ABSTRACT
Dehydroepiandrosterone (DHEA) is a testosterone/oestrogen precursor and known modulator of vertebrate aggression. Male song sparrows (Melospiza melodia morphna) show high aggression during breeding and nonbreeding life-history stages when circulating DHEA levels are high, and low aggression during molt when DHEA levels are low. We previously showed that androgen receptor and aromatase mRNA expression are higher during breeding and/or nonbreeding in brain regions associated with reproductive and aggressive behaviour, although the potential role of DHEA in mediating these seasonal changes remained unclear. In the present study, nonbreeding male song sparrows were captured and held in the laboratory under short days (8 : 16 h light/dark cycle) and implanted with s.c. DHEA-filled or empty (control) implants for 14 days. DHEA implants increased aggression in a laboratory-based simulated territorial intrusion. Brains of DHEA-implanted birds showed higher aromatase mRNA expression in the preoptic area (POA) and higher androgen receptor mRNA expression in the periventricular nucleus of the medial striatum (pvMSt) and ventromedial nucleus of the hypothalamus. The DHEA-induced increases in aromatase expression in the POA and androgen receptor expression in the pvMSt are consistent with previously reported seasonal increases in these markers associated with naturally elevated DHEA levels. This suggests that DHEA facilitates seasonal increases in aggression in nonbreeding male song sparrows by up-regulating steroid signalling/synthesis machinery in a brain region-specific fashion.
Subject(s)
Aggression/physiology , Aromatase/metabolism , Avian Proteins/physiology , Brain/physiology , Dehydroepiandrosterone/physiology , Receptors, Androgen/metabolism , Sparrows/physiology , Animals , Male , RNA, Messenger/metabolismABSTRACT
Autophagy, the process of self-degradation of cellular components, has an important role in neurodegenerative diseases, such as Alzheimer's disease. In this study, we investigated the effects of SP600125 as c-Jun N-terminal kinase (JNK) inhibitor and bucladesine as a cyclic adenosine 3',5'-monophosphate (cAMP) analog on spatial memory and expression of autophagic factors in Aß-injected rats. Male Wistar rats were used. Rats were randomly allocated into five groups as following: amyloid beta (Aß)-only group, Aß + SP600125 (30 µg/1 µ/side, n = 7) and/or bucladesine (100 µM/1 µl/side, n = 7), and the normal control (vehicle only) group. The treatments were administered bilaterally to the CA1 sub-region of the hippocampus stereotaxically. Spatial reference memory was performed using Morris Water Maze 21 days later. The expression of authophagy markers (beclin1, Atg7, Atg12, and LC3 II/LC3 I) in the hippocampus was evaluated using western blotting. Compared to the vehicle group, Aß administration reduced spatial reference learning (P < 0.001) and memory (P < 0.01) and upregulated the expression of beclin1, Atg7, Atg12, and LC3 II/I (P < 0.0001). Compare to Aß-only group, the administration of SP600125 and/or bucladesine improved spatial reference learning (P < 0.001) and memory (P < 0.01). Compared to the Aß-only group, the treatment with SP600125 and/or bucladesine also reduced beclin1, Atg7, Atg12, and LC3 II/I (P < 0.0001) which was similar to amount of normal rats. In summary, it seems that the improvement of spatial memory by SP600125 and/or bucladesine in Aß-injected rats is in relation with normalizing of autophagy to the physiologic level, possibly through neuroprotection and/or neuroplasticity.
Subject(s)
Anthracenes/therapeutic use , Bucladesine/therapeutic use , JNK Mitogen-Activated Protein Kinases/antagonists & inhibitors , Memory Disorders/drug therapy , Neuroprotective Agents/therapeutic use , Protein Kinase Inhibitors/therapeutic use , Alzheimer Disease/drug therapy , Alzheimer Disease/metabolism , Amyloid beta-Peptides , Animals , Anthracenes/pharmacology , Autophagy/drug effects , Autophagy-Related Protein 12/metabolism , Autophagy-Related Protein 7/metabolism , Beclin-1/metabolism , Bucladesine/pharmacology , Disease Models, Animal , Drug Therapy, Combination , Male , Maze Learning/drug effects , Memory Disorders/metabolism , Microtubule-Associated Proteins/metabolism , Neuroprotective Agents/pharmacology , Protein Kinase Inhibitors/pharmacology , Rats, Wistar , Spatial Memory/drug effectsABSTRACT
BACKGROUND: Our goal was to identify the clinical criteria for requesting the chest X-ray in patients with blunt trauma and whether its findings such as clinical signs with a high sensitivity could be used to codify the final criteria. MATERIALS AND METHODS: 386 patients with multiple trauma or blunt chest trauma examined by a physician and the injury mechanism, vital signs, O(2) saturation, auscultation findings, abrasions and ecchymosis, crepitation, tenderness on palpation, and pain on lateral compression were noted. The physician's clinical judgment on the necessity of a chest X-ray was also noted in a questionnaire. After taking the X-ray, a digital photo was taken and showed to a radiologist to report any significant chest injury. Data were collected and the positive and negative predictive values, sensitivity and specificity were estimated. RESULTS: 350 males (90.9%) and 35 females (9.1%) with the mean age of 47.1 ± 15.5 years old were evaluated. Falling down (37.7%) was the major mechanism of injury and chest pain (48%) the first complaint of patients. In 87.3% of the chest X-rays, there was no abnormal finding. Among several pathological findings in the chest X-rays, hemothorax, and rib fracture (each with 3.4% prevalence) had a higher prevalence. Tenderness on palpation with clinical judgment had a higher sensitivity about 95% and higher specificity about 100% in crepitation detected. CONCLUSION: Results showed the combination of positive chest pain and tachypnea in the patients could identify a significant chest injury with 100% sensitivity. More studies on this issue are warranted.
