Prognostic Value of Procalcitonin, CRP, Serum Amyloid A, Lactate and IL-6 Markers in Liver Transplant Patients Admitted to ED with Suspected Infection.

BACKGROUND/AIM: Infections are one of the most important causes of mortality and morbidity after liver transplantation as in all transplantations. Infectious complications are known to be among the preventable causes with appropriate diagnosis and treatment. So early prediction of the risk of infections will provide an effective approach to determine the local antimicrobial resistance and prevention of specific risk factors. The aim of this study was to deterimne whether specific markers are useful or not to deterimne a suspected infection in patients that have undergone liver transplantation. PATIENTS AND METHODS: The study included 65 patients with liver transplantation admitted to emergency room with suspicion of infection. These patient's CRP, procalsitonin (PCT), lactate, SAA and IL-6 levels were initially measured in the emergency department. The patients were classified to three categories according to culture results; culture-negative, culture-positive and control group. Studying parameters were investigated according to whether the culture was positive or negative in these patients. RESULTS: CRP, PCT, lactate, SAA and IL-6 levels were significanlty high in patients with suspected infeciton when compared to the control group (p<0.05). CRP, PCT and IL-6 levels were higher in the culture-positive group than in the culture-negative group and there was a significant variation (p<0.05). When suspecting an infection evaluating the parameters CRP, PCT and IL-6 was very meaningfull (p<0.05). CONCLUSION: We can use CRP, PCT, lactate, SAA and IL-6 parameters to identify presence of infection at the liver transplantation patients admitted to the emergency department with suspected infection. If CRP, PCT and IL-6 levels are significantly high we can guess the patient's positive culture.

Histopathological evaluation of melatonin as a protective agent in heart injury induced by radiation in a rat model.

INTRODUCTION: Melatonin is a hormone which is known to be a powerful cardioprotective agent due to its free radical-scavenging properties. This study was carried out to evaluate whether melatonin administration prior to irradiation would have a protective effect on cardiac histopathological changes in an experimental rat model. METHODS: Rats were divided into four groups. Single dose of 18 Gy radiation and sham radiation exposure were used in related groups. 50mg/kg dose of melatonin were injected intraperitonally 15 min prior to radiation exposure. Analyses and assessments were performed 6 months after radiation exposure. RESULTS: Severe myocardial fibrosis was observed prominently in three regions: the apex, tips of papillary muscles and adjacent to the atrioventricular valves. Inflammation was found to be more in irradiated groups. Increased inflammation and fibrosis were in concordance. The number of mast cells was found to be decreased in irradiated groups. Myocyte necrosis and fibrosis were diminished with melatonin while vasculitis was prevented. CONCLUSIONS: Elementary pathological lesions of radiation-induced heart disease (RIHD) are fibrosis, vascular damage, vasculitis and myocyte necrosis. Development of vasculitis was prevented by the use of melatonin. Fibrosis and necrosis were prominently decreased. Prevention of RIHD with the use of melatonin at the long term is encouraging according to the histopathological results.

Oxidative stress in the in vivo DMBA rat model of breast cancer: suppression by a voltage-gated sodium channel inhibitor (RS100642).

Breast cancer (BCa) was induced in vivo in female rats with 7,12-dimethylbenz(a)anthracene (DMBA). Two main questions were addressed. Firstly, would the carcinogenesis be accompanied by oxidative stress as signalled by superoxide dismutase, glutathione peroxidase, malondialdehyde and total nitrate? Secondly, would treating the rats additionally with a blocker of voltage-gated sodium channel (VGSC) activity, shown previously to promote BCa progression, affect the oxidative responses? The DMBA-induced increases in the antioxidant systems were completely blocked by the VGSC inhibitor RS100642, which also significantly prolonged the lifespan. We conclude that VGSC inhibition in vivo can significantly protect against oxidative stress and improve survival from tumour burden.

Case report of a traumatic abdominal wall hernia resulting from falling onto a flat surface.

This article reports a case of high-energy type traumatic abdominal wall hernia (TAWH) associated with multiple organ injuries including pelvic fractures, liver laceration and ascending colon perforation. The cause of the trauma was falling to the ground from a height of approximately 8 meters. Since the forces affecting the abdomen are unique when falling on a flat surface, the mechanism of defect may be different between a low-energy type handlebar hernia and high-energy type TAWH. Only a few cases of high-energy type TAWH exist in the literature, all reporting falling on or hitting an angled or curved material. To our knowledge, this is the only report of TAWH resulting from falling onto a flat surface. The diagnosis and management are summarized, the literature data are reviewed, and the mechanism of action is discussed.

Does pinealectomy affect the recovery rate after spinal cord injury?

Previous reports documented demonstrated that melatonin, a free radical scavenger, is important in protecting against oxidative stress-induced tissue damage after spinal cord injury (SCI). This study was undertaken to investigate the effects of pinealectomy (PX) and administration of exogenous melatonin after SCI in rats. These animals were randomized into six groups, each having 12 rats. Group 1 underwent laminectomy alone. Group 2 underwent laminectomy followed by SCI and received no medication. Group 3 underwent laminectomy followed by SCI and received melatonin. Group 4 underwent PX and laminectomy alone. Group 5 underwent PX and laminectomy followed by SCI and received no medication. Group 6 underwent PX and laminectomy followed by SCI and received melatonin. Melatonin (100 mg/kg) was given intraperitoneally immediately after trauma to the rats in the groups 3 and 6. PX caused a significant increase in the malondialdehyde (MDA), nitrite oxide (NO), glutathione (GSH), xanthine oxidase (XO) levels and decrease in GSH levels as compared with the control group. Trauma to the spinal cord results in significantly higher oxidative stress. Melatonin administration significantly reduced MDA, XO and NO levels, and increased GSH levels in the spinal cord after trauma. Exogenous melatonin treatment after trauma attenuated tissue lesion area and accelerated motor recovery rate. These findings suggest that reduction in endogenous melatonin after PX makes the rats more vulnerable to trauma and exogenous melatonin administration has an important neuroprotective effect on the level of the spinal cord.

The histopathological evaluation of the effectiveness of melatonin as a protectant against acute lung injury induced by radiation therapy in a rat model.

PURPOSE: This study presents the histopathological evaluation of the effectiveness of melatonin as a protectant against acute lung injury induced by radiation therapy. MATERIALS AND METHODS: Thirty-two Wistar rats were divided into four groups. The rats in Group 1 received melatonin and underwent radiation therapy. The rats in Group 2 received no melatonin and underwent radiation therapy. The rats in Group 3 received melatonin and underwent sham radiation therapy. The rats in Group 4 received no melatonin and underwent sham radiation therapy. Melatonin was administered at a dose of 100 mg/kg using an intraperitoneal injection. Radiation therapy was delivered on a Cobalt-60 unit using a single fraction of 18 Gy through an anterior portal covering the right lung in entirety. The rats underwent euthanasia at 6 weeks following radiation therapy. The lungs were dissected and blinded histopathological evaluation was performed. RESULTS: Concerning the right lung, a decrease in intra-alveolar edema and intra-alveolar erythrocytes was observed despite an increase in activated macrophages, intra-alveolar fibrosis, hyaline arteriosclerosis and alveolar wall thickness for the rats in Group 1 as compared to the rats in Group 2. Concerning the left lung, a decrease in alveolar neutrophils and intra-alveolar erythrocytes was evident despite an increase in activated macrophages, hyaline arteriosclerosis and alveolar wall thickness for the rats in Group 1 as compared to the rats in Group 2. CONCLUSIONS: This study puts forward the histopathological evidence regarding the effectiveness of melatonin as a protectant against acute lung injury induced by radiation therapy through restrained inflammation, regrettably at the expense of promoted fibrosis. The effectiveness of melatonin as a protectant against acute lung injury induced by radiation therapy needs to be evaluated further for the unresolved concerns regarding the safety.

Central nervous system protection by resveratrol in streptozotocin-induced diabetic rats.

The objective of the present study was to investigate the possible neuroprotective effect of resveratrol against streptozotocin-induced hyperglycaemia in the rat brain and medulla spinalis. Thirty adult male Wistar rats were divided into three groups as follows: control group, streptozotocin-induced diabetic-untreated group, and streptozotocin-induced diabetic resveratrol-treated group. Diabetes was induced by a single injection of streptozotocin (STZ) (60 mg/kg body weight). Three days after streptozotocin injection, resveratrol (10 mg/kg) was injected intraperiteonally daily over 6 weeks to the rats in the treatment group. Six weeks later, seven rats from each group were killed and the brain stem and cervical spinal cord were removed. The hippocampus, cortex, cerebellum, brain stem and spinal cord were dissected for biochemical studies (lipid peroxidation measuring malondialdehyde [MDA], xanthine oxidase [XO], nitric oxide [NO] and glutathione). MDA, XO and NO levels in hippocampus, cortex, cerebellum, brain stem and spinal cord in the streptozotocin-induced diabetic-untreated group increased significantly. Treatment with resveratrol significantly reduced MDA, XO and NO production and increased glutathione levels when compared to the streptozotocin-induced diabetic-untreated group. This study demonstrates that resveratrol is a potent neuroprotective agent against diabetic oxidative damage.

Neuroprotection by resveratrol against traumatic brain injury in rats.

Oxidative stress after traumatic brain injury may contribute to many of the pathophysiologic changes. Resveratrol, naturally present at high concentration in grape skin, seeds, and red wine, has significant antioxidant properties in a variety of in vitro and in vivo models. In this study, we investigate the effect of resveratrol on oxidative stress after traumatic brain injury in rat model.A total of 54 adult Wistar albino male rats weighing 250-300 g were used. The rats were allocated into three groups. The first group was control (sham-operated) group in which only a craniotomy was performed, the others were trauma and resveratrol groups. A 100 mg/kg single dose of resveratrol, freshly prepared by dissolving in 50% ethanol and diluted in physiological saline (2%), for resveratrol group, and 1 ml ethanol (2%) for trauma group, was administered intraperitoneally immediately after trauma. Weight-drop method was used for achieving head trauma. Then, all groups were separated into three subgroups for biochemical analysis, brain water content and histopathological assessment following trauma. Twenty-four hours after trauma brain water content and malondialdehyde (MDA), glutathione (GSH), nitric oxide (NO), xanthine oxidase (XO) levels of traumatic hemisphere were evaluated. Quantitative histopathological analysis was performed on 14th day postinjury. Trauma caused a significant increase in MDA, XO, NO levels and decrease in GSH level as compared to control group. Resveratrol administration significantly reduced MDA, XO and NO levels, increased GSH level, and also attenuated tissue lesion area. Our results indicate that treatment with resveratrol immediately after traumatic brain injury reduce oxidative stress and lesion volume. Future studies involving different doses and the dose-response relationship could promise better results.

The effects of granulocyte colony-stimulating factor on the healing of tracheal anastomosis following radiation therapy in rats.

OBJECTIVE: This study evaluates the effects of granulocyte colony-stimulating factor on the healing of tracheal anastomosis following radiation therapy in rats. METHODS: Fifty-six male Wistar rats were divided into four groups. Group 1 underwent tracheal anastomosis. Group 2 underwent radiation therapy followed by tracheal anastomosis. Group 3 underwent radiation therapy followed by tracheal anastomosis and received granulocyte colony-stimulating factor. Group 4 underwent sham radiation therapy followed by sham tracheal anastomosis. At 10 days following radiation therapy, the trachea was dissected for histopathological, mechanical and biochemical evaluation. RESULTS: Median scores for inflammation were three points for Group 1, two points for Group 2, two points for Group 3 and one point for Group 4. Median scores for angiogenesis were four points for Group 1, two points for Group 2, three points for Group 3 and one point for Group 4. Median scores for connective tissue regeneration were four points for Group 1, two points for Group 2, three points for Group 3 and one point for Group 4. Median scores for epithelial regeneration were two points for Group 1, one point for Group 2, one point for Group 3 and one point for Group 4. Mean anastomotic bursting pressures were 853 mmHg for Group 1, 293 mmHg for Group 2, 417 mmHg for Group 3 and 966 mmHg for Group 4. Mean hydroxyproline concentrations were 159 microg/mg for Group 1, 177 microg/mg for Group 2, 120 microg/mg for Group 3 and 117 microg/mg for Group 4. CONCLUSIONS: This study suggests that granulocyte colony-stimulating factor contributes to the healing of tracheal anastomosis following radiation therapy through improved connective tissue regeneration.

Effect of pinealectomy and melatonin replacement on morphological and biochemical recovery after traumatic brain injury.

Numerous studies showed that melatonin, a free radical scavenger, is neuroprotective. In this study, we investigated the effect of pinealectomy and administration of exogenous melatonin on oxidative stress and morphological changes after experimental brain injury. The animals were divided into six groups, each having 12 rats. Group 1 underwent craniotomy alone. Group 2 underwent craniotomy followed by brain trauma and received no medication. Group 3 underwent craniotomy followed by brain trauma and received melatonin. Group 4 underwent pinealectomy and craniotomy alone. Group 5 underwent pinealectomy and craniotomy followed by brain injury and received no medication. Group 6 underwent pinealectomy and craniotomy followed by brain trauma and received melatonin. Melatonin (100 mg/kg) was given intraperitoneally immediately after trauma to the rats in Groups 3 and 6. Pinealectomy caused a significant increase in the malondialdehyde (MDA), nitric oxide (NO), glutathione (GSH), and xanthine oxidase (XO) levels, and a decrease in GSH levels as compared to the control group. Trauma to pinealectomized rats causes significantly higher oxidative stress. Exogeneous melatonin administration significantly reduced MDA, XO and NO levels, increased GSH levels, and attenuated tissue lesion area. These findings suggest that reduction in endogenous melatonin after pinealectomy makes the rats more vulnerable to trauma, and exogenous melatonin administration has an important neuroprotective effect.

Effects of resveratrol and methylprednisolone on biochemical, neurobehavioral and histopathological recovery after experimental spinal cord injury.

AIM: To investigate the neuroprotective effect of resveratrol in an experimental spinal cord injury (SCI) model in rats. METHODS: Male Wistar albino rats weighing 200-250 g were randomized into six groups. Weight-drop trauma was performed for SCI. Group 1 underwent laminectomy alone. Group 2 underwent laminectomy followed by SCI. Groups 3, 4, 5, and 6 underwent laminectomy followed by SCI and received resveratrol (100 mg/kg), methylprednisolone (MP) (30 mg/kg), resveratrol (100 mg/kg) plus MP (30 mg/kg), and ethanol (2%), respectively. The rats were divided into two subgroups for biochemical analysis (killed at 24 h after surgery) and for neurobehavioral and histopathological evaluation (killed at 6 weeks after surgery). Posttraumatic neurological recovery after surgery was recorded weekly. RESULTS: Groups 3 and 5 revealed significantly lower malon-dialdehyde, nitric oxide, xanthine oxidase, and higher glutathione levels than group 4 (P<0.05). Neurological recovery rates were significantly better in groups 3 and 5 than group 4 (P<0.05). When spinal trauma size ratios were compared, there was no significant difference between treatment groups. CONCLUSION: Resveratrol treatment revealed better biochemical recovery in the acute stage of trauma than MP treatment. Although resveratrol and combined treatment revealed better neurobehavioral recovery than MP treatment; resveratrol, MP, and combined treatment modalities improved histopathological recovery at the same level in the final stage of the experiment. Future studies involving different doses of resveratrol and different doses combinations with MP could promise better results as each drug has a different anti-oxidative mechanism of action.

Neuroprotective effect of etomidate in the central nervous system of streptozotocin-induced diabetic rats.

It is well known that hyperglycaemia due to diabetes mellitus leads to oxidative stress in the central nervous system. Oxidative stress plays important role in the pathogenesis of neurodegenerative changes. In the present study we investigated the possible neuroprotective effect of etomidate against streptozotocin-induced (STZ-induced) hyperglycaemia in the rat brain and spinal cord. A total of 40 rats were used in this study. Rats were divided into four groups: sham-control, diabetic, diabetic-etomidate treated and vehicle for etomidate treatment group. Diabetes mellitus was induced by a single injection of streptozotocin (60 mg/kg body weight). Three days after streptozotocin injection, etomidate (2 mg/kg) was injected intraperitoneally for etomidate group and lipid emulsion (10%) for vehicle group was injected with corresponding amount intraperitoneally every day for 6 weeks. Six weeks after streptozotocin injection, seven rats from each group were killed and brain, brain stem and cervical spinal cord were removed. The hippocampus, cortex, cerebellum, brain stem and spinal cord were dissected for the biochemical analysis (the level of malondialdehyde [MDA], total nitrite, reduced glutathione [GSH], and xanthine oxidase [XO] activity). STZ-induced diabetes resulted in significantly elevation of MDA, XO and nitrite levels in the hippocampus, cortex, cerebellum, brain stem and spinal cord of the rats (P < 0.05) while etomidate treatment provided significantly lower values (P < 0.05). This study demonstrated that etomidate have neuroprotective effect on the neuronal tissue against the diabetic oxidative damage.

Evaluation of the neuroprotective effects of citicoline after experimental spinal cord injury: improved behavioral and neuroanatomical recovery.

Spinal cord injury (SCI) caused by trauma mainly occurs in two mechanisms as primary and secondary injury. Secondary injury following the primary impact includes various pathophysiological and biochemical events. Methylprednisolone is the only pharmacological agent having clinically proven beneficial effects on SCI. Citicoline has been shown to have clinical and experimental beneficial effects on brain ischemia. This study aims to investigate the neuroprotective effect of citicoline in an experimental SCI model in rats. Sixty adult Wistar albino rats were randomized into five groups. SCI was performed by the weight-drop model. Group 1 underwent laminectomy alone. The Group 2 underwent laminectomy followed by SCI and received no medication. Group3, Group 4 and Group 5 underwent laminectomy followed by SCI and received medication. Group 3 and Group 5 received citicoline and Group 4 and Group 5 received methylprednisolone. The rats were divided into two subgroups for biochemical analysis (sacrificed at 24 h after surgery) and neurobehavioral and histopathological evaluation (sacrificed at 6 weeks after surgery). Malondialdehyde levels, nitric oxide levels and trauma size ratios were lower and reduced glutathione levels were higher in Group 3, Group 4 and Group 5 as compared to Group 2. Posttraumatic neurological recovery after surgery was significantly better in Group 3, Group 4 and Group 5 compared to Group 2. In conclusion, this study demonstrates that citicoline is as effective as methylprednisolone. The efficacy of citicoline combined with methylprednisolone is not superior to either citicoline or methylprednisolone alone.

Neuroprotective effect of etomidate on functional recovery in experimental spinal cord injury.

OBJECTIVE: Primary impact to the spinal cord causes rapid oxidative stress after injury. To protect neural tissue, it is important to prevent secondary pathophysiological mechanisms. Etomidate, a strong antiexcitotoxic agent, stimulates the gamma aminobutyric acid (GABA) receptors. The purpose of this study was to investigate neurobehavioral and histological recovery and to evaluate the biochemical responses to treatment of experimental spinal cord injury (SCI) in rats with etomidate or methylprednisolone (MP) or both etomidate and MP. MATERIAL AND METHODS: Seventy-two rats were randomly allocated into six groups: a control group (laminectomy alone), a trauma group (laminectomy+trauma), a methylprednisolone group (30 mg/kg MP), an etomidate group (2 mg/kg), a methylprednisolone and etomidate combined treatment group (30 mg/kg MP and 2 mg/kg etomidate) and a vehicle group. Six rats from each group were killed at the 24th hour after the injury. Malondialdehyde, glutathione, nitric oxide and xanthine oxidase levels were measured. Neurological functions of the remaining rats were recorded weekly. Six weeks after injury, all of those rats were killed for histopathological assessment. RESULTS: Etomidate treatment revealed similar neurobehavioral and histopathological recovery to MP treatment 6 weeks after injury. Combined treatment did not provide additional neuroprotection. CONCLUSION: Etomidate treatment immediately after spinal cord injury has similar neuroprotection to MP. In spite of different neuroprotection mechanisms, combined treatment with MP and etomidate does not provide extra protection.