post-traumatic stress disorder/albumin

All patients sustaining major trauma exhibit increased capillary permeability, manifested as micro-albuminuria. Urinary albumin excretion rate (AER) measured on intensive care units (ICU) can predict early post-traumatic acute respiratory distress syndrome (ARDS). This prospective study sought to

OBJECTIVE Human albumin may be effective in the treatment of posttraumatic brain edema due to its hyperoncotic features. Therefore, the aim of the experimental study presented in this paper has two points: the first is to evaluate the efficacy of intraventricular hyperoncotic human albumin on

OBJECTIVE To observed the pathological changes of closed diffuse brain injury in the rats died immediately and 15 min to 5 days after the injury. METHODS H.E. staind and esterification-silver stain were applied to investigate the closed diffuse brain injury. RESULTS In rats died immediately after

Mortality is high among patients developing post-traumatic brain oedema and increased intracranial pressure following severe head injury. Although routine treatment varies from one centre to another it often includes one or more of such measures as hyperventilation, high-dose barbiturate therapy,

OBJECTIVE To evaluate the application value of percutaneous endoscopic gastrostomy (PEG) for home nutrition support in patients with stroke and post-traumatic brain. METHODS We retrospectively analyzed the clinical data of the 16 patients with stroke and post-traumatic brain, including cerebral

Anions of fatty acids infused intravenously into dogs clearly duplicate the clinical syndrome of post-traumatic pulmonary insufficiency (congestive atelectasis, shock lung, traumatic wet lung). Neutral fat embolized to the lungs is incapable of producing this syndrome within the time investigated.

Previous studies have shown that severe sepsis after major trauma results in the reprioritization of release of hepatic acute-phase proteins (APP). They suggest competition for leucine for nutritional utilization may be responsible. To test this hypothesis, a branched-chain enriched (46.6%) amino

BACKGROUND The incidence and risk factors for post-traumatic cervical epidural hematoma are not well described in the current literature. Our aim was to determine the incidence and associated risk factors for post-traumatic cervical spine epidural hematoma (SEH). METHODS We performed a retrospective

OBJECTIVE Traumatic joint injury induces chondrocyte dysfunction and progressive breakdown of articular cartilage, leading to post-traumatic osteoarthritis (PTOA). In this condition, dysfunctional fibroblast-like chondrocytes (FLCs) no longer express proteins required for cartilage maintenance, such

The purpose of this study was to determine if serum microRNA (miRNA) signatures were biomarkers of early cartilage degeneration in preclinical mouse models of post-traumatic osteoarthritis (OA) and inflammatory arthritis. Cartilage degeneration was induced in 10-12 week old male C57BL6 mice by

BACKGROUND Traumatic brain injury (TBI) confers a high risk of venous thrombosis, but early prevention with heparinoids is often withheld, fearing cerebral hematoma expansion. Yet, studies have shown heparinoids not only to be safe but also to limit brain edema and contusion size after TBI. Human

Muscle trauma during preliminary denervation stimulates generation and differentiation of satellite cells. There are two types of posttraumatic cells with different types of albumin synthesis (intracellular and extracellular) under the sarcolemma of the muscle fibers. It is assumed that either two

Renal tolerance of the preparation beta-aescin (Reparil) was tested in cases of oedema following fresh soft tissue crush injuries of the extremities and surgical and reconstructive operations on the hand. Forty in-patients with healthy kidneys were treated with 10 mg beta-aescin intravenously twice

Traumatic brain injury (TBI) is accompanied with enhanced matrix metalloproteinase-9 (MMP-9) activity and elevated levels of plasma fibrinogen (Fg), which is a known inflammatory agent. Activation of MMP-9 and increase in blood content of Fg (i.e. hyperfibrinogenemia, HFg) both contribute to