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Eighteen patients (11 renal tumours, 3 bronchogenic carcinomas, 4 others) with 24 different bone metastases were embolized for preoperative devascularization (11 x) or for intractable pain (7 x). Metastases were localized in the spine (17 x), pelvis (5 x), and shoulder girdle (2 x). All metastases were hypervascularized. ⋯ Intraoperative blood loss was minimized to 2100 ml (600 ml-4200 ml). Pain relief was achieved in 6 out of 7 patients. Eight of 18 patients died as a result of underlying diseases (follow-up 7 months).
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CA1 pyramidal neurons receive two distinct excitatory inputs that are each capable of influencing hippocampal output and learning and memory. The Schaffer collateral (SC) input from CA3 axons onto the more proximal dendrites of CA1 is part of the trisynaptic circuit, which originates in Layer II of the entorhinal cortex (EC). The temporoammonic (TA) pathway to CA1 provides input directly from Layer III of the EC onto the most distal dendrites of CA1 pyramidal cells, and is involved in spatial memory and memory consolidation. ⋯ However, in young adults CA3-CA1 synapses still exhibit more facilitation than TA-CA1 synapses during physiologically-relevant activity, suggesting that the two pathways are each poised to uniquely modulate CA1 output in an activity-dependent manner. Finally, we show that there is a developmental decrease in the initial release probability at TA synapses that underlies their developmental decrease in facilitation, but no developmental change in release probability at SC synapses. This represents a fundamental difference in the presynaptic function of the two major inputs to CA1, which could alter the flow of information in hippocampus during development.
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Mediators of inflammation · Jan 2008
Inhibitory effect on cerebral inflammatory response following traumatic brain injury in rats: a potential neuroprotective mechanism of N-acetylcysteine.
Although N-acetylcysteine (NAC) has been shown to be neuroprotective for traumatic brain injury (TBI), the mechanisms for this beneficial effect are still poorly understood. Cerebral inflammation plays an important role in the pathogenesis of secondary brain injury after TBI. However, it has not been investigated whether NAC modulates TBI-induced cerebral inflammatory response. ⋯ Measures of IL-6 showed no change after NAC treatment. NAC administration reduced brain edema, BBB permeability, and apoptotic index in the injured brain. The results suggest that post-TBI NAC administration may attenuate inflammatory response in the injured rat brain, and this may be one mechanism by which NAC ameliorates secondary brain damage following TBI.
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The goal of this study was to investigate the short-term outcomes in patients older than 60 years with isolated rib fractures and admitted to emergency hospital. ⋯ Elderly patients sustaining blunt chest trauma had significant morbidity and potential for mortality.
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J Infect Dev Ctries · Jun 2010
Comparative StudyTopical treatment of Klebsiella pneumoniae B5055 induced burn wound infection in mice using natural products.
Burn wound infection remains the principal cause of death in burn patients. Efficacy of honey and aloe vera gel was evaluated in the treatment of burn wound infection induced with Klebsiella pneumoniae B5055 and their efficacy was compared with an isolated and well-characterized Klebsiella specific phage Kpn5. ⋯ The results of this study strongly suggest that phage Kpn5 has therapeutic value in treating burn wound infection in mice as a single topical application of this phage was able to rescue mice from infection caused by K. pneumoniae B5055 in comparison to multiple applications of honey and aloe vera gel.