 63, s. 210-223
  • Forskningsöversikt (refereegranskat)abstract
    • The perinatal period has often been described as immune deficient. However, it has become clear that immune responses in the neonate following exposure to microbes or as a result of tissue injury may be substantial and play a role in perinatal brain injury. In this article we will review the immune cell composition under normal physiological conditions in the perinatal period, both in the human and rodent. We will summarize evidence of the inflammatory responses to stimuli and discuss how neonatal immune activation, both in the central nervous system and in the periphery, may contribute to perinatal hypoxic-ischemic brain injury.
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2908.
  • Laine, Saara, et al. (författare)
  • Effects of Different Exercise Training Protocols on Gene Expression of Rac1 and PAK1 in Healthy Rat Fast- and Slow-Type Muscles.
  • 2020
  • Ingår i: Frontiers in Physiology. - : Frontiers Media S.A.. - 1664-042X. ; 11
  • Tidskriftsartikel (refereegranskat)abstract
    • Purpose: Rac1 and its downstream target PAK1 are novel regulators of insulin and exercise-induced glucose uptake in skeletal muscle. However, it is not yet understood how different training intensities affect the expression of these proteins. Therefore, we studied the effects of high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) on Rac1 and PAK1 expression in fast-type (gastrocnemius, GC) and slow-type (soleus, SOL) muscles in rats after HIIT and MICT swimming exercises.Methods: The mRNA expression was determined using qPCR and protein expression levels with reverse-phase protein microarray (RPPA).Results: HIIT significantly decreased Rac1 mRNA expression in GC compared to MICT (p = 0.003) and to the control group (CON) (p = 0.001). At the protein level Rac1 was increased in GC in both training groups, but only the difference between HIIT and CON was significant (p = 0.02). HIIT caused significant decrease of PAK1 mRNA expression in GC compared to MICT (p = 0.007) and to CON (p = 0.001). At the protein level, HIIT increased PAK1 expression in GC compared to MICT and CON (by ∼17%), but the difference was not statistically significant (p = 0.3, p = 0.2, respectively). There were no significant differences in the Rac1 or PAK1 expression in SOL between the groups.Conclusion: Our results indicate that HIIT, but not MICT, decreases Rac1 and PAK1 mRNA expression and increases the protein expression of especially Rac1 but only in fast-type muscle. These exercise training findings may reveal new therapeutic targets to treat patients with metabolic diseases.
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2909.
  • Lambert, G W, et al. (författare)
  • Influence of voluntary exercise on hypothalamic norepinephrine.
  • 1998
  • Ingår i: Journal of applied physiology. - 8750-7587. ; 85:3, s. 962-6
  • Tidskriftsartikel (refereegranskat)abstract
    • We combined hypothalamic tissue and plasma determinations of norepinephrine, dihydroxyphenylalanine, and dihydroxyphenylglycol with measurements of abdominal fat in voluntary running rats to examine the relationship among exercise training, hypothalamic and sympathetic nervous function, and body fat stores. The hypothalamic concentrations of norepinephrine, dihydroxyphenylalanine, and dihydroxyphenylglycol were reduced after exercise training (P < 0.01), with the amount of norepinephrine being strongly associated with the plasma norepinephrine (r = 0.58, P < 0.05) and dihydroxyphenylglycol (r = 0.65, P = 0.01) concentrations. Exercise training resulted in a diminution in abdominal fat mass (P < 0.01). A strong relationship existed between fat mass and hypothalamic norepinephrine content (r = 0.83, P < 0.001). The presence of a positive relationship between the arterial and hypothalamic norepinephrine levels provides presumptive evidence of an association between noradrenergic neuronal activity of the hypothalamus and sympathetic nervous function. The observation that abdominal fat mass is linked with norepinephrine in the hypothalamus raises the possibility that alterations in body fat stores provide an afferent signal linking hypothalamic function and the activity of the sympathetic nervous system.
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2910.
  • Landén, Mikael, 1966, et al. (författare)
  • Dyslipidemia and high waist-hip ratio in women with self-reported social anxiety.
  • 2004
  • Ingår i: Psychoneuroendocrinology. - : Elsevier BV. - 0306-4530. ; 29:8, s. 1037-46
  • Tidskriftsartikel (refereegranskat)abstract
    • Previous research has indicated that phobic anxiety is associated with coronary heart disease. In this study, the possible association between social anxiety and various anthropometric, metabolic, and endocrine measurements known to be associated with cardiovascular disease were studied in a population-based cohort of 216 women 41-42 years old. Each participant was assessed by means of a DSM-IV based self-report questionnaire regarding social anxiety and related psychiatric diagnoses. Waist-to-hip ratio (WHR), body mass index (BMI), and serum levels of lipids and hormones were assessed. The prevalence of social anxiety was 14% (n=31). The social anxiety group displayed higher serum levels of triglycerides (1.3+/-0.9 vs. 1.0+/-0.5, P=0.003) and low-density lipoprotein (LDL) (3.3+/-0.8 vs. 3.0+/-0.7, P=0.03), but lower high-density lipoprotein (HDL) (1.4+/-0.3 vs. 1.6+/-0.4, P=0.04) and HDL/LDL ratio (0.46+/-0.15 vs. 0.57+/-0.22, P=0.008) than the other women. Serum levels of total testosterone (1.6+/-0.8 vs. 2.2+/-1.1, P=0.013) and free thyroxin (14+/-2 vs. 16+/-4, P=0.04) were lower in subjects confirming social anxiety. While WHR was significantly higher in the social anxiety group (0.83+/-0.06 vs. 0.80+/-0.07, P=0.016), BMI did not differ between the groups. Our data suggest that self-reported social anxiety is associated with two established risk factors for cardiovascular disease: dyslipidemia and increased WHR.
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